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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
6401.0 - Consumer Price Index, Australia, Dec 2001
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 23/01/2002
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6401.0 - Consumer Price Index, Australia
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
3301.0 - Births, Australia, 2009 Quality Declaration
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 03/11/2010
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CHARACTERISTICS OF PARENTS
Indigenous status
Around one-third (31%) of Aboriginal and Torres Strait Islander births registered in 2009 were births for which both parents identified themselves as being of Aboriginal and Torres Strait Islander origin on the birth registration statement, while for 42% of Aboriginal and Torres Strait Islander births only the mother identified herself as being of Aboriginal and Torres Strait Islander origin (including births where paternity was not acknowledged and those where the father's Indigenous status was unknown). The remaining 27% of Aboriginal and Torres Strait Islander births were to an Aboriginal and Torres Strait Islander father and a non-Indigenous mother (including births where the mother's Indigenous status was not stated).
3.5 Indigenous status of parents, Australia - 1999 to 2009
Median age
Overall, Aboriginal and Torres Strait Islander women have children at younger ages than all women. The median age of Aboriginal and Torres Strait Islander women who registered a birth in 2009 was 24.5 years, six years lower than the median age of all mothers (30.6 years). Of the states and territories, Aboriginal and Torres Strait Islander mothers living in the Northern Territory had the lowest median age (24.1 years), followed by Aboriginal and Torres Strait Islander mothers in Western Australia (24.2 years).
For Australia, where the age of the father was known, fathers of Aboriginal and Torres Strait Islander births in 2009 were younger than all fathers, with a median age of 27.8 years compared with 33.0 years for all fathers. Western Australia recorded the lowest median age of fathers of Aboriginal and Torres Strait Islander births (27.1 years), followed by Queensland, South Australia and the Northern Territory (all 27.6 years).
Nuptiality
In 2009, 85% of Aboriginal and Torres Strait Islander births were ex-nuptial (that is, births to women who were not in a registered marriage at the time of birth) compared with 35% of all births. Ex-nuptial births where the father did not sign the birth registration statement (that is, births where paternity was not acknowledged) accounted for 15% of all Aboriginal and Torres Strait Islander births, compared with 3% of all births.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
6291.0.40.001 - Labour Force, Selected Summary Tables, Australia, Nov 1998
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 17/12/1998
Past Releases
First Release
• First Issue: Jan 1998
© Commonwealth of Australia 2013
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Research article
Socioeconomic inequality in domains of health: results from the World Health Surveys
Ahmad R Hosseinpoor1*, Jennifer A Stewart Williams2, Lynn Itani3 and Somnath Chatterji1
Author Affiliations
1 Department of Health Statistics and Information Systems, World Health Organization, Geneva, Switzerland
2 Research Centre for Gender, Health & Ageing, University of Newcastle, Australia
3 Institute for Development, Research, Advocacy and Applied Care, Beirut, Lebanon
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BMC Public Health 2012, 12:198 doi:10.1186/1471-2458-12-198
The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2458/12/198
Received:7 September 2011
Accepted:19 March 2012
Published:19 March 2012
© 2012 Hosseinpoor et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background
In all countries people of lower socioeconomic status evaluate their health more poorly. Yet in reporting overall health, individuals consider multiple domains that comprise their perceived health state. Considered alone, overall measures of self-reported health mask differences in the domains of health. The aim of this study is to compare and assess socioeconomic inequalities in each of the individual health domains and in a separate measure of overall health.
Methods
Data on 247,037 adults aged 18 or older were analyzed from 57 countries, drawn from all national income groups, participating in the World Health Survey 2002-2004. The analysis was repeated for lower- and higher-income countries. Prevalence estimates of poor self-rated health (SRH) were calculated for each domain and for overall health according to wealth quintiles and education levels. Relative socioeconomic inequalities in SRH were measured for each of the eight health domains and for overall health, according to wealth quintiles and education levels, using the relative index of inequality (RII). A RII value greater than one indicated greater prevalence of self-reported poor health among populations of lower socioeconomic status, called pro-rich inequality.
Results
There was a descending gradient in the prevalence of poor health, moving from the poorest wealth quintile to the richest, and moving from the lowest to the highest educated groups. Inequalities which favor groups who are advantaged either with respect to wealth or education, were consistently statistically significant in each of the individual domains of health, and in health overall. However the size of these inequalities differed between health domains. The prevalence of reporting poor health was higher in the lower-income country group. Relative socioeconomic inequalities in the health domains and overall health were higher in the higher-income country group than the lower-income country group.
Conclusions
Using a common measurement approach, inequalities in health, favoring the rich and the educated, were evident in overall health as well as in every health domain. Existent differences in averages and inequalities in health domains suggest that monitoring should not be limited only to overall health. This study carries important messages for policy-making in regard to tackling inequalities in specific domains of health. Targeting interventions towards individual domains of health such as mobility, self-care and vision, ought to be considered besides improving overall health.
Background
Inequities in health constitute one of the main challenges for public health globally. In all countries people of lower socioeconomic status (SES), as measured by social determinants such as education, income or occupation, are in a worse state of health compared to those from higher SES across the entire range. Health is defined by the World Health Organization (WHO) as "a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity" [1]. However, for the purposes of measurement, health must be operationalized as an individual's intrinsic capacity to function in a range of domains and aggregated in order to quantify and compare levels of health across individuals and populations. Uniform approaches to measuring levels and distributions of health allow targeted approaches by policy makers to tackle health inequalities and researchers to monitor the impact of these interventions [2-7].
Self-rated health (SRH) [8,9] is widely used in population surveys to measure health status. Empirically SRH is a strong predictor of mortality risk, even after accounting for known socioeconomic and medical risk factors [10-14]. Responses to a single-item question, such as, "how would you rate your health in general" summarize an individual's overall self-report of their health combining the individual's aggregation of her functioning without a way of determining the relative problems in different domains [10,15]. However for monitoring population health over time, and particularly for analyses of socioeconomic disparities, the overall SRH question may create comparability problems [16].
A common theme that has emerged from efforts to develop an operational definition of "health" is the view that health state reported by individuals consists of a series of values indicating levels on domains such as mobility, pain, sleep, cognition and vision [2]. While overall measures of SRH are important, understanding the key components of health can help inform policies and interventions to improve the different aspects of health and health outcomes in general.
In recent decades the measurement of health and its core elements has been operationalized through a set of elements, or domains, that together constitute an understanding of overall health [17]. The WHO developed eight core domains of health that have been widely accepted as being of fundamental importance to all human beings irrespective of their social or socioeconomic circumstances. These domains are: mobility; self-care; pain and discomfort; cognition; interpersonal activities; vision; sleep and energy, and affect [2,17]. Questions referring to the domains of health are used in many population survey instruments. For measurement purposes self-reported health in each domain is characterized by a single cardinal scale [2]. Although there are methodological challenges pertaining to the comparability of health status data across populations and cultures, research has shown that the WHO health domains are highly consistent across countries and cultures [18]. The availability of multi-domain health state measurement instruments makes it possible to measure the different attributes of health in population surveys conducted across many countries [2,19,20].
A few studies have demonstrated associations between SES and physical, functional, mental, cognitive and behavioral aspects of health [9,21-24]. However mostly these studies focus only on specific sub-populations in high income countries so the results are often not generalizable. We know of no work that has comprehensively "un-packed" socioeconomic associations separately within the WHO domains of health at a multi-country level. The aim of this study is to compare and assess socioeconomic inequalities in each of the individual health domains and in a separate measure of overall health.
Methods
Study population
The study population comprises a multi-country dataset drawn from the World Health Survey (WHS). The WHS was conducted by the World Health Organization in 2002-2004 to provide valid, reliable, representative and comparable population data on the health status of adults, aged 18 years and older, in 70 countries from all regions of the world [25]. All samples were probabilistically selected with every individual being assigned a known non-zero probability of being selected. The samples were nationally representative except in China, Comoros, Congo, Côte d'Ivoire, India, and the Russian Federation, where the WHS was carried out in geographically limited regions. To adjust for the population distribution represented by the UN Statistical Division http://unstats.un.org/unsd/default.htm webcite and also non-response, post-stratification corrections were made to sampling weights [26].
Data
This study includes 57 countries drawn from all national income groups as defined by the World Bank [27]. Thirty seven low- and lower middle-income countries and twenty upper middle- and high-income countries were further combined into the lower-income and the higher-income country groups, respectively. Inclusion at the country level required complete information on sampling weights and key covariates. Eleven of the thirteen excluded countries had insufficient data on sampling weights and two had insufficient data to create the household wealth index. The study included 247,037 respondents, aged 18 and over. Appendix table 1 gives the sample size by country. Separate analyses were undertaken for pooled data sets of 57 countries, 37 lower-income countries, and 20 higher-income countries. The data used here are openly available.
Table 1. Prevalence of self-reported poor health across health domains and overall health among adults aged 18+, by wealth and education; pooled analysis of 57 countries WHS (2002-2004)
Variables
Respondents to the WHS Individual Questionnaire were asked to self-rate the extent to which they were having difficulties in each of eight health domains using a five point scale: none; mild; moderate; severe, and extreme/cannot do. In addition respondents were asked to rate their overall health as either: very good; good; moderate; bad, or very bad.
The outcome variable in this study is the dichotomy poor health (comprising the health domain responses "severe" and "extreme/cannot do" and the overall health responses "bad" or "very bad") vs. good health (comprising the health domain responses "none", "mild" or "moderate" and the overall health responses "very good", "good" and "moderate"). This binary outcome variable was calculated for each health domain and for overall health.
Education and wealth are independent variables used here as categorical measures of SES. For education, individuals were assigned an educational ranking that was either: no formal schooling; less than primary school; completion of primary school; completion of secondary school, or completion of high school or above. For wealth, a dichotomous hierarchical ordered probit model was used to develop an index of the household economic status or wealth. This indicated individuals' economic status and was based on owning selected assets and/or with access to certain services [28-30]. The index was divided into quintiles within each country, where quintile one represented the poorest wealth quintile and quintile five the richest.
Methods of analysis
Prevalence estimates of poor health were calculated for each domain of health and for overall health (overall prevalence) according to wealth quintiles and education level. In addition, relative socioeconomic inequalities in SRH were measured for each of the eight health domains and for overall health using the relative index of inequality (RII). The RII summarized the extent to which perceived poor health varied separately by education and wealth in each of the health domains, by taking into account the distribution of poor health as well as the distribution of the population according to our measures of education and wealth [31]. To calculate RII, individuals were cumulatively ranked (ranging from zero to one) according to descending socioeconomic status (i.e. highest wealth or education level to lowest). The RII represents the ratio reporting poor health between those at the top rank (i.e. the lowest level of education or wealth) and those at rank zero (i.e. the highest level of education or wealth). Thus RII > 1 indicates a higher proportion rating poor health among populations of lower socioeconomic status. We refer to this situation as pro-rich inequality; pro-poor inequality exists when the prevalence of poor health is higher among those with higher socioeconomic status [32].
Data were adjusted for respondents' country of residence and age (expressed categorically as 18-29, 30-39, 40-49, 50-59, 60-69 and 70+ years) in Model 1. In Model 2 adjustments were also made for: sex; urban/rural area of residence; marital status (married/cohabiting vs. never married vs. divorced/separated/widowed), and wealth or education as possible confounders.
The Poisson regression model with a robust variance was used to assess associations in each health domain and in overall health and to generate prevalence ratio values and 95% confidence intervals (CIs) [33].
All analyses were weighted to account for individual survey sample designs and adjustments were made to allow for the fact that observations within survey clusters were not necessarily independent. Analyses were carried out using STATA V11 (StataCorp, 2009).
Results
Prevalence of reporting poor health
Table 1 gives prevalence of poor health across the health domains and overall health, by wealth and education for all countries. Tables 2 and 3 give prevalence estimates for the lower- and higher-income country groups respectively. On average, the prevalence of poor health was lowest for self-care (2.9% for all countries, 3.4% for the lower-income country group, and 1.7% for the higher-income country group) and highest for pain and discomfort (10.8% for all countries, 11.2% for the lower-income country group, and 9.7% for the higher-income country group). The prevalence of reporting poor overall health was 9.4% for all countries, 10.1% for the lower-income country group and 7.2% for the higher-income country group.
Table 2. Prevalence of self-reported poor health across health domains and overall health among adults aged 18+, by wealth and education; pooled analysis of 37 lower-income countries WHS (2002-2004)
Table 3. Prevalence of self-reported poor health across health domains and overall health among adults aged 18+, by wealth and education; pooled analysis of 20 higher-income countries WHS (2002-2004)
Wealth-related inequality in poor health
Poor health was more prevalent in the poorest wealth quintile than in the richest. There was a descending gradient in the prevalence of poor health, moving from the poorest wealth quintile to richest, in all the domains of health and in overall health.
Figures 1, 2 and 3 show wealth-related relative inequalities, in poor health in the domains of health, and overall health, for all countries, the lower-income country group, and the higher-income country group respectively. In each of the country groups, the RII was greater than one and statistically significant in all domains and in overall health indicating pro-rich inequalities. Model 1 was adjusted for age and country of residence. Inequalities attenuated after controlling for age, sex, education, marital status, place and country of residence in Model 2.
Figure 1. Wealth-related inequality in poor health by health domains and overall health in adults aged 18+; pooled analysis of 57 countries WHS (2002-2004).
Figure 2. Wealth-related inequality in poor health by health domains and overall health in adults aged 18+; pooled analysis of 37 lower-income countries WHS (2002-2004).
Figure 3. Wealth-related inequality in poor health by health domains and overall health in adults aged 18+; pooled analysis of 20 higher-income countries WHS (2002-2004).
In the combined countries data set poor health was twice as prevalent in the poorest, compared with the richest adults in the mobility, self-care, cognition, interpersonal activities and vision domains in Model 1. The prevalence of poor overall health was twice as high in the richest, compared with the poorest wealth quintile, in both Models 1 and 2.
In the lower-income country group (Model 1) poor health was twice as prevalent in the poorest, compared with the richest adults in the self-care domain and in overall health. In the higher-income country group (Model 1) poor health was at least twice as prevalent in the poorest compared with the richest adults in all the domains except sleep and energy.
Education-related inequality in poor health
Poor health was more prevalent in the lowest compared with the highest education level. There was a descending gradient in the prevalence of poor health, moving from the lowest to the highest education level, in all the domains of health and in overall health.
Figures 4, 5 and 6 show education-related relative inequalities, in poor health in the domains of health, and overall health for all countries, the lower-income country group, and the higher-income country group, respectively. For each country group, the RII was greater than one and statistically significant in all domains and in overall health indicating pro-rich inequalities (Model 1). Inequalities attenuated after controlling for age, sex, wealth, marital status, place and country of residence in Model 2. The RII was not significant in the vision and affect domains in Model 2 for the lower-income country group.
Figure 4. Education-related inequality in poor health by health domains and overall health in adults aged 18+; pooled analysis of 57 countries WHS (2002-2004).
Figure 5. Education-related inequality in poor health by health domains and overall health in adults aged 18+; pooled analysis of 37 lower-income countries WHS (2002-2004).
Figure 6. Education-related inequality in poor health by health domains and overall health in adults aged 18+; pooled analysis of 20 higher-income countries WHS (2002-2004).
In the combined countries data set (Model 1) poor health was at least three times as prevalent in adults in the lowest, compared with the highest education rank in the mobility, self-care, pain and discomfort, cognition, interpersonal activities and vision domains. Poor overall health was over three times as prevalent in the lowest, compared with the highest education rank in Model 1 and twice as high in Model 2.
In the lower-income country group (Model 1) poor health was at least three times as prevalent in adults in the lowest, compared with the highest education rank in the self-care, and interpersonal activities domains. In the higher-income country group (Model 1) poor health was at least three times as prevalent in adults in the lowest, compared with the highest education rank in all of the health domains except affect and sleep and energy.
Discussion
Pro-rich health inequalities, which favor groups who are advantaged either with respect to education or wealth, are consistent and statistically significant in each of the domains of health and in health overall. There was a descending gradient in the prevalence of poor health, moving from the poorest wealth quintile to richest, and moving from the lowest to the highest educated groups.
In the combined countries data set, in all the domains and in overall health, the education-related inequality in poor health was higher than the wealth-related inequality in poor health. Adjusting for the effects of sex, urban/rural area, marital status and education or wealth as other possible confounders on top of age and country of residence attenuated our measured inequalities, but all of the inequalities remained statistically significant. These findings are consistent with the literature reporting positive associations between SES (measured by education, income and wealth) and SRH [8,34].
Reports of health status incorporate complex combinations of an individual's assessment about their health and health conditions [6]. Considered alone, summary measures of overall health mask differences in the domains of health that may be important to know about in order to target specific interventions. This study takes the additional step of assessing socioeconomic inequalities in the individual domains of health and comparing these measures with inequalities in overall health measured separately. The findings contribute to current evidence of health inequalities by reporting statistically significant inequalities in poor health separately within the widely used domains of health developed by the WHO.
In the combined countries data set and for both country income groups, inequalities were highest for self-care, cognition, vision and mobility. It is possible that correlations between the domains to some extent influence these results, for example persons reporting poor self-care may also report poor mobility and poor cognition. Sadana et al. [17] assessed correlations between six WHO health domains (affect, cognition, mobility, pain, self-care and usual activities) and overall health from 66 surveys carried out by the WHO and showed relatively high correlations between self-care and mobility and self-care and cognition (Rho: 0.76 and 0.59, respectively).
Associations between SES and aspects of SRH [22,35,36] are widely documented. The ageing of populations has increased interest in cognitive function as a public health issue. There is now a mounting body of evidence that low SES, measured by education, occupation, income, and ownership of financial assets, predicts decline in cognitive function in older adults [37-41].
Internationally there is a recognized need to address the "social determinants of health" [4,42,43]. Yet taking action to reduce inequalities and inequities in health within countries requires understanding of how social and economic factors are associated with all of the key components of health, as well as health overall. This is the first study of its kind to provide evidence of associations between education and wealth specifically in all eight domains of health at a pooled multi-country level, and also by comparing groups of lower- and higher-income countries. The analysis by country income groups provides additional insights into the patterning of relative socioeconomic inequalities in the domains of health. Although, on average, health is better in the higher-income countries, the distribution of individual health states in accordance with educational rank as well as wealth rank is more unequal in this group.
Study strengths
The large multi-country dataset allowed us to assess socioeconomic inequalities in the health domains and in overall health. We have ensured comparability of data between countries by using the WHS. Inequalities in health are measured here by SRH. Self-rated health instruments are applicable within many cultural, demographic and socioeconomic settings [10,44-46] and are strong predictors of health care utilization, morbidity and mortality outcomes [12-14,16,34,47].
This work is based on the domains of health developed by the WHO. They provide a consistent validated way of describing and comparing population health within and between countries [2,17].
Higher SES is associated with better living standards, the most direct (and popular) measures of which are income and consumption expenditure. However measuring income and consumption expenditure can be problematic. In high-income countries, consumption expenditure patterns are very complex and income can be a better measure, and in developing countries, where formal employment is less common and home production widespread, consumption expenditure can be a more accurate measure of living standards [48]. This study uses a method to estimate household wealth that is based on the premise that wealthier households are more likely to own a given set of assets. In addition to being consistent with a broader definition of poverty, this approach provides a way of drawing international comparisons when analyzing health inequalities [28-30].
It is important to consider evidence of socioeconomic inequalities when developing interventions that target specific domains (e.g. mobility, pain and cognition), otherwise interventions may widen inequalities in health. The results from this study are of relevance to public health policy-makers and others because they identify inequalities in the individual health domains.
Limitations
The data are cross sectional and so can only describe associations between socioeconomic factors and health. The results show that health inequalities according to education and wealth exist after adjusting for age, at a point in time, but they do not explain casual relationships or health change over time. There is a need for research that examines ways in which socioeconomic factors mediate changes in health domains as well as overall health.
The results of this study are based on self-reported information about health. Future studies need to incorporate health examinations and biomarkers within household surveys in order to improve the validity of self-reported health states and to detect and correct systematic reporting biases.
The countries were not probabilistically selected and therefore not necessarily representative of the world or of similar groups of countries (e.g. defined by geography or income). The use of pooled data masks possibly important variation between countries. For example, in order to tailor intervention programs aimed at improving health it is important to understand SRH within local context and culture and these aspects are not captured in our data [44]. Although it was not the purpose of this study to examine inter-country variation, we did include a "country" variable to control for any potential confounding effects related to individual countries.
There is evidence that relative to advantaged groups, disadvantaged groups may fail to perceive and report the presence of illness or health deficits which may result in misleading assessments of population health [9,34,49]. However if such bias exists in our study, then it is likely that the results underestimate the true size of education-and wealth-related inequalities in the domains of health and health overall.
Lastly, we used RII which is a relative measure of inequality that is adjusted for variation in average prevalence of poor health across health domains. As such, information on the absolute size of differences in prevalence of poor health between socioeconomic groups is not reflected in RII [50]. To address this we have provided prevalence estimates of poor health by wealth quintile and educational level.
Deconstructing inequalities in health in different domains, separately by wealth and education in lower- and higher-income country groups, paints a much more nuanced picture than would be otherwise visible. Major differences between the country groups highlight the complex interaction between health, a country's level of economic development and individual socioeconomic status.
Conclusions
In order to understand drivers of inequality in the distribution of health status within country settings, one needs to examine not just overall self-reported health (as the inequality in this overall item does not change much by wealth or education) but the individual domains of health status and disentangle them by different SES stratifiers. Future studies should attempt to improve our understanding of the drivers of these varying patterns. This will then provide the evidence required for specific areas to be addressed in targeted population sub-groups.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
AH designed the study with input from SC, JSW and LI. LI conducted the literature review. AH did the statistical analysis. JSW wrote the first draft with inputs from AH and SC. All co-authors read and approved the final draft.
Acknowledgements
The views expressed in this paper are those of the author(s) and do not necessarily represent the views or policies of the World Health Organization. The authors thank the reviewers for the excellent feedback they provided.
References
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3. Mackenbach JP, Stirbu I, Roskam AR, Schaap MM, Menvielle G, Leinsalu M, Kunst AE: Socioeconomic inequalities in health in 22 European countries.
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Pre-publication history
The pre-publication history for this paper can be accessed here:
http://www.biomedcentral.com/1471-2458/12/198/prepub
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Research
Significance of lobular intraepithelial neoplasia at margins of breast conservation specimens: a report of 38 cases and literature review
Sophia K Apple*, Mahan Matin, Eric P Olsen and Neda A Moatamed
Author Affiliations
Department of Pathology & Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A. BOX 951732, 1P-244 CHS Los Angeles, CA 90095-1732 USA
For all author emails, please log on.
Diagnostic Pathology 2010, 5:54 doi:10.1186/1746-1596-5-54
Published: 20 August 2010
Abstract
Background
Presence of lobular intraepithelial neoplasia (LIN) is not routinely reported as part of margin assessment in breast conservation therapy (BCT) as in ductal carcinoma in situ (DCIS). With new emerging evidence of LIN as possible precursor lesion, the hypothesis is that LIN at the margin may increase the risk of local recurrence with BCT. The aim is to determine whether there is an increase incidence of recurrence when LIN is found at surgical margins on BCT.
Methods
We retrospectively reviewed a total of 1,334 BCT at a single institution in a 10 year period. Inclusion criteria are positive margin with LIN from primary BCT containing invasive and/or in situ carcinoma with comparison to the negative control group who had similar diseases with negative margin for LIN.
Results
We identified 38 cases (2.8%) with LIN either lobular carcinoma in situ/atypical lobular hyperplasia (LCIS/ALH) at a margin on initial BCT with 36% recurrence rate. Of the 38 cases: 5 (13%) were lost to follow-up, 12 (32%) had no further procedures performed and 21 (55%) had re-excision. Out of 21 patients who had re-excisions, 12 (57%) had residual invasive carcinoma or DCIS, three (14%) had pleomorphic LCIS and 4 (19%) showed residual classic type LCIS. 71% had significant residual disease (local recurrence) and 29% had no residual disease. A negative control group consisted of 38 cases. We found two patients with bone or brain metastasis and one local recurrence. Clinical follow up periods range from 1 to 109 months.
Conclusions
LIN found at a margin on BCT showed a significant recurrent ipsilateral disease. Our study supports the view that LIN seen at the margin may play a role in recurrence.
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Category:Virginia RepositoriesEdit This Page
From FamilySearch Wiki
Revision as of 18:37, 13 November 2012 by Sandralpond (Talk | contribs)
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Pages in category "Virginia Repositories"
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lightbox in IE
Newbie Member
7Jan2009,21:44 #1
The browser won't run the page on which i am using lightbox. and I get an error report saying "would not complete the operation due to error" can someone please help? I think perhaps there is a piece of code that i can use to make the page run lightbox??
here is the link ... fishpondmedia.com/windsor/gallery.html
Team Leader
8Jan2009,10:38 #2
I checked in IE, works fine.
Go4Expert Founder
8Jan2009,18:28 #3
Moved to HTML forum
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About this Journal Submit a Manuscript Table of Contents
Evidence-Based Complementary and Alternative Medicine
Volume 2011 (2011), Article ID 873672, 9 pages
doi:10.1093/ecam/nep055
Original Article
Feldenkrais Method Balance Classes Improve Balance in Older Adults: A Controlled Trial
1Rehabilitation Sciences Research Centre, School of Physiotherapy, University of Melbourne, Parkville, VIC 3010, Australia
2Calvary Health Care Bethlehem, Caulfield South, Australia
3Austin Health, Heidelberg, Victoria, Australia
Received 25 September 2008; Accepted 19 May 2009
Copyright © 2011 Karol A. Connors et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
The objective of this study was to investigate the effects of Feldenkrais Method balance classes on balance and mobility in older adults. This was a prospective non-randomized controlled study with pre/post measures. The setting for this study was the general community. A convenience sample of 26 community-dwelling older adults (median age 75 years) attending Feldenkrais Method balance classes formed the Intervention group. Thirty-seven volunteers were recruited for the Control group (median age 76.5 years). A series of Feldenkrais Method balance classes (the 33312Getting Grounded Gracefully33313 series), two classes per week for 10 weeks, were conducted. Main outcome measures were Activities-Specific Balance Confidence (ABC) questionnaire, Four Square Step Test (FSST), self-selected gait speed (using GAITRite instrumented gait mat). At re-testing, the Intervention group showed significant improvement on all of the measures (ABC, P = .016, FSST, P = .001, gait speed, P < .001). The Control group improved significantly on one measure (FSST, P < .001). Compared to the Control group, the Intervention group made a significant improvement in their ABC score (P = .005), gait speed (P = .017) and FSST time (P = .022). These findings suggest that Feldenkrais Method balance classes may improve mobility and balance in older adults.
1. Introduction
Various forms of exercise have aimed to improve balance in older adults, generally to attempt to reduce the incidence of falls [14]. Exercise has also been proposed as a preventative strategy to slow the decline from pre-frailty to frailty in older adults [5]. Exercise approaches to achieve these aims have varied from strength and balance training [6] to specific balance exercises [3] to Tai Chi [79]. As yet, no single approach has emerged as being definitively more effective than another. However, a recent systematic review and meta analysis of studies using exercise to prevent falls, suggests that balance training may be more effective in lowering falls risk than other exercise components such as strength or endurance training [10].
The Feldenkrais Method has the potential to be a useful tool for balance retraining. The Feldenkrais Method was developed over several decades by Dr. Moshe Feldenkrais (1904–1984), an Israeli scientist and Judo master [11] with a pioneering interest in human movement from a dynamics systems perspective. Dr. Feldenkrais combined his understanding of human movement from his martial arts training, with extensive reading from Eastern and Western sources to develop a unique approach to improving movement. This approach is currently practised by thousands of registered Feldenkrais Method practitioners working in over 20 countries. The lessons are based on martial arts principles, but have been devised to address improvement in all aspects of human function, from an actor performing on stage to a disabled person turning over in bed [12]. The Feldenkrais Method `Awareness Through Movement' classes use an exploratory learning approach, in which participants are verbally guided through movement sequences aimed at improvement of body awareness and movement organization [13]. Stephens [14] has proposed that “this process facilitates the learning of strategies for improving organization and coordination of body movement by developing spatial and kinesthetic awareness of body-segment relationships” (page 1642). Among the hundreds of lessons which Dr. Feldenkrais created [12], many are suitable for balance retraining.
Recent investigations into the nature of balance have revealed its complexity [15]. Achieving effective balance is a multi-system and multi-dimensional task [16]. Not only are the motor, sensory (including proprioception, vision and vestibular systems) and cognitive systems of the body involved, but the ability to dynamically interact with the environment must also be included [15]. The Feldenkrais Method is an approach to balance retraining that is multi-dimensional. All parts of the body are potentially involved in the movements, including the eyes, the feet and the trunk, which are all important contributors to balance [17]. There is also involvement of the senses in the lessons, including tactile sensation, proprioception, vestibular stimulation and vision. A fundamental principle of the Feldenkrais Method is that the processes of thinking, feeling, sensing and doing are all interrelated components of human functioning, and to address any one component is to address them all [13]. It is this concept of the unity of the mind and body that distinguishes the Feldenkrais Method from most mainstream approaches to movement improvement.
There has been little high quality research into the Feldenkrais Method. A randomized controlled trial comparing the Feldenkrais Method to Tai Chi and a non-treatment control group, in a sample of 59 older women, found significant improvement in several measures of function and balance in the Feldenkrais Group and on one measure in the Tai Chi group and none in the control group [18]. However, statistical analysis did not extend to between group comparisons, so interpretation of the results is limited. The study also did not include any assessment of balance confidence, which is an important aspect of balance retraining. These results support the need for further studies into this approach to improving balance.
The most effective way to investigate the dynamic properties of balance and mobility, is to use dynamic balance tests [15]. The three primary outcome measures used in the current study were the Four Square Step test (FSST) [19], gait speed (measured using the GAITRite electronic walkway, CIR systems, Inc) and the Activities-specific Balance Confidence (ABC) questionnaire [20]. These three measures have been found to have moderate to high reliability and validity in samples of older people [1922]. The FSST is a test of stepping and changing direction which has been found to discriminate between non-fallers, occasional fallers and frequent fallers [19]. The ABC questionnaire is a self-rating scale used to assess balance confidence in performing a range of everyday tasks. It has been well documented that not only is balance confidence related to mobility functioning [20, 23], but decreased confidence may be related to diminished activity due to a fear of falls [24, 25]. Higher scores have been found to correlate with better mobility and lower scores with less mobility [20]. The GAITRite electronic walkway is a portable device capable of measuring many gait parameters [21]. Gait speed was selected as a primary outcome measure as a slower gait speed in older adults has been found to correlate with increased risk of falls and poorer balance [26]. Exploratory analysis of the gait data was also undertaken to investigate which gait parameters were affected by the classes.
The purpose of this study was to investigate whether community dwelling older adults undertaking a series of Feldenkrais Method balance classes improved on measures of mobility and balance. This was a pragmatic study which compared a group of older adults already enrolled in Feldenkrais Method balance classes, with a similar group who received no intervention. Both groups were tested and re-tested on balance and mobility measures at a 3-month time interval, and the changes within and between the groups were compared.
2. Methods
2.1. Ethics
The project was approved by the Human Research Ethics Committees at the University of Melbourne and the Caulfield General Medical Centre.
2.2. Participants
The Intervention group was a sample of convenience drawn from community dwelling older adults, who had enrolled to attend a series of Feldenkrais Method balance classes [27], in a community health setting, as part of a falls prevention program. The Control group was recruited from community dwelling older adults who volunteered in response to an advertisement for participants in a balance study.
Inclusion criteria included being aged over 65, able to walk independently in the community (with or without a gait aid), able to perform the balance tests without a walking frame (a walking stick was permissible) and able to participate in a series of balance classes. All participants provided informed consent. Those currently receiving any additional intervention related to mobility were excluded from the study.
2.3. Procedures
The Intervention group participants were assessed on balance and mobility measures prior to starting the classes and at completion of the program. The Control group were tested and retested on the same measures, at an interval of three months, with no intervention.
Testing was performed by one of the investigators and a research assistant trained in the use of the GAITRite instrumented walkway. Testers were not blinded to group allocation, but were blinded to previous results on retesting. Three trials of the FSST were conducted and the fastest speed of the final two trials was used for analysis (as recommended in the protocol described by the developers of the test [19]). Participants performed three trials walking on the GAITRite walkway, and an average speed from the three trials calculated. On each trial, they were instructed to walk at a comfortable pace. Exploratory analysis of gait data was performed, including stride length, cadence (steps/minute), double support time (percentage of the gait cycle when both feet were in contact with the ground) and variability of step length (calculated by dividing the variability on each step length by the mean step length for each participant, to arrive at a coefficient of variability). The ABC score was calculated by adding the score for each question on the questionnaire and dividing by the number of questions, as per protocol [20].
After the completion of the classes, participants in the Intervention group were asked: “Do you think the classes had any effects on you? If yes, what were they?” These questions were asked at the re-testing session by the researcher.
2.4. Intervention
A series of Feldenkrais Method balance classes, “Getting Grounded Gracefully” [28] was delivered to the Intervention group by the Feldenkrais Practitioner who devised the program. Classes were conducted for 1 h, twice weekly for 10 weeks. All classes were conducted in sitting, standing or moving within the room. Each of the 20 classes engaged the participants in different movement tasks, such as sit to stand or weight shift in standing. Several postural control themes were continued through the classes. These themes included: control of the pelvis over the base of support in many variations, flexibility and movement control in the ankles and the trunk, enhancing body awareness (such as awareness of the contact of the feet on the floor and paying attention to which parts of the body were engaged in particular movement tasks) and building balance confidence.
2.5. Data Analysis
Descriptive statistics were calculated for all outcome measures. The groups were compared at baseline to determine if there were any significant differences between the groups. Parametric tests were used for gait speed, while non-parametric tests were used for FSST, ABC and age as these data were not normally distributed [29].
To evaluate the effect of the intervention for the normally distributed variables (gait speed), an ANCOVA was used to compare post intervention scores, with baseline gait speed as the covariate. This approach has been recommended by Vickers [30] for non-normally distributed data (FSST and ABC), change scores were calculated for each subject, and Mann-Whitney U-tests compared change scores between the groups. The mean treatment effect (and 95 CI) of the classes were calculated for each variable. Within group changes, between initial and re-testing, were analyzed using repeated measures statistical tests. All tests were two-tailed tests.
Exploratory analysis of the gait variables: The effect of the intervention was evaluated using an ANCOVA to compare post intervention scores, with baseline scores as the covariate for normally distributed data (cadence, double support and stride variability) and Mann Whitney U tests for data not normally distributed (stride length). There was also an investigation of relationships between the variables using Spearman correlation tests as the testing involved data that were not normally distributed. SPSS Graduate Pack v.15.0 was used for all statistical analysis.
3. Results
Figure 1 shows the flow chart for recruitment and attrition. There were no significant differences on baseline measures between those who dropped out of the study and those who presented for re-testing. Two participants in the Control group were not re-tested on the GAITRite, so there were 35 subjects in this group with data on gait speed for analysis.
Figure 1: Flow chart of participant recruitment and retention.
3.1. Baseline Comparisons
There was no significant difference in age between the Intervention group [median = 75.0 (IQR = 8.0) years] and the Control group [median = 76.5 (IQR = 10.0) years] (). At baseline, all participants were asked about their current health status. Table 1 displays the co-morbidities reported by both groups. The Control group reported an average of 1.3 (48/37) conditions per person, while the Intervention group reported 1.6 (42/26), indicating similar levels of health status.
Table 1: Health status of participants at baseline.
Table 2 displays the baseline scores for both groups on the three main outcome measures. Despite being similar in age, the Control group displayed a non-significant trend towards being more mobile than the Intervention group, both on the FSST () and on gait speed (). The Control group displayed significantly higher scores on the ABC questionnaire ().
Table 2: Comparison between groups at baseline, re-testing and difference between groups (95% CI) for Intervention group (n = 26) and Control group (n = 37).
3.2. ABC Score
Results of the initial and post-tests are provided in Table 2. Non-parametric tests were used as data were not normally distributed. Change scores were found to be significantly different between the Intervention and Control groups (Z = 2.80, ), as illustrated in Figure 2. The Intervention group was found to have significantly improved between initial and re-testing (Z = 2.41, ). The Control group had a small though non-significant deterioration in score over this period (Z = 1.01, ).
Figure 2: Box plot displaying ABC change scores between initial and retesting for both groups.
3.3. Gait Speed
Results of the initial and post tests are provided in Table 2. Change scores were found to differ significantly between groups (F = 5.98, ), using ANCOVA to test for the main effect of group. Using paired-samples t-tests, these changes were found to be significant within the Intervention group (df = 25, t = 3.75, ), but not within the Control group (df = 36, t = 1.01, ) as illustrated in Figure 3.
Figure 3: Box plot displaying gait speed change scores between initial and retesting for both groups.
3.4. FSST
Results of the initial and post-tests are provided in Table 2. Change scores were significantly different between the Intervention and Control groups (Z = 2.28, ) as illustrated in Figure 4. Wilcoxon Signed Ranks tests showed that both the Intervention group (Z = 3.43, ) and the Control group (Z = 3.9, ) improved significantly on this measure.
Figure 4: Box plot displaying FSST change scores between initial and retesting for both groups.
3.5. Exploratory Analysis of Gait Data
Analysis of several gait variables, comparing changes both within groups and between groups is presented in Table 3. Compared to the Control group, the Intervention group significantly increased their cadence by 5.02 steps/min (95% CI 1.49–8.62, F = 9.59, ). The intervention group made significantly more improvement in stride length than the Control group (Z = 2.17, ). Neither double support time (F = 0.09, ) nor stride variability (F = 0.023, ) change scores were found to differ significantly between groups, using ANCOVA to test for the main effect of group.
Table 3: Exploratory gait variables.
3.6. Participant Comments
The Intervention group participants made comments on several aspects of balance and mobility that had been affected by the classes. Twenty-one of the participants had noticed changes which they felt were related to the classes, and five said they had noticed no changes. Eight people commented on improvements in walking. Seven commented on feeling more confident. Thirteen commented on changes to body image, such as “Makes you think about the soles of the feet on the ground”. Ten mentioned improvement in functional activities, including walking on slopes and taking the dog for a walk.
4. Discussion
Results of this study showed that participants attending the Feldenkrais Method classes made statistically significant improvements on a number of balance measures compared to a non-intervention Control group. The Feldenkrias Method may therefore be a useful approach to improving balance in older adults. The group attending the classes made improvements in both psychological and physical domains of balance measurement.
4.1. Balance Confidence
The improvement in scores on the self-rated ABC questionnaire suggested that the Intervention group felt more confident in their balance while performing a variety of tasks. This increased confidence in undertaking everyday activities was substantiated by the participants' comments about the effects of the classes. These comments suggested there had been a translation from skills learnt in the classes to improvement in everyday functional activities.
The median ABC score, for the Intervention group in the current study, increased from 68.7 to 81.7 (18.9%). These results compare well to Sattin and Wolf's study of Tai Chi to improve balance [7], which found an increase of five points on the ABC, over a 4-month period, or Liu-Ambrose's study of Tai Chi and balance [31] which recorded a 6% improvement in ABC score (from a mean of 78.3 points to 83.2 points).
The difference in the ABC scores between groups at baseline may have affected the results, as perhaps the Intervention group, who scored lower at initial testing, were more likely to score higher on retesting due to a regression to the mean. To investigate this possibility, the authors examined the results of a subgroup of the Control group who scored a median of 74.7 (IQR = 18.3) on the ABC. This score was not significantly different from the Intervention group median score at baseline of 68.7 (IQR = 18.2). This lower-scoring subgroup of the Control group, who were similar to the Intervention group in initial scores, made a slight decrease in score over time [1.3 (IQR = 16.3)], unlike the Intervention group who improved over time. This provides some support to the contention that the improvement observed in the Intervention group was probably not a regression to the mean.
4.2. Gait Speed and Other Gait Parameters
For gait speed, the mean treatment effect of 0.11 m represented a 9.7% increase in speed attributable to the classes. Wayne's 2004 [9] review of 30 Tai Chi studies included one study which measured gait speed, and Gardner's 2000 [32] review of exercise as a balance intervention included two studies, neither of which found a significant change in gait speed. The 9.7% increased speed in the Intervention group in the current study compares favorably to a 6% increase in gait speed observed in people who had participated in Tai Chi sessions [8].
The increased gait speed was achieved through both longer step lengths and increased cadence, with an associated decrease in double support time. The faster gait speed in the Intervention group may have been due to increased confidence [23]. Fear of falling has been shown to alter postural control to produce “stiffer” movement patterns [33], so decreased fear may have enabled a “freer” gait style, with longer steps and increased speed. The faster speed may also have resulted from improved intersegmental control between the lower limbs, pelvis, trunk and head.
4.3. Dynamic Balance
Both groups made significant improvements between initial and retesting sessions on the FSST. The improvement by almost all participants suggests that there may be a learning effect on the task, and that caution should be exercised if it is used as an outcome measure for clinical trials. Despite both groups improving significantly, the Intervention group still made significantly more improvement than the Control group on this measure, suggesting that their ability to step in all directions and change direction in space had improved.
4.4. A Novel Approach to Balance Training
The Feldenkrais Method differs from other exercise approaches in several ways. Firstly it is an exploratory learning approach based on dynamics systems principles [34]. Participants are allowed to progress at their own pace, gradually expanding their “perceptual-motor workspace” or “movement envelope” as described by Karl Newell [35]. These ideas about dynamic systems and human movement control have been recently discussed by Bardy et al. [36], in relation to the “self-organizing” capacity of biological systems such as the human. He states that “behavior emerges from the interaction of multiple sub-systems, including experience” (page 500). The relevance of this thinking to the current study is that participants were not taught specific strategies to improve their balance, but were presented with many opportunities for learning and allowed to work out solutions for themselves. There was no “right" way to do each movement, but instead each repetition was viewed as an exploration. Participants gained confidence in exploring the space around themselves in their own way and time, resulting in expanded perceived limits of stability as they practice moving their centre of mass close to the edge of the base of support in many directions. This approach allows older people the time to gradually build their movement skills and repertoire of solutions to movement challenges.
Another difference between the Feldenkrais Method balance classes and other approaches to balance retraining is the variability of the training. It has been stated that “ when practice is varied by changing aspects of the environmental context or the task, the motor skill that develops is more flexible and generative in type” [37] (page 96). Feldenkrais Method balance classes have greater variety and variability than standard balance training programs such as that described by Gardner [3], which consisted of about 12 balance exercises repeated over many sessions (with grading for increasing the difficulty of most of these exercises). In Tai Chi balance classes certain forms of movement are practiced over and over again [7, 8]. The Feldenkrais Method balance classes consisted of a series of individual lessons, each one different. Within each lesson, the movement tasks were systematically varied after about twenty repetitions of each action, including variations to direction, speed, amplitude and intersegmental timing of the action. For example, rotation was practiced first with the eyes leading the movement, then the shoulders leading, then the pelvis, then the knees, then different combinations of the above body parts. This variability of practice has been considered an important principle to be included in motor skill acquisition training [35].
Finally, the Feldenkrais Method, influenced by its martial arts origins, seeks to engage every part of the person in the movements, from the toes, to the trunk, to the eyes and the breath. The movement classes also have an emphasis on improving movement control of the pelvis, to improve both power in movement and the control of the centre of gravity. This concept is again related to martial arts principles [11], and translates well into training to improve balance in everyday function. Indeed the “practice of controlled movements of the centre of mass” has been identified as one of the most important components of a balance training program for older adults to prevent falls [10] (page 2234).
4.5. Study Limitations
One limitation of this study was the lack of randomization between groups, due to the pragmatic nature of this pilot study. The Intervention group was a sample of convenience, recruited from people already enrolled into a series of Feldenkrais Method balance classes. Although the researchers attempted to recruit a similar group to act as a control, the Control group was more confident in their balance than the Intervention group. This limitation led to the baseline differences between the groups, which has already been discussed.
The lack of blinding of the testers to the group allocation of the subjects was a potential source of bias. This was countered by the assessors giving exactly the same instructions to all participants on all occasions, and the assessors were blinded to baseline results at re-test. As with many interventions in the rehabilitation setting, it was impossible to blind subjects to the intervention in this type of clinical trial.
There were no adverse effects such as falls or reports of injuries during the classes.
5. Conclusion
Participants in Feldenkrais Method balance classes improved in several measures of balance and mobility compared a Control group who received no intervention. It appears that the Feldenkrais Method, which uses an exploratory learning approach based on an understanding of dynamic systems, may add some useful dimensions to the retraining of balance.
Funding
National Health Medical Research Council of Australia, Health Professionals Training Fellowship Grant (to C.S.) (grant number 310612).
Acknowledgments
The authors wish to thank Robert Webb for his assistance with organization of participants and venues for data collection, and Cameron Wilson for his assistance with data collection. This trial was registered on the NIH Clinical Trials website (http://www.clinicaltrials.gov/). The trial identifier is NCT00222287.
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Pune, September 16 Army hurdle over, natural gas by first week of October
Pune is all set to get piped Compressed Natural Gas (CNG) in time for the Commonwealth Youth Games (CYG).
With the Army having given clearance for the Dehu Road stretch of the pipeline project, Gas Authority of India Limited (GAIL) and Maharashtra Natural Gas Limited (MNGL) are hopeful that 50 city buses would be able to run on CNG by October, as scheduled.
Pune, September 15 The Pune Municipal Corporation
Pune, September 15 Used syringes, needles, bandages, body parts pile up at city hospitals, with no place to dump the waste in
It was a crackdown on a racket involved in the disposal of spray cans, but it is hospitals that are suffering
Pune, September 10 The latest to join the green brigade in the city, the jewellers may gift every customer, who purchase gold from them on Dassera (buying gold on Dassera is considered auspicious), a Shami tree sapling.
The Department of Social Forestry has proposed to distribute about one lakh saplings of Shami tree to the Pune Jewellers Association, which is considering gifting the saplings to those who buy gold from them on Dassera which will fall on October 9. The idea is to urge people to plant more trees and save the dwindling Shami trees from vanishing.
Mumbai, September 09 Publishes pamphlets asking people to use artificial ponds;
Pune, September 07 Glitch at Loni terminal server cuts off supply, repair staff work on holiday
A technical glitch at the Hindustan Petroleum Corporation Limited (HPCL) server at the Loni terminal affected diesel supply to the city, creating a sudden shortage. The glitch happened on Saturday and forced officials at the terminal to work on Sunday as well to restore regular supply.
Pune, September 05 Kumar Sublime, a project by Kumar Builders at Kondhwa, received the prestigious five-star eco-housing rating certificate from Municipal Commissioner at a function held recently. Arun Nigvekar and Prashant were among those presenton the occasion.
The certification has been initiated for the first time in the city. For the 5 star eco housing rating, the minimum criteria is 800 points. This is an interim certification till the completion of the project, said a press release.
Pune, September 4 Here
Pune, August 27 Use soluble clay and vegetable dyes to make 20,000 idols for festival
The forthcoming Ganesh festival may be an environment-friendly one, thanks to the efforts of the Directorate of Social Forestry through its National Green Corps (NGC).
Over 800 schools across the state have made 20,000 eco-friendly Ganesh idols
Pune, August 25 Civic body proposes to raise Rs 2,600-crore urban transport fund for metro, Rs 2,300 crore for ring road land acquisition
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Bibliography: Future on Ice
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Title: Future on Ice
Editor: Orson Scott Card
Year: 1998
Type: ANTHOLOGY
Language: English
ISFDB Record Number: 35132
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Copyright (c) 1995-2011 Al von Ruff.
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Nano Express
Charge transfer magnetoexciton formation at vertically coupled quantum dots
Willian Gutiérrez1*, Jairo H Marin2 and Ilia D Mikhailov1
Author Affiliations
1 Escuela de Física, Universidad Industrial de Santander, A. A. 678, Bucaramanga, Colombia
2 Escuela de Física, Universidad Nacional de Colombia, A.A. 3840, Medellín, Colombia
For all author emails, please log on.
Nanoscale Research Letters 2012, 7:585 doi:10.1186/1556-276X-7-585
Published: 23 October 2012
Abstract
A theoretical investigation is presented on the properties of charge transfer excitons at vertically coupled semiconductor quantum dots in the presence of electric and magnetic fields directed along the growth axis. Such excitons should have two interesting characteristics: an extremely long lifetime and a permanent dipole moment. We show that wave functions and the low-lying energies of charge transfer exciton can be found exactly for a special morphology of quantum dots that provides a parabolic confinement inside the layers. To take into account a difference between confinement potentials of an actual structure and of our exactly solvable model, we use the Galerkin method. The density of energy states is calculated for different InAs/GaAs quantum dots’ dimensions, the separation between layers, and the strength of the electric and magnetic fields. A possibility of a formation of a giant dipolar momentum under external electric field is predicted.
Keywords:
Magnetoexciton; Vertically coupled quantum dots; Giant dipolar momentum; Galerkin method; Density of energy states.
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Groups Policy Implementation
Posted by & filed under Site News.
Dear Community,
On December 20th, the General Assembly consensed that all groups must provide the following information in order to make it easier for people to join the movement:
1. A mission statement which does not violate the Principles of Solidarity
2. A working email or phone number
3. Day and time of a weekly open meeting (this should be listed as a recurring event, so that it shows up on the daily schedule)
4. Minutes from a weekly meeting, which demonstrate at least 5 people in attendance.
You can see the list of groups and their current status here. The list is updated once a month.
If you are a member of a group that no longer appears on the website, don’t worry! Your group isn’t gone forever, it can be reactivated once you make sure these guidelines are met.
You’ll need to get in touch with us at [email protected] with the updated info for your group’s website. If you need assistance bringing your group into compliance, please be in touch and InfoHub will be happy to help out.
In solidarity,
-InfoHub Working Group Team
You must be logged in to post a comment.
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Endy:Reprints
From OpenWetWare
Revision as of 19:53, 19 February 2013 by Endy (Talk | contribs)
Jump to: navigation, search
Add to My Links
Home Lab Members Research Notebooks Publications Internal Contact
• Note: We also publish thesis proposals, dissertations, and technical reports via DSpace, an online digital repository operated by the MIT Library.
• Note: PDF reprints are provided below within the context of fair use. Please obtain copies from the publisher if appropriate.
• Note: Search "endy d" via PubGet for a third-party automatically generated set of PubMed-listed publications from the lab.
Contents
Student Dissertations
Barry Canton
Engineering the interface between cellular chassis and synthetic biological systems
MIT PhD, 2008 dissertation (PDF), doi: 1721.1/44918
Jeff Gritton
Architecture and evolutionary stability of yeast signaling pathways
MIT MS, 2006 thesis (PDF), doi: 1721.1/37258
Jason Kelly
Tools and reference standards supporting the engineering and evolution of synthetic biological systems
MIT PhD, 2008 dissertation (PDF), doi: 1721.1/44917
Nicolas Koutsoubelis
Quantitative in silico and in vivo characterization of the recombinase addressable data storage
University of Freiburg Bachelor's thesis (PDF)
Sriram Kosuri
Simulation, models, and refactoring of bacteriophage T7 gene expression
MIT PhD, 2007 dissertation (PDF), doi: 1721.1/39912
Alex Mallet
Analysis of Targeted and Combinatorial Approaches to Phage T7 Genome Generation
MIT MS, 2007 thesis (PDF), doi: 1721.1/35880
Reshma Shetty (co-advisee with Tom Knight
Applying engineering principles to the design and construction of transcriptional devices
MIT PhD, 2008 dissertation (PDF), doi: 1721.1/44921
Francois St-Pierre
Determination of cell fate selection during phage lambda infection
MIT PhD, 2009 dissertation (PDF), doi: pending
Samantha Sutton
Engineering phosphorylation-dependent post-translational protein devices
MIT PhD, 2008 dissertation (PDF), doi: 1721.1/45205
Ty Thompson
Models and analysis of yeast mating response: tools for model building, from documentation to time-dependent stimulation
MIT PhD, 2008 dissertation (PDF), doi: 1721.1/45206
Peer Reviewed Research Articles
A survey of enabling technologies in synthetic biology
submitted
Linda J. Kahl & Drew Endy
Living digital logic via engineered genetic transistors
in re-review
Jerome Bonnet et al.
Measurement and modeling of intrinsic transcription terminators
revised & resubmitted
Guillaume Cambray et al.
Precise and reliable gene expression via standard transcription and translation initiation elements
Nature Methods, in press
Vivek Mutalik et al.
URL pending PDF reprint pending
Quantitative estimation of activity and quality for collections of functional genetic elements.
Nature Methods, in press
Vivek Mutalik et al.
URL pending PDF reprint pending
Design and analysis of genetically encoded counters
Procedia Computer Science, v11 (2012) pp.43-54
Palpoom Subsoontorn and Drew Endy
URL PDF reprint
A fully decompressed synthetic bacteriophage øX174 genome assembled and archived in yeast
Virology, published online 15 October 2012, doi: 10.1016/j.virol.2012.09.020
Paul Jaschke, Erica Lieberman, Jon Rodriguez, Adrian Sierra, Drew Endy
URL PDF reprint
Engineered cell-cell communication via DNA messaging
Journal of Biological Engineering Sept 2012, 6:16 doi:10.1186/1754-1611-6-16
Monica Ortiz and Drew Endy
URL Final PDF pending
Refactored M13 bacteriophage as a platform for tumor cell imaging and drug delivery
ACS Synthetic Biology, doi:10.1021/sb300052u, August 17, 2012
Debadyuti Ghosh, Aditya Kohli, Felix Moser, Drew Endy, and Angela Belcher
URL PDF reprint
Rewritable digital data storage in live cells via engineered control of recombination directionality
PNAS USA, 21 May 2012, doi: 10.1073/pnas.1202344109
Jerome Bonnet, Pakpoom Subsoontorn and Drew Endy
URL PDF reprint
Scaffold number in yeast signaling system sets tradeoff between system output and dynamic range
PNAS USA, 2011 November; doi: 10.1073/pnas.1004042108
Ty Thomson, Kirsten Benjamin, Alan Bush, Tonya Love, David Pincus, Orna Resnekov, Richard Yu, Andrew Gordon, Alejandro Colman-Lerner, Drew Endy, Roger Brent
URL | PDF reprint
Gemini, a bifunctional enzymatic and fluorescent reporter of gene expression
PLoS ONE 4(11): e7569. doi:10.1371/journal.pone.0007569
Lance Martin, Austin Che, Drew Endy
URL PDF reprint
Measuring the activity of BioBrick promoters using an in vivo reference standard
Journal of Biological Engineering, 2009 March 20;3:4
Jason R Kelly, Adam J Rubin, Caroline M Ajo-Franklin, John Cumbers, Michael J. Czar, Kim de Mora, Aaron L Glieberman, Dileep D Monie, Drew Endy
URL PDF reprint
Determination of cell fate selection during phage lambda infection
PNAS USA, 2008 December; 105(52), 20705-20710
Francois St-Pierre, Drew Endy
URL PDF reprint
Refinement and standardization of synthetic biological parts and devices
Nature Biotechnology, 2008 July; 26(6), 787-93
Barry Canton, Anna Labno, Drew Endy
URL PDF reprint News & Views
Engineering BioBrick vectors from BioBrick parts
Journal of Biological Engineering, 2008 Apr 14;2:5
Reshma Shetty, Drew Endy, Tom Knight
URL
Stimulus design for model selection and validation in cell signaling
PLoS Comput Biol. 2008 Feb 15;4(2):e30
Josh Apgar, Jared Toettcher, Drew Endy, Forest White, Bruce Tidor
URL
TABASCO: A single molecule, base-pair resolved gene expression simulator
BMC Bioinformatics 2007, 8:480
Sriram Kosuri, Jason R Kelly, Drew Endy
URL
DNA synthesis and biological security
Nature Biotechnology June 2007
Hans Bugl, John P Danner, Robert J Molinari, John T Mulligan, Han-Oh Park, Bas Reichert, David A Roth, Ralf Wagner, Bruce Budowle, Robert M Scripp, Jenifer A L Smith, Scott J Steele, George Church & Drew Endy
URL PDF reprint
Synthetic genomics: Options for governance
Biosecur Bioterror 2007 Dec;5(4):359-62
Michele Garfinkel, Drew Endy, Gerald Epstein, Robert Friedman
URL (Full Report)
Foundations for engineering biology
Nature 24 November 2005 doi:10.1038/nature04342
Drew Endy
URL PDF reprint
Refactoring bacteriophage T7
Nature/EMBO Molecular Systems Biology 13 September 2005 doi:10.1038/msb4100025
Leon Y. Chan, Sriram Kosuri and Drew Endy
URL PDF reprint News & Views October 2004 version
Regulated cell to cell variation in a cell fate decision system
Nature 18 September 2005 doi:10.1038/nature03998
Alejandro Colman-Lerner, Andrew Gordon, Eduard Serra, Tina Chin, Orna Resnekov, Drew Endy, C. Gustavo Pesce and Roger Brent
URL PDF reprint News & Views
Modelling cellular behaviour (insight feature)
Nature 409, 391-395
Drew Endy and Roger Brent
PDF reprint
Computation, prediction, and experimental test of fitness for bacteriophage T7 mutants with permuted genomes
Proceedings of the National Academy of Sciences USA 97, 5375-5380
Drew Endy, Lingchong You, John Yin and Ian Molineux
PDF reprint
Toward antiviral strategies that resist viral escape
Antimicrobial Agents & Chemotherapy 44, 1097-1099
Drew Endy and John Yin
PDF reprint
Intracellular kinetics of a growing virus: A genetically-structured simulation for bacteriophage T7
Biotechnology & Bioengineering 55, 375-389
Drew Endy, Deyu Kong, and John Yin
PDF reprint
Transcribed Lectures
Synthetic biology: Can we make biology easy to engineer? <--note: transcription was not proofed
Industrial Biotechnology' 1 December 2008, 4(4): 340-351
Drew Endy
URL PDF reprint
Other Articles, edited but not peer reviewed
Switches, switches, every where, in any drop we drink
Molecular Cell, 25 January 2013
Jerome Bonnet, Drew Endy
URL pending, PDF reprint pending
Cribsheet #16: Synthetic Biology
SEED July 2008
Lee Billings, Drew Endy
Illustrator: Thomas Porostocky
URL PDF reprint
Reconstruction of the genomes
Science 2008 Feb 29;319(5867):1196-7
Drew Endy
URL PDF reprint
Building a fab for biology
Scientific American June 2006
David Baker, George Church, Jim Collins, Drew Endy, Joe Jacobson, Jay Keasling, Paul Modrich, Christina Smolke, Ron Weiss
PMID: 16711359
A biological engineer searches for simplicity
Nature 449, 5
Drew Endy
URL
Useful construction
The Scientist January 2006
Drew Endy
URL (login likely req'd.)
URL (login not req'd., as of 24 March 2009)
2003 Synthetic Biology study
US Government October 2003
Drew Endy, Patrick Lincoln, Richard Murray
doi:1721.1/38455
Molecular monogamy
Nature 426, 614-615
Drew Endy and Michael B. Yaffe
PDF reprint
Decoding NF-kB signaling
Science 298, 1189-1190
Alice Y. Ting and Drew Endy
PDF reprint
A standard parts list for biological circuitry
DARPA white paper October 1999
Drew Endy, Adam Arkin
doi:1721.1/29794
Books
Adventures in synthetic biology
Nature 24 November 2005 Cover & Online
Drew Endy, Isadora Deese and Chuck Wadey
PDF, links, and background information
For a reprint, please download a free .PDF from the link above
Edited Book Chapters
Synthetic Biology
Bioethics Briefing Book, The Hastings Center, 2008, Chapter 35
Michele Garfinkel, Drew Endy, Gerald Epstein, Robert Friedman
Free Online
Towards a predictive biology: The example of bacteriophage T7
Evolution as Computation, Landweber & Winfree (eds.), DIMACS Workshop, Princeton, 1999, 201-209 (book chapter).
Drew Endy
no e-print currently available (sorry!)
Selected Online Lectures or Debates
Synthetic Biology Debate with Jim Thomas, moderated by Stewart Brand
The Long Now Foundation, 17 November 2008
Cowell Theater, Fort Mason Center, San Francisco
Online w/ transcription via FORA.tv, DVD for purchase via Whole Earth Films
Programming DNA: A 2-bit language for engineering biology
24C3, The 24th Chaos Communication Congress, 27 December 2007
Berliner Congress Center, Berlin
Online via Google video
Personal tools
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So he said: and vast Earth rejoiced greatly in spirit, and set and hid him in an ambush, and put in his hands [175] a jagged sickle, and revealed to him the whole plot. And Heaven came, bringing on night and longing for love, and he lay about Earth spreading himself full upon her.1Then the son from his ambush stretched forth his left hand and in his right took the great long sickle [180] with jagged teeth, and swiftly lopped off his own father's members and cast them away to fall behind him. And not vainly did they fall from his hand; for all the bloody drops that gushed forth Earth received, and as the seasons moved round [185] she bore the strong Erinyes and the great Giants with gleaming armour, holding long spears in their hands and the Nymphs whom they call Meliae2all over the boundless earth. And so soon as he had cut off the members with flint and cast them from the land into the surging sea, [190] they were swept away over the main a long time: and a white foam spread around them from the immortal flesh, and in it there grew a maiden. First she drew near holy Cythera, and from there, afterwards, she came to sea-girt Cyprus, and came forth an awful and lovely goddess, and grass [195] grew up about her beneath her shapely feet. Her gods and men call Aphrodite, and the foam-born goddess and rich-crowned Cytherea, because she grew amid the foam, and Cytherea because she reached Cythera, and Cyprogenes because she was born in billowy Cyprus, [200] and Philommedes3 because she sprang from the members. And with her went Eros, and comely Desire followed her at her birth at the first and as she went into the assembly of the gods. This honor she has from the beginning, and this is the portion allotted to her amongst men and undying gods,— [205] the whisperings of maidens and smiles and deceits with sweet delight and love and graciousness.
1 The myth accounts for the separation of Heaven and Earth. In Egyptian cosmology Nut （the Sky） is thrust and held apart from her brother Geb （the Earth） by their father Shu, who corresponds to the Greek Atlas.
2 Nymphs of the ash-trees （μέλιαι）, as Dryads are nymphs of the oak-trees. Cp. note onWorks and Days, l. 145.
3 “Member-loving”: the title is perhaps only a perversion of the regularφιλομειδής（laughter-loving）.
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[3] For I could wish that I myself were accursed from Christ for my brothers' sake, my relatives according to the flesh,
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CMD sent two reporters to track ALEC in Oklahoma
Click here to help support our future investigations.
Peter F. Geithner
From SourceWatch
Jump to: navigation, search
Peter F. Geithner "is an advisor to the Asia Center at Harvard University and a consultant to the Asia Pacific Philanthropy Consortium, Rockefeller Foundation, Sasakawa Peace Foundation, and other organizations. He serves on the boards of the National Committee on United States-China Relations, the China Center for Economic Research (Peking University), the Center for the Advanced Study of India (University of Pennsylvania), lemente (Holdings) Asia, Inc., and the Institute of Current World Affairs.
"Mr. Geithner was with The Ford Foundation for 28 years, where he held program management positions mainly concerned with Asia. He was Director of Asia Programs from 1990 to 1996. Prior to assuming that position, he served for two and a half years as the Foundation’s first representative in Beijing, China. His earlier assignments with the Foundation included Program Officer in Charge, Developing Country Programs (New York), Representative for Southeast Asia (Bangkok), Deputy Head, Asia Pacific (New York), and Deputy Representative for India, Nepal, and Sri Lanka (New Delhi).
"Prior to joining The Ford Foundation, Mr. Geithner served with the U.S. Agency for International Development in Zimbabwe, Zambia, and Washington, D.C. He was also Assistant to the President of a private international company, and served for four years as a Naval Aviator.
"Mr. Geithner is a graduate of Dartmouth College (BA) and the Johns Hopkins University School of Advanced International Studies (MA). He is a member of Phi Beta Kappa, a recipient of the State Department Distinguished Service Award, and the Royal Thai Government Order of the White Elephant.“ [1]
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Person:Theodorick Bland (1)
Watchers
Browse
Theodorick Bland
d.16 July 1783/90 Amelia County, Virginia
m. 11 February 1701
1. Mary Bland1704 - 1764
2. Elizabeth Bland1705 -
3. Richard Bland1710 - 1776
4. Theodorick Bland1719 - 1783/90
m. 1739
• HTheodorick Bland1719 - 1783/90
1. Frances Bland1744 - 1788
Facts and Events
Name Theodorick Bland
Gender Male
Alt Birth[1] 2 Dec 1708
Birth? 19 December 1719 of Kippax, Prince George County, Virginia
Marriage 1739 of Kippax, Prince George County, Virginiato Frances Elizabeth Bolling
Death? 16 July 1783/90 Amelia County, Virginia
Alt Death[1] 1784
the text in this section is copied from an article in Wikipedia
Theodorick Bland (December 2, 1708 – 1784), also known as Theodorick Bland, Sr. or Theodorick Bland of Cawsons, was a member of the Virginia House of Burgesses, a clerk of the court of Prince George County, Virginia, and the father of Congressman Theodorick Bland.
This page uses content from the English Wikipedia. The original content was at Theodorick Bland of Cawsons. The list of authors can be seen in the page history. As with WeRelate, the content of Wikipedia is available under the Creative Commons Attribution/Share-Alike License.
References
1. 1.0 1.1 Theodorick Bland of Cawsons, in Wikipedia: The Free Encyclopedia. (Online: Wikimedia Foundation, Inc.).
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Catalogue Number
2012.0 - 1996 Census of Housing and Population, 1996
Latest ISSUE Released at 11:30 AM (CANBERRA TIME) 02/10/1995
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Tell me more ×
Answers OnStartups is a question and answer site for entrepreneurs looking to start or run a new business. It's 100% free, no registration required.
So the idea for my startup which we have been also sharing with few incubators wasn't well received during the last 3 months. And now we find out that during this time the same has been developed by a startup in Netherlands.
Surprisingly, they have done everything so similar to our plan, in fact they have same set of features and implementation. Looking at their detailing gives me a feel as if I am reading my own document that we have been working on.
Has my idea been stolen or is it just a bizzare coincidence. Whatever the case may be I never had a copyright on it since we were only just starting to build it.
SO the question is what now? Continue building or abandon.
share|improve this question
5 Answers
up vote 2 down vote accepted
Congratulations, this just proves that your "idea" is actually worth pursuing, you are not the only one who thinks is a good idea and that is a good thing.
Unless you are building the next Facebook or Twitter (and chances are you are not), having other startups developing the same product is not a bad thing, on the contrary, it usually suggests there is a big enough market for that product or service.
share|improve this answer
Continue building.
With several billions people on the planet and most of them living interconnected it is to be expected that same ideas arise.
Having said that it's most times of no consequence who's built it first. The winner will be decided based on many other criteria, such as the quality of the service, quality of support, perception, marketing etc.
How can you know? Perhaps they will screw up and you will excel?
Go ahead and try it.
share|improve this answer
You may find that you now get more interest from incubators when they know a similar service has launched elsewhere. It demonstrates proof of concept to some extent.
If you feel you still have a market, go ahead. Make sure you learn from everything they do/have done and use it to improve your business. Show potential investors how you are improving on the execution and how you can capture a viable market.
share|improve this answer
If someone else has done what you wanted, that proves that you are not so crazy after all. There are more people that think that your idea is worth investing in. Like Ricardo said, congratulations!
Now, you have been going through this for some time, so you should be able to make improvements. Even more, you get to see where they fail.
I would only worry about not making a copy of this product. Yes, I know, it's not a copy because you had the idea, but since you'll be launching after them you are the one who has to make himself apart. Try to give it a twist, maybe go after a different market.
share|improve this answer
There are over billion computer users in the world, you have huge markets to look for. Considering other company is also a startup they also will have to pitch their ideas faster and spread so it would be better if you can finish your product and compete, possibly in other markets. For example their focus may be in Europe right now, you can try expanding in US or India. Their is Amazon in US does not means there can't be more flipkarts or infibeams in India.
share|improve this answer
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1 reputation
bio website emekadavid-solvingit.blogspot.com
location Lagos, Nigeria
age
visits member for 8 months
seen Sep 13 '12 at 18:36
stats profile views 2
I love exchanging ideas. Interestingly, although many persons find maths and economics boring, I believe they are essential to the modern age. I like those subjects like I like rice and a plate of chicken. Thanks everyone. I love stackoverflow also.
0 Questions
This user has not asked any questions
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Research article
MicroRNA-125b regulates the expression of aggrecanase-1 (ADAMTS-4) in human osteoarthritic chondrocytes
Tetsuya Matsukawa1,2, Tadahiro Sakai1*, Tomo Yonezawa2,3, Hideki Hiraiwa1, Takashi Hamada1, Motoshige Nakashima1, Yohei Ono1, Shinya Ishizuka1, Hiroyuki Nakahara2, Martin K Lotz2, Hiroshi Asahara2,4 and Naoki Ishiguro1
Author affiliations
1 Department of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan
2 Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
3 Department of System Biomedicine, Tokyo Medical and Dental University, 1-5-45 Tsushima, Bunkyo-ku, Tokyo 113-8510, Japan
4 Department of System Biomedicine, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157-8535, Japan
For all author emails, please log on.
Citation and License
Arthritis Research & Therapy 2013, 15:R28 doi:10.1186/ar4164
Published: 13 February 2013
Abstract
Introduction
Increased expression of aggrecanase-1 (ADAMTS-4) has emerged as an important factor in osteoarthritis (OA) and other joint diseases. This study aimed to determine whether the expression of ADAMTS-4 in human chondrocytes is regulated by miRNA.
Methods
MiRNA targets were identified using bioinformatics. Chondrocytes were isolated from knee cartilage and treated with interleukin-1 beta (IL-1β). Gene expression was quantified using TaqMan assays and protein production was determined by immunoblotting. Luciferase reporter assay was used to verify interaction between miRNA and target messenger RNA (mRNA).
Results
In silico analysis predicted putative target sequence of miR-125b on ADAMTS-4. MiR-125b was expressed in both normal and OA chondrocytes, with significantly lower expression in OA chondrocytes than in normal chondrocytes. Furthermore, IL-1β-induced upregulation of ADAMTS-4 was suppressed by overexpression of miR-125b in human OA chondrocytes. In the luciferase reporter assay, mutation of the putative miR-125b binding site in the ADAMTS-4 3'UTR abrogated the suppressive effect of miR125.
Conclusions
Our results indicate that miR-125b plays an important role in regulating the expression of ADAMTS-4 in human chondrocytes and this identifies miR-125b as a novel therapeutic target in OA.
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Combining Assemblies Using ILMerge
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Combining Assemblies Using ILMerge (Unpublished)
When creating solutions that include multiple projects, Visual Studio creates an assembly for each project. This can lead to libraries that are complicated to use, needing many references. Using ILMerge, the assemblies can be combined into a single file.
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Tool: Creating a custom MachineKey in ASP.NET
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Tool: Creating a custom MachineKey in ASP.NET (Unpublished)
"There are many times when it is worthwhile to create a custom machineKey for your web.config file. This is worthwhile on a webfarm but also worthwhile on a stand-alone server so that your machineKey remains the same after an iisreset or application pool recycle. "
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Flameman/ipaq/status
From eLinux.org
Revision as of 10:14, 7 March 2009 by Flameman (Talk | contribs)
Jump to: navigation, search
daily updated
Contents
user land progress
• @16-02-2009, the stage3 armv4l has been started
• @18-02-2009, ready to boot a minimal stage1 with init=/bin/bash root=/dev/hda3
• @23-02-2009, stage3 has been finished, tested, well running and able to compile
• @23-02-2009, stage3 is OK, stage4 has been started wirh xorg-x11 in mind (QT embedded is under studying)
• @02-03-2009, stage4 has branched into microwindows stuff, nanoX has been compiled, tested, well running
• @03-03-2009, wonder about an other branch to "QT-extended" ...
• @04-03-2009, echo "2.6-hh is dead, If you are scared of building things, then this isn't the project for you" > /etc/motd
• @05-03-2009, stage4 has also branced into xorg-base/xserver stuff, long emerge time
kernel last report
• @ 05-2009, 2.6.29.colie
** lcd: working
** backlight : NOT working
** touchscreen : NOT working
** buttons: NOT working
** battery: NOT working (new battery device interface)
** sound: NOT working
** usb: NOT working
** RTC: working
** compactflash: not working
** pcmcia: sleeve 1xpcmcia is working with pATA-pcmcia-16bit/5V
• @ 05-2009, 2.6.19-hh4 && 2.6.19.my
** lcd: working
** backlight : working
** touchscreen : working, but it seems there is no handler
** buttons: working
** battery: NOT working (new battery device interface)
** sound: NOT working
** usb: NOT working
** RTC: working
** compactflash: not working
** pcmcia: sleeve 1xpcmcia is working with pATA-pcmcia-16bit/5V, sleeve 2xpcmcia NOT working
old info at http://www.handhelds.org/moin/moin.cgi/KernelStatus
kernel proof
@ 05-03-2009
2.6.19.my has been derived from 2.6.19.hh4
2.6.19.my is used as my current working branch
download
• working one
kernel-ipaq-3600.gz
2.6.19: it has a bit of issues with the touch screen, it doesn't work at all with the sleeve dual pcmcia, it works with sleeve single pcmcia ... it is configured to have rootfs on pcmcia pATA disk
• experimental proof
version:
kernel-ipaq-3600-proof.gz
miscellanea
back light
how to switch it on/off ? using the sysfs class
touch screen
used: micro_ts + devts kernel module
mmm devts seems to produce too much noise, nano-X doesn't appreciate it
SA1100_BITSY seems to be missing: dunno why (why hasn't been removed from the tree ?), where is the missing stuff ... dunno at all, i will remove it
config TOUCHSCREEN_BITSY
33 tristate "Compaq iPAQ H3600 (Bitsy) touchscreen"
34 depends on SA1100_BITSY
35 select SERIO
36 help
37 Say Y here if you have the h3600 (Bitsy) touchscreen.
38
39 If unsure, say N.
40
41 To compile this driver as a module, choose M here: the
42 module will be called h3600_ts_input.
an other branch
issued
Current status:
* booting works
* PCMCIA mostly works (tested with CF and 1xPCMCIA sleeves,
don't have 2xPCMCIA) It Oopses on suspend (probably patch from
Thomas Kunze posted at linux-arm should help, but didn't check)
* Serial console works
* Framebuffer works
* USB gadget (UDC) - mostly worked last time I tried, using hackish
driver by Nick Bane. I cleaned it up a bit, but it's still a mess,
and probably should be rewritten from scratch.
* Flash works (R/W tested with sa11xx_flash, R/O with physmap)
* Buttons/Touchscreen works (with both patching mainline driver and
using forward-ported MFD-drivers by Gremlin)
* IRDA - code exists, but not tested
* Battery - level-reading driver by Gremlin kinda works, but values
are strange. Charging works without any drivers.
* Backlight - seems to work with driver by Gremlin
* Sound - driver exists in mainline kernel, but it's broken, as it
depends on L3 code from 2.4 kernel. It appears that in hh.org 2.6.21
kernel this code exists, but I didn't try to check if it can be used.
In fact I even didn't check if this driver works in 2.6.21-hh
(but something tells me that it doesn't).
5-3-2009: this branch is under deep evaluation
history
just to have an idea of what was done http://www.handhelds.org/hypermail/kernel-discuss/attachment.html
11-2005
new MACHINE_START definition for ipaq h3600
From: Alessandro GARDICH <gremlin_at_gremlin.it>
Date: Mon, 14 Nov 2005 21:11:35 +0100
Nothing change, just to follow the new way for the definition.
* text/x-patch attachment: handhelds-sa-26.patch
ipaq h3600 - patch for new egpio functions
From: Alessandro GARDICH <gremlin_at_gremlin.it>
Date: Sat, 19 Nov 2005 18:30:22 +0100
Nothing change, just to follow the new way *_egpio function.
Remain out only micro that have to be full rewriten and uda1341 OSS
driver, alsa one should work.
01-2006
From: Alessandro GARDICH <gremlin_at_gremlin.it>
Date: Fri, 06 Jan 2006 18:23:16 +0100
Hi to all,
another patch for iPAQ h3600
epiphany patch :
* arch/arm/common/ipaq/micro.c :
- estetic code clean-up
- support for keys device
- backlight device definition
- backlight are now restored after framebuffer blank/resume
* arch/arm/common/ipaq/micro_key.c :
- support for keys (5 application keys and 4 directions pad)
* arch/arm/common/pxa_keys.c :
- moved from arch/arm/mach-pxa/pxa_keys.c
- small changes to be used also for h3600 device
* arch/arm/mach-sa1100/h3600.c
- add support for power and action keys
- backlight device definition moved in micro.c
* include/asm-arm/arch-pxa/pxa_keys.h
- to not break existing pxa code it only include hardware/pxa_keys.h
* include/asm-arm/arch-sa1100/h3600_gpio.h
- add definition for GPIO number (not bit) for action button
* include/asm-arm/arch-sa1100/h3600.h
- add definition for GPIO number (not bit) for power button
* include/asm-arm/arch-sa1100/irqs.h
- macro to get IRQ for a giver GPIO
* include/asm-arm/hardware/pxa_keys.h
- moved from include/asm-arm/arch-pxa/pxa_keys.h
There are still some issues with micro* modules after sustend/resume and
when unloading.
This is really the epyphany patch, the end of xmas vacation.
From monday work and pool start again and so spare time will be just
few hours for day. :)
But i'll continue ...
I'm also looking on ebay if I can find a cheap h37xx and h38xx to take
care of such iPAQs also.
Re: [PATCH] RTC classdev: Add sysfs support for wakeup alarm (r/w)
From: David Brownell <david-b_at_pacbell.net>
Date: Mon, 18 Dec 2006 16:59:11 -0800
On Monday 18 December 2006 4:54 pm, David Brownell wrote:
> > http://handhelds.org/cgi-bin/cvsweb.cgi/linux/kernel26/drivers/rtc/rtc-sa1100.c.diff?r1=1.5&r2=1.6&f=h
>
> That patch you applied looks right to me -- why don't you forward it
> to Alessandro as a bugfix for 2.6.20-rc2, and save me the effort?
Actually, correction: it'd be correct if you ripped out the buggy
calls to manage the irq wake mechanism. A later message will show
how those need to work. (The IRQ framework will give one helpful
hint when it warns about mismatched enable/disable calls ...)
- Dave
10-2006
iPAQ h3600 - patch for 2.6.19
From: Alessandro GARDICH <gremlin_at_gremlin.it>
Date: Sun, 10 Dec 2006 18:07:13 +0100
Hi all
With this patch also h3600 will compile and run kernel 2.6.19
- irq calling loose registers parameter
- platform device/driver in h3600_lcd
- minor cleanup
see u soon
Re: Funky breakage with w100fb imageblit patch
* This message: [ Message body ] [ Respond ] [ More options ]
* Related messages: [ Next message ] [ Previous message ] [ In reply to ] [ Next in thread ]
From: Manuel Teira <manuel.teira_at_telefonica.net>
Date: Sun, 10 Dec 2006 20:54:32 +0100
A fast note about performance:
It seems that the performance problem is not the imageon itself. After
one of my tests, I found in my dmesg lines like:
<4>Alignment trap: font (1269) PC=0x4002f9f4 Instr=0xe592c000 Address=0x00012726 FSR 0x013
The problem is the font itself: as any character is 14 bytes (for the
7x14 font) not all the char pointers fall in a word boundary and so,
we're forcing the cpu to correct the missalignment.
I have a little libw100 test program, to fill the screen with a given
text. This is what I got when I use a nonaligned char, like "1":
root_at_c7x0:/media/card/libw100/bin$ ./font 0 1 "1"
Written 3094 characters in 19 seconds. Rate: 162.422116 cps
And using an aligned one, like "2":
root_at_c7x0:/media/card/libw100/bin$ ./font 0 1 "2"
Written 3094 characters in 0 seconds. Rate: 16563.169165 cps
This is like the performance I got using the 8x16 font, so, the problem
seems to be the misalignment of the font, and not the imageon itself.
Regards.
El dom, 10-12-2006 a las 19:33 +0100, Manuel Teira escribió:
> El dom, 10-12-2006 a las 19:29 +0200, Paul Sokolovsky escribió:
> > Hello Manuel,
> >
> > Sunday, December 10, 2006, 11:26:45 AM, you wrote:
> >
> > > Hello.
> >
> > > After a fast review of the code, I think that the problem could be
> > > caused by an error in the w100_hostdata function, while calculating the
> > > amount of data entries needed to feed the data to the card. At the
> > > beginning of that function, the line:
> >
> > > u32 left = width * height * depth / 32;
> >
> > > is just giving 0 entries for one of your 4x6 characters, neither for non
> > > 8 bit multiples. This can likely be the cause of the hangs.
> >
> > > Please, could you try changing that line with:
> >
> > > u32 left = width * height * depth / 32 + (((width * height * depth) %
> > > 32) ? 1 : 0);
> >
> > Just in case, "(width * height * depth + 31) / 32" would be more
> > canonical way to express that, no? ;-)
>
> Yes. Better and more compact. ;-)
>
> >
> > > and try without applying your patch for checking the dimensions of the
> > > image?
> >
> > Ok, I tried. It draws characters now, but in rather distorted form,
> > mostly. It appears that either some special alignment of bitmaps is
> > required (unlikely, as some substrings of different lengths are
> > rendered properly), or there's some internal counter misinitialized,
> > which causes slant and corruption. I made an fb shot:
> > http://handhelds.org/~pfalcon/w100fb-7x14fon-corrupt.png
> >
>
> Thanks for the screenshot. I think that the problem is related with how
> data is packed into the font bitmaps. The former calculation is
> supposing that the data is packed, and a font scanline is using just the
> bits it needs. So, for example, for a 4x6 character, the function is
> thinking that any scanline is only 4 bits, but perhaps it's padded to
> expand to a byte boundary. Anyway, the screenshot is really funny,
> because it seems that, as you say, always a set of adjacent chars (and
> not always the same length) are drawn correctly.
>
> I've just made some test with that same 7x14 font and I managed it to
> render correctly. I've just changed the patch to always assume that the
> data scanlines are aligned to byte boundaries. I've also made the
> counterpart changes in libw100 and made some tests. It seems to draw
> correctly, but perfomance is worse than for a 8x16 font.
>
> I'm attaching a new w100-extaccel.patch with the changes.
>
> Regards.
rework has been re-started at 03-2009
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Coffee County, GeorgiaEdit This Page
From FamilySearch Wiki
United States Georgia Coffee County
Guide to Coffee County Georgia genealogy. Birth records, marriage records, death records, census records, family history, and military records.
Georgia
Online Records
Coffee County, Georgia
Map
Location of Georgia in the U.S.
Facts
Founded February 9, 1854
County Seat Douglas
Courthouse
Address Coffee County Courthouse
101 So Peterson Avenue
Douglas, GA 31533
Phone: 912.384.4799
Coffee County Website
Contents
Coffee County Georgia Courthouse
Clerk Superior Court has divorce and land recors from 1854
and some military discharge records from 1919; Probate Court
has marriage and probate records; County Health Department
has birth and death records[1]
Coffee County Georgia History
Local histories are available for Coffee County, Georgia. County histories may include biographies, church, school and government history, and military information. For more information about local histories, see the wiki page section Georgia Local Histories.
Parent County
1854--Coffee County was created 9 February 1854 fromClinch, Irwin, Telfair andWare Counties.
County seat: Douglas [2]
Boundary Changes
Record Loss
1898 and 1938 -- Courthouse burned and many records were damaged.
For further information on researching in burned counties, see the following:
Coffee County Georgia Places/Localities
Populated Places
Neighboring Counties
Coffee County Georgia Genealogy Resources
Cemeteries
Church
LDS Ward and Branch Records
• Douglas
Court
Land
Land and property records can place an ancestor in a particular location, provide economic information, and reveal family relationships. Land records include: deeds, abstracts and indexes, mortgages, leases, grants and land patents.
See Georgia Land and Property for additional information about early Georgia land grants from the government. After land was transferred to private ownership, subsequent transactions (generally buying and selling deeds) were usually recorded at the county courthouse and where records are currently housed.
Local Histories
• Ward, Warren P. Ward's History of Coffee County: A Story Dealing with the Past and Present of Coffee County, Beginning with the Early Settlers about the Year 1800, Discussing the Creek Indians and the Pioneers, Leading Up to the Creation of Coffee County in 1854, Old Families, Old Schools and Churches, Showing the Conditions During the Civil War and Ending Up with the Spirit of Progress, which is Evident in Better Schools, and a More Intelligent Civilization: Showing that Coffee County in South Georgia is God's Country and a Good Place to Live in the Year 1930.. Atlanta: Press of Foote & Davies Co., c1930. Digital version at Ancestry ($).
Maps
Military
Newspapers
Newspapers Extracts and Abstracts
Newspapers abstracts can sometimes be found using search phrases such as Coffee County, Georgia newspapers in online catalogs like:
Probate
Taxation
Taxes were levied on free white males over 21 and slaves aged 21 to 60. These persons are referred to as "polls." Tax listings, or digests, of a county generally list the taxable landowners and other polls and the amount of tax. The records for each county are divided by militia district.
Vital Records
Colonial courts kept some early probate records. From 1777 to 1798 and since 1852, the court of ordinary or register of probates has kept probate and guardianship records. The inferior court handled probate and guardianship matters from 1798 to 1852.
Many probate records to the 1930s and 1940s are at the Georgia Department of Archives and History and the Family History Library on microfilm.
Content: Probate Records may give the decedent's date of death, names of his or her spouse, children, parents, siblings, in-laws, neighbors, associates, relatives, and their place of residence.
Record types: Wills, estates, guardianships, naturalizations, marriage, adoption, and birth and death records (not all years).
Marriage
• 1871-1897 - Coffee County Marriage Index 1871-1897. Batch M723491 at FamilySearch - free.[3]
• 1885-1904 - Coffee County Marriage Index 1885-1904. Batch M723492 at FamilySearch - free.[3]
Death
• 1859-60, 1879-80 - Coffee County, Georgia Mortality Schedules at Ancestry ($).
Coffee County Georgia Genealogy Societies and Libraries
Family History Centers
Coffee County Georgia Genealogy Websites
Coffee County Georgia Genealogy References
1. Handybook for Genealogists: United States of America, 10th ed. (Draper, Utah: Everton Pub., 2002), Coffee County, Georgia. Page 153 At various libraries (WorldCat); FHL Book 973 D27e 2002.
2. The Handybook for Genealogists: United States of America,10th ed. (Draper, UT:Everton Publishers, 2002).
3. 3.0 3.1 Genealogical Society of Utah, Parish and Vital Records List (July 1998). Microfiche. Digital version at https://www.familysearch.org/learn/wiki/en/images/0/09/Igigeorgiaad.pdf.
Need additional research help? Contact our research help specialists.
Need wiki, indexing, or website help? Contact our product teams.
Did you find this article helpful?
You're invited to explain your rating on the discussion page (you must be signed in).
• This page was last modified on 18 May 2013, at 02:12.
• This page has been accessed 1,630 times.
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Bristol Parish, VirginiaEdit This Page
From FamilySearch Wiki
Revision as of 22:41, 9 February 2011 by Murphynw (Talk | contribs)
United States Virginia Bristol Parish
Contents
History
Bristol Parish has served Charles City, Henrico, Prince George, Dinwiddie counties.
Founded
Boundary
Resources
Parish History
Parish Records
References
1. Freddie Spradlin, "Parishes of Virginia," VAGenWeb, accessed 29 January 2011; Hening's Statutes at Large; Emily J. Salmon and Edward D.C. Campbell Jr., The Hornbook of Virginia History (Richmond: Library of Virginia, 1994).
Need additional research help? Contact our research help specialists.
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Research
Genomic features of Bordetella parapertussis clades with distinct host species specificity
Mary M Brinig1,2*, Karen B Register3, Mark R Ackermann4 and David A Relman1,2,5
Author Affiliations
1 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA
2 VA Palo Alto Health Care System, Palo Alto, California 94304, USA
3 USDA/ARS/National Animal Disease Center, Respiratory Diseases of Livestock Research Unit, Ames, Iowa 50010, USA
4 Department of Veterinary Pathology, Iowa State University, Ames, Iowa 50011, USA
5 Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
For all author emails, please log on.
Genome Biology 2006, 7:R81 doi:10.1186/gb-2006-7-9-r81
Published: 6 September 2006
Abstract
Background
The respiratory pathogen Bordetella parapertussis is a valuable model in which to study the complex phenotype of host specificity because of its unique two-species host range. One subset of strains, including the sequenced representative, causes whooping cough in humans, while other strains infect only sheep. The disease process in sheep is not well understood, nor are the genetic and transcriptional differences that might provide the basis for host specificity among ovine and human strains.
Results
We found 40 previously unknown genomic regions in an ovine strain of B. parapertussis using subtractive hybridization, including unique lipopolysaccharide genes. A microarray survey of the gene contents of 71 human and ovine strains revealed further differences, with 47 regions of difference distinguishing the host-restricted subgroups. In addition, sheep and human strains displayed distinct whole-genome transcript abundance profiles. We developed an animal model in which sheep were inoculated with a sheep strain, human strain, or mixture of the two. We found that the ovine strain persisted in the nasal cavity for 12 to 14 days, while the human strain colonized at lower levels and was no longer detected by 7 days post-inoculation. The ovine strain induced less granulocyte infiltration of the nasal mucosa.
Conclusion
Several factors may play a role in determining host range of B. parapertussis. Human- and ovine-associated strains have differences in content and sequence of genes encoding proteins that mediate host-pathogen contact, such as lipopolysaccharide and fimbriae, as well as variation in regulation of toxins, type III secretion genes, and other virulence-associated genes.
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An unofficial blog that watches Google's attempts to move your operating system online.
Send your tips to [email protected].
March 21, 2008
Google Analytics Benchmarks
Two weeks ago, Google Analytics added a new feature that lets you compare your site's traffic with average data for other similar sites. To make this feature possible, you need to enable data sharing with the benchmarking service. "Google will remove all identifiable information about your website, then combine that data with hundreds of other anonymous sites in comparable industries and report them in an aggregate form." There's also an option to enable data sharing with other Google services that will allow a better integration between Analytics, AdWords and other services.
The benchmarking data is now live and you can see it if you go to Visitors > Benchmarking (Beta). Google compares the following values for the last 30 days: visits, page views, pages/visit, bounce rate, average time on site and new visits. By default, your site is compared with other sites of similar size, but you can restrict the benchmark to general categories like: Internet, Travel, Shopping, Reference etc. Since the data is aggregated from the sites that agreed to participate in the program, it may not be representative. Google says it will add new categories once more sites will enable the data sharing option.
"When benchmarking is enabled, Google crawls the websites in the account then categorizes them by vertical and the amount of visits. The data is then made anonymous through aggregation. For sites of a similar size, a category of industry verticals can be chosen when there is a sufficient number of accounts in that category."
It's interesting to compare your site's traffic with these aggregate data as it will help you put things in perspective, but you shouldn't be disappointed if the comparison is not favorable. Each site is unique and has a different raison d'être.
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My apologies for all of the gaming posts recently, but I wanted to let any World of Warcraft players know that we are starting a new all-Orc guild on Khadgar. We plan to run every Saturday evening US time, Sunday morning Japan time. Each run will start approximately at 6PM Eastern, 3PM Pacific, 7AM Japan time. We'll start today. I'm just setting up the guild now.
The guild will be called "We Orc" and is the Horde affiliate of "We Know".
We'll play only once a week and anyone who misses a run can try to catch up to the level that we all go to during the run. We'll post the current level on the wiki. The idea is to try to see whether and how much more fun it is to have everyone at the same level collaborating.
My Orc character is named "Tasmanian". Whisper me if you want to join. I'll be hanging out at the spawn point to rendezvous with the new characters. Orcs all the way down... see you there.
UPDATE: Until we get the guild going, do a "/join weorc" to join the chat channel.
UPDATE: We got the guild started. Thanks! Here's a group photo.
About this Archive
This page is an archive of recent entries in the Business and the Economy category.
Books is the previous category.
Computer and Network Risks is the next category.
Find recent content on the main index.
Monthly Archives
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Changes between Version 25 and Version 26 of Changelog
Ignore:
Timestamp:
May 3, 2012 8:57:15 AM (13 months ago)
Author:
Don-vip
Comment:
my svncomment was bad for r5185, it's of course scrollable now :)
Legend:
Unmodified
Added
Removed
Modified
• Changelog
v25 v26
1616 * Allow MapCSS to style right and left side casings differently (r5206)
1717* sub-minor enhancements
18 * Non-scrollable menu for Imagery offset (r5185)
18 * Scrollable menu for Imagery offset (r5185)
1919 * remote control: increase the possible request size (from 1KiB to 1MiB) (r5189)
2020 * Style: icons for building entrances (r5190)
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Restriction digest
From OpenWetWare
Jump to: navigation, search
Contents
General Information
Restriction digest involves the cutting of DNA at specific recognition sequences by enzymes.
General Procedure
Specific Protocols
Enzyme selection for BioBricks digest
Endy:Restriction Digest
Knight:Restriction Digest
Silver: Restriction Digest
Griffitts:Restriction digest
Richard Lab:Restriction Digest
Notes
• For help with specific enzymes, see Restriction enzymes
• For buffer composition, see Restriction digest/Buffers
• If you are interested in cutting near the ends of the linear DNA fragment, note that some enzymes do not cut efficiently at the ends of linear DNA. So include extra bases to increase the efficiency of cutting. Many enzymes work with 4 bases supposedly but XhoI was found to require more than 4 bases (8 bases was used successfully). Thus, to be on the safe side, use 8 bases whenever possible. NEB has more information here. Read the information at NEB carefully ... they recommend adding 4 bases to the numbers listed in their table.
• Tom was once having some trouble with failed restriction digests. He called NEB and they recommended doing the digest in a larger volume. Therefore, the Knight lab typically does digests in either 50 μL or 100 μL volumes rather than the 20 μL volume that the Endy lab uses. If the sample needs to be concentrated, some method of DNA purification is used.
Personal tools
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Quotation added by staff
Why not add this quote to your bookmarks?
Don't be dismayed at good-byes. A farewell is necessary before you can meet again. And meeting again, after moments or lifetimes, is certain for those who are friends. Bach, Richard
This quote is about farewells · Search on Google Books to find all references and sources for this quotation.
A bit about Bach, Richard ...
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Revision history of "Thread:User talk:WaitingforGodot/"No such thing as atheists."/reply (14)"
Jump to: navigation, search
Diff selection: Mark the radio boxes of the revisions to compare and hit enter or the button at the bottom.
Legend: (cur) = difference with latest revision, (prev) = difference with preceding revision, m = minor edit.
Personal tools
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Community
Toolbox
support
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The Truth: “… we’re going to win it all.”
Chuck - Red's Army September 25, 2009 Uncategorized 46 Comments
Via Marc Spears of Yahoo! Sports:
“Before the season even started last year, I was asked, ‘What is
going to stop y’all from winning it all?’ ” Pierce said in a phone
interview on Thursday. “The first thing I said was, ‘If we’re healthy,
we’re going to win it all.’ And I’m going to say it again: ‘If we are
healthy, we are going to win it all.’
“I honestly believe that. I think we’re the best team in the NBA, healthy.”
Anyone have an issue with his bold statement? I sure don't, because he's right. I'm sure these commits well upsit a lot of Lakerz fanz (the mere thought of our Laker trolls and their stupidity dilutes my intelligence), but we can't expect them to admit the truth.
Pierce also said Kevin Garnett played "a couple of days" last week:
“It wasn’t like he was out there [screaming] and dunking,” Pierce said. “No, none of that. But he was out there on the court.”
And one other thing; don't bring up the 2008 championship:
“When someone brings it up, I don’t want to hear it. That’s in the past.”
Like this Article? Share it!
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(Roughly) Daily
“I hope I die before I get old (Talkin’ ’bout my generation)”…
From illustrator Bruce Worden and writer Clare Cross, a children’s classic for the new millennium (albeit, about the last one), Goodnight Keith Moon.
[TotH to Tyler Hellard, aka Pop Loser]
###
As we prepare to explore the teenage wasteland, we might spare a thought for Sophia Cecelia Kalos (who later became much better known by her stage name, Maria Callas); she died on this date in 1977. The pre-eminent bel canto soprano of the Twentieth Century, Callas was known by her legion of fans as “La Divina,” (“The Goddess”), a superlatively-specific appropriation of the approbation reserved by opera aficionados for the very finest female singers. The term “diva” (while it dates back to the late Nineteenth Century as a descriptor of a “fine lady”), emerged among Callas’ following as a shorthand for “divina”– making her the first singer who was a diva.
source
Written by LW
September 16, 2012 at 1:01 am
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"A REALLY INTELLIGENT INTERVIEWER." -- Lance Henriksen
"QUITE SIMPLY, THE BEST HORROR-THEMED BLOG ON THE NET." -- Joe Maddrey, Nightmares in Red White & Blue
**Find The Vault of Horror on Facebook and Twitter, or download the new mobile app!**
**Check out my other blogs, Standard of the Day, Proof of a Benevolent God and Lots of Pulp!**
Tuesday, November 10, 2009
Barnes & Noble Lets You Talk to Anne Rice
Barnes & Noble will be doing something very special tomorrow for fans of the most important vampire novelist since Bram Stoker. And yes, I'm talking about Anne Rice, not what's-her-name. The author of Interview with the Vampire, Queen of the Damned and the rest of the Vampire Chronicles, as well as the Witches of Mayfair series and many other books, will be stopping by B&N's Facebook page tomorrow to chat online with her fans.
The live chat will take place from 1pm-5:30pm EST. Visitors must go to this thread link to participate. For more info on the event itself, the Facebook event page is right here.
Rice is promoting her new novel, Angel Time, which is the beginning of her new Songs of the Seraphim series. The series looks to be a combination of her past in thrillers and her more recent religious-themed work.
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Help Wikitravel grow by contributing to an article! Learn how.
Saint-Pierre (Martinique)
From Wikitravel
Jump to: navigation, search
Saint-Pierre is a community of about 5,000 people in on the island of Martinique. The settlement was wiped out in 1902 by the volcano Mount Pelée.
[edit] Get in
[edit] Get around
[edit][add listing] See
• Volcano Museum, (Musée Vulcanologique)
[edit][add listing] Do
• Scuba dive at wrecks in the harbor. During the 1902 volcanic eruption, all but one of the ships in the harbor sunk, leaving many wrecks as dive sites.
[edit][add listing] Buy
[edit][add listing] Eat
[edit][add listing] Drink
[edit][add listing] Sleep
[edit] Contact
[edit] Get out
This article is an outline and needs more content. It has a template, but there is not enough information present. Please plunge forward and help it grow!
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Catalogue Number
6281.0 - Work in Selected Culture and Leisure Activities, Australia, Apr 2007
Latest ISSUE Released at 11:30 AM (CANBERRA TIME) 19/12/2007 Final
Page tools: Print Page Print All RSS Search this Product
NOTES
ABOUT THIS PUBLICATION
This publication presents results from the Survey of Work in Selected Culture and Leisure Activities, conducted in April 2007. It presents information on the number and basic demographic characteristics of persons involved in paid or unpaid work in selected culture and leisure activities over a 12 month period.
Information about hobby activities is included only in Table 12. All other information in this publication relates to persons involved in culture and leisure activities for other than their own, family's or friends' use.
ABOUT THIS SURVEY
The 2007 Survey of Work in Selected Culture and Leisure Activities was conducted throughout Australia as part of the Australian Bureau of Statistics' (ABS) Monthly Population Survey (MPS). The survey was previously conducted in 1993, 1997, 2001 and 2004.
Data from those years are included in some tables for comparative purposes. The survey collected information on the types of activities undertaken, the time spent on activities, whether any payment was received, the amount of payment received, and whether those activities were part of the person's main job. The survey also asked about relevant qualifications for selected culture and leisure acvitivies. For a list of the culture and leisure activities included in the survey, refer to the Glossary.
Unless otherwise specified, differences between data items highlighted in the Summary of Findings are statistically significant. See Technical Note (paragraphs 15 to 17) for further details.
ROUNDING
As estimates have been rounded, discrepancies may occur between sums of the component items and totals.
INQUIRIES
For further information about these and related statistics, contact the National Information and Referral Service on 1300 135 070.
SUMMARY COMMENTARY
INTRODUCTION
During the 12 months prior to April 2007, an estimated 3.5 million (22%) of Australians aged 15 years and over were involved in some form of paid or unpaid work relating to the selected culture and leisure activities covered in the survey. (Table 1) The overall participation rate for persons involved in culture and leisure activities increased from 17% in 2004 to 22% in 2007. (Table 14) Since 2001 the number of persons involved in culture and leisure activities increased by 52% from 2.3 million. (Table 13) Persons undertaking hobby activities for their own, family's or friends' use, or who only attended culture and leisure events, are not included in these figures.
CHARACTERISTICS OF PERSONS INVOLVED
Sex
Overall, while a higher percentage of females (24%) than males (19%) aged 15 years and over worked in a culture or leisure field, the participation rates for paid involvement were similar for males and females (7%). Females had a higher rate of unpaid involvement than males, with 17% of females (1.4 million) having unpaid involvement only, compared with 12% of males (1 million). (Table 2)
PARTICIPATION RATE, By sex
Age
Involvement in culture and leisure activities was lowest in the oldest age group, with 15% of those aged 65 years and over participating. In comparison, the participation rate for those aged 15 to 24 years was 25%, and for those aged 25 to 34 years was 23%. (Table 2)
PARTICIPATION RATE, By age
The proportion of people with paid involvement in culture and leisure activities was highest for those aged 25 to 34 years (9%), 35 to 44 years (8%) and 45 to 54 years (8%). Unpaid involvement only was highest for persons aged 15 to 24 years (19%). (Table 2)
Birthplace
Persons born in Australia had a participation rate of 23%, compared with 18% for persons born overseas. Persons born overseas in main English speaking countries had a similar rate (25%) to that for those born in Australia, while those born overseas from other than main English speaking countries had a participation rate of 14%. Of those born in Australia, 7% received some payment for working in a culture or leisure activity, compared with 5% for those born overseas. (Table 2)
Geographic location
The participation rates for the states and territories ranged from 21% for New South Wales to 30% for the Australian Capital Territory. (Table 1)
The participation rate for residents in the state capital cities (21%) was similar to that for residents outside the state capital cities (22%). However, there was a difference in rates for paid and unpaid involvement, with 7% of persons in the state capital cities reporting a paid involvement compared with 5% for those outside the state capital cities. Persons outside the state capital cities had a higher rate of unpaid only involvement - 17% compared with 14% for persons in the state capital cities. (Table 2)
PARTICIPATION RATE, By state or territory
The participation rate increased since 2004 for all the states and territories except the Australian Capital Territory. The largest increase was observed in the Northern Territory (57%) followed by Tasmania (37%). (Table 14)
Labour force status
Of persons who were employed in the week prior to interview, 24% (or 2.5 million persons) were involved in a culture or leisure activity at some time during the 12 months prior to interview. Unemployed persons and those not in the labour force had participation rates of 21% (100,700 persons) and 17% (928,200 persons), respectively. Persons employed part-time (28%) had a higher participation rate than persons employed full-time (23%). (Table 2)
TYPE OF ACTIVITIES
Information was collected for a variety of culture and leisure activities in this survey (see the Glossary for a full list of activities).
Some 1.4 million persons had an involvement in visual art activities in the previous 12 months. This represents an increase of 79% from 2004 when there were 789,900 persons reporting an involvement in visual art activities. (Table 13)
In 2007, large numbers of persons reported involvement in the following visual art activities:
638,600 in photography (300,100 in 2004)
558,000 in drawing (288,700 in 2004)
552,500 in creating artworks with a computer (286,300 in 2004)
463,000 in painting (262,400 in 2004). (Table 13)
In 2007, there were 960,800 persons (or 27% of all persons involved) who had an involvement in craft activities. In comparison, there were 542,700 persons (or 20% of all persons involved) who reported an involvement in craft activities in 2004. The craft activities attracting large numbers of participants in 2007 were furniture-making and wood crafts (316,800 persons, up from 204,500 in 2004) and textiles (282,400 persons, up from 144,300 in 2004). (Table13)
Other activities with large numbers of persons involved in 2007 were:
506,300 in performing arts, an increase of 19% from 2004
459,200 in design, an increase of 24% from 2004
409,800 in festival organising, an increase of 62% from 2004
335,100 in music, with no statistically significant change from 2004
606,500 in writing, with no statistically significant change from 2004. (Table 13)
Patterns of involvement in particular culture and leisure activities were quite different for males and females. During 2007, there were more males than females involved in furniture-making and wood crafts (266,000 males compared with 50,800 females), designing websites (165,000 and 89,200), and designing computer games and other interactive software (62,600 and 12,800). Females outnumbered males by more than two to one for the activities of art and craft show organising (149,600 females compared with 50,300 males), performing arts (345,000 and 161,200), painting (335,300 and 127,700) and library and archive involvements (78,200 and 30,300). A noticeably higher number of females than males were also involved in craft activities (628,800 females compared with 332,100 males) and cultural teaching activities (154,800 and 101,900), which excludes primary and secondary school teaching. (Table 3)
PERSONS INVOLVED, In 5 most popular activities, By sex
NATURE OF INVOLVEMENT
Payment status
More people had some paid involvement in visual art activities (281,900), design (279,800) and writing (240,700) than any other culture or leisure activity in the survey (note: paid involvement also includes persons who received goods and services as payment). Cinema and video distribution (64%) was among the activities with the highest proportion of persons involved receiving payment, along with zoos and aquaria (62%), design (61%), and television (56%). (Table 4)
Of the 1.1 million persons who received some payment, 39% were paid less than $5,000 over the year, 26% were paid between $5,000 and $39,999 and 24% were paid $40,000 or more. (Table 8)
The proportion of people being paid for their involvement has decreased from 35% in 2004 to 30% in 2007. (Table 14)
PARTICIPATION RATE 2004 and 2007, By payment status
Duration of activities
Most people involved in culture and leisure activities had only a short-term involvement (up to 13 weeks of the year) or were involved for less than 10 hours per week over the 12 month period. For all activities except architecture, the majority of persons were involved for less than 10 hours per week. The activities with the highest proportion of persons involved for less than 10 hours per week were photography (91%), jewellery making (88%), painting (87%), and drawing (87%). (Table 9)
The activities that were most likely to be short-term were festival organising (81%), art and craft show organising (81%), national parks and reserves (72%) and television (72%). Architecture was one activity which tended to have involvements of a longer duration. Around 67% of persons involved in architecture did so for 10 hours or more per week and 69% of persons involved in architecture did so for more than 13 weeks of the year. (Table 9)
Income from activities
Annual income from culture and leisure activities was reasonably low because most people involved in culture and leisure activities had only a short-term or part-time involvement. For example, of the 118,800 persons with paid involvement in music, almost two-thirds (74,600 or 63%) received an annual income from this activity of less than $5,000. Conversely, 22,500 (63%) persons received an annual income of $5,000 or more from their paid involvement in libraries and archives. (Table 7)
Involvement as part of main job
Of the 1.1 million persons who received some payment for their involvement in culture and leisure activities, 66% (701,800 persons) stated their involvement was part of their main job they held last week. The activities with the highest proportion of persons where the activity was part of their main job held last week, were museums (8,400 persons or 86%), pottery and ceramics (14,400 or 85%), designing computer games and other interactive software (33,500 or 84%) and print-making (21,800 or 84%). (Table 6)
QUALIFICATIONS
People involved in selected activities (visual art, craft, writing, publishing, performing arts, music, designing websites, designing computer games and design) were asked whether they had qualifications relevant to these activities. Of the 3.1 million persons involved in these activities, 30% had relevant qualifications. The most commonly reported areas where persons had relevant qualifications were design (185,800) and writing (150,200), while fewer persons had relevant qualifications for activities such as glass crafts (8,800) and pottery and ceramics (20,200). Higher proportions of persons who had relevant qualifications were paid for their involvement (53%) than those without relevant qualifications (22%). (Table 11)
HOBBIES
Activities which were undertaken solely for the person's own use or for the use of their family or friends were classified as hobby activities. For this survey, data on hobby activities were only collected for art and craft, writing and music.
Around 2.0 million persons had a work involvement in arts and crafts, 606,500 had a work involvement in writing, and 335,100 in music. These figures include persons with both a work and hobby activity involvement. In addition, there were 2.1 million persons who were involved in art and craft as a hobby activity only, 356,900 persons were involved in writing as a hobby activity only, and 265,000 persons were involved in music as a hobby activity only. (Table 12)
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Topic > Culture and Leisure
Statistics by Topic
Participation in Culture Sport and Leisure
A Directory of Education and Training Statistics, 2009 (cat no. 1136.0)
Aboriginal and Torres Strait Islander Australians: Involvement in Arts and Culture, 2001 and 2002 (cat no. 4721.0)
Arts and Culture in Australia: A Statistical Overview, 2012 (cat no. 4172.0)
Australian Social Trends, April 2013 (cat no. 4102.0)
Children's Participation in Cultural and Leisure Activities, Australia, Apr 2012 (cat no. 4901.0)
Children's Participation in Sport and Leisure Time Activities, 2003 - 2012 (cat no. 4901.0.55.001)
Culture and Recreation News, Mar 2013 (cat no. 4147.4.55.001)
General Social Survey: States and Territories, 2010 (cat no. 4159.0.55.003)
Information Paper: Arts and Cultural Heritage - An Information Development Plan, 2008 (cat no. 4915.0.55.002)
Information Paper: Defining Sport and Physical Activity, A Conceptual Model, 2008 (cat no. 4149.0.55.001)
Involvement in Organised Sport and Physical Activity, Australia, April 2010 (cat no. 6285.0)
Labour Statistics: Concepts, Sources and Methods, 2013 (cat no. 6102.0.55.001)
Measures of Australia's Progress, 2010 (cat no. 1370.0)
Measures of Australia's Progress: Summary Indicators, 2009 (cat no. 1383.0.55.001)
Microdata: General Social Survey, CURF, Australia, 2010 (cat no. 4159.0.30.003)
Microdata: Multipurpose Household Survey, Expanded CURF, Australia, 2008-09 (cat no. 4100.0.55.001)
Microdata: National Aboriginal and Torres Strait Islander Social Survey, Expanded CURF, 2008 (cat no. 4720.0.55.001)
Microdata: Participation in Sport and Physical Recreation, Australia, 2011-12 (cat no. 4177.0.55.002)
National Aboriginal and Torres Strait Islander Social Survey, 2008 (cat no. 4714.0)
National Aboriginal and Torres Strait Islander Social Survey, Australia, 2002 (cat no. 4714.0.55.001)
National Aboriginal and Torres Strait Islander Social Survey, Australia: Summary Booklet, 2008 (cat no. 4714.0.55.003)
National Aboriginal and Torres Strait Islander Social Survey: Users' Guide, 2008 (cat no. 4720.0)
NSW State and Regional Indicators, Dec 2010 (cat no. 1338.1)
Participation in Selected Cultural Activities, Australia, 2010-11 (cat no. 4921.0)
Participation in Sport and Physical Recreation, Australia, 2011-12 (cat no. 4177.0)
Public Attitudes to the Arts, Australia, Nov 1997 (cat no. 4157.0)
Spectator Attendance at Sporting Events, 2009-10 (cat no. 4174.0)
Sport and social capital, Australia, 2010 (cat no. 4917.0)
Sports and Physical Recreation: A Statistical Overview, Australia, 2012 (cat no. 4156.0)
Statistics Victoria, Jun 2011 (cat no. 1100.2)
Technical Manual: Multipurpose Household Survey, Expanded CURF, Australia, 2008-09 (cat no. 4100.0)
Technical Manual: Participation in Sport and Physical Recreation, Expanded CURF, Australia, 2009–10 (cat no. 4177.0.55.001)
The Health and Welfare of Australia's Aboriginal and Torres Strait Islander Peoples, Oct 2010 (cat no. 4704.0)
Time Use on Recreation and Leisure Activities, 2006 (cat no. 4173.0)
Work in Selected Culture and Leisure Activities, Australia, Apr 2007 (cat no. 6281.0)
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Beaufort Sea
Oceans and seas:
Beaufort Sea
This article has been reviewed by the following Topic Editor: C Michael Hogan
The Beaufort Sea is a marginal sea consisting of the waters off the northern coast of Alaska and Canada.
This is bounded to the east by Banks Island of the Canadian Arctic Archipelago and on the west by the Chukchi Sea.
The bathymetric characteristics include the narrowest continental shelf found anywhere in the Arctic Ocean. This shelf is dissected by three submarine valleys, the largest of which is 45 kilometers wide, and drops off rapidly to the Beaufort Deep, whose maximum depth is 3940 meters (m).
Source: Wikimedia Commons
Although it is geographically identified as a separate entity, the Beaufort Sea is oceanographically an integral part of the Arctic Ocean and as such cannot be described in isolation.
Hydrography
Substantially different circulation regimes are found on the inner and outer shelf regions, with the demarcation line corresponding approximately to the 50 m isobath. The inner shelf is strongly wind driven in summer, with a westward water motion driven by the prevailing easterly winds. This circulation varies seasonally, responding rapidly to large changes (including even an occasional reversal in prevailiing wind direction), and is far less energetic in the winter (with wind effects persisting even under the fast ice close to the shore). The outer shelf circulation is energetic at subtidal frequencies throughout the year, with the dominant feature being the Beaufort Undercurrent, a bathymetrically steered mean eastward flow extending from around the 50 m isobath to at least the base of the continental slope. This relatively strong current apparently increases with depth to around 10 centimeters per second (cm s−1), and is probably not locally driven but rather part of the large scale circulation in the Canadian Basin, although the portion of the Undercurrent overlying the shelf can be modified by local wind forcing. Frequent cross–shelf motions are found near the inshore edge of the Undercurrent, with daily means exceeding five cm/sec and durations typically three days or more. These serve to transport materials between the inner and outer shelf regions.
The most prominent hydrographic feature on the shelf is a subsurface summer temperature maximum generally found seaward of around 40–50 m depth which disappears during the winter. This is associated with an eastward flow of water originating in the Bering Sea. The warm water enters via the eastern Bering Strait and follows the Alaskan coast around Point Barrow. It is composed of two water masses called Alaskan Coastal Water (ACW) and Bering Sea Water (BSW). The ACW has summer temperatures of five to ten degrees Celsius (C) west of Barrow with salinities less than 31.5. It mixes rapidly with local surface water as it moves eastward and is not clearly identifiable east of around 147 to 148 degrees W. The BSW is more saline and has a density range from 25.5–26.0 σt, and can be traced as far east as Barter Island at 143 degrees W.
See Also
Further Reading
• Rhodes W. Fairbridge, editor. The Encyclopedia of Oceanography. Van Nostrand Reinhold Co., 1966.
• Knut Aagaard. The Beaufort Undercurrent. In P. W. Barnes, D. M. Schell, and E. Reimnitz, editors, The Alaskan Beaufort Sea, pages 47–71. Academic Press, Inc., 1984.
Citation
Steve Baum (Lead Author);Peter Saundry (Contributing Author);C Michael Hogan (Topic Editor) "Beaufort Sea". In: Encyclopedia of Earth. Eds. Cutler J. Cleveland (Washington, D.C.: Environmental Information Coalition, National Council for Science and the Environment). [First published in the Encyclopedia of Earth March 30, 2010; Last revised Date May 14, 2013; Retrieved May 18, 2013 <http://www.eoearth.org/article/Beaufort_Sea?topic=49523>
The Author
Assistant Research Scientist, Physical Section Department of Oceanography Texas A&M University ... (Full Bio)
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Haiti Earthquake, January 12, 2010
Hazards & Disasters:
Haiti Earthquake, January 12, 2010
Damaged Haitian national palace, Port-au-Prince. Source: UN
This article has been reviewed by the following Topic Editor: C Michael Hogan
On January 12, 2010 at 4:53 p.m. local time, Haiti experienced a major earthquake of magnitude 7.0 on the Richter Scale, centered 10 miles (15 km) southwest of the capitol city of Port-au-Prince at a depth of 13 km (8.1 miles). (18.457°N, 72.533°W)
While the country experiences earthquakes frequently, this was the largest earthquake experienced by the island in over a century and occurred near a heavily populated area with few buildings designed or built to withstand significant earthquakes. The US Geological Survey (USGS) estimated that nearly three million people were exposed to severe shaking. Because the earthquake occurred inland, there was no related tsunami, however landslides related to the earthquake are expected.
According to official estimates by the Haitian government::
• 316,000 people were killed,
• 300,000 injured,
• 1.3 million displaced,
• 97,294 houses destroyed and 188,383 damaged in the Port-au-Prince area and in much of southern Haiti.
Other estimates suggest substantially lower numbers of casualties, perhaps as low as fewer than 100,000. The casualties include at least 4 people killed by a local tsunami in the Petit Paradis area near Leogane.
The United Nations Office for Coordination of Humanitarian Affairs estimated the fatalities at 222,570.
Background
Haiti occupies the western part of the Caribbean island of Hispaniola, one of the Greater Antilles islands, situated between Puerto Rico and Cuba. The eastern two-thirds of Hispaniola is occupied by the Dominican Republic. Much of the island of Hispaniola sits on the Gonave microplate, a small strip of the earth’s crust in the boundary region between two major tectonic plates - the Caribbean plate and the North America plate. The Caribbean plate is moving eastward with respect to the North America plate.
Two major east-west trending, "strike-slip fault systems" cross the island as shown in Figure 2. -- the Septentrional fault system to the north and the Enriquillo-Plaintain Garden fault system (EPGFZ) to the south. This earthquake occurred in the Enriquillo-Plaintain Garden fault system.
The Enriquillo-Plaintain Garden fault system is so named because it extends from the Enriquillo Valley of the Dominican Republic the east to the region of the Plantain Garden River in Jamaica to the west.The fault crosses the southern peninsula of Haiti, crosses the Jamaica Passage between the islands of Jamaica and Hispaniola and along the southern edge of the Blue Mountains of eastern Jamaica.
The Enriquillo-Plaintain Garden fault system marks the southern edge of the Gonave microplate. This fault system accommodates movement of about 7 mm/year, nearly half the overall motion between the Caribbean plate and North America plate.
The Enriquillo-Plaintain Garden fault system has not produced a major earthquake in recent decades. The EPGFZ is the likely source of historical large earthquakes in 1860, 1770, 1761, 1751, 1684, 1673, and 1618, though none of these has been confirmed in the field as associated with this fault.
According to French historian Moreau de Saint-Méry (1750–1819), "only one masonry building had not collapsed" in Port-au-Prince following an earthquake on 18 October 1751, while "the whole city collapsed" during the earthquake of 3 June 1770. Another earthquake destroyed the city of Cap-Haïtien and other towns in the north of Haiti and the Dominican Republic on 7 May 1842; this earthquake also destroyed the Sans-Souci Palace.[11] In 1946, a magnitude-8.0 earthquake struck the Dominican Republic and also shook Haiti, producing a tsunami that killed 1,790 people and injured many others.[12]
In 2008, a group led by Paul Mann of the University of Texas, noted the risk of a 7.2 earthquake if the strain built up in the fault were released in a single event. They reported:
The linearity of the fault and its association with en echelon folds, pull-apart basins, and restraining bends indicates that motion is left-lateral and late Quaternary in age. Historical earthquakes indicate that the last major ruptures of the fault occurred in an east to west time-space progression that began in 1751 in south-central Hispaniola and perhaps culminated in the Kingston, Jamaica , event in 1907. Recorded seismicity over the past 40 years is sparse as expected from a fully locked fault plane. GPS-constrained block models with elastic strain accumulation give ~8 mm/year of slip rate on the fault. Since the last major event in south-central Dominican Republic was in 1751, that yields ~2 meters of accumulated strain deficit, or a Mw=7.2 earthquake if all is released in a single event today. The two largest cities within 30 km of the fault zone are Port-au-Prince, Haiti , and Kingston, Jamaica , with a combined population of 3.65 million inhabitants. We present initial results from a paleoseismic study of the Jamaica segment of the EGPGFZ conducted in January, 2008, to determine the chronology of its historic and prehistoric ruptures. Such studies should be considered high priority in Jamaica, Haiti and the Dominican Republic given the seismic hazards posed by the fault.
Felt Reports
Figure 3. Source time function, describing the rate of moment release with time after earthquake origin. Source: Gavin Hayes, National Earthquake Information Center (NEIC), US Geological Survey
According to official estimates, 316,000 people killed, 300,000 injured, 1.3 million displaced, 97,294 houses destroyed and 188,383 damaged in the Port-au-Prince area and in much of southern Haiti. Other estimates suggest substantially lower numbers of casualties, perhaps as low as fewer than 100,000. The casualties include at least 4 people killed by a local tsunami in the Petit Paradis area near Leogane.
Tsunami waves were also reported at Jacmel, Les Cayes, Petit Goave, Leogane, Luly and Anse a Galets. The tsunami had recorded wave heights (peak-to-trough) of 12 cm at Santo Domingo, Dominican Republic and 2 cm at Christiansted, US Virgin Islands.
Uplift was observed along the coast from Leogane to L'Acul and subsidence was observed along the coast from Grand Trou to Port Royal.
Felt:
• (VIII - Severe) at Leogane, 29 km (18 mi) west of Port-au-Prince.;
• (VII - Very Strong) at Carrefour, Port-au-Prince and Petionville;
• (VI - Strong) at Vieux Bourg d'Aquin;
• (V - Moderate) at Port-de-Paix, La Vega, Moca and San Cristobal;
• (IV - Light) at Bani, Bonao, Luperon, Nagua, Puerto Plata, Santiago, Santo Domingo and Sosua, Dominican Republic, and at Santiago de Cuba
• (III -Weak) at Oranjestad, Aruba; at Guantanamo, Cuba; at Cockburn Harbour, Turks and Caicos Islands; and at Maracaibo, Venezuela
• (II) - Weak) in the Kingston-Mona area, Jamaica;at Carolina and San Juan, Puerto Rico; at Cockburn Town, Turks and Caicos Islands; and at Caracas, Venezuela.
• Felt in parts of The Bahamas, Puerto Rico and the US Virgin Islands and as far as southern Florida, northern Colombia and northwestern Venezuela.
Tectonic Summary
The January 12, 2010, Haiti earthquake occurred in the boundary region separating the Caribbean plate and the North America plate. This plate boundary is dominated by left-lateral strike slip motion and compression, and accommodates about 20 mm/y slip, with the Caribbean plate moving eastward with respect to the North America plate.
Haiti occupies the western part of the island of Hispaniola, one of the Greater Antilles islands, situated between Puerto Rico and Cuba. At the longitude of the January 12 earthquake, motion between the Caribbean and North American plates is partitioned between two major east-west trending, strike-slip fault systems -- the Septentrional fault system in northern Haiti and the Enriquillo-Plantain Garden fault system in southern Haiti.
The location and focal mechanism of the earthquake are consistent with the event having occurred as a combination of reverse and left-lateral strike slip faulting on the Enriquillo-Plantain Garden fault system. The overall Enriquillo-Plantain Garden fault system accommodates about 7 mm/y of motion, nearly half the total oblique convergence between the Caribbean and North America plates. The January 12 main shock did not produce observable surface displacement on the geomorphologically well-expressed main-strand of the Enriquillo-Plantain Garden fault system, but appears instead to have primarily involved rupture of a fault or faults distinct from the previously mapped principal strand, causing significant uplift of the Léogâne delta.
The Enriquillo-Plantain Garden fault system has not produced a major earthquake in recent decades. The EPGFZ is the likely source of historical large earthquakes in 1860, 1770, and 1751, though none of these has been confirmed in the field as associated with this fault.
Sequence of events possibly associated with the Enriquillo fault in 1751-1860 are as follows.
October 18, 1751: a major earthquake caused heavy destruction in the gulf of Azua (the eastern end of the Enriquillo Fault) which also generated a tsunami. It is unclear if the rupture occurred on the Muertos thrust belt or on the eastern end of Enriquillo Fault.
Nov. 21, 1751: a major earthquake destroyed Port-au-Prince but was centered to the east of the city on the Plaine du Cul-de-Sac.
June 3, 1770: a major earthquake destroyed Port-au-Prince again and appeared to be centered west of the city. As a result of the 1751 and 1770 earthquakes and minor ones in between, the authorities required building with wood and forbade building with masonry.
April 8, 1860: there was a major earthquake farther west accompanied by a tsunami.
"Haiti Mission Report"
In a "Haiti Mission Report" by the United Nations Environment Programme released two months after the eathquake, the impacts was sumarrized as follows:
According to official United Nations (UN) estimates, the earthquake killed 222,570 people, injured an estimated 300,000 and left 1,000,000 homeless, making it comparable, in terms of human tragedy, to the South-East Asian tsunami of 2004 (which caused 230,000 deaths spread across fourteen countries). This catastrophic event was also characterized by severe damage to the capital city, where the majority of casualties were incurred, and by the enormity of its impact on humanitarian response mechanisms, due to the destruction of all lifeline buildings (ranging from the presidential palace to schools and hospitals).
In addition to the severe damage in Port-au-Prince, several cities and villages in the south of the island were impacted, resulting in extensive death and destruction. The Government has estimated that some 250,000 residences and 30,000 commercial buildings collapsed or were badly damaged. The earthquake has thus led to significant population displacement, with many people, including some whose homes were not damaged, vacating the city and moving out into the open. The United Nations estimates that up to 1.9 million people are in need of food aid for the foreseeable future.
and,
. . . all the fatalities in this case occurred within 100 kilometers of Port-au-Prince in an area covering only about 25 percent of the total geographical area of Haiti. The earthquake killed 222,570 people – one in every 45 Haitians – which is perhaps one the largest such ratios in history (major tragedies have typically occurred in more populated places). In addition, it devastated the capital city, demolished the presidential palace (along with numerous other ministries and Government buildings), destroyed the office of the United Nations (killing 92 UN staff including the Head of the Mission), and killed the leader of the opposition party and the capital’s archbishop.
Images
Port-au-Prince, the downtown core shows the damage after the earthquake. Source: United Nations Development Programme
Port-au-Prince, the Haitian national palace shows heavy damage after earthquake. Source: United Nations Development Programme
Port-au-Prince, a poor neighbourhood shows the damage after earthquake. Source: United Nations Development Programme
A Haitian boy receives treatment at an ad hoc medical clinic following the earthquake. Source: United Nations Development Programme
Further Reading
• Magnitude 7.0 - HAITI REGION US Geological Survey (accessed January 16, 2010)
• [http://www.ig.utexas.edu/jsg/18_cgg/Mann3.htm. "Entiquillo-Plantain Garden Strike-Slip Fault Zone: A Major Seismic Hazard Affecting Dominican Republic, Haiti and Jamaica"], Mann, Paul, Calais, Eric, Demets, Chuck, Prentice, Carol S., and Wiggins-Grandison, Margaret (March 2008). 18th Caribbean Geological Conference. Retrieved 2010-01-13.
Citation
U.S. Geological Survey (Lead Author);Peter Saundry (Contributing Author);C Michael Hogan (Topic Editor) "Haiti Earthquake, January 12, 2010". In: Encyclopedia of Earth. Eds. Cutler J. Cleveland (Washington, D.C.: Environmental Information Coalition, National Council for Science and the Environment). [First published in the Encyclopedia of Earth January 26, 2010; Last revised Date July 6, 2012; Retrieved May 18, 2013 <http://www.eoearth.org/article/Haiti_Earthquake,_January_12,_2010?topic=49565>
The Author
The U.S. Geological Survey (USGS) is the primary research arm of the Department of the Interior. As the Nation's largest water, earth, and biological science and civilian mapping agency, the USGS collects, monitors, analyzes, and provides scientific understanding about natural resource conditions, issues, and problems. The USGS serves the Nation by providing reliable scientific information to describe and understand the Earth; minimize loss of life and property from natural disasters; manage ... (Full Bio)
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Changes related to "Virgin Islands"
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"url": "www.go4expert.com/forums/importing-class-bean-jsp-page-t26264/",
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Importing class (not bean) in jsp page
Newbie Member
12Jul2011,13:45 #1
I am importing a class using the command:
<%@ page import="user.UserLoggedIn" %>
I am able to work on the methods but my query is:
Quote:
If I have static variables inside it, do they retain the value throughout the whole session or even after closing the session?
I just want to store these variables throughout the session and then reset them
In a bean, I can use scope="session"
Is there any similar way to do it in classes?
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hdqymcklelvroy5uj2ty5vyubav36jji
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Heroin
From Grand Theft Wiki
Jump to: navigation, search
The Triads unloading the heroin from the Platypus.
The heroin is a part of Grand Theft Auto IV's storyline including The Lost and Damned and The Ballad of Gay Tony. Like the diamonds, it also has a large part of the game involving the protagonists Niko Bellic, Johnny Klebitz and Luis Fernando Lopez. Below are scenarios that takes place involving different people that gain possession of the heroin and the heroin itself.
Contents
Description
Arrival in Liberty City, and Angels of Death theft
When the Platypus arrived in Liberty City, the heroin, which belonged to the Triads and brought in from the east, was smuggled into the city together with the diamonds and Niko Bellic. The Angels of Death soon stole it, and it was in their hands until Johnny Klebitz and The Lost Brotherhood came, destroyed the AoD clubhouse and stole it themselves.
Elizabeta's assistance to offload it
The Lost, along with Elizabeta Torres tried to offload the heroin, but the deal turned out to be an LCPD sting. Niko Bellic and Playboy X managed to escape, Johnny also escaped with the heroin and took it back to the Lost MC clubhouse.
The Lost MC's attempt to sell it to the Triads
The Lost MC decide they will try and sell the heroin back to the Triads. Billy Grey tells Johnny and Jim to do the deal. Billy had previously conspired with the Triad leader to kill Johnny once he arrived, and while Johnny and Jim are being jumped, the police arrive and arrest Billy. Johnny, Jim and Brian Jeremy escape while the Triads take back their heroin. In a side note, Luis Lopez and Tony Prince had previously met with the Triad leader to discuss some licensing arrangements for the planning department on behalf of Rocco Pelosi.
Phil Bell and Niko Bellic's involvement
Phil Bell, an associate of the Pegorino Crime Family hires Niko Bellic to ambush the Triads and steal the heroin before the Triads can offload it. Niko does so and hijacks the truck, then transports it to an abandoned house in Westdyke, where Phil's nephew, Frankie Gallo would "sit" on the heroin until it was safe to sell it. After some time, Niko and Phil went to the house to move the heroin, however, the house was being monitored by the FIB. The three of them fought off numerous members of the NOOSE before hiding the heroin again in a house in Leftwood.
Eventually, Jimmy Pegorino made a deal with Dimitri Rascalov, and joined forces. Pegorino gave all the heroin to Dimitri to sell and asked Niko to accompany Phil when overseeing the deal. Niko is reluctant due to his personal grudge against Dimitri, but Jimmy manages to talk him round. However, Niko is again left unsure when his cousin Roman and girlfriend Kate advise him in opposite directions, Roman urging him to do the deal, with Kate telling him to cut his ties with Dimitri altogether due to his previous betrayal.
Niko then either does the deal, and is again betrayed when Dimitri kills the buyers and steals the heroin, or he takes revenge by ambushing Dimitri on the Platypus, which is being used by the Russians to move the heroin.
Niko Bellic's Choice
Deal
If Niko does the deal with Dimitri, Dimitri kills the buyers, takes the heroin and escapes. Phil and Niko pursue one of his men with the money and retrieve it. Dimitri, fearing a retaliation from Niko, sends a hitman to kill him at Roman's wedding, but Roman is killed instead during the struggle. Dimitri then tries to escape, and kills Pegorino in another act of betrayal. Niko then pursues Dimitri to Happiness Island, and after a fire-fight, Dimitri dies of his injuries.
"Deal" effect on The Ballad Of Gay Tony
After Dimitri's death, Bulgarin now has ownership of the heroin at Funland. Luis Lopez goes to Funland in pursuit of Bulgarin, he kills Timur and destroys all the heroin. He then chases and kills Bulgarin on his private jet, which explodes in mid-air.
Revenge
If Niko chooses to take revenge, he carries out a full-blown assault and slaughters Dimitri's men on the Platypus, which Dimitri is using to import/export the heroin that Pegorino had given him to sell. After killing Dimitri, Niko leaves the scene, and the heroin is left on the ship. Niko's revenge leaves the Pegorinos ruined, without the money or the heroin. Niko then attends Roman's wedding, but Pegorino interferes and tries to kill Niko by firing on the guests, but Kate McReary is killed instead. Niko then pursues Pegorino to Happiness Island, and after a fire-fight, Niko finishes Pegorino with a shot to the head.
"Revenge" effect on The Ballad Of Gay Tony
After Niko killed Dimitri aboard the Platypus, Bulgarin and Timur claimed ownership of the heroin and took it Funland in Broker to be unloaded. Luis carries out an attack and destroys the heroin. He then races to the airport to catch Bulgarin after learning from Timur that he was planning to flee back to Russia. Finally, Luis kills Bulgarin, who drops a grenade causing his jet to explode over Firefly Island.
Consequences
Niko Bellic
After the Triads took back their heroin, which they believe is cursed, they later attempt to ship it. The Pegorinos hear about this and so Niko, under orders from Phil Bell steals the heroin and hides it in a abandoned house. When Niko and Phil went to go pick up the heroin, the FIB attempt to bust them. After they escaped the FIB, the Pegorinos ally with the Russians and try to sell it to another Mafia Family. Pegorino gives the heroin to Dimitri who says he has found a buyer. But Dimitri kills the buyers and steals the heroin for himself in the "Deal" ending, whilst in the "Revenge" ending he never gets a chance to try and sell it due to Niko's ambush on the Platypus.
Johnny Klebitz
Johnny and the Lost MC steal the heroin from the AoD clubhouse, unaware that the AoD had stole it from the Triads to begin with. First, Johnny arranges for Elizabeta Torres to help him offload it. Elizabeta uses Playboy X and Niko Bellic to oversee the deal. However, it turns out to be an LCPD sting, the three of them escape, and Johnny takes the heroin back to the Lost MC clubhouse. When the Lost MC discover the heroin belonged to the Triads, Billy sends Jim and Johnny to sell it back to them. However, it is revealed that Billy arranged for the Triads to ambush and kill Johnny when he arrived. Johnny and Jim survive the ambush however, and the triads take back their heroin, the the cops show up and arrest Billy and Johnny does not see or hear of the heroin afterwards.
Luis Lopez
After Dimitri was killed Luis destroyed all of the heroin, and killed Bulgarin soon after. In "Deal", Luis does this after Dimitri's death on Happiness Island. In "Revenge", Luis does this at roughly the same time Niko kills Pegorino.
Mission appearances
Note the following missions are sorted in chronological order of the timeline.
See Also
• Drugs for other uses of heroin in the Grand Theft Auto series.
• Diamonds
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About this Journal Submit a Manuscript Table of Contents
Clinical and Developmental Immunology
Volume 2012 (2012), Article ID 152546, 11 pages
doi:10.1155/2012/152546
Research Article
Clinical Isolates of Mycobacterium tuberculosis Differ in Their Ability to Induce Respiratory Burst and Apoptosis in Neutrophils as a Possible Mechanism of Immune Escape
1IMEX-CONICET-ANM, Academia Nacional de Medicina, 1425 Buenos Aires, Argentina
2Servicio de Micobacterias, Hospital Malbrán, Pacheco de Melo 3081, 1425 Buenos Aires, Argentina
Received 4 April 2012; Accepted 29 April 2012
Academic Editor: Eyad Elkord
Copyright © 2012 María M. Romero et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Tuberculosis pathogenesis was earlier thought to be mainly related to the host but now it appears to be clear that bacterial factors are also involved. Genetic variability of Mycobacterium tuberculosis (Mtb) could be slight but it may lead to sharp phenotypic differences. We have previously reported that nonopsonized Mtb H37Rv induce apoptosis of polymorphonuclear neutrophils (PMNs) by a mechanism that involves the p38 pathway. Here we evaluated the capability to induce PMN apoptosis of two prevalent Mtb lineages in Argentina, the Latin America and Mediterranean (LAM), and Haarlem, using the H37Rv as a reference strain. Results showed that LAM strains strongly induced apoptosis of PMN which correlated with the induction of reactive oxygen species (ROS) production and p38 activation. Interestingly, the highly prosperous multidrug-resistant M strain, belonging to the Haarlem lineage, lacked the ability to activate and to induce PMN apoptosis as a consequence of (1) a weak ROS production and (2) the contribution of antiapoptotic mechanisms mediated at least by ERK. Although with less skill, M is able to enter the PMN so that phenotypic differences could lead PMN to be a reservoir allowing some pathogens to prevail and persist over other strains in the community.
1. Introduction
Polymorphonuclear neutrophils (PMNs) are key components of the first line of defense against bacterial and fungal pathogens. In tuberculosis (TB), the influx of PMN to the lung is one of the first events in the pathogenesis of the disease. Bacterial products elicit the upregulation of the β2 integrin, CD11b, as well as the release of pronflammatory cytokines by PMN contributing to the recruitment of leukocytes at the site of infection and amplifying the immune response [1, 2]. Microbicidal mechanisms of PMNs include the release of proteolytic enzymes and antimicrobial peptides as well as the rapid production of reactive oxygen species (ROS) essential for bacterial killing which also enhance inflammatory reactions [3].
We have previously demonstrated that nonopsonized virulent Mycobacterium tuberculosis (Mtb) strain H37Rv induces PMN activation and accelerates their apoptosis in vitro at a low Mtb : PMN ratio [4]. Moreover, in infected individuals circulating PMN become activated [5] and are recruited to the lungs in the early infection, where they underlie apoptosis [6]. Accelerated apoptosis has been observed in PMN after mycobacterial internalization, possibly dependent on oxidative processes [4, 7], enhanced by high concentrations of TNF-alpha [8], and mediated via TLR2- and mitogen-activated protein kinase (MAPK) p38- dependent pathways [9]. Along these lines, it has been demonstrated that PMN response to cytokines and other released pro-inflammatory agents as well as activation of PMN involves the MAPK pathway [10]. In the context of mycobacterial infection, the mode of PMN cell death could influence disease outcome: if a PMN cannot kill an ingested organism, then necrosis could offer an inflammatory reaction whereas, if PMN became apoptotic, then PMN-dendritic cell cross-presentation and increased lymphocyte proliferation occurs in response to Mtb, directly influencing the development of an acquired immune response [11].
In Argentina a total of 11,464 new cases of TB were reported in 2006, with an incidence of 29.1 per 100,000 inhabitants. As in other South American countries [2, 12] the vast majority of Mtb strains circulating in Argentina belong to the Latin American and Mediterranean (LAM) and the Haarlem lineages [2, 13, 14]. Within the Haarlem lineage, the multidrug-resistant (MDR) M strain is highly prosperous in Argentina and is able to build up further drug resistance without impairing its ability to spread [15]. The genetic variability of Mtb strains might lead to sharp phenotypic differences which could be responsible for a differential modulation of host immune response impacting in the onset and progression of the disease [16]. In this context, differential immune responses among resistant Mtb strains have been reported [17, 18].
Therefore, in this work we evaluated whether clinical isolates of Mtb differ in their capability to induce PMN apoptosis, in order to evaluate apoptosis as a possible mechanism that leads to pathogen survival inside PMN allowing some strains to prevail and persist over other strains in the community.
2. Methods
2.1. Isolate Selection and Preparation of Bacterial Strains
Mtb isolates representative of prevalent LAM and Haarlem lineages were obtained from sputum-culture-positive patients with TB in Argentina. The isolates had been previously submitted to drug susceptibility testing and genotyping by IS6110 DNA fingerprinting and spoligotyping using standardized protocols. The following strains were evaluated: a drug-susceptible strain (LAM, 10406) and a drug-resistant strain (Ra, 11608) from the LAM lineage and a drug-susceptible Haarlem strain (H, 12425) and an MDR strain from the Haarlem lineage (isolate 6548 as representative of the outbreak strain M). Spoligotyping and IS6110 restriction fragment length polymorphism pattern profiles of Mtb strains used as antigens are depicted in Figure 1. The strains belonged to the collection kept at the Reference Laboratory for Mycobacteria at the Instituto Nacional de Enfermedades Infecciosas ANLIS “Carlos G. Malbran” in Buenos Aires, Argentina. Laboratory reference strain H37Rv from T family was kindly provided by I. N. de Kantor (Former Head of TB Laboratory, INPPAZ PAHO/WHO) (Figure 1). All strains were grown in Middlebrook 7H9 broth (Difco Laboratories, Detroit, MI, USA) at 37°C in 5% CO2 until log phase. Mycobacteria were harvested, washed three times, and suspended in phosphate-buffered saline (PBS) free of pyrogen. Bacteria were killed by gamma irradiation or heat-killed and suspended in PBS at an OD600 nm of 1 (~108 bacteria/mL) and stored at −20°C until their use. LPS from Escherichia coli 0111:B4 was purchased from Sigma Chemicals Co. (St. Louis, USA).
Figure 1: Spoligotyping and IS6110-RFLP pattern profiles of Mtb strains used as antigens in this study: reference virulent strain H37Rv, local-drug-sensitive (LAM, 10406) and drug-resistant (Ra, 11608) LAM strains, drug-sensitive Haarlem strain (H, 12425), and MDR Haarlem strain, M (6548).
2.2. Antibodies and Reagents
Oxidase inhibitor, diphenylene iodonium DPI, was provided by Cayman Chemical (Michigan, USA), the specific inhibitor of p38, SB203580, and the specific inhibitor of ERK, PD98059, were purchased from Calbiochem-Behring (La Jolla, CA, USA). DMSO (Sigma Co.) was added to cultures at 0.1% (vol/vol) as a solvent control.
Mouse antibodies (Abs) against Caspase-3 (BD Biosciences Pharmingen, California, USA) phospho (Thr202/Tyr204)-ERK1/2, and phosphor (Thr180/Tyr182)-p38 were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA). Mouse antihuman CD11b, CD66b and CD16 were purchased from eBioscience (San Diego, CA, USA).
2.3. PMN Purification and Culture
PMNs were isolated from heparinized venous blood from healthy donors by Ficoll-Hypaque gradient centrifugation [19] followed by sedimentation in 3% dextran (Sigma Chem. Co, St. Louis Mo, USA). The PMN-rich supernatant was then collected and residual red blood cells were removed by hypotonic lysis. The cells were washed immediately and resuspended at 3 × 106 cells/mL in RPMI-1640 medium (Gibco, NY, USA) supplemented with 1% heat-inactivated Fetal Calf Serum (FCS) (Gibco) and 50 μg/mL gentamycin (complete media, CM). The viability was consistently >95% as determined by trypan blue dye exclusion. The purity of the final PMN preparation was up to 95% as assessed by morphological examination by staining with Wright-Giemsa and by FACS light scatter patterns. Cultures were performed by incubating 1 mL of a PMN suspension (3 × 106 cell) in Falcon 2063 tubes stimulated with Mtb strains, at different Mtb : PMN ratios.
2.4. Surface Cell Staining
Cell surface expression of CD11b and FcRIIIb (CD16) in recently isolated or 3 and 18-h-cultured PMN was evaluated by direct immunofluorescence using saturating concentrations of monoclonal mouse antihuman CD11b-PE- and -CD16-FITC-conjugated antibodies. Briefly, 5 × 105 cells were incubated with the antibody for 20 min on ice. Cells were washed, fixed in 500 μL of 1% paraformaldehyde. Using a FACScan (Becton-Dickinson Immunocytometry Systems, San Jose, CA), 10,000 events were collected in linear mode for forward scatter (FSC) and side scatter (SSC), and log amplification for FL-1 and FL-2. Analysis was performed using the CellQuest software (Becton-Dickinson) and isotype-matched controls were used to determine autofluorescence and nonspecific staining. Results were expressed as percentages of positive cells and as mean fluorescence intensity (MFI).
2.5. Intracellular Cell Staining
The activated cytoplasmic protein caspase-3 was measured in PMN by using a Fix and Perm kit (Caltag, Burlingame, CA, USA). Briefly, 3 × 106 PMNs were incubated with different Mtb strains at 1 : 2 Mtb : PMN ratio for 5 h and thereafter cells were washed and resuspended in 100 μL solution A (fixation) for 15 min at room temperature. After washing with PBS containing 1% Na azide and 5% FCS, cells were resuspended in solution B (permeabilization) and mouse antihuman FITC-conjugated caspase-3 antibody specific for active caspase-3 (BD Pharmingen). After 20-min incubation on ice in the dark, cells were washed, resuspended in isoflow, and analyzed in the same manner as mentioned above.
Phosphorylated form of p38 and ERK cytoplasmic proteins were measured in permeabilized cells as described above. PMNs were incubated with Mtb strains at a 1 : 2 Mtb : PMN ratio for 1 h. Thereafter, cells were washed with PBS and resuspended in 100 μL solution A (fixation) for 15 min at room temperature. After washing with PBS containing 1% Na azide and 5% FCS, cells were suspended in solution B (permeabilization) and the mouse anti-human p-p38 IgM anti-p-p38-FITC- or anti-human p-ERK-conjugated antibody (Santa Cruz Biotechnology, Santa Cruz, CA., USA). After 20-min incubation on ice in the dark, cells were washed, resuspended in isoflow and acquired in a flow cytometry and analyzed as previously described.
2.6. Detection of Apoptosis Using Annexin-FITC by FACS
The percentage of apoptotic PMN was assessed based on the Annexin V-FITC (Sigma) protein-binding assay. Briefly, 5 μL of Annexin V-FITC (10 μg/mL) and 5 μL of propidium iodide (PI) (250 mg/mL) (Sigma) were added to 1.2 × 106 cells in 500 μL of binding buffer and incubated for 15 min at room temperature in the dark, as previously described [4]. Cells were washed, resuspended in binding buffer acquired in a flow cytometry, as previously described. AV/PI cell population was regarded as alive, AV+/PI was considered as an early apoptotic population, and the AV+/PI+ population represented late stage apoptotic or necrotic cells. Alternatively, to modify cellular p38 and ERK activity, SB20358 (20 μM) or PD98059 (50 μM) inhibitors was added to 1 mL PMN suspension before culture, at 37°C for 30 min. When indicated, 10 mM H2O2 were added 15 min after Mtb treatment.
2.7. Assay for Oxidative Burst Using Dihydrorhodamine 123 (DHR)
Intracellular ROS levels were measured by Dihydrorhodamine assays 123 (DHR). DHR was dissolved in DMSO at a concentration of 20 μg/mL and stored in aliquots at −70°C until use. Briefly, 5 × 105 PMNs were incubated with 100 μl DHR (5 μg/mL) for 15 min at 37°C. Afterward, gamma-irradiated Mtb strains (1 × 106 bacilli/mL) were added to the culture at 1 : 2, 5 : 1, 20 : 1, and 50 : 1 Mtb : PMN ratios for additional 90 min. When indicated, heated-killed MtbMtb) were employed.
2.8. Phagocytosis Assay
As an indirect measure of phagocytosis ROS production induced by DHR-labeled Mtb was performed. Briefly, Mtb were incubated with 5 μg/mL DHR for 30 min at 37°C followed by an extensive washing to remove free DHR and suspended in RPMI 1640 plus 10% FCS. Thereafter, 5 × 105 PMNs were incubated with DHRMtb strains at a 50 : 1 ratio for 90 min at 37°C, washed and centrifuged at 100 g evaluated immediately in a flow cytometer as previously described.
Direct measure of phagocytosis, was performed by the method described by Busetto et al. [20]. Briefly, 3 × 106/mL PMNs were suspended in media 10% FSC and were incubated at 37°C in a shaking water bath with nonopsonized FITC-labeled Mtb strains. PMN-Mtb mixtures (ratio 10 : 1) were incubated for 2 hr at 37°C. To stop phagocytosis, aliquots of the incubation mixtures were withdrawn into the tubes used for cytometric analysis containing an equal volume of 250 μg/mL Trypan Blue (TB) dissolved in ice-cold 0.1 M citrate buffer, pH 4.0. After 1 min incubation in ice, the samples were analyzed by flow cytometry. Each sample was collected for 30 seconds at the slowest flow rate to minimize the coincidental appearance of free bacteria and PMN in the laser beam. The data were then analyzed by using CellQuest software from Becton Dickinson. The mean number of ingested bacteria per neutrophil was assessed (i.e., both attached and internalized particles).
2.9. Statistics
The statistical analysis of the data was performed using one-way ANOVA followed by Tukey’s multiple comparison tests to compare more than two groups followed by Wilcoxon test to compare two groups. The significance was considered as . The graphical representation of the values is given by mean ± SEM.
3. Results
3.1. PMN Apoptosis Induced by Different Mtb Strains
We have previously described that nonopsonized strain Mtb H37Rv is able to induce PMN apoptosis at low Mtb : PMN ratio [4]. In order to evaluate whether Mtb strains differ in their capability to induce apoptosis, PMNs were incubated at 1 : 2 Mtb : PMN ratio for 18 h and, thereafter, apoptosis were evaluated by measuring the percentage of cells expressing FITC-conjugated Annexin V (AV+). Flow cytometric analysis shows that all strains, except M, induced significant increase of AV+ PMNs respect to spontaneous apoptosis. Furthermore, clinical isolates belonging to LAM lineage (LAM and Ra) were the highest inducers of apoptosis (Figure 2(a)). LPS, that exerts an antiapoptotic effect on cultured PMN [21], was used as a control in the apoptosis assay (data not shown). Most apoptotic signaling pathways are originated from death receptor linkage or stress stimuli converging on activation of caspases, key executors of apoptosis. To assess the involvement of Caspase-3 (casp-3) in Mtb-induced PMN apoptosis, expression of the activated form of Casp-3 was evaluated in PMN incubated with different Mtb strains (Mtb : PMN 1 : 2) for 5 h. As it is shown in Figure 2(b), all strains, except M, induced Casp-3 activation being LAM and Ra the highest inducers. These results are consistent with those obtained in the apoptosis assay. In addition, no differences were observed in the loss of FcγRIIIb receptor (CD16) expression among strains. As it is known, the loss of CD16 expression on PMN surface correlates with spontaneous apoptosis in culture [22] so that our results show differences in Mtb-induced apoptosis whereas CD16 shedding was independent of the Mtb strain (Figure 2(c)).
Figure 2: PMN apoptosis induced by different Mtb strains. PMNs (3 × 106/mL) were cultured in media alone (control, —) or stimulated with Mtb strains (H37Rv, LAM, Ra, H, and M) at 1 : 2 Mtb : PMN ratio and parameters of apoptosis were evaluated by flow cytometric analysis. (a) Expression of Annexin V-FITC (AV-FITC) on PMN cultured for 18 h. Results are expressed as media ± SEM of percentage of positive cells (). Control (—) versus LAM, Ra, and H: ; H37Rv: ; LAM and Ra versus other strains: . (b) Intracellular expression of activated cytoplasmic protein caspase-3 in PMN after 5 h culture with or without Mtb stimulation. Results are expressed as media ± SEM of MFI. Control (—) versus LAM and Ra: ; H37Rv: ; H ; LAM and Ra versus other strains: . (c) The percentage of fresh (0 h) and 16 h cultured cells expressing FcRIIIb (CD16) was measured. 0 h versus control: ; control vesrus Mtb strains: .
3.2. CD11b, CD66b, and p-p38 Expression Induced by Mtb Strains
CD11b and CD66b are proteins found in the membrane of the various PMN granules and appear on the cell surface after exocytosis and release of granular contents upon activation [23]. Indeed, the CD11b receptor is dramatically upregulated at the surface of activated PMN which extravasate through the vessels and migrate to the site of infection, thereby enhancing the effectors’ functions of these cells. As shown in Figure 3, all Mtb strains enhanced CD11b and CD66b expression in 3 h culture PMN. Particularly, we found that susceptible and drugs-resistant LAM strains showed the highest activation level, while M showed the lowest one (Figures 3(a) and 3(b)). As previously demonstrated, activation- and apoptosis-induced H37Rv involves the activation of mitogen-activated protein kinase p38 [4, 9]. In this work, flow cytometric analysis of the activated form of p38 (p-p38) showed that susceptible and drugs resistant LAM induced the highest expression of p-p38 whereas, with M, p-p38 was not detectable. These results suggest a different participation of p38 in apoptosis induced by Mtb strains (Figure 3(c)). From now on, we will refer to both LAM and Ra as “LAM,” because no differences were found between susceptible or drugs-resistant LAM clinical isolates.
Figure 3: CD11b, CD66b, and p-p38 MAPK expression in PMN induced by Mtb strains. PMNs (3 ×106/mL) were cultured in media alone (control, —) or stimulated with Mtb strains at 1 : 2 Mtb : PMN ratio for 3 h. (a) and (b) Surface expression of activation markers was evaluated by flow cytometry and results are expressed as media ± SEM of MFI (). Statistical differences: CD11b and CD66b: control (—) versus H37Rv, LAM, Ra and H: ; control versus M: ; LAM and Ra versus other strains: ; (c) PMNs (3 × 106/mL) were cultured in media alone (control, —) or stimulated with Mtb strains at 1 : 2 Mtb : PMN ratio for 1 h. Intracellular activated form of p38 (p-p38) was measured by flow cytometry. Results are expressed as media ± SEM (). Statistical differences: control versus H37Rv, LAM, Ra, and H: ; LAM and Ra versus other strains: .
3.3. Role of p-p38, ERK, and ROS in Differential Mtb-Induced PMN Apoptosis
To evaluate if Mtb strains differ in the mechanisms underlying the apoptotic process, PMNs were cultured with Mtb in presence of different inhibitors for 18 h and apoptosis was evaluated by AV expression. According to our previous results obtained with H37Rv [9], SB203580, a specific p38 inhibitor, only inhibited the apoptosis induced by LAM and H (Figure 4(a)). Considering that ROS are involved in the regulation of MAP-kinase-dependent apoptotic pathway [24], we used an oxidase inhibitor (DPI) to assess the participation of ROS in apoptosis and we observed that generation of ROS was essential for triggering apoptosis induced by all strains (Figure 4(a)). Strikingly, M was able to induce apoptosis when PMNs were incubated with a specific ERK inhibitor, PD98059, suggesting that this strain could be triggering anti-apoptotic mechanisms, which involve ERK (Figure 4(a)). In order to evaluate the grade of participation of anti-apoptotic signals, H2O2 was added to the culture before challenging with different Mtb strains and apoptosis was measured by AV. Interestingly, apoptosis induced by all strains was enhanced in the presence of H2O2. However this effect was lower for the Haarlem strains, in particular M, which effect was not enough to reach high levels of apoptosis (Figure 4(b)), supporting the idea that anti-apoptotic mechanisms could be involved.
Figure 4: Role of MAP kinases and reactive oxygen species in PMN apoptosis induced by Mtb strains. (a) PMN (3 × 106/mL) were cultured in media alone (control, —) or stimulated with Mtb strains at 1 : 2 Mtb : PMN ratio for 18 h, in the presence or absence of specific inhibitors for p38 and ERK (SB203580 and PD98059, resp.), and an oxidase inhibitor DPI. Thereafter, Annexin V-FITC (AV-FITC) binding was measured by flow cytometry. Results are expressed as media ± SEM (). Statistical differences: Control versus LAM: , control versus H: , control versus H37Rv: ; H37Rv, LAM and H versus SB: ; H37RV, LAM and H versus DPI: ; M versus PD: . (b) PMN were treated with 10 mM H2O2 15 min before Mtb challenge and thereafter PMN were cultured as described in (a). After 18 h-culture, Annexin V-FITC (AV-FITC) positive PMN was measured by flow cytometry. A representative experiment out of four is displayed.
3.4. Role of p-p38, ERK, and ROS in CD11b UpRegulation by Mtb Strains
Previously we have shown that H37Rv-induced apoptosis depends on PMN activation as Mtb induced also CD11b expression [4]. CD11b is a receptor that serves in nonopsonic recognition of microbes which may confer an advantage in the alveolar space, where serum opsonins are limited. We further evaluated whether the activation of p38 is involved in the upregulation of CD11b expression and, as observed in Table 1, SB203580 abolished CD11b upregulation by all strains. Besides, PD inhibited M-induced C11b enhancement suggesting that ERK was also required for M. This data is in accordance with that observed to apoptosis. However, CD11b expression was not abrogated by DPI suggesting that ROS did not participate in CD11b upregulation.
Table 1: CD11b expression on 3 h-cultured PMN stimulated with Mtb strains and treated or not with MAPK or ROS inhibitors.
3.5. ROS Production Induced by Mtb Strains in PMN
Considering that apoptosis in human PMN may be related to ROS production [25] we wondered if M, that fails in induce PMN apoptosis, would exhibit any deficiency to induce ROS. Therefore, we evaluated the conversion of nonfluorescent dihydrorhodamine123 (DHR) to rhodamine123 as a measure of H2O2 production. DHR freely enters the cell; it binds to cellular and mitochondrial membranes and emits a bright fluorescent signal mainly localized inside the cell [26]. As it is shown in Figure 5(a), all Mtb strains induced ROS production in a dose-dependent manner. At low Mtb : PMN ratio (1 : 2), LAM, H, and H37Rv strains were able to induce significant amount of ROS whereas M did not (Figure 5(b)). Besides, at high doses (50 : 1 Mtb : PMN) all Mtb strains were able to induce ROS, being LAM the highest inducer (Figure 5(c)).
Figure 5: ROS production induced by Mtb strains in PMN. (a) PMNs treated with DHR were incubated with Mtb strains and MFI of 123rodhamine was measured by flow cytometry. Different Mtb : PMN ratios were tested (1 : 2, 5 : 1, 20 : 1, and 50 : 1) and a representative experiment out of three is shown. (b) ROS production induced at low Mtb : PMN ratio (1 : 2); results are expressed as media ± SEM (), statistical differences: control versus LAM, H37Rv, and H: . (c) ROS production induced at 50 : 1 Mtb : PMN ratio; results are expressed as media ± SEM (), statistical differences: control versus LAM ; H37Rv and H ; M . (d) ROS production was induced with gamma-irradiated or heat-killed (Ø) Mtb strains at 1 : 2 Mtb : PMN ratio. Statistical differences: control (—) versus LAM ; LAM versus LAMØ . A representative experiment is embedded. In all cases PMNs were washed, and 10,000 events were collected in a flow cytometer as described in Section 2.
3.6. Phagocytosis of Mtb Strains by PMN
On the other hand, it is known that certain pathogens fail to trigger ROS and apoptosis in PMN and enter the cell at a low rate [27], so that we wondered whether Mtb strains exhibited a disparity in their entrance to the PMN. In this purpose, PMNs were incubated with FITC-labeled Mtb during two hours and the percentage of PMN expressing FITC-Mtb was evaluated by flow cytometry. As shown in Figure 5(d), M was less engulfed than LAM, H37Rv, and H. Similar results were obtainedinPMNinfected withlive bacteria (data not shown).
Besides, in order to determine if low ROS production was associated with a low entrance, we quantified ROS with DHR-labeled Mtb (DHRMtb), so that oxidized DHR represents the levels of ingested bacteria. Figure 5(e) shows that while M was not able to induce ROS, LAM was the highest inducer. Although H and H37Rv showed a similar phagocytosis rate as LAM, these two strains induced less ROS production, suggesting that the differences seem not to be related to their efficiency to enter in PMN. In particular, the fact that M was not able to induce ROS in this condition might be related to the low phagocytic rate and a poor ability to induce ROS (Figure 6).
Figure 6: Phagocytosis of Mtb strains by PMN (a) As direct measure of phagocytosis, PMN were incubated with FITC-labeled Mtb (ratio 10 : 1). Then all Mtb-FITC bound/not ingested by PMN were quenched with Trypan Blue. Results represents bound/ingested plus ingested and are expressed as media ± SEM of MFI (). Statistical differences: Control (—) versus H37Rv, LAM and H: control versus M ; M versus other strains . (b) Phagocytosis was indirectly measured by ROS production induced with DHR labeled Mtb (DHRMtb). PMN were incubated with DHRMtb (50 : 1 ratio) for 90 min. at 37°C and 123rhodhamine emission was evaluated immediatly in a flow cytometer. Results are expressed as media ± SEM of MFI (). Statistical differences: control (–) versus H37Rv, LAM and H: ; LAM versus H37Rv and H ; LAM versus M . In all cases PMN were washed, and 10,000 events were collected in a flow cytometer as described in Section 2.
4. Discussion
The outcome of tuberculosis infection has long been considered dependant mainly on the ability of the host to deal with the pathogen. Now it is becoming clear that in addition to host factors, phenotypic differences among Mtb strains are also involved in key aspects of pathogenesis and latency as transmissibility, virulence, and immunogenicity among Mtb strains, determined by the genetic background of the organisms [15, 2830]. In this context, the Mtb envelope contains diverse lipids and glycolipids that are likely to mediate specific host interactions [31].
PMNs are the first defensive cells recruited into infected tissue, where their role has been thought to be the elimination of invading pathogens via mechanisms such as the generation of ROS [32] and the release of preformed oxidants and proteolytic enzymes from granules [33]. In this way, PMN apoptosis induced by bacteria is likely beneficial to the host because it reduces the release of cytotoxic components [34] and promotes PMN removal by macrophages from sites of infection, reducing tissue destruction during necrosis. Microorganisms that evade killing survive and disseminate to cause disease [35].
The aim of this work was to evaluate the prevalent Mtb strains in Argentina in their capability to induce PMN apoptosis compared with H37Rv. As we showed here, except M, all Mtb strains induced a significant increase in PMN apoptosis at Mtb : PMN ratio (1 : 2). The very high level of apoptosis induced by LAM, both sensible (LAM) and multidrugs-resistant (Ra) strains, was in accordance with a marked activated phenotype of PMN, as well as Casp-3 and p-p38 expression, and moreover, Mtb-induced apoptosis has correlated with ROS production. In the same way, M, that fails to induce PMN apoptosis, also fails at inducing expression of Casp-3 and p-p38 and ROS production.
Today it is known that ROS can act as signaling molecules [36] modulating diverse receptor-ligand intracellular signaling pathways, such as the MAPK-dependent apoptotic pathway and NF-kB pathways [2, 24]. In this context it has been described that PPD induces the rapid activation of MAPKs, ROS, and apoptosis signal-regulating kinase 1 (ASK1) in monocytes in a TLR2-dependent manner [37] and ASK1 could also be activated by oxidant stress, involving p38 pathway. A strong evidence for the involvement of ROS in PMN apoptosis is the fact that phagocytes from patients with chronic granulomatous disease that are unable to produce ROS due to a defect in NADPH oxidase are predisposed to recurring bacterial and fungal infections and develop granulomas linked to altered PMN apoptosis [38]. Patients with chronic granulomatous disease are also susceptible to TB and complications of vaccination with the bacillus Calmette-Guérin [39].
Here we show that both ROS and p38 are involved in the apoptosis triggered at low Mtb : PMN rate. Remarkably, M was able to trigger apoptosis when ERK was abrogated suggesting that M activates anti-apoptotic mechanisms which could also impact on final apoptosis outcome in PMN. This result was supported by the fact that addition of H2O2 allowed a partial induction of apoptosis by M. The involvement of ERK in signaling triggered by M was also evident as both p38 and ERK were involved in CD11b expression induced by M, whereas other strains only activated p-p38 (Table 1). Although p-p38 induced by M was not detectable, it could be enough to activate PMN but not to overcome antiapoptotic mechanisms triggered by this strain.
It has been described that PMN uptake of the obligated intracellular pathogen Anaplasma phagocytophilum occurs at a slow rate compared with other bacteria [27], and even more, PMN infection with this pathogen fails to trigger ROS and delays PMN spontaneous apoptosis [2, 25]. In this context, albeit M was ingested at a lower rate, no differences were observed among LAM, H37Rv, and H (Figure 5(d)), suggesting that differences in ROS production were not related to the efficiency in bacterial entry. Consistently, albeit M was able to induced ROS at high Mtb : PMN ratio, it was not able to induce ROS when DHR came from Mtb that has been ingested (MtbPMN), because of the sum of the low phagocytic rate and a poor ability to induce ROS. Therefore, we can assume that LAM is more efficient in entering PMN and also has a major capability to induce ROS than other strains. Moreover, it is possible that Mtb strains would not be qualitatively different in their capacity to induce ROS but merely show a quantitatively different dose-response curve that is finally reflected in apoptosis outcome.
Pathogens have developed strategies to counteract NADPH oxidase function and suppress generation of phagosomal ROS. The nuo G gene encodes the NuoG subunit of the type I NADH (nicotinamide adenine dinucleotide)-dehydrogenase of Mtb. Deletion of this gene leads to elevated ROS levels and apoptosis following infection of primary macrophages [40]. Similarly, deletion of the secA2 gene, which encodes a protein required for the secretion of superoxide dismutase A, results in enhanced ROS production and apoptosis. Superoxide dismutase A breaks down superoxide leading to diminished ROS generation, which is a mechanism that Mtb uses to prevent apoptosis [41]. Nevertheless, our data obtained with heat-killed bacteria suggest that the mechanism exerted by M might not involve those enzymes, but structural differences between clinical isolates leads to different ROS/apoptosis rate.
LAM and Haarlem are the two main families circulating in Latin American countries [2, 13, 14]. Among them, two clinical isolates differently interact with PMN in the host. In particular, M strain of the Haarlem family can be regarded as a highly successful genotype in Argentina because it has been able to prevail and persist over other MDR Mtb strains in the community [42, 43] being able to build up further drug resistance without impairing its ability to spread [15]. In this context, it has been described that, when killing is absent, not only could the disease progress locally, but the infected PMN could also traffic organisms to distal sites, in particular if bacilli reach the systemic circulation. Indeed, a granulocytic “Trojan horse” has been proposed by several authors in the context of mycobacterial infection [44]. Therefore, though less skillfully, M is able to enter the PMN and in turn generate fewer ROS. As a result, PMNs have less capacity to kill M and greater capacity to prolong its life, becoming a reservoir for this strain or another strain that uses this mechanism.
5. Conclusion
In conclusion, here we show that, independently of the ability to entering PMN, certain Mtb strains (as LAM) induce high PMN apoptosis by triggering signaling mechanisms that involves ROS generation via p38 activation, leading to enhanced effectors’ functions whereas others fail in activating PMN to kill pathogen as well as inducing apoptosis as a consequence of no. (1) a slight ROS production and (2) contribution of anti-apoptotic mechanism mediated at least by ERK, making PMN a “Trojan horse,” which could be a beneficial mechanism allowing some strains to prevail and persist over other strains in the community.
Abbreviations
Mtb :Mycobacterium tuberculosis
PMN: polymorphonuclear neutrophils
ROS: Reactive Oxygen Species
TB: tuberculosis
DHR: dihydrorhodamine
MAPK: mitogen-activated protein kinase.
Acknowledgments
This work was supported by Grants from the Agencia Nacional de Promoción Científica y Tecnológica, ANPCyT (PAE-PICT 2007–2329 and PAE-PICT 2007–2328), Consejo Nacional de Investigaciones Científicas y Técnicas, CONICET (PIP 112-200801-01476), and Fundación Alberto J Roemmers. The authors thank to the National Commission of Atomic Energy (CONEA) for Mtb irradiation and they specially thank Dr. Marta Finiazs for helpful comments and critical reading of the paper.
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Bibliography: Stern der Ungeborenen
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Title: Stern der Ungeborenen
Author: Franz Werfel
Year: 1946
Type: NOVEL
Language: German
ISFDB Record Number: 1353553
Note: WorldCat, OCLC 30733181 and 742525251 say that the 1946 first edition of this book was published by "S. Fischer" in Frankfurt, while OCLC 930118, 492948357, and 243738547 claim it was published by "Bermann-Fischer" in Stockholm. The Frankfurt records may be in error, or it may be that both companies were claiming the rights to this book.
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Water 2010, 2(3), 363-380; doi:10.3390/w2030363
Article
The Occurrence of Cold Spells in the Alps Related to ClimateChange
1 Department of General Physics “Amedeo Avogadro”, University of Torino, Via Pietro Giuria 1 10125, Torino (TO), Italy 2 Department of Environmental Science and Engineering, Severe Storm Research Center and Center for Climate/Environment Change Prediction Research, Ewha Womans University, Seoul 120-750, Korea
* Author to whom correspondence should be addressed.
Received: 23 June 2010; in revised form: 27 July 2010 / Accepted: 27 July 2010 / Published: 2 August 2010
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Abstract: Climate change is not only a likely prospect for the end of this century, but it is already occurring. Part of the changes will include global warming and increasing temperature variability, both at global and regional scales. This increased variability was investigated in this paper from the point of view of the occurrence of cold spells in the Alps in the future climate (2071–2100), compared with the present climate (1961–1990). For this purpose, a regionalisation of the climate change effects was performed within the Alps. To avoid possible errors in the estimate of the 2m air temperature, the analysis was performed on the soil surface temperature. To get realistic values for this variable, a land surface scheme, UTOPIA, has been run on the selected domain, using the output of the Regional Climate Model (RegCM3) simulations as the driving force. The results show that, in general, the number of cold breaks is decreasing over the Alps, due to the temperature increment. However, there are certain zones where the behaviour is more complicated. The analysis of the model output also allowed a relationship to be found between the number of cold breaks and their duration. The significance of these results over the whole area was assessed.
Keywords: cold spells; climate change; LSPM; UTOPIA; climate extremes
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Cite This Article
MDPI and ACS Style
Galli, M.; Oh, S.; Cassardo, C.; Park, S.K. The Occurrence of Cold Spells in the Alps Related to ClimateChange. Water 2010, 2, 363-380.
AMA Style
Galli M, Oh S, Cassardo C, Park SK. The Occurrence of Cold Spells in the Alps Related to ClimateChange. Water. 2010; 2(3):363-380.
Chicago/Turabian Style
Galli, Marco; Oh, Seungmin; Cassardo, Claudio; Park, Seon Ki. 2010. "The Occurrence of Cold Spells in the Alps Related to ClimateChange." Water 2, no. 3: 363-380.
Water EISSN 2073-4441 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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Contributors : Mohamed Hussein
Analyzed 7 days ago based on code collected 7 days ago.
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All-time Commits: 2
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Names in SCM: Mohamed Hussein
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User:Elaine Marie Robbins/Notebook/Capstone/2012/06/01
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Citrate AuNP Elongation Main project page
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Methods
1. Add 1 μL of diluted thiol-modified TS primer to 5.6 mL of citrate AuNP solution.
2. Mix 3 μL AuNP/TS primer, 0.5 μL 50x dNTP mix, 16 μL sterile water, 2.5 μL 10x PCR buffer, and 2 μL cell extract in a PCR tube.
3. Incubate in heat block at 30°C for 30 min.
Personal tools
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[59] And I have been induced by their testimony in his behalf, and by their entreaties, to offer him my service now, which he has so well deserved, and which on my part is only a repayment of just and reasonable gratitude. And I hope, O judges, as you love and consider dear to you those men who were the chief agents in my preservation and safety, and in the restoration of my dignity, that so also the things which were done by this man to the extent of his power and of the opportunities which were afforded him, will be grateful to and approved of by you. He, then, is not now attacked by his own enemies, for he has none, but by those of his friends; enemies who are both numerous and powerful; men whom yesterday Cnaeus Pompeius, in a very eloquent and dignified oration, desired to come forward and contend with him if they chose, but to abandon the unequal contest and unjust persecution which they were carrying on against this man.
This work is licensed under a Creative Commons Attribution-ShareAlike 3.0 United States License.
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PubCon Live: SEO Design & Organic Site Structure
Nov 11, 2009 • 4:20 pm | (0) by | Filed Under WebmasterWorld PubCon 2009 Las Vegas
Below is live coverage of the SEO Design & Organic Site Structure from the PubCon 2009 conference.
This coverage is provided by Brian Ussery - Beu Blog.
We are using a live blogging tool to provide the real time coverage, please excuse any typos. You can also interact with us and while we are live blogging, so feel free to ask us questions as we blog. We will publish the archive below after the session is completed.
Previous story: PubCon Live: Viral and Video - Two Good Things That Go Great Together
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Place:Lynwood, Cook, Illinois, United States
Watchers
NameLynwood
TypeVillage
Coordinates41.526°N 87.548°W
Located inCook, Illinois, United States
source: Getty Thesaurus of Geographic Names
the text in this section is copied from an article in Wikipedia
Lynwood is a village in Cook County, Illinois, United States. The population was 7,377 at the 2000 census.
Lynwood was founded in 1959. The Village is surrounded by Lansing to the north, Glenwood to the west, Sauk Village to the south, and Munster and Dyer, Indiana to the east. The Indiana state line borders the entire eastern edge of Lynwood. Lynwood is currently a mix of suburban neighborhoods with a substantial amount of remaining farmland.
Research Tips
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Place:Portage, Cambria, Pennsylvania, United States
Watchers
NamePortage
TypeBorough
Coordinates40.387°N 78.674°W
Located inCambria, Pennsylvania, United States
source: Getty Thesaurus of Geographic Names
source: Family History Library Catalog
the text in this section is copied from an article in Wikipedia
Portage is a home rule municipality, formerly a borough, within Portage Township in Cambria County, Pennsylvania, southeast of Ebensburg and west-southwest of Altoona. It is part of the Johnstown, Pennsylvania Metropolitan Statistical Area. Coal mining was the lifeblood of Portage. In 1900, 816 people lived there, and in 1910, there were 2,954 residents. The population was 2,837 at the 2000 census.
Research Tips
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Looking for a Store/Retail Deal? Search here.
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Tuesday, October 9, 2012
68% Off Photo Canvases + Free Shipping Exp 10/13
Now is a great time to start watching for deals that you can use for gifts for Christmas and the Holidays. A Photo Canvas is a wonderful personalized gift. Check out these deals today via Plum District. Shipping is Free on this offer Exp 10/13.
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Australian Bureau of Statistics
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Tell me more ×
Answers OnStartups is a question and answer site for entrepreneurs looking to start or run a new business. It's 100% free, no registration required.
X was working part-time on an idea and after about a year and a basic demo in hand, he talked to two potential people (A and B) who would become co-founders but would work part-time just like X. The split that they talked about was 20% for A and 30% for B (two years vesting) and X retained 50%.
After about a year they worked and build a MVP and have potential customers who are interested in using this. But for some really weird reason A and X can not continue working on it (they are not leaving by choice), leaving it to only B. X has completed almost two years and A and B have completed about a year.
Given the two year vesting schedule, X has 50% and A has 10% (due to vesting) and B has 15% (he will get the next 15% in the coming year).
How do they now carry things forward? How should B's work be valued for each that we works on this project. There is a potential plan to bring developers / business guys as and when needed.
The proposal: For each year that B works on this (part-time), he gets 15%, 12.5%, 10%, 7.5% and so on %. The idea is that the more the contribution from others including B, the more the share they get and the original % of X and A keeps going down. This is a way to penalize X and A because they are not working on it any more. For all the others joining the team, it would be a 2 year vesting for whatever share they get (until company is ready to pay salary)
As an example:
P 0.00 15.00 12.50 10.00 07.50 <- extra % for B
Y 01.00 02.00 03.00 04.00 05.00 <- Year
B 30.00 40.50 47.94 53.14 56.66 <- % for B
X 50.00 42.50 37.19 33.47 30.96 <- % for X
A 20.00 17.00 14.88 13.39 12.38 <- % for A
What do you think of this proposal? Is it reasonable for B to work on these terms, given his past contribution is same as present
share|improve this question
1 Answer
B should continue to work at his per-week labor value unless the value of that labor increases. As it stands, for each week B has worked to date, he has earned 0.288% of the business (after one year, he owned 15%; after two years he would own 30%). That amounts to a little less than 1.25% per month. This portion should be deducted from both X's and A's shares, either equally or proportionate to their remaining share value (which is easy to calculate with a spreadsheet).
I suspect this is fair because the "penalty" charged to X and A will be the decreased acceleration of the company's value due to the loss of their labor. You don't anticipate B to make up for both X and A in terms of productivity, do you?
If a larger portion is given to B in exchange for B's labor, then that extra is exceptionally generous. It wouldn't be unfair to give that interest to B, except perhaps unfair to X and A.
By the way, I think that X currently owns 75% of the company, not 50%. If A owns 10% and B owns 15%, the remaining 75% probably belongs to X (if it doesn't belong to some other unnamed entity).
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Research article
Anemia and the onset of gout in a population-based cohort of adults: Atherosclerosis Risk in Communities study
Mara A McAdams-DeMarco1,2*, Janet W Maynard3, Josef Coresh1 and Alan N Baer3
Author affiliations
1 Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, 615 N. Wolfe St, Baltimore, MD 21205, USA
2 Department of Surgery, Johns Hopkins University School of Medicine, 720 Rutland Ave, Baltimore, MD 21205, USA
3 Division of Rheumatology, Johns Hopkins University School of Medicine, 5200 Eastern Avenue, Mason F. Lord Building, Center Tower, Suite 4100; Baltimore, MD 21224, USA
For all author emails, please log on.
Citation and License
Arthritis Research & Therapy 2012, 14:R193 doi:10.1186/ar4026
Published: 20 August 2012
Abstract
Introduction
There is a growing prevalence of gout in the US and worldwide. Gout is a recognized risk factor for cardiovascular disease (CVD). It is unclear whether other risk factors for CVD are also associated with increased risk of gout. Anemia is one such CVD risk factor. No studies have evaluated the relationship between anemia and gout. We tested whether anemia was associated with incident gout independent of comorbid conditions in Atherosclerosis Risk in the Communities.
Methods
This population-based cohort recruited 15,792 individuals in 1987 to 1989 from four US communities and contained nine years of follow-up. Anemia was defined as hemoglobin <13.5 g/dL for men and <12 g/dL for women. Using a Cox Proportional Hazards model, we estimated the hazard ratio (HR) and confidence intervals (CI) of incident gout by baseline anemia, adjusted for confounders (sex, race, estimated glomerular filtration rate, body mass index and alcohol intake) and clinical factors (coronary heart disease, congestive heart failure, diabetes, hypertension, diuretic use and serum urate level).
Results
Among the 10,791 participants, 10% had anemia at baseline. There were 271 cases of incident gout. Patients with anemia had a two-fold increased risk of developing gout over nine years (HR = 2.01, 95% CI: 1.46, 2.76). Anemia was associated with incident gout independent of known gout risk factors, confounders and clinical risk factors (HR = 1.73, 95% CI: 1.24, 2.41). This association persisted after additionally adjusting for serum urate level (HR = 1.83, 95% CI: 1.30, 2.57).
Conclusion
We identified anemia as a novel risk factor for gout. Anemia was associated with an approximately two-fold increased risk of gout-independent kidney function and serum urate. These findings suggest that anemia is a risk factor for gout on par with other chronic conditions such as obesity and diabetes. The biological mechanism linking anemia to gout remains unclear.
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Notes from Nagios World Conference 2012
Ashish Vijayaram
1
Nagios World Conference 2012 was held between Sep 23 and Sep 28th at St. Paul, MN. I represented Mozilla IT/SRE along with Sheeri Cabral, who spoke about MySQL plugins. I wanted to share some observations and my best takeaways from the conference. I attended 11 talks in all and spoke to various speakers and other attendees about our setup and some tricky monitoring problems we’ve had to face.
My list of items to address at the conference were:
1. Discuss our Nagios setup – pros and cons. Do we have a sound setup? Do we use best practices and abide by guidelines, etc. How do we compare to other setups of similar magnitude?
2. Are there good ideas to reduce the number of actionable as well as unactionable alerts?
3. How are we scaling up? Can we scale better? Are there any tools that will help us deal with problems of scale?
4. Are we harnessing Nagios to the best of its capabilities? Are there more features that Nagios can provide that we lack?
5. General monitoring best practices and ideas.
Here are my notes for each of the above:
1. (Pros/Cons) Our Nagios setup is pretty well thought out and aligns very well with the best practices and recommendations that were suggested to the audience. Amongst the suggestions were to use hostgroups as much as possible over configuring hosts individually, separate out instances for better scalability (which we do on a per-DC basis), setup the Nagios servers on highly available clusters (most of our instances are VMs, which inherently provide availability and reliability), use chef/puppet/…, “play” with checkcommands instead of adding more plugins for similar functionality (see the number of check_http derivatives and our use of “-p <port number>” in http service checks) among others. There were some specific performance tuning tips (liveblog) that were given and I will work on implementing them.
2. (Reduce noise) This vastly depends on infrastructure stability. My assessment is that Mozilla IT is in a state of upward scale and it is difficult to “stabilise” in the traditional sense. I think it will take us a year or two to get to a state where most of our alerts mean real problems not not just potential problems or the ones that could cause problems if left unacknowledged over a period of time. This also requires an overhaul of service and operational SLAs. tl;dr we’ll get there in time. We can surely work on reducing unactionable alerts in the meantime and that should be a significant goal.
3. (Scale) We are scaling up pretty well. Our idea of an instance-per DC works very well. We are presently missing some form of an aggregation (think MNTOS, but better. Thruk maybe?), if at all. We currently monitoring less than 1500 hosts per instance and the (mostly) stock configuration has held up pretty well. As such I don’t find a lot of benefit in investing much time and effort into scaling (see Mod Gearman).
4. (Utilizing Nagios) We are using Nagios very very well. Between two-way communication using IRC bots and the assortment of alerting mechanisms we have, we are making pretty good use of what Nagios provides and adding more to it. I believe we’re still far from hitting the limits of what Nagios can do and even then we can leverage the tools that work with Nagios to extend it further (addons, plugins like check_mk and multisite). The beauty of Nagios lies in its simplicity. It does not have every. single. thing. a monitoring solution should have. Rather, it follows the UNIX philosophy of “do it less, do it well”. ’nuff said!
5. (Best practices) We are missing some good-to-have features such as performance graphing of Nagios itself as well as everything it monitors, analytics, trending (one word but super important, can make a world of difference. /me waves to Corey Shields who had proposed this earlier this year) and other good-to-have things. This is going to be an ongoing goal and something we should refine all the time. It’s also a little hard to work towards since defining specific items are itself tricky.
We were also introduced to Nagios Incident Manager (liveblog), an upcoming product which integrates with Nagios and is useful for handling high severity incidents. I would like to see this setup, since Bugzilla might not always be the best tool for such cases.
Lastly, I realized more than once that we have a kickass setup at Mozilla. Particularly, our puppet module is awesome and utilizes many sound principles. I strongly believe there is a *lot* of value in open-sourcing our manifests and templates. This is surely going to help a whole lot of people and earn us tons of goodwill amongst IT.
The guys from Nagios are great too – a good pack of developers and it’s very interesting to hear about monitoring crazy stuff, like Microsoft Word macros(!). Overall, I’d recommend being part of the Nagios Conferences if you’re serious about monitoring your stuff (and you should be)!
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A New Combined Approach of Technology Acquisition Using Priority Setting, A Case Study of Membrane Technology
Mostafa Jafari, Mahdi Sahafzadeh
Abstract
In this paper an overall approach of technology acquisition by using a priority setting method is proposed. In the management of technology literature, different methods of Technology Acquisition were developed. We categorized them into three levels: mode, mechanism and operational models. In this paper we developed an algorithm for choosing the best mode of technology acquisition in the specific technology. The algorithm is combination of critical technologies method and some criteria such as cost of technology acquisition mode. Concurrently priorities of technologies will be set. Finally we applied this approach to membrane technology in Iranian petrochemical industry.
Full Text: PDF
This work is licensed under a Creative Commons Attribution 3.0 License.
Asian Social Science ISSN 1911-2017 (Print) ISSN 1911-2025 (Online)
Copyright © Canadian Center of Science and Education
To make sure that you can receive messages from us, please add the 'ccsenet.org' domain to your e-mail 'safe list'. If you do not receive e-mail in your 'inbox', check your 'bulk mail' or 'junk mail' folders.
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Error!
Success!
Dependency Injection
0
kicks
Dependency Injection (Unpublished)
Dependency Injection is a design principle to create independent code blocks. DI identifies each object dependencies and removes it by injecting the object externally to the class. In this post I gave you a sample implementation of DI and DI Containers.
Kicked By:
Drop Kicked By:
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RPi FAQ
From eLinux.org
Revision as of 07:57, 25 February 2012 by Jim Manley (Talk | contribs)
Jump to: navigation, search
The Rpi beta board (model B)
A 3D rendering of the Raspberry Pi logo by forum user Antario. Source
Contents
INTRODUCTION
What’s a Raspberry Pi?
The Raspberry Pi is a credit-card sized computer that plugs into your TV and a keyboard. It’s a capable little PC which can be used for many of the things that your desktop PC does, like spreadsheets, word-processing and games. It also plays high-definition video. We want to see it being used by kids all over the world to learn programming.
Can I buy shares in the Raspberry Pi Foundation?
We’re a charity, so you can’t buy shares in the company. If you want to support us, we’d love you to buy one. We’ll also be offering a package where you can do a buy-one-give-one purchase, and we’ll be accepting donations too once we start shipping.
BUYING AND SHIPPING
When can I buy one?
We are hoping to have the Raspberry Pi available to order at the end of February 2012. The initial production run will be 10,000 uncased development-style boards with further productions runs starting once these have been sold.
Where can I buy one?
The Raspi will initially only be available to purchase through RaspberryPi.org – if you sign up to the mailing list on the home page you’ll be notified as soon as we’re ready to start shipping.
How many can I buy in one go?
For the first batch we are limiting orders to one per person. This restriction will be relaxed as production gets in to full swing, and we can be sure of getting boards to all who want them. This should prevent eBay scalping (to some extent – we will also be auctioning some boards ourselves to try to make sure there’s no market for scalpers), and ensure that as many different individuals as possible get their Raspberry Pi!
How much will it cost?
The Model A will cost $25 and the Model B $35, plus local taxes.
How can I pay for it?
We will accept most major cards, PayPal, and offline payments.
What will I get when I buy one?
A Raspberry Pi. Leads, a power supply or SD cards are not included but can be purchased at the same time from the store. You will be able to buy preloaded SD cards too. The first batch (February 2012) will not have a case.
Why is the price in US Dollars? You’re a UK company!
The components we buy are priced in dollars, and we negotiate manufacturing in dollars. Because currency markets are so volatile at the moment, we price the final board in dollars too so we don’t have to keep changing the price.
Will there be a buy-one-give-one program?
Yes. We plan to implement a program of this sort, but you can also just buy one if you prefer.
Will the device be available internationally?
We intend to ship worldwide from launch. We may establish a distribution network in due course.
How much will it cost to ship to [country X]?
We don’t know yet; we're still negotiating about logistics. The people we're talking to have local distribution points all over the world, so you can have your Raspberry Pi shipped from somewhere closer than the UK.
Will there be a minimum order quantity?
The minimum order quantity will be one unit.
Do you accept pre-orders?
No. We are adequately funded, and don’t want to take your money until we have finished hardware.
I want to be a Raspberry Pi reseller.
We are not taking requests for people to be resellers at the moment.
Can I join the mailing list?
You certainly can. Head to the home page, and you’ll see a form at the top right you can fill in. People who are signed up will get an e-mail as soon as we have confirmed a release date.
GENERAL
What’s the difference between Model A and Model B?
Model A has 128Mb of RAM, one USB port and no Ethernet (network connection). Model B has 256Mb RAM, two USB ports and a 100Mbits/sec Ethernet port.
What are the dimensions of the Raspberry Pi?
The Raspberry Pi measures 85.60mm x 53.98mm x 17mm, with a little overlap for the SD card and connectors which project over the edges. It weighs 45g.
What SoC are you using?
The SoC is a Broadcom BCM2835. This contains an ARM1176JZFS, with floating point, running at 700Mhz, and a Videocore 4 GPU. The GPU is capable of BluRay quality playback, using H.264 at 40M bits/s. It has a fast 3D core accessed using the supplied OpenGL ES 2.0 and OpenVG libraries.
Why did you select the ARM11?
Cost and performance.
How powerful is it?
The GPU provides Open GL ES 2.0, hardware-accelerated OpenVG, and 1080p30 H.264 high-profile decode.
The GPU is capable of 1 Gpixel/s, 1.5 Gtexel/s or 24 GFLOPs of general purpose compute and features a bunch of texture filtering and DMA infrastructure.
That is, graphics capabilities are roughly equivalent to Xbox 1 level of performance. Overall real-world performance is something like a 300MHz Pentium II, only with much, much swankier graphics.
Will it overclock?
There’s a little overclocking headroom – most devices will run happily at 800MHz. There’s no BIOS per se, but we do support booting bare metal code, so something could be done.
Will it blend?
Yes. We have conducted extensive virtual simulations. No Raspberry Pis were harmed in the testing.
How does it boot?
You have to boot from SD but a USB HD can “take over” after the initial boot. You cannot boot without an SD card.
Where’s the on / off switch?
To switch on: just plug it in!
To switch off: remove power.
Why is there no real time clock (RTC)?
The expectation is that non-network connected units will have their clocks updated manually at startup. Adding an RTC is surprisingly expensive, once you’ve factored in batteries, area and componentry and would have pushed us above our target price. You can add one yourself using the GPIO pins if you’re after an interesting electronics project.
Will you sell a self-assembly kit?
No. It would be too expensive for us to provide kits alongside finished boards, which would mean introducing another step in manufacturing; and a kit would be impossible to hand solder. We use special equipment (robots!) to solder on the BGA package and other tiny components.
Can I add extra memory?
No. The RAM is a POP package on top of the SoC, so it’s not removable or swappable.
What hardware documentation will be available?
Broadcom don’t release a full datasheet for the BCM2835, which is the chip at the heart of the Raspberry Pi. We will release a datasheet for the SoC which will cover the hardware exposed on the Raspi board e.g. the GPIOs. We will also release a board schematic later on.
But I want documentation for <hardware X>!
Other documentation may be released in future but this will be at the Foundation’s discretion.
But I demand the documentation for the chip. Give it to me!
To get the full SoC documentation you would need to sign an NDA with Broadcom, who make the chip and sell it to us. But you would also need to provide a business model and estimate of how many chips you are going to sell.
Why doesn’t the Raspberry Pi include <insert name> piece of hardware or <insert name> sort of port?
Our main function is a charitable one – we’re trying to build the cheapest possible computer that provides a certain basic level of functionality, and keeping the price low means we’ve had to make hard decisions about what hardware and interfaces to include.
Can you test it to make sure that it is suitable for <X>?
If you want to use it for something that we haven’t tested, and that it’s not intended for (i.e. anything but the educational work we’re planning for it), then that development work is up to you.
How do I connect a mouse and keyboard?
Model A has one USB port and Model B has two. Beyond this, mice, keyboards, network adapters and external storage will all connect via a USB hub.
CASES
Will it have a case?
Not for the first batch. We’ll be making and selling cases by the summer; you'll be able to buy a unit with or without a case, or a case on its own. The education release later in 2012 will have a case by default. There are lots of homebrew case discussions on the forum.
Will it fit in an Altoids tin?
Doesn’t quite work, I’m afraid – because we don’t round off the edges of the board, it’s a little too big to fit the tin.
GRAPHICS
What display can I use?
There is composite and HDMI out on the board, so you can hook it up to an old analog TV, to a digital TV or to a DVI monitor (using a cheap adapter for the DVI). There is no VGA support, but adaptors are available, although these are relatively expensive.
Why is there no VGA support?
The chip specifically supports HDMI. VGA is considered to be an end-of-life technology, so supporting it doesn’t fit with our plans at the moment.
Is there a GPU binary?
Yes. The GPU binary also contains the first stage bootloader.
Can I add a touchscreen?
We haven’t experimented with any touchscreens yet, but there’s no electronic reason why it shouldn’t work. There’s lots of discussion about this on the forums. The main issue people are encountering seems to be one of cost; touchscreens are very pricey!
What is the usable temperature range?
The Raspberry Pi is built from commercial chips which are qualified to different temperature ranges; the LAN9512 is specified by the manufacturers being qualified from 0°C to 70°C, while the AP is qualified from -40°C to 85°C. You may well find that the board will work outside those temperatures, but we’re not qualifying the board itself to these extremes.
AUDIO
Is sound over HDMI supported?
Yes.
What about standard audio in and out?
There’s a standard 3.5mm jack for audio out. You can add any supported USB microphone for audio in.
POWER
What are the power requirements?
The device is powered by 5v micro USB. You can read more about it here. Power supplies will be available at launch.
Can I run power Raspberry Pi from batteries as well as from a wall socket?
Yes. The device should run well off 4 x AA cells.
Is power over Ethernet (PoE) possible?
Not in the base device, but it’s been a very commonly requested feature, so we’re examining options for later releases.
SOFTWARE
What operating system (OS) does it use?
We’ll be using Fedora as our recommended distribution. It’s straightforward to replace the root partition on the SD card with another ARM Linux distro if you want to use something else. The OS is stored on the SD card.
Does it have an official programming language?
By default, we’ll be supporting Python as the educational language.
Any language which will compile for ARMv6 can be used with the Raspberry Pi, though; so you’re not limited to using Python.
Will it run WINE (or Windows, or other x86 software)?
No.
What Linux distros will be supported at launch?
Fedora, Debian and ArchLinux will be supported from the start. We hope to see support from other distros later. (Because of issues with newer releases of Ubuntu and the ARM processor we are using, Ubuntu can’t commit to support Raspberry Pi at the moment.) You will be able to download distro images from us as soon as the Raspberry Pi is released, and we will also be selling pre-loaded SD cards shortly after release.
Will it run Android?
If someone in the community can port a version of Android to work with 256MB of RAM, then it’ll run on the Raspberry Pi.
Will it run <insert name of program here>?
In general, you need to look to see whether the program you want can be compiled for the ARMv6 architecture. In most cases the answer will be yes. Specific programs are discussed on our forum, so you might want to look there for an answer.
Will it run the new Windows 8 ARM version?
We are not partners with Microsoft, and their support would be required for porting Windows 8.
SD cards and storage
We have tried cards up to 32GB and most cards seem to work OK. The Wiki has more information about which makes and models work best. You can also attach a USB stick or USB hard drive for storage.
What happens if I brick the device?
You can restore the device by reflashing the SD card.
NETWORKING, USB AND WIRELESS
Does the device support networking? Is there Wi-Fi?
The Model B version of the device includes 10/100 wired Ethernet. There is no Ethernet on the Model A version (which we expect to be taken up mostly by the education market), but Wi-Fi will be available via a standard USB dongle.
Will there be a WiFi option?
Not in the first version, though you can add a dongle. ARM Linux WiFi support can be a bit patchy; there’s a list of tested dongles on the wiki.
Why no Gigabit Ethernet?
The Ethernet is driven via USB 2.0, so the upstream bandwidth would not support Gigabit.
Does the device have support for any form of netbooting or pxe?
No. However, it’s such a low power device that we expect it to be left on much of the time!
How do you connect more than two USB devices?
Use a hub to increase the number of ports. Some keyboards have hubs built in which would work well.
EDUCATIONAL USES
What educational material will be available?
We’re working with partners to get software materials developed, as well as with the open source community. Computing at School are writing a user guide and programming manual, we’re aware of a few books being planned and written around the Raspberry Pi, and others have already started to produce some excellent tutorials including video. We’re also working with partners to use it as a teaching platform for other subjects, including languages, math, and so on.
Once we launch, we hope that the community will help bodies like Computing at School put together teaching material such as lesson plans and resources and push this into schools. In due course, the foundation hopes to provide a system of prizes to give young people something to work towards.
There’s lots of discussion of educational uses and resources in our forums – come and have a chat!
GLOSSARY
BGA: ball grid array. A type of surface mount packaging for electronics.
SoC: system on chip. A computer on a single chip.
GPIO: General purpose input/output. A pin that can be programmed to do stuff.
GPU: graphics processing unit. The hardware the handles the graphics.
Distro: a specific package (“flavor”) of Linux and associated software.
Brick: to accidentally render a device inoperative by making changes to software or firmware.
Pxe: preboot execution environment. A way to get a device to boot via the network.
PoE: power over ethernet. Powering a device via an ethernet cable.
R-Pi_Personal_FAQs
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Difference between revisions of "Yocto Project Introduction"
From eLinux.org
Jump to: navigation, search
(The main parts)
(Build output)
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distribution.
distribution.
The directory where the software resides after a typical build is: <build_top_dir>/tmp/deploy
+
The directory where the software resides after a typical build is: <build_top_dir>/tmp/deploy and <build_top_dir>/tmp/sysroots.
+
The 'sysroots' directory contains the directory structure and contents for the root filesystem for a target build.
+
(Except it seems to be missing /dev, and it doesn't have root ownership - it probably needs pseudo to see the full contents). The 'deploy' directory has the images or packages that are ready to be installed on the device.
Revision as of 19:33, 3 August 2012
This is an introduction about the Yocto Project, written from the point of view of someone somewhat familiar with embedded Linux development and embedded Linux distribution maintenance. In my own investigation of the Yocto Project, I found that there were a few key concepts that I didn't find discussed or presented anywhere. I'd like to fix that with this page. The purpose of this page is to give a broad overview of how the project technically works, so that the learning curve for people approaching the Yocto Project for the first time is lessened.
Contents
The big picture
The Yocto Project is a collection of tools and meta-data (defined in a bit) that allows a developer to build their own custom distribution of Linux for their embedded platform. This could be a developer at a semi-conductor company, who wishes to develop board support for one of their hardware platforms, or it could be an independent developer writing a complete software stack for a product they are making. It could also be a group of engineers developing a distribution for use in multiple devices or products -- such as an embedded Linux distribution company, or the "systems" team at a company that produces multiple embedded Linux products.
The main parts
The main parts of the Yocto Project are the build system, the package meta-data, and the developer tools. The build system uses a tool called "bitbake" to process the meta-data and produce a complete Linux distribution. By design, the build system produces not just the software that will run on the target, but also the development tools used to build that software. It basically starts completely from scratch, building all the tools needed to construct the software, and then using those to build the kernel, libraries, and programs that comprise a Linux distribution. Finally, it prepares the resulting software by placing it into appropriate bundles (including packages, images, or both) for deployment to the target device and in preparation for application development and debugging. The Yocto Project also includes various additional tools used to develop embedded Linux or applications on top of it. This includes things such as emulators, IDEs and host/target (cross) agents and debug tools.
Let's start by describing some of the concepts of the build system...
Build system
The primary tool used in the build system is called 'bitbake'. Bitbake has a user-manual at http://docs.openembedded.org/bitbake/html/ . (As of August, 2012, this document appears to be a bit dated, and missing a few items of importance.) Basically, bitbake can be thought of as "make" on steroids. It basically performs the same type of functionality as make - which is: determining the actions to perform based on 1) what the user requests at the command line, 2) the project data and 3) the existing build state, and then performing those actions.
Bitbake uses it's own new syntax for expressing:
• the tasks to perform
• the relationships (dependencies) between those tasks
• the variables that control how the tasks are performed
• the actual build instructions (e.g. compiler commands, linker commands, packaging commands, etc.)
Bitbake differs from 'make' in several key ways. The first is that it has a global view of the task list for a distribution. That is, it reads the entire set of files related to the distribution, and determines the global task list for a particular high-level build operation. This is considerably different from 'make', which processes just a single Makefile at a time. (Admittedly, 'make' can be made to work with extremely large projects, using complex include schemes and nested invocations. However, even these types of system are rarely used for something as complex as a complete Linux distribution build.)
Another apparent difference is that the syntax of the files that bitbake processes allows for a very high degree of flexibility in defining the tasks that should be performed and the variables that control the build process and output.
[note to consider: maybe too much flexibility?]
A variety of mechanisms (described in the bitbake manual) are used to control what operations are performed and what variables are used to control them. bitbake supports inheritance mechanisms, to allow for a class-like definition of common operations which can be customized for specific situations. It also supports the conditional definition of new tasks, and has the ability to customize or eliminate (mask) tasks based on variables computed during the build.
Bitbake is written in Python, and some aspects of the build system can be written using short Python snippets as well. Many aspects of the system are written in snippets of shell code as well.
The meta-data
A key element of the Yocto Project is the meta-data which is used to construct a Linux distribution.
Meta-data refers to the build instructions themselves, as well as the data used to control what things get built and to affect how they are built. The meta-data also includes commands and data used to indicate what versions of software are used, where they are obtained from. The meta-data also consist of changes or additions to the software itself (patches or auxiliary files), used to fix bugs or customize the software for use in a particular situation.
The build instructions consists of commands to execute the compiler, linker, archiver, packaging tools and other programs.
The Yocto Project provides the build tool (bitbake) and meta-data itself, for a few distributions. Much of this meta-data can be re-used when someone is building their own distribution. The Yocto Project is related to the OpenEmbedded project, where the bitbake tool, much of the meta-data, and many of the meta-data concepts originated.
Each software component on the system (such as an individual program) has associated with it one or more files to express it's meta-data (dependencies, patches, build instructions). A top-level (usually single) file that defines the 'tasks' for the software is provided in a ".bb" (bitbake) file. This is referred to as that component's "recipe" file. This file may be terse, as the system allows for inheritance and inclusion. Class files (.bbclass) are used to express the meta-data for commonly-used types of build and packaging operations. These files are 'inherit'ed into a recipe. Include files (.inc) are sometimes used to provide a common set of definitions, which can be customized for a particular version of the software. These files are included into a recipe using a 'require' command. Finally, patches and auxiliary files may be associated with recipe. These files can be referenced by the build instructions (eg. applied to the software after fetching it and before compiling it in the case of patches) of the recipe.
A set of bitbake files that are related to a particular feature area can be organized into a "layer". This represents a collection of software or build tasks that can included into an overall distribution.
Finally, a user selects the individual bitbake files to include, or sets of files from different layers, by referencing them in their local configuration (conf/bblayers.conf) and expressing build controls, also in their local configuration (conf/local.conf).
Build stages
The recipes for a distribution define a number of discreet tasks that are performed to accomplish the build. The tasks have names such as 'fetchall', 'configure', 'compile'. Internally, these tasks are prefixed with 'do_' (eg. do_configure)
There can be a large number of tasks associated with a software component. By default, bitbake performs all tasks associated with building a software component and preparing it for deployment. However, bitbake can be used to perform just a single task relative to a component, using the '-c' command line option.
For example, to just perform the 'configure' task for the busybox software, you can do the following:
bitbake busybox -c configure
Note that is busybox has already been built, this command might not do anything (because bitbake avoids re-running tasks that are not needed, like 'make'). To force it, you could use the '-f' option:
bitbake busybox -c configure -f
Not every software component needs every build stage, so some might not be defined for a component. To see the list of tasks that a recipe defines for a component, execute the 'listtasks' task for that component:
bitbake busybox -c listtasks
This is a list of the tasks associated with busybox (as of Poky version 7.0)
do_fetchall
do_build
do_devshell
do_cleansstate
do_configure
do_cleanall
do_populate_lic
do_package_write
do_populate_sysroot
do_buildall
do_package_write_rpm
do_menuconfig
do_populate_lic_setscene
do_patch
do_listtasks
do_compile
do_package_setscene
do_fetch
do_checkuri
do_clean
do_package_write_rpm_setscene
do_package
do_unpack
do_install
do_populate_sysroot_setscene
do_checkuriall
Build work areas
The area where each software component is built is dependent on the recipe name, the distro name, build tool and whether the target architecture for the component. During the build, some items are built for the host machine and some are built for the target machine. In embedded Linux these are often different architectures.
The directory used for an individual component is something like:
<build_top_dir>/tmp/work/<arch-distro-tool-dir>/<package_name_and_version>
For example, in a build of the busybox code for the ARM qemu emulator platform with yocto version 7.0 was located in: <build_top_dir>/tmp/work/armv5te-poky-linux-gnueabi/busybox-1.19.4-r2
The build directory for the sqlite database tool, for use on my Ubuntu 12.04 (x86_64) host, was located at: <build_top_dir>/tmp/work/x86_64-linux/sqlite3-native-3.7.10-r2
The work directory for a software component contains not only the source code for the item, but additional data related to building it, staging it for installation into a package or image, and a 'temp' directory which has logs of the various build tasks. The work directory is useful to know if you want to customize the software (for example if you need to make a bugfix or apply some external patch), or determine why some build operation (such as fetching, compiling, packaging, etc.) is failing.
In the 'temp' directory under the work directory are both 'run' files and log files. The 'run' files are actually shell scripts or python scripts that are executed during the different build stages. The log files have the output from the commands that were used to build the software.
Other directories under the work directory are used for packaging the software's output files, or staging them for inclusion in a system image, or for staging other information about the package, such as it's software license.
Build output
The software for an embedded device can be packaged multiple different ways, in preparation for deployment to the actual device. For some systems, the built software is packaged into kernel and filesystem images, which can then be directly written to flash or storage media on the device. For other systems, the software may be bundled as packages (similar to the way desktop distributions of Linux are delivered). These might require developer or even end-user installation on the target device. The Yocto Project build system is capable of producing images and packages in several formats, that are selectable by the developer in the local configuration for the distribution.
The directory where the software resides after a typical build is: <build_top_dir>/tmp/deploy and <build_top_dir>/tmp/sysroots. The 'sysroots' directory contains the directory structure and contents for the root filesystem for a target build. (Except it seems to be missing /dev, and it doesn't have root ownership - it probably needs pseudo to see the full contents). The 'deploy' directory has the images or packages that are ready to be installed on the device.
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{
"content_type": "text/html",
"provenance": "cccc-CC-MAIN-2013-20-0000.json.gz:6600",
"uncompressed_offset": 91152095,
"url": "familysearch.org/learn/wiki/en/Newton_County,_Arkansas",
"warc_date": "2013-11-22T14:52:20.000Z",
"warc_filename": "<urn:uuid:6665fd01-f1d9-4202-9b85-a205e59b6354>",
"warc_url": "http://familysearch.org/learn/wiki/en/Newton_County,_Arkansas"
}
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Newton County, ArkansasEdit This Page
From FamilySearch Wiki
United States Arkansas Newton County
Guide to Newton County Arkansas genealogy. Birth records, marriage records, death records, census records, family history, and military records.
Arkansas
Online Records
Newton County, Arkansas
Map
Location in the state of Arkansas
Location of Arkansas in the U.S.
Facts
Founded December 14, 1842
County Seat Jasper
Courthouse
Address Newton County Courthouse
Court Street
Jasper, AR 72641-0435
Phone: 870.446.5125
Adopt-a-wiki page
This page adopted by:
ARGenWeb Project
who welcome you to contribute.
Adopt a page today
Contents
County Courthouse
Newton County Courthouse
Court Street
Jasper, AR 72641-0435
Phone: 870.446.5125
County Clerk has marriage and land records
from 1866, probate and court records from 1880[1]
History
Parent County
• 1842--Newton County was created 14 December 1842 from Carroll County. County seat: Jasper [2]
Boundary Changes
See an interactive map of Newton County boundary changes.
Record Loss
Places/Localities
Populated Places
Neighboring Counties
Resources
Cemeteries
Church
Church records and the information they provide vary significantly depending on the denomination and the record keeper. They may contain information about members of the congregation, such as age, date of baptism, christening, or birth; marriage information and maiden names; and death date. For general information about Arkansas denominations, view the Arkansas Church Records wiki page.
Court
Land
Land and property records can place an ancestor in a particular location, provide economic information, and reveal family relationships. Land records include: deeds, abstracts and indexes, mortgages, leases, grants and land patents.
See Arkansas Land and Property for additional information about early Arkansas land grants. After land was transferred to private ownership, subsequent transactions were usually recorded at the county courthouse and where records are currently housed.
Local Histories
Local histories are available for Newton County, Arkansas. County histories may include biographies, church, school and government history, and military information. For more information about local histories, see Arkansas Local Histories.
Maps
Military
Civil War
• Men from Newton County served in the 1st Regiment, Arkansas Infantry (Union) 1 and in the 3rd Regiment, Arkansas Cavalry (Union)2. 1Arkansas. Adjutant General's Office.Report of the Adjutant General of Arkansas, for the period of the late rebellion, and to November 1, 1866 (Bethesda, Maryland : University Publications of America, c1990) .
2Allen, Desmond Walls. The Third Regiment, Arkansas Cavalry (Union) Infantry (Arkansas Research: Conway, Arkansas,1987).
Newspapers
Additional newspapers abstracts can sometimes be found using search phrases such as Newton County, Arkansas newspapers in online catalogs like:
Probate
Probate records of Arkansas have been kept by the probate or county courts. You can obtain copies of the original records by contacting the clerk's office in the county courthouse.
The Family History Library has microfilm copies of many Arkansas probate records. See Arkansas Probate Records for more information about Probate records in Arkansas, including statewide indexes.
Taxation
Arkansas tax records replace missing censuses and provide lists of residents during years between censuses. There may be gaps of several years for some counties. For more information see Arkansas Taxation.
Vital Records
Vital Records consist of births, adoptions, marriages, divorces, and deaths recorded on registers, certificates, and documents. A copy or an extract of most original records can be purchased from the Arkansas Vital Records State Department of Health or the County Clerk's office of the county where the event occurred. See also Arkansas Vital Records Online and Arkansas Statewide Indexes and Collections at the Family History Library.
Marriage
Societies and Libraries
Family History Centers
Web Sites
References
1. The Handybook for Genealogists : United States of America, 10th ed., (Draper, UT: Everton Publishers, 2002), p. 69.
2. The Handybook for Genealogists: United States of America,10th ed. (Draper, UT:Everton Publishers, 2002).
3. FamilySearch Wiki contributors, "Arkansas County Marriages (FamilySearch Historical Records)," in FamilySearch Wiki, accessed 18 April 2013.
4. Genealogical Society of Utah, Parish and Vital Records List (July 1998). Microfiche. Digital version at https://www.familysearch.org/learn/wiki/en/images/d/d7/Arkansasnz.pdf.
Need additional research help? Contact our research help specialists.
Need wiki, indexing, or website help? Contact our product teams.
Did you find this article helpful?
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• This page was last modified on 17 May 2013, at 20:53.
• This page has been accessed 1,574 times.
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{
"content_type": "text/html",
"provenance": "cccc-CC-MAIN-2013-20-0000.json.gz:6611",
"uncompressed_offset": 109351908,
"url": "genomebiology.com/2007/8/2/R23/abstract",
"warc_date": "2013-11-22T14:52:20.000Z",
"warc_filename": "<urn:uuid:6665fd01-f1d9-4202-9b85-a205e59b6354>",
"warc_url": "http://genomebiology.com/2007/8/2/R23/abstract"
}
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Method
Clustering of phosphorylation site recognition motifs can be exploited to predict the targets of cyclin-dependent kinase
Alan M Moses*, Jean-Karim Hériché and Richard Durbin
Author Affiliations
Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1HH, UK
For all author emails, please log on.
Genome Biology 2007, 8:R23 doi:10.1186/gb-2007-8-2-r23
Published: 22 February 2007
Abstract
Protein kinases are critical to cellular signalling and post-translational gene regulation, but their biological substrates are difficult to identify. We show that cyclin-dependent kinase (CDK) consensus motifs are frequently clustered in CDK substrate proteins. Based on this, we introduce a new computational strategy to predict the targets of CDKs and use it to identify new biologically interesting candidates. Our data suggest that regulatory modules may exist in protein sequence as clusters of short sequence motifs.
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2hanksbz5r6eobwnau5oilu2oezcspfe
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{
"content_type": "text/html",
"provenance": "cccc-CC-MAIN-2013-20-0000.json.gz:6612",
"uncompressed_offset": 109363551,
"url": "genomebiology.com/2012/13/12/181/abstract",
"warc_date": "2013-11-22T14:52:20.000Z",
"warc_filename": "<urn:uuid:6665fd01-f1d9-4202-9b85-a205e59b6354>",
"warc_url": "http://genomebiology.com/2012/13/12/181/abstract"
}
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Research highlight
Irreconcilable differences: divorcing geographic mutation and recombination rates within a global MRSA clone
Todd J Treangen1,2 and Adam M Phillippy1,2*
Author Affiliations
1 National Biodefense Analysis and Countermeasures Center, Frederick, MD 21702, USA
2 Center for Bioinformatics and Computational Biology, University of Maryland, College Park, MD 20742, USA
For all author emails, please log on.
Genome Biology 2012, 13:181 doi:10.1186/gb-2012-13-12-181
Published: 27 December 2012
Abstract
A growing resource of methicillin-resistant Staphylococcus aureus (MRSA) genomes uncovers intriguing phylogeographic and recombination patterns and highlights challenges in identifying the source of these phenomena.
See related Research: http://genomebiology.com/2012/13/12/R126 webcite
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{
"content_type": "text/html",
"provenance": "cccc-CC-MAIN-2013-20-0000.json.gz:6616",
"uncompressed_offset": 111860840,
"url": "globalvoicesonline.org/-/world/western-europe/vatican-city/",
"warc_date": "2013-11-22T14:52:20.000Z",
"warc_filename": "<urn:uuid:6665fd01-f1d9-4202-9b85-a205e59b6354>",
"warc_url": "http://globalvoicesonline.org/-/world/western-europe/vatican-city/"
}
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GlobalVoices in Learn more »
Vatican City
Country archive · 2 posts
Latest stories about Vatican City
10 February 2009
Italy: In Defense of the “Right to die”
A legal battle over a young woman's 'right to die' after 17 years in a coma has spurred both vast online commentary and activism in Italy. Mostly in defense of "Eluana Englaro's choice", Italian netizens have signed petitions, organized protests, and made YouTube videos of their own 'living will' testimonies, in defiance of both prime minister Silvio Berlusconi and the Vatican.
22 April 2008
U.S. Papal Visit: The World Reacts
As Pope Benedict XVI makes his first papal visit to the United States, the media and blogosphere are in a frenzy - primarily due to the sexual abuse scandal that shook the foundation of the American Catholic church six years ago. The Pope addressed the issue in Washington D.C. on Thursday, speaking with victims of sexual abuses, which pleased some bloggers but for others was too little too late.
World regions
Countries
Languages
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{
"content_type": "text/html",
"provenance": "cccc-CC-MAIN-2013-20-0000.json.gz:6628",
"uncompressed_offset": 138301863,
"url": "josm.openstreetmap.de/ticket/7291",
"warc_date": "2013-11-22T14:52:20.000Z",
"warc_filename": "<urn:uuid:6665fd01-f1d9-4202-9b85-a205e59b6354>",
"warc_url": "http://josm.openstreetmap.de/ticket/7291"
}
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Modify
#7291 closed defect (fixed)
Can't use WMS layer in 4818
Reported by: jezevec Owned by: jezevec
Priority: critical Component: Core
Version: latest Keywords:
Cc: jttt
Description (last modified by skyper)
Josm report bug after wms use attempt (I test few different sources)
Repository Root: http://josm.openstreetmap.de/svn
Build-Date: 2012-01-19 02:33:08
Last Changed Author: bastiK
Revision: 4818
Repository UUID: 0c6e7542-c601-0410-84e7-c038aed88b3b
URL: http://josm.openstreetmap.de/svn/trunk
Last Changed Date: 2012-01-18 20:43:48 +0100 (Wed, 18 Jan 2012)
Last Changed Rev: 4818
Identification: JOSM/1.5 (4818 cs)
Memory Usage: 151 MB / 989 MB (70 MB allocated, but free)
Java version: 1.6.0_29, Sun Microsystems Inc., Java HotSpot(TM) Client VM
Operating system: Windows Vista
Dataset consistency test: No problems found
Plugin: ElevationProfile (27285)
Plugin: Tracer (27354)
Plugin: buildings_tools (27355)
Plugin: download_along (27289)
Plugin: licensechange (27472)
Plugin: measurement (27289)
Plugin: multipoly-convert (27289)
Plugin: openstreetbugs (27355)
Plugin: plastic_laf (26605)
Plugin: reverter (27393)
Plugin: turnrestrictions (27355)
Plugin: undelete (27395)
Plugin: utilsplugin2 (27426)
Plugin: waydownloader (27289)
java.lang.NullPointerException
at org.openstreetmap.josm.data.imagery.WmsCache.removeNonReferencedFiles(WmsCache.java:246)
at org.openstreetmap.josm.data.imagery.WmsCache.loadIndex(WmsCache.java:219)
at org.openstreetmap.josm.gui.layer.WMSLayer.<init>(WMSLayer.java:173)
at org.openstreetmap.josm.gui.layer.ImageryLayer.create(ImageryLayer.java:133)
at org.openstreetmap.josm.actions.AddImageryLayerAction.actionPerformed(AddImageryLayerAction.java:45)
at javax.swing.AbstractButton.fireActionPerformed(Unknown Source)
at javax.swing.AbstractButton$Handler.actionPerformed(Unknown Source)
at javax.swing.DefaultButtonModel.fireActionPerformed(Unknown Source)
at javax.swing.DefaultButtonModel.setPressed(Unknown Source)
at javax.swing.AbstractButton.doClick(Unknown Source)
at javax.swing.plaf.basic.BasicMenuItemUI.doClick(Unknown Source)
at javax.swing.plaf.basic.BasicMenuItemUI$Handler.mouseReleased(Unknown Source)
at java.awt.AWTEventMulticaster.mouseReleased(Unknown Source)
at java.awt.Component.processMouseEvent(Unknown Source)
at javax.swing.JComponent.processMouseEvent(Unknown Source)
at java.awt.Component.processEvent(Unknown Source)
at java.awt.Container.processEvent(Unknown Source)
at java.awt.Component.dispatchEventImpl(Unknown Source)
at java.awt.Container.dispatchEventImpl(Unknown Source)
at java.awt.Component.dispatchEvent(Unknown Source)
at java.awt.LightweightDispatcher.retargetMouseEvent(Unknown Source)
at java.awt.LightweightDispatcher.processMouseEvent(Unknown Source)
at java.awt.LightweightDispatcher.dispatchEvent(Unknown Source)
at java.awt.Container.dispatchEventImpl(Unknown Source)
at java.awt.Window.dispatchEventImpl(Unknown Source)
at java.awt.Component.dispatchEvent(Unknown Source)
at java.awt.EventQueue.dispatchEventImpl(Unknown Source)
at java.awt.EventQueue.access$000(Unknown Source)
at java.awt.EventQueue$1.run(Unknown Source)
at java.awt.EventQueue$1.run(Unknown Source)
at java.security.AccessController.doPrivileged(Native Method)
at java.security.AccessControlContext$1.doIntersectionPrivilege(Unknown Source)
at java.security.AccessControlContext$1.doIntersectionPrivilege(Unknown Source)
at java.awt.EventQueue$2.run(Unknown Source)
at java.awt.EventQueue$2.run(Unknown Source)
at java.security.AccessController.doPrivileged(Native Method)
at java.security.AccessControlContext$1.doIntersectionPrivilege(Unknown Source)
at java.awt.EventQueue.dispatchEvent(Unknown Source)
at java.awt.EventDispatchThread.pumpOneEventForFilters(Unknown Source)
at java.awt.EventDispatchThread.pumpEventsForFilter(Unknown Source)
at java.awt.EventDispatchThread.pumpEventsForHierarchy(Unknown Source)
at java.awt.EventDispatchThread.pumpEvents(Unknown Source)
at java.awt.EventDispatchThread.pumpEvents(Unknown Source)
at java.awt.EventDispatchThread.run(Unknown Source)
Attachments (0)
Change History (20)
comment:1 Changed 16 months ago by skyper
• Description modified (diff)
comment:2 follow-up: Changed 16 months ago by jttt
• Cc jttt added
comment:3 Changed 16 months ago by jezevec
comment:4 in reply to: ↑ 2 Changed 16 months ago by rickmastfan67
comment:5 follow-up: Changed 16 months ago by simon04
comment:6 in reply to: ↑ 5 Changed 16 months ago by rickmastfan67
comment:7 Changed 16 months ago by akks
comment:9 follow-ups: Changed 16 months ago by landwirt@…
comment:10 in reply to: ↑ 9 Changed 16 months ago by landwirt@…
comment:11 Changed 16 months ago by bastiK
• Resolution set to fixed
• Status changed from new to closed
comment:12 in reply to: ↑ 9 Changed 16 months ago by bastiK
comment:13 Changed 16 months ago by akks
comment:14 follow-up: Changed 16 months ago by navmaps_eu
• Resolution changed from fixed to invalid
comment:15 Changed 16 months ago by navmaps_eu
• Resolution invalid deleted
• Status changed from closed to reopened
comment:16 in reply to: ↑ 14 Changed 16 months ago by simon04
comment:17 Changed 16 months ago by navmaps_eu
comment:18 Changed 16 months ago by simon04
comment:19 Changed 16 months ago by skyper
• Owner changed from team to jezevec
• Status changed from reopened to needinfo
comment:20 Changed 16 months ago by navmaps_eu
comment:21 Changed 16 months ago by simon04
• Resolution set to fixed
• Status changed from needinfo to closed
Modify Ticket
Change Properties
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as closed .
as The resolution will be set. Next status will be 'closed'.
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Note: See TracTickets for help on using tickets.
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rkcdbsb2xshb4hjvyjne4r7f7stttube
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{
"content_type": "text/html",
"provenance": "cccc-CC-MAIN-2013-20-0000.json.gz:6637",
"uncompressed_offset": 151923014,
"url": "lists.maemo.org/pipermail/maemo-developers/2005-November/001673.html",
"warc_date": "2013-11-22T14:52:20.000Z",
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}
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[maemo-developers] [maemo-developers] Questions to HOWTO:Set up CPU transparency with your device and sbrsh
From: Riku Voipio rvoipio+maemo at movial.fi
Date: Thu Nov 3 16:37:47 EET 2005
On Wednesday 02 November 2005 19:54, Timo Steuerwald wrote:
> - I've set my new target to sbrsh and the rest the same as described in
>http://www.maemo.org/platform/docs/tutorials/Maemo_tutorial.html#Building-for-ARM
how did you configure sbrsh (in sbox) and sbrshd (on target machine) ?
You need to follow this document:
http://scratchbox.org/download/files/sbox-releases/0.9.8/doc/installdoc.html#cputransp
> checking whether the C compiler works... configure: error: cannot run C
> compiled programs.
> If you meant to cross compile, use `--host'.
> See `config.log' for more details.
So what does config.log say?
You can also try "sbrsh targetname --mount" directly to see if you have
problem in nfs mounting or somewhere else. If mounting works, but apps still
dont, try tcp networking or
More information about the maemo-developers mailing list
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{
"content_type": "text/html",
"provenance": "cccc-CC-MAIN-2013-20-0000.json.gz:6673",
"uncompressed_offset": 206245985,
"url": "quotationsbook.com/book/KDAVIS144/",
"warc_date": "2013-11-22T14:52:20.000Z",
"warc_filename": "<urn:uuid:6665fd01-f1d9-4202-9b85-a205e59b6354>",
"warc_url": "http://quotationsbook.com/book/KDAVIS144/"
}
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KDAVIS144's bookmarks
"A woman is like a teabag -- only in hot water do you realize how strong she is."
Reagan, Nancy on women
14 fans of this quote
"The trouble with some women is they get all excited about nothing, and then they marry him."
Cher on women
8 fans of this quote
"Nothing real can be threatened. Nothing unreal exists. Herein lies the peace of God."
A Course In Miracles on peace
30 fans of this quote
KAWANA's quote collection
I'm female and made my book on 16th October 2011.
My book as a pdf
My feed
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{
"content_type": "text/html",
"provenance": "cccc-CC-MAIN-2013-20-0000.json.gz:6674",
"uncompressed_offset": 206251434,
"url": "quotationsbook.com/book/mpwilson/page=3/",
"warc_date": "2013-11-22T14:52:20.000Z",
"warc_filename": "<urn:uuid:6665fd01-f1d9-4202-9b85-a205e59b6354>",
"warc_url": "http://quotationsbook.com/book/mpwilson/page=3/"
}
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mpwilson's bookmarks
"Honest winter, snow clad and with the frosted beard, I can welcome not uncordially; but that long deferment of the calendar's promise, that weeping loom of March and April, that bitter blast outraging the honor of May -- how often has it robbed me of heart and hope."
Gissing, George Robert on hope
"In all things it is better to hope than to despair."
Goethe, Johann Wolfgang Von on hope
16 fans of this quote
"Hope is definitely not the same thing as optimism. It is not the conviction that something will turn out well, but the certainty that something makes sense, regardless of how it turns out."
Havel, Vaclav on hope
32 fans of this quote
"Men and women are limited not by the place of their birth, not by the color of their skin, but by the size of their hope."
Johnson, John on hope
16 fans of this quote
"We must accept finite disappointment, but never lose infinite hope."
King Jr. Martin Luther on hope
36 fans of this quote
"Hope is the feeling you have that the feeling you have isn't permanent."
Kerr, Jean on hope
13 fans of this quote
"Neither should a ship rely on one small anchor, nor should life rest on a single hope."
Epictetus on hope
24 fans of this quote
"There is a crack in everything, that's how the light gets in."
Cohen, Leonard on hope
53 fans of this quote
"To give a generous hope to a man of his own nature, is to enrich him immeasurably."
Channing, William Ellery on hope
8 fans of this quote
"Where there is no vision, there is no hope."
Carver, George Washington on hope
32 fans of this quote
"Hope is the best part of our riches."
Bovee, Christian Nevell on hope
10 fans of this quote
This quotation can be viewed in the context of a book
"When people grow gradually rich their requirements and standard of living expand in proportion, while their present-giving instincts often remain in the undeveloped condition of their earlier days. Something showy and not-too-expensive in a shop is their only conception of the ideal gift."
Munro, Hector Hugh on giving
"Plant a kernel of wheat and you reap a pint; plant a pint and you reap a bushel. Always the law works to give you back more than you give."
Norvell, Anthony on giving
"The test of our progress is not whether we add more to the abundance of those who have much; it is whether we provide enough for those who have too little."
Roosevelt, Franklin D. on giving
6 fans of this quote
"We should give as we would receive, cheerfully, quickly, and without hesitation; for there is no grace in a benefit that sticks to the fingers."
Seneca on giving
"Blessed are those who give without remembering. And blessed are those who take without forgetting."
Meltzer, Bernard on giving
9 fans of this quote
"The gifts that one receives for giving are so immeasurable that it is almost an injustice to accept them."
Mckeun, Rod on giving
"I do not believe one can settle how much we ought to give. I am afraid the only safe rule is to give more than we can spare."
Lewis, C. S. on giving
10 fans of this quote
"In the long run, we get no more than we have been willing to risk giving."
Kopp, Sheldon on giving
3 fans of this quote
"While you have a thing it can be taken from you... but when you give it, you have given it. No robber can take it from you. It is yours then for ever when you have given it. It will be yours always. That is to give."
Joyce, James on giving
4 fans of this quote
"The more sympathy you give, the less you need."
Forbes, Malcolm S. on giving
"You give but little when you give of your possessions. It is when you give of yourself that you truly give."
Gibran, Kahlil on giving
10 fans of this quote
"Complete possession is proved only by giving. All you are unable to give possesses you."
Gide, Andre on giving
3 fans of this quote
"The human contribution is the essential ingredient. It is only in the giving of oneself to others that we truly live."
Andrus, Ethel Percy on giving
5 fans of this quote
"No matter what age you are, or what your circumstances might be, you are special, and you still have something unique to offer. Your life, because of who you are, has meaning."
Angelis, Barbara De on giving
8 fans of this quote
"From what we get, we can make a living; what we give, however, makes a life."
Ashe, Arthur on giving
13 fans of this quote
"Sharing is sometimes more demanding than giving."
Bateson, Mary on giving
"Nature does not give to those who will not spend..."
Baughan, R.J. on giving
4 fans of this quote
"Give, and it shall be given to you. For whatever measure you deal out to others, it will be dealt to you in return."
Bible on giving
"It is possible to give without loving, but it is impossible to love without giving."
Braunstein, Richard on giving
12 fans of this quote
"The most satisfying thing in life is to have been able to give a large part of oneself to others."
Chardin, Pierre Teilhard De on giving
3 fans of this quote
"Try a thing you haven't done three times. Once, to get over the fear of doing it. Twice, to learn how to do it. And a third time to figure out whether you like it or not."
Thomson, Virgil on fear
3 fans of this quote
"To live with fear and not be afraid is the final test of maturity."
Weeks, Edward on fear
4 fans of this quote
"I've been absolutely terrified every moment of my life - and I've never let it keep me from doing a single thing I wanted to do."
O'Keeffe, Georgia on fear
"Never turn your back on fear. It should always be in front of you, like a thing that might have to be killed."
Thompson, Hunter S. on fear
"Curiosity will conquer fear even more than bravery will."
Stephens, James on fear
This quotation can be viewed in the context of a book
"We are more often frightened than hurt; and we suffer more from imagination than from reality."
Seneca on fear
10 fans of this quote
"He who is afraid of a thing gives it power over him."
Proverb, Moorish on fear
3 fans of this quote
"If we take the generally accepted definition of bravery as a quality which knows no fear, I have never seen a brave man. All men are frightened. The more intelligent they are, the more they are frightened."
Patton, George S. on fear
"Half the things that people do not succeed in are through fear of making the attempt."
Northcote, James on fear
But wait... my book has more: prev 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20 next
Mike Wilson's quote collection
I'm male, single from the United States and made my book on 13th September 2010.
My book as a pdf
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Quotes by Leverson, Ada
Ada Leverson (1862-August 1933), nee Beddington, was a British writer, now known as a novelist. She began writing during the 1890s, as a contributor to Black and White, Punch, and The Yellow Book. She was a loyal friend to Oscar Wilde, who called her Sphinx; in the 1997 film Wilde she is played by Zoe Wanamaker. She was a wit, and a friend of Max Beerbohm; her writing has been compared to Beerbohm's, and the stories of Saki. She was also a friend of George Moore; Osbert Sitwell in Great Morning has an anecdote in which she tries, unsuccessfully, to get Moore to see the young William Walton. Of the Sitwells' circle - Sacheverall Sitwell dedicated a poetry collection to her, while she was hopelessly in love with Osbert - she lived out her old age in the Hotel Porta Rossa in Florence..
"Before he left, Aunt William pressed a sovereign into his hand guiltily, as if it were conscience money. He, on his side, took it as though it were a doctor's fee, and both ignored the transaction."
Leverson, Ada on giving
"You don't know a woman until you have received a letter from her."
Leverson, Ada on women
4 fans of this quote
Take a look at recent activity on QB!
Search Quotations Book
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Ocean
From RationalWiki
Jump to: navigation, search
— Outline Only —
This article is only a brief description of the subject, and is not intended to give a full explanation.
Check out the "see also" or "references" sections, or Wikipedia's article for more detail.
Oceans are big wet colorless (though they look blue) things that cover quite a lot of the earth. They are very salty, extremely polluted and contain many delicious[Citation Needed] edibles.
Contents
[edit] History
A salt mine reveals the massive deposits left behind by the evaporation of former seas million of years ago.
Oceans formed over the course of millions of years after the shiny new Earth cooled enough for water to settle on its surface and fill up the holes. As the crust drifted about, continents and supercontinents formed and moved around; the spaces in between these land masses would be individual seas. Pangea was the most recently formed of these supercontinents and split 250-150 million years ago,[1] dividing the large Tethys ocean into several smaller oceans. The Atlantic Ocean is the youngest of these; as measured by the record of changes in the magnetic field in the rocks below it - it is thought to date back less than a hundred millon years.
In historic times, the oceans posed an insurmountable barrier to most cultures. During the Middle Ages, better shipbuilding techniques finally enabled regular, safe crossings. The result of this was that five or six small countries on the northeastern Atlantic coast were able to carve up most of the world into a few massive empires, the consequences of which are still readily apparent today.
According to some young-Earthers, the amount of salt in the ocean suggests they formed 62 million years ago[2]. The young Earthers make their argument based on a starting point of zero salt, which isn't true - the oceans actually used to be saltier than they are today. This is due to the fact that a large amount of salt is deposited on the shore when seawater evaporates outside of the ocean - the first great lowering of salinity occurred in the late Precambrian, when huge amounts of salt were deposited in Neoproterozoic evaporite basins. These deposits result in a mineral known as "evaporite".[3]
In other evidence for the extreme age of the oceans, not long after they formed, iron-manganese nodules started forming, incredibly slowly - see here for more information.
[edit] Life
Lovecraftian Horror
The greatest variety of life occurs in coral reefs, but the vast open ocean has the most productivity.
There are plenty of fish in the sea - the oceans contain more than (insert really big number here) species. They also teem with plant life and invertebrate animals, and many species of aquatic mammal, including dolphins and whales. Most of the really weird stuff, however, is in the deep sea trenches.[4] The deepest recorded sea trench is the Mariana Trench which is thought to be roughly just under 11,000 m, or about 36,000 ft.
[edit] Non-conservation
The oceans have also provided food for seagoing communities (a resource currently being depleted faster than it can be replaced), and are also used as a huge rubbish dump. Both of these may well have a permanent effect on sea life - it is possible that jellyfish may become the sea's dominant life form after all the fish have been eaten or choke on plastic bags.[5]
Whales are probably the most famous example of overfishing (overmammaling?). The result is this:
Extinct
Critically Endangered
Endangered
Vulnerable
Lower Risk
(Conservation Dependent)
Lower risk
(Near Threatened)
Lower Risk
(Least Concern)
None*
• Blue whale
(Antarctic)[6]
• Gray whale
(Northwest Pacific)[7]
• Blue whale[8]
• Fin whale[9]
• North Pacific right whale[10]
• North Atlantic right whale[11]
• Sei whale[12]
• Beluga[13]
• Blue whale
musculus subspecies (Atlantic)[14]
• Sperm whale[15]
• Antarctic minke whale
• Arnoux's beaked whale
• Baird's beaked whale
• Blue whale (North Pacific)[16]
• Bowhead whale[17]
• Gray whale
(Northeast Pacific)[18]
• Northern bottlenose whale
• Southern bottlenose whale
• Short-finned pilot whale
• Southern right whale[19]
• Minke whale[20]
• Dwarf sperm whale[21]
• Pygmy right whale
• Long-finned pilot whale
• Humpback whale[22]
• Pygmy sperm whale[23]
• Melon-headed whale
• Gray whale (species)[20]
* The Atlantic population of gray whales went extinct in the late 17th Century. It is not listed as a part of IUCN's red list.[24]
Despite the mess whaling made of the marine mammal population, people still do it (even though commercial whaling is banned by international law). As of 1987, Japan has been whaling for "scientific purposes", which apparently include distributing the meat of what may be the second most intelligent species on Earth to school children for lunch, and (one can safely assume) resurrecting commercial whaling.[25]
[edit] Sea also
[edit] Footnotes
1. This is the duration of various phases of breaking up, not a ridiculous uncertainty. After all, drift is slow, you don't wake up to find the Earth completely resurfaced overnight!
2. A young Earth indeed.
3. ScienceDirect
4. Weird stuff. From Greenpeace. It's just a video, so just open it.
5. Invasion of the jellyfish
6. http://www.iucnredlist.org/search/details.php/41713/all
7. http://www.iucnredlist.org/search/details.php/8099/all
8. http://www.iucnredlist.org/details/2477
9. http://www.iucnredlist.org/search/details.php/2478/summ
10. http://www.iucnredlist.org/search/details.php/41711/summ
11. http://www.iucnredlist.org/search/details.php/41712/summ
12. http://www.iucnredlist.org/search/details.php/2475/summ
13. http://www.iucnredlist.org/search/details.php/6335/summ
14. http://www.iucnredlist.org/search/details.php/2483/all
15. http://www.iucnredlist.org/search/details.php/41755/summ
16. http://www.iucnredlist.org/search/details.php/2482/all
17. http://www.iucnredlist.org/search/details.php/2467/summ
18. http://www.iucnredlist.org/search/details.php/8098/all
19. http://www.iucnredlist.org/search/details.php/8153/summ
20. 20.0 20.1 http://cmsdata.iucn.org/downloads/cetacean_table_for_website.pdf
21. http://www.iucnredlist.org/search/details.php/11048/summ
22. http://www.iucnredlist.org/search/details.php/13006/summ
23. http://www.iucnredlist.org/search/details.php/11047/summ
24. Eschrichtius robustus (Grey whale) Geographic Range IUCN Red list of threatened species
25. Greenpeace
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From the GreenLab: Quis Defending Melo
Jay December 27, 2011 Uncategorized 1 Comment
When it was all said and done, Carmelo Anthony torched the Celtics to the tune of 37 points, leading the way to a victory for his Knicks. The game tying three-pointer with about three minutes to go sticks out most, as do the two free throws on the questionable foul called on Marquis Daniels. Without Paul Pierce to check Melo, the burden fell mostly on Sasha Pavlovic and Quis. Sasha struggled heavily, but while going through film in the GreenLab, Quis did a solid job on Melo.
When Quis was able to be aggressive and establish his position on Melo first, he did a good job defending him. When Melo went into his offense quickly, being a spot up jumper or drive to the basket, he was able to score. Check the videos below for a detailed examination of Quis' defense from each half.
Quis First Half Defense on Melo
• 0:00-0:18 - Quis picks up Melo at half court, and follows him to the high post. Here, he's able to fight and establish his position first, denying Melo the ball and making him work to get it. He angles Melo to the middle, cutting off the baseline as well as the option of driving with his strong hand. Quis doesn't bite on Melo's fakes, and Melo is forced to kick it out.
• 0:19-0:30 – Off an out-of-bounds set, Melo inbounds the ball and cuts to the right three-point line. As he does this, Quis fights through a Bill Walker screen and is able to establish position as Melo hesitates again. Quis again cuts off the baseline, forcing Melo to the middle and dribbling with his left hand. As he funnels him in, he successfully slap-steals the ball from Melo, creating the turnover.
• 0:31 – 0:40 – Again off the inblunds play, Melo receives the ball back, but this time in the low post, hoping to get better position on Quis. Quis again cuts off the baseline as well as his strong dribble side. Melo attempts a swipe fake but kicks it out to Walker who travels.
• 0:41 – 0:50 – Even as Quis leaves Melo to hedge out and help, he recovers quickly enough to get his left hand at Melo's three-point attempt. He also jumps to the side of Melo, eliminating any shot of getting a foul drawn.
• 0:51 – 1:05 – Here we see one of the mistakes by Quis. As he successfully fights through a series of screens, he eventually overplays Melo who quickly cuts to the basket. Quis immediately realizes his gambling mistake by giving the "my bad" signal.
• 1:06 – 1:25 – With the half coming to a close, Melo is waiting on the post again, with Quis having his arms up, angling his body to a slight overplay to Melo's right side to make the post-entry pass difficult. Melo uses his size advantage to eventually get the ball, but Quis again cuts off the baseline and forces him to the middle. Melo pushes off a little, but Quis again contests the shot with the left hand as Melo misfires.
Quis 2nd Half Defense on Melo
• 0:00 – 0:17 – Picking up Melo 3/4 court, Quis fights through a soft screen at half court. Here, all he needs to do is create even a little pressure to Melo as the ball handler to give Rondo enough time to snake in for the steal and breakaway lay-up.
• 0:18 – 0:27 – Melo is again trying to do work on Quis in the low post. Quis again does a good job with the lower body and forces him to the middle. Not a bad approach by Marquis to try and take a charge, but he gets whistled for the block. Debatable.
• 0:28 – 0:36 – Melo gets the ball on the left elbow. Marquis again establishes his position first as the aggressor. And once again, Melo has a tough time making anything out of it and Quis gets a hand up (albeit the incorrect one) and forces Melo to pass.
• 0:37 – 0:50 – The Knicks try to get Melo going on the low post again. Once again, Marquis has already established ownership of the spot, and Melo hesitates for a second and misfires on the turn-around fade-away jumper.
• 0:51 – 1:00 – As Toney Douglas passes to Melo on the run, Melo tries to go baseline but Quis cuts him off. KG is helping towards the middle, so Melo retreats back to the baseline after spotting KG. Quis uses excellent footwork in combination with one arm up to avoid a cheap foul. As Quis gives him the baseline this time (because KG is there to help) Melo has no place to go and has to kick it out. It turns out to be a smart play as Douglas drills a three. Still, you can't ask for better defense on Melo than what Quis provided.
• 1:01 – 1:39 – Melo is bringing the ball up, but backing his way into Quis. This is a trick ball handlers will use as an extra precaution to protect the ball and avoid getting pick-pocketed straight up. It also shows an obvious screen is being set for Melo. As Amare Stoudemire sets the screen, KG is able to show and recover (one of the best in the business at this), avoiding the switch that NY was hoping for. This would allow Melo to be at the top of the key, straight up with KG, creating an advantage for Melo to take KG off the dribble. But Quis doesn't switch and smartly stays with Melo. Again, Quis is fronting Melo, creating a tough angle for Douglas to pass him the ball. As Melo gets the ball, he quickly makes his move and Quis pulls a Rondo-gamble-poke and steals it. Except he's whistled for the foul. Again, this is quite debatable, but to me, he's called for the foul because it looks like a foul based on Melo's reaction.
So we can see here how important Quis' defense is. It's amazing that he's even back on the court this season but with the loss of Jeff Green, and Paul Pierce for the time being, Marquis will have his hands full. Next up: LeBron James and possibly Dwyane Wade.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
1384.6 - Statistics - Tasmania, 2006
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 10/02/2006
Page tools: Print Page Print All RSS Search this Product
Contents >> Environment >> Land >> World Heritage listings
Natural and cultural properties that are considered to be of ‘outstanding universal value’ and that meet the criteria of the World Heritage Convention may be entered on the World Heritage List. The list is compiled by the United Nations Educational, Scientific and Cultural Organisation (UNESCO) World Heritage Committee. Signatories to the Convention (such as Australia) undertake to identify, protect, conserve, present and transmit to future generations the properties entered on the World Heritage List.
There are two World Heritage properties in Tasmania: the Tasmanian Wilderness and Macquarie Island.
THE TASMANIAN WILDERNESS
• listed in 1982
• covers 1.38 million hectares (approximately 20% of Tasmania)
• features a diverse array of both natural and cultural features of global significance, e.g. pristine habitats for plants and animals that are found nowhere else in the world and the most significant and extensive glacially modified landscapes in Australia.
Further information can be found on the
Tasmania Parks and Wildlife Service web site at http://www.parks.tas.gov.au/wha/whahome.html
MACQUARIE ISLAND
• listed in 1997
• a site of major geoconservation significance, being the only place on earth where rocks from the earth's mantle (6 km below the ocean floor) are being actively exposed above sea-level.
Further information can be found on the following web sites:
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Unless otherwise noted, content on this website is licensed under a Creative Commons Attribution 2.5 Australia Licence together with any terms, conditions and exclusions as set out in the website Copyright notice. For permission to do anything beyond the scope of this licence and copyright terms contact us.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
2901.0 - Census Dictionary, 2006 (Reissue)
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 17/11/2006 Reissue
Page tools: Print Page RSS Search this Product
Contents >> Glossary >> Customised geographic reports
Customised geographic reports
The 2006 Census customised geographic data reports provide clients with tabular geographic data which relate specifically to the Census Geographic Areas. The data available in these reports are taken from the Collection District Record Database (CDRD).
Three types of common geographic data reports can be provided using the following standardised reports:
• direct queries - data from any number of nominated geographic areas can be drawn directly from the CDRD, (for example, the area in square kilometres for a number of SLAs).
• geographic conversions - a listing of all the geographic areas of a particular type (for example, an SLA) that are contained within, or share any common territory with, specified geographic areas of another type (for example, a State Electoral Division) can be taken from the CDRD.
• comparability listings - a set of Collection Districts (CDs) from a previous Census year can have the CDs from the 2006 Census which correspond to them identified and listed. Alternatively, a list of 2006 Census CDs can have the CDs from previous Censuses which correspond to them identified and listed. In each comparability listing there is a comparability indicator.
Clients who have data requirements that cannot be met by these three standard reports, or a combination thereof, can have their requests serviced though a special data query facility which is also available.
To place an order for a customised geographic data report, contact ABS Information Consultancy. Contact details for Information Consultancy are provided on the back cover of this publication.
See also Australian Standard Geographical Classification (ASGC), Collection District Record Database (CDRD) 2006, Census Geographic Areas.
Previous PageNext Page
© Commonwealth of Australia 2013
Unless otherwise noted, content on this website is licensed under a Creative Commons Attribution 2.5 Australia Licence together with any terms, conditions and exclusions as set out in the website Copyright notice. For permission to do anything beyond the scope of this licence and copyright terms contact us.
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Case report
Giant pulmonary artery aneurysm in a patient with vasoreactive pulmonary hypertension: a case report
Inês Araújo*, Pilar Escribano, María J Lopez-Gude, Carmen J Lopez-Guarch, Maria A Sanchez, Maria J Ruiz-Cano, Juan Delgado and Jose Cortina
BMC Cardiovascular Disorders 2011, 11:64 doi:10.1186/1471-2261-11-64
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mona19
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Editorial
Editorial Announcement
Ravi P Agarwal
Author affiliations
Florida Institute of Technology, USA
Citation and License
Boundary Value Problems 2011, 2011:1 doi:10.1186/1687-2770-2011-1
Published: 17 May 2011
First paragraph (this article has no abstract)
I am excited to inform all previous and future contributors, as well as readers, that the journal Boundary Value Problems has been transferred to the international publisher Springer, Science + Business Media, to continue publication as part of the new SpringerOpen range of fully open access journals.
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(December 2011)
DC, 2011 Series
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Price:
2.99 USD
Pages:
36
Indicia frequency:
monthly
On-sale date:
2011-10-12
Indicia Publisher:
DC Comics
Brand:
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Barcode:
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Editing:
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Color:
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Dimensions:
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Binding:
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Issue Notes
"Rated T Teen."
The Menace of Brainstorm! (Table of Contents)
Mister Terrific / cover / 1 page (report information)
Credits
Pencils:
J. G. Jones (signed)
Inks:
J. G. Jones (signed)
Colors:
Lovern Kindzierski
Letters:
typeset
Content Information
Genre:
superhero
Characters:
Mister Terrific [Michael Holt]; Brainstorm
Blinded by Science (Table of Contents)
Mister Terrific / comic story / 20 pages (report information)
Credits
Script:
Eric Wallace
Pencils:
Gianluca Gugliotta
Inks:
Wayne Faucher
Colors:
Mike Atiyeh
Letters:
Dave Sharpe
Content Information
Genre:
superhero
Characters:
Mister Terrific [Michael Holt]; Karen Starr; Aleeka Okafur; Jamaal Mason; Dr. Phillip Lyong; Nola; Senator Gonzalez; Donald Leeson; Michael's college roommate; Brainstorm
Synopsis:
Mr. Terrific regains control over his own mind and stabilizes the situation at the Conscientia Institute with Karen's help. Later, Michael traces his foe to an outdoor mall in Los Angeles. When Brainstorm reveals himself and proves powerless against the hero, he makes the denizens of the mall attack Mr. Terrific.
Reprints:
Editing
Table of Contents
1. 0. The Menace of Brainstorm!
Mister Terrific
2. 1. Blinded by Science
Mister Terrific
This issue was most recently modified by:
• Jochen G.
• R. J. Roper
• Dwayne Best
• Gregory Fischer
• Bob Hughes
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View of the Unisphere from the FotP.
[↑ Index ↑]
This document (source) is part of Crummy, the webspace of Leonard Richardson (contact information). It was last modified on Sunday, December 27 2009, 18:19:46 Nowhere Standard Time and last built on Saturday, May 18 2013, 07:00:07 Nowhere Standard Time.
Crummy is © 1996-2013 Leonard Richardson. Unless otherwise noted, all text licensed under a Creative Commons License.
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East Deccan dry-evergreen forests
East Deccan dry-evergreen forests
This article has been reviewed by the following Topic Editor: Mark McGinley
Introduction
Satellite View of the Southeast coast of India (Source: USGS)
The vegetation in the East Deccan Dry Evergreen Forests has an unusual physiognomy that makes it distinctive from most of the other dry forests. Unlike other dry forests of the Indo-Pacific region that lose their leaves for part of the year (i.e., during the nonmonsoonal season), these forests stay green during the long dry season.
Location and General Description
The ecoregion extends as a narrow strip along the southern coastal areas of Andhra Pradesh and Tamil Nadu states in India, where it represents the narrow strip of dry evergreen forest formation.
Geologically, this ecoregion has Gondwanaland origins. The average rainfall is 800 millimeters (mm). Most of the precipitation occurs during the brief northeast monsoon between October and December. Maximum temperatures during the long dry season can reach a stifling 44° Celsius (°C).
The original vegetation had emergent species of deciduous elements, such as Albizzia amara and Chloroxylon spp. But the original canopy-forming deciduous species have succumbed to human pressures, and the shrubby evergreen species now form a closed evergreen understory. Therefore, the existing vegetation type represents a low forest (up to 10 meters [m]) with a complete, closed canopy consisting of mostly small leathery-leaved evergreen trees with short trunks and spreading crowns. A large number of climbers are present, but bamboos are completely absent.
The characteristic floristic elements are Manilkara hexandra, Mimusops elengi, Diospyros ebernum, Strychnos nux-vomica, Eugenia spp., Drypetes sepiaria, and Flacourtia indica. The degraded stages of this forest have been categorized as tropical dry evergreen scrub by Puri et al. and are typically dominated by thorny species such as Zyzyphus glabarrima, Dicrostachys cinerea, Randia dumetorum, and Carissa spinarum.
Biodiversity Features
The ecoregion does not contain any endemic mammals or birds. But the sixty-six known mammal species include two threatened species: the wild dog (Cuon alpinus) and sloth bear (Melursus ursinus). Other species that deserve conservation attention in this ecoregion include its largest predator, the common leopard (Panthera pardus), and some of the smaller predators such as the jungle cat (Felis chaus) and leopard cat (Prionailurus bengalensis). The mammal community includes several ungulates of conservation importance such as the blackbuck (Antilope cervicapra), the chinkara (Gazella bennettii), and the small Indian chevrotain or mouse deer (Moschiola meminna). The Sriviliputhur (Kamarajar District in Tamil Nadu) and Amaravathy Nagar (Coimbatore District) have the largest remaining populations of the threatened grizzled giant squirrel (Ratufa macroura).
Bird richness is greater, with 230 species. The Jerdon's courser (Rhinoptilus bitorquatus) is endangered, and the spot-billed pelican (Pelecanus philippensis) and lesser florican (Eupodotis indica) are globally threatened. Some other birds that deserve conservation attention as focal species because of their need for relatively intact habitat and low tolerances of disturbance include the woolly-necked stork (Ciconia episcopus), white-bellied sea-eagle (Haliaeetus leucogaster), and Indian grey hornbill (Ocyceros birostris).
Current Status
Table 1. WCMC (1997) Protected Areas That Overlap with the Ecoregion.
Protected Area Area (km2) IUCN Category
Vettangudi 30 IV
Nelapattu 130 IV
Total 160
Ecoregion numbers of protected areas that overlap with additional ecoregions are listed in brackets.
Hundreds of years of human impact have taken a heavy toll on the natural habitat of this ecoregion, and more than 95 percent of the ecoregion is deforested. The remaining forests are scattered small fragments. The two small, protected areas cover less than 200 square kilometers (km2) (Table 1), which is less than 1 percent of the ecoregion's area. Marakanam, a sacred grove near Pondicherry, is fairly well protected and represents an important example of this vegetation type.
Types and Severity of Threats
Like most of the other ecoregions in the Indian Subcontinent, this ecoregion is also subjected to heavy deforestation and grazing pressure from domestic livestock. The stunted scrub vegetation present throughout most of the ecoregion is indicative of long years of grazing practices. The remnant sal (Shorea robusta) forests are being rapidly lost to podu, or shifting cultivation.
Invasion by Prosopsis, a thorny exotic plant that is unpalatable to domestic livestock, is being used extensively in reforestation programs and will certainly usurp the preferred habitat of the Jerdon's courser.
Poaching is rampant in areas with Naxalite conflicts, especially in the Satmala Hills, Pakla Wildlife Sanctuary, and Etunagaram. The ground situation makes patrolling by the forest department staff nearly impossible.
Justification of Ecoregion Delineation
During previous analyses of conservation units, Rodgers and Panwar and MacKinnon divided the largest biogeographic unit in India, the Deccan Peninsula, into five subunits or biotic provinces. Each of these units contained several distinct habitat types. In keeping with our rules for defining ecoregions as conservation units that represent distinct habitat types, we identified the distinct dry evergreen forests along the southeastern coast of the Deccan Peninsula as the East Deccan Dry Evergreen Forests.
Additional Information on this Ecoregion
Disclaimer: This article is taken wholly from, or contains information that was originally published by, the World Wildlife Fund. Topic editors and authors for the Encyclopedia of Earth may have edited its content or added new information. The use of information from the World Wildlife Fund should not be construed as support for or endorsement by that organization for any new information added by EoE personnel, or for any editing of the original content.
Citation
World Wildlife Fund (Lead Author);Mark McGinley (Topic Editor) "East Deccan dry-evergreen forests". In: Encyclopedia of Earth. Eds. Cutler J. Cleveland (Washington, D.C.: Environmental Information Coalition, National Council for Science and the Environment). [First published in the Encyclopedia of Earth August 25, 2008; Last revised Date August 25, 2008; Retrieved May 18, 2013 <http://www.eoearth.org/article/East_Deccan_dry-evergreen_forests>
The Author
Known worldwide by its panda logo, World Wildlife Fund (WWF) leads international efforts to protect endangered species and their habitats. Now in its fifth decade, WWF works in more than 100 countries around the globe to conserve the diversity of life on Earth. With nearly 1.2 million members in the U.S. and another 4 million worldwide, WWF is the world's largest privately financed conservation organization. WWF directs its conservation efforts toward three global goals: 1) saving endangered ... (Full Bio)
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Victoria Archives and Libraries
From FamilySearch Wiki
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== [[Australia]] ==
== [[Australia]] ==
Revision as of 21:56, 26 February 2013
State Library at Night.
Australia
The following is a list of archives and libraries that have genealogical material.
The State Library of Victoria is Victoria's premier research library and helps family historians find their ancestors in our dedicated Genealogy Collection and unique Victorian heritage records.
Public Record Office Victoria is the archives of the State Government of Victoria which hold records from the late 1830s to today. These include indexes to passengers from inwards assisted from 1839 to 1871 and unassisted from 1852 to 1923, outward passengers from 1852 to 1901, and Wills, Probates and Administrations from 1841 to 1925. There are other records available online including education and teachers, court in quest records, insolvency, prisoners and convicts and much more.
Australia Institute of Genealogical Studies Inc. promotes and encourages the study of genealogy, heraldry, family history and allied subjects throughout Australia and to assist members and others in genealogical research.
The Genealogical Society of Victoria is conveniently located in the city offering an extensive world-wide reference library, research assistance and large bookshop.
Bendigo Regional Archive Centre is a is a unique partnership between Public Record Office Victoria, City of Greater Bendigo and Goldfields Library Corporation.
The Victorian Government Gazette thia archive of historic government gazettes provides access to over 160 years of official information published in and about Victoria. It contains images of every relevant page in the Victoria Government Gazette produced since 1836, as well as searchable indexes for each publication.
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About this Journal Submit a Manuscript Table of Contents
Case Reports in Emergency Medicine
Volume 2013 (2013), Article ID 459453, 3 pages
http://dx.doi.org/10.1155/2013/459453
Case Report
Renal Abscess in a Patient Presenting with Persistent Hiccups
Division of Emergency Medicine, Medical University of South Carolina, 169 Ashley Avenue, MSC 300, Room 294, Charleston, SC 29425, USA
Received 30 November 2012; Accepted 23 December 2012
Academic Editors: A. K. Exadaktylos, E. Kagawa, and F. Natale
Copyright © 2013 Mark Flanagan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Hiccups are common, typically limited, and rarely present with adverse complications. In the context of persistent or intractable episodes, however, hiccups may signal a more serious underlying cause. Here, we present an unexpected and pathologic case of hiccups in a patient who was ultimately diagnosed with renal abscesses.
1. Introduction
Hiccups are also known as “hiccoughs”, synchronous diaphragmatic flutter (SDF), and “singultus”, from the Latin word singult, which roughly translates as “catch one’s breath while sobbing” [1, 2]. Hiccups have usually been characterized as a benign annoyance and in most cases this proves true. However, persistent or intractable episodes are reported to have an organic cause approximately 80% of the time with the remaining 20% thought to be psychogenic in nature. Therefore, it is important to maintain a high index of suspicion in those patients to search for an underlying disease process.
2. Case Report
A 47-year-old male presented to the emergency department (ED) complaining of nausea, vomiting, diarrhea, stomach pain, and constant hiccups for three days. He had attributed his symptoms to having the flu and had been self-medicating with DayQuil and NyQuil without relief. The nausea and vomiting were not associated with eating or drinking and emesis was described as nonbloody and nonbilious. His past medical history was significant for previously treated tuberculosis. He denied any medications, allergies, or past surgeries. He lived alone and denied any current use of alcohol, tobacco, or illicit drug use but endorsed prior abuse of alcohol, cocaine, and marijuana. He was an unemployed construction worker with no recent travel.
Review of systems revealed increased fatigue over the prior 4-5 days, an estimated 30 pound unexpected weight loss over the past three months, peeling of palms and recent upper respiratory infection symptoms, but was otherwise negative.
Upon arrival, his vital signs were as follows: oral temperature 97.3°F, blood pressure 123/78, heart rate 72, respiration rate 20, and an oxygen saturation of 96% on room air. He was noted to be persistently hiccupping, although in no acute distress and generally well appearing. Examination of the ENT, neck, chest, and cardiovascular system were within normal limits. Abdominal exam was soft and exhibited normal bowel sounds. There was mild epigastric tenderness to palpation, no guarding, no rebound, and no masses. Rectal exam revealed guaiac positive stool. He was noted to have mild desquamation of his palms bilaterally.
ED laboratory results were significant for WBC 28 K/cumm, hemoglobin 12 gm/dL, hematocrit 32%, and platelets of 84 K/cumm. Sodium was 125 mmol/L, bicarbonate 20 mmol/L, BUN 121 mg/dL, and creatinine 5.3 mg/dL. An ED visit 4 years prior demonstrated a creatinine of 1.0 mg/dL. Bilirubin was 4.9 mg/dL, AST 185 IU/L, ALT 93 IU/L, and ALP 158 IU/L. The urinalysis revealed 11–20/HPF WBCs, positive nitrates, and many bacteria but was otherwise negative. A KUB X-ray was obtained demonstrating a 1.2 × 0.7 cm rounded opacity overlaying the expected course of the left ureter.
The patient was administered normal saline IV fluids and chlorpromazine 25 mg IV with temporizing affect of the hiccups. A workup for postobstructive uropathy was initiated, including a renal ultrasound which showed mild left hydronephrosis with a proximal 1.1 cm ureteral stone (Figure 1).
Figure 1: Renal ultrasound demonstrating mild left hydronephrosis.
Urology was consulted and a CT IVP was obtained. In addition to prior findings of hydronephrosis and a 1.1 cm ureteral stone, a subcapsular fluid collection concerning for an abscess was noted overlying the left kidney (Figure 2). The patient was started on empiric IV ciprofloxacin and admitted to the Internal Medicine service. An emergent percutaneous nephrostomy tube was placed.
Figure 2: Enlarged left kidney with a ventral superior hypodensity concerning for a subcapsular fluid collection.
During the patient’s hospital admission, he was converted to an oral antibiotic regimen which initially responded well to therapy. It was noted, however, that the patient continued to experience persistent hiccups. A subsequent increased leukocytosis and recurrent fever prompted a repeat CT IVP which demonstrated another left subcapsular fluid collection concerning for abscess. A second percutaneous nephrostomy tube was placed and an additional course of IV antibiotics started, with subsequent resolution of the patient’s hiccups and normalization of his renal function. He was discharged in good condition 3 days later and subsequently lost to followup.
3. Discussion
Hiccups are not known to serve any physiological purpose and are known to start in vitro. Episodes of hiccups are typically brief and may be bothersome but are rarely of serious consequence. As episodes lengthen and increase in frequency, they may signal a more serious underlying condition. Persistent hiccups are defined as those lasting greater than 48 hours whereas intractable hiccups are defined as lasting more than 1 month. Persistent and intractable hiccups occur more frequently with the adult, male population for as yet unrecognizable reasons [13].
The pathophysiology of hiccups remains somewhat poorly understood. There is general consensus that they are a reflex pattern of “sudden contraction of the diaphragmatic inspiratory muscles followed by an abrupt closure of the glottis” [1, 2]. The hiccup reflex arc is comprised of an afferent limb emanating from the phrenic and vagus nerves and the sympathetic chain from T6 to T12. It then passes through a “hiccup center” located in a nonspecific region of the C3 to C5 cervical segments. An efferent limb of the hiccup arc routes primarily through the phrenic nerve, affecting the diaphragm and causing muscular contraction, though recent studies [2, 3] ascribe there may be several different as yet identified components of the efferent limb. Fluoroscopy has shown that hiccups typically affect only one hemidiaphragm with the left hemi-diaphragm being affected about 80% of the time.
There are many causes of hiccups. The etiology of benign or self-limited hiccups is often attributed to gastric distention, sudden changes in ambient or gastric temperature, consumption of alcohol, or smoking tobacco [1]. The pathologic etiologies can be subdivided into central or peripheral processes, toxic or metabolic processes, or pharmacologic processes.
Central causes of hiccups can be structural, vascular, or infectious in nature. Etiologies include, but are not limited to: central neoplasms, multiple sclerosis, cerebrovascular accidents, arteriovenous malformations, encephalitis, and meningitis [13].
Peripheral causes are far vaguer and numerous in nature, including any process which can irritate the vagus or phrenic nerves and its branches. These include, but are not limited to, pharyngitis, retropharyngeal, or paratonsillar abscess, goiters, tumors of the neck or mediastinum, irritation of the tympanic membranes, myocardial infarction, pericarditis, and aortic aneurysm, or dissection. Any process that causes pulmonary or intra-abdominal irritation, which can then precipitate irritation of the diaphragm, must be included in this very long list of differential diagnoses. It should also be noted that foreign bodies, such as aberrant pacemaker lines, may cause diaphragmatic irritation.
Toxic and metabolic causes include alcohol ingestion, uremia, hyponatremia, and hypocalcaemia. Some drugs are also known to lead to hiccups, prompting a thorough evaluation of the patient’s medication list. These pharmacologic agents include IV steroids, barbiturates, benzodiazepines, and alpha-methyldopa.
Management of hiccups should center on a thorough history and physical as well as the inclusion of pertinent laboratory and radiographic studies in order to rule out an organic cause if suspected. Treatment of an organic cause of hiccups usually resolves the hiccups. There are a large percentage of patients for whom no etiology can be found. For those, there are a multitude of potential nonpharmacologic and pharmacologic treatments.
Few nonpharmacologic treatments have been medically well-studied but may be worth attempting for shorter bouts, if no contraindication exists. Two common techniques include breath holding or bag breathing. Both serve to increase arterial pCO2. This may decrease the hiccup frequency but will not stop them completely. Irritation of the nasopharynx is thought to interrupt the hiccup reflex arc. This may be accomplished by direct means through nasopharyngeal suction or uvular stimulation, or by more indirect means of swallowing a spoonful of granulated sugar or gargling with cold water [2]. Other methods such as acupuncture and hypnosis have been attempted with reported success [15]. More severe cases have also been treated with phrenic nerve blockade or surgical interruption [1].
Pharmacological treatments for the management of hiccups continues to evolve. Some of the more common drugs utilized include nifedipine, haloperidol, phenytoin, metoclopramide, and gabapentin. The two most commonly utilized medications are chlorpromazine and baclofen. Chlorpromazine is the most widely used medication for persistent hiccups [6]. The recommended starting dose is 25–50 mg IV. It may also be administered orally or intramuscularly but with reduced effectiveness. This dose may be repeated up to three times. If successful, chlorpromazine may be continued orally as an outpatient at a dose of 25–50 mg up to 3-4 times a day for 10 days [7]. Baclofen also has been demonstrated to be effective in moderating or terminating persistent hiccups with no demonstrable organic cause. Its mechanism of action in terminating hiccups is unclear, but presumably central [8]. Dosing may be done in conjunction with famotidine when a gastrointestinal cause is suspected [9]. Recommended initial dosing is 10 mg orally, three times a day [10].
4. Summary
The evaluation of a patient with the chief complaint of persistent or intractable hiccups can be a daunting process given the broad list of differential diagnoses to consider. Though many patients will leave the ED with the diagnosis of idiopathic singultus, it is vital to maintain a high index of suspicion in order to rule out a potentially life threatening etiology.
Disclosure
The authors of this paper have no financial disclosure or conflict of interests to resolve.
References
1. P. W. Kolodzik and M. A. Eilers, “Hiccups (singultus): review and approach to management,” Annals of Emergency Medicine, vol. 20, no. 5, pp. 565–573, 1991. View at Scopus
2. J. H. Lewis, “Hiccups: causes and cures,” Journal of Clinical Gastroenterology, vol. 7, no. 6, pp. 539–552, 1985. View at Scopus
3. R. PauL, “Hiccups,” Southern Medical Journal, vol. 88, no. 2, pp. 175–181, 1995. View at Publisher · View at Google Scholar
4. J. Dietzel, M. Grundling, D. Pavlovic, and T. I. Usichenko, “Acupuncture for persistent postoperative hiccup,” Anaesthesia, vol. 63, no. 9, pp. 1021–1022, 2008. View at Publisher · View at Google Scholar · View at Scopus
5. M. Bobele, “Nonmedical management of intractible hiccups: a brief review of the literature,” Psychological Reports, vol. 61, no. 1, pp. 225–226, 1987. View at Scopus
6. I. Gilson and M. Busalacchi, “Marijuana for intractable hiccups,” The Lancet, vol. 351, no. 9098, p. 267, 1998. View at Publisher · View at Google Scholar · View at Scopus
7. J. E. Tintinalli, D. Gabor, and J. Stephan, Stapczynski, Emergency Medicine: A Comprehensive Study Guide, 6th edition, 2004.
8. K. Marsot-Dupuch, V. Bousson, J. Cabane, and J. M. Tubiana, “Intractable hiccups: the role of cerebral MR in cases without systemic cause,” American Journal of Neuroradiology, vol. 16, no. 10, pp. 2093–2100, 1995. View at Scopus
9. C. Guelaud, T. Similowski, J. L. Bizec, J. Cabane, W. A. Whitelaw, and J. P. Derenne, “Baclofen therapy for chronic hiccup,” European Respiratory Journal, vol. 8, no. 2, pp. 235–237, 1995. View at Publisher · View at Google Scholar · View at Scopus
10. K. Marien and D. Havlak, “Baclofen with famotidine for intractable hiccups,” European Respiratory Journal, vol. 10, no. 9, p. 2188, 1997. View at Publisher · View at Google Scholar · View at Scopus
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About this Journal Submit a Manuscript Table of Contents
Journal of Oncology
Volume 2012 (2012), Article ID 703858, 9 pages
doi:10.1155/2012/703858
Review Article
Advancements in the Treatment of Metastatic Breast Cancer (MBC): The Role of Ixabepilone
Department of Medical Oncology, G. Morris Dorrance Jr. Endowed Chair in Medical Oncology, Fox Chase Cancer Center, 333 Cottman Avenue, Room C315, Philadelphia, PA 19111-2497, USA
Received 6 January 2012; Accepted 18 February 2012
Academic Editor: Thomas Rutherford
Copyright © 2012 Massimo Cristofanilli. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Successful management of breast cancer in the metastatic setting is often confounded by resistance to chemotherapeutics, in particular anthracyclines and taxanes. The limited number of effective treatment options for patients with more aggressive biological subtypes, such as triple-negative metastatic breast cancer, is especially concerning. As such, a therapy clinically proven to be effective in this subtype would be of great value. Ixabepilone, a novel synthetic lactam analog of epothilone B, demonstrated better clinical outcomes in metastatic disease, particularly in triple-negative breast cancer. Most recently, studies have shown the activity of ixabepilone in the neoadjuvant setting, suggesting a role for this drug in primary disease. Notably, treating in the neoadjuvant setting might allow clinicians to explore the predictive value of biomarkers and response to treatment, as pharmacogenomic approaches to therapy continue to evolve. In this article, we review the efficacy and safety data of ixabepilone as a monotherapy and as a component of combination therapy for metastatic and primary breast cancer.
1. Introduction
Breast cancer is the most prevalent malignancy in women and in its metastatic state, the second most common cause of mortality [1]. In 2011, an estimated 230,480 of women were diagnosed with new cases of invasive breast cancer in the United States and 39,520 died from the disease [2]. Despite advances in treatment strategies, metastatic breast cancer (MBC) remains incurable and the goals of therapy range from symptom palliation to extending survival. Treatment selection is based on a series of factors including performance status, site of metastasis, and subtype of disease [3]. Breast tumors can be classified into 5 intrinsic subtypes based on differences in patterns of gene expression: (1) basal-like; (2) human epithelial receptor-2-positive (HER2)/neu, also known as ErbB2+; (3) luminal-like A; (4) luminal-like B; and (5) the normal breast tissue-like subtype [4]. As such, breast cancer treatments can be categorized as: (a) estrogen receptor (ER)-positive and thus, treatable by endocrine therapy; (b) HER2 overexpressed/amplified, treatable with trastuzumab or other HER2-targeted therapies; or (c) triple-negative (TN), with no current specific therapeutic biomarker, typically treated with cytotoxic chemotherapy. This review will outline the treatment strategies in the management of MBC and focus on the role of novel cytotoxic agents, particularly ixabepilone, in this disease.
2. The Management of MBC
Breast cancer tumor subtypes are characterized by different clinical outcomes [5]. Basal-like tumors are primarily ER-negative, strongly associated with mutations in the breast cancer susceptibility gene 1 (BRCA1), and have a very poor clinical outcome. BRCA1 is a tumor suppressor that functions in many DNA damage response pathways (i.e., homologous recombination and nonhomologous end-joining during DNA double-strand break repair). HER2/neu tumors are typified by overexpression of ErbB2 and genes involved in the ras pathway [6]. Similar to basal-like tumors, they are primarily ER-negative and associated with a poor clinical outcome. Conversely, luminal-like A and B tumors are primarily ER-positive, with luminal-like A providing the best clinical outcome of all subtypes, whereas luminal-like B tumors are associated with an intermediate outcome. Tumors from patients with the normal breast tissue-like subtype tend to have the lowest expression of genes associated with cell proliferation and thus would be expected to have a favorable clinical outcome [7].
Managing MBC can be extremely challenging, as resistance to standard-of-care chemotherapeutics (i.e., anthracyclines and taxanes) is a major cause of treatment failure [810]. Moreover, the widespread use of anthracycline and taxane in the adjuvant setting theoretically contributes to an increase of the proportion of patients with resistance to these drugs for whom other effective agents are necessary for treatment of recurrent disease. This condition is particularly relevant for patients with TN breast cancer, a subset of disease associated with more aggressive features and higher recurrence rate [11]. The most recent investigations explored the various mechanisms of drug resistance and attempted to develop agents that could target those survival pathways. Several preclinical models identified overexpression of neuronal-β tubulin III and IV isotopes associated with resistance to taxanes [12, 13]. These observations were confirmed in subsequent clinical studies in patients with MBC treated with first line paclitaxel further confirming the critical role of β tubulin in the development of drug resistance [14, 15]. More recently, poly(ADP-ribose) polymerase (PARP) inhibitors were extensively evaluated for their activity and clinical benefit especially for women with TN disease, as PARP inhibitors have shown promising results in mammary tumor models [16, 17].
Although typically regarded as pro-survival under physiological conditions, studies in which PARP1 was inhibited during S-phase in BRCA1- and BRCA2-deficient cells have shown that PARP1 inhibition causes genomic instability, cell-cycle arrest, and apoptosis, as these cells were defective in homology-directed double-strand break repair mechanisms [1719] imparted by unmutated BRCA1. Importantly, hereditary breast cancers due to mutations in BRCA1 are mainly of the basal-like or TN subtypes suggesting the utility of PARP1 inhibitors in treatment of patients with TN breast cancer.
Early clinical results with the PARP1 inhibitor iniparib (BSI-201) in 123 patients with TN breast cancer were encouraging and showed that the addition of iniparib to treatment with gemcitabine plus carboplatin significantly increased median overall survival (OS, 12.3 versus 7.7 months; ), median progression-free survival (PFS, 5.9 versus 3.6 months; ), and objective response rate (ORR, 52% versus 32%; ) [20]. However, recent results from a randomized phase 3 trial with 519 patients with TN breast cancer did not confirm these data; patients receiving iniparib with gemcitabine and carboplatin experienced no improvement in OS (11.8 versus 11.1 months; ) and only minor improvement in PFS (5.1 versus 4.1 months; ) compared with patients receiving chemotherapy alone [21]. This study did not meet the prespecified significance criteria for PFS and OS; ongoing molecular analyses of patients’ tumor samples may identify cancer subtypes sensitive to PARP1 inhibition.
Novel cytotoxic agents would be particularly useful for patients with anthracycline and/or taxane-resistant disease. Eribulin and ixabepilone are microtubule-targeting agents that have recently expanded the armamentarium of available cytotoxic drugs in treatment of MBC.
Eribulin, a synthetic analog of the marine macrolide halichondrin B, was approved by the US Food and Drug Administration (FDA) and the European Medicines Agency for the treatment of patients with MBC who have received at least 2 prior chemotherapy regimens for late-stage disease. The approval was based on results from a phase 3 trial (EMBRACE) which compared eribulin monotherapy with the physician’s choice of treatment in 762 patients with anthracycline- and taxane-pretreated locally recurrent breast cancer or MBC [22]. Patients received 2 to 5 previous chemotherapy regimens, including at least 2 regimens for recurrent or MBC. The physician’s choice included any monotherapy, most commonly vinorelbine, gemcitabine, or capecitabine. Eribulin significantly improved median OS compared with the physician’s treatment choice (13.1 versus 10.6 months; ) and also produced a higher response rate (12% versus 5%; ) but did not show longer PFS (3.7 versus 2.2 months; ) on independent review. EMBRACE was the first phase 3 study demonstrating a survival benefit for single-agent therapy in heavily-pretreated MBC patients.
Ixabepilone is a semi-synthetic lactam analog of epothilone B, which belongs to a class of naturally occurring, pro-apoptotic, antineoplastic microtubule-stabilizing compounds [23, 24]. The epothilones, although structurally unrelated to the taxanes, bind to the taxane-binding domain of microtubules. However, the mechanism by which each agent binds to these sites is different [25] and ixabepilone thus maintains activity against paclitaxel-resistant cell lines [26, 27]. Moreover, ixabepilone demonstrated potent activity in a xenograft model with βIII-tubulin overexpression (Pat-21 breast cancer), and in two xenograft models with an overexpression of drug efflux transporters (Pat-7 ovarian cancer and HCTVM46 colon cancer) [2830].
3. Ixabepilone and Its Approved Indications
Among the epothilones, ixabepilone has undergone the most extensive clinical development [31]. Preclinical trials in mouse xenograft models demonstrated that the maximum tolerated dose for ixabepilone was 10 mg/kg [32]. Results from clinical trials of patients treated with ixabepilone 40 mg/m2 demonstrated that the exposure was comparable to that of mice treated with ixabepilone 10 mg/m2, and that 40 mg/m2 offered clinically significant antitumor activity [33]. After determining a clinically effective dose, phase I/II trials in patients with solid tumors investigated several dosing schedules of the Cremophor-based ixabepilone formulation [34]. Subsequent trials described in the next section have identified doses that led to the FDA approval of ixabepilone for the treatment of metastatic or locally advanced breast cancer in patients after failure of an anthracycline and a taxane (in combination with capecitabine) and as a monotherapy after failure of an anthracycline, a taxane, and capecitabine [35].
4. Ixabepilone as a Monotherapy or in Combination with Capecitabine: Trials 081, 046, and 048
Three pivotal clinical trials, a phase 2 trial (081) and 2 phase 3 trials (046 and 048), have investigated the efficacy of ixabepilone as a monotherapy and in combination with capecitabine in patients with MBC [3638].
4.1. Trial 081
The single-arm phase 2 trial 081 assessed the efficacy of ixabepilone (40 mg/m2 intravenous [IV] over 3 hours every 3 weeks) in women with MBC who were heavily pretreated with an anthracycline, a taxane, and capecitabine. In this trial, patients had significant baseline disease and the majority (88%) had received up to 3 prior therapies in the metastatic setting. Ixabepilone demonstrated ORR among 113 response-assessable patients of 11.5% (95% confidence interval [CI], 6.3%–18.9%) as determined by an independent radiology facility. The investigator-assessed ORR among all 126 patients was 18.3% (95% CI, 11.9%–26.1%). Additional 13% (95% CI, 7.6%–20.9%) of treated patients demonstrated durable (≥6 months) stable disease. Median PFS was 3.1 months (95% CI, 2.7–4.2 months) [36]. The tolerability profile of ixabepilone was acceptable, as treatment-related adverse events were manageable and mostly grade 1 to 2. Selected grade 3 to 4 hematologic, treatment-related adverse events included neutropenia (54%) and fatigue/asthenia (14%), whereas peripheral neuropathy was the most common nonhematologic adverse event. In summary, the results demonstrated that ixabepilone monotherapy has clinically meaningful antitumor activity with a manageable safety profile in patients with MBC resistant to an anthracycline, a taxane, and capecitabine.
4.2. Trials 046 and 048
These 2 randomized, open-label phase 3 trials assessed the efficacy of ixabepilone (40 mg/m2 IV over 3 hours every 3 weeks) in combination with capecitabine (2000 mg/m2 orally on days 1–14 every 3 weeks) versus capecitabine alone (2500 mg/m2) on the same schedule. In total, 1973 ( and ) patients with MBC heavily pretreated and previously exposed to an anthracycline and/or resistant to a taxane, were assessed [37, 38]. The primary endpoint of these studies was PFS.
In trial 046, PFS associated with ixabepilone in combination with capecitabine was superior to capecitabine as a single agent (hazard ratio [HR] = 0.75; 95% CI, 0.64–0.88; stratified log-rank ). Median PFS was prolonged to 5.8 months (95% CI, 5.45–6.97 months) for ixabepilone in combination with capecitabine compared with 4.2 months (95% CI, 3.81–4.50) for capecitabine alone; these data were consistent with investigator-assessed median PFS (5.3 versus 3.8 months; ). The ORR was also greater in the combination arm by independent assessment (35% versus 14%; ) and by investigator assessment (42% versus 23%) [38]. In trial 048, median PFS (6.2 versus 4.4 months; ) for ixabepilone in combination with capecitabine, compared with capecitabine alone, was similar to the median PFS observed in trial 046 [37]. Investigator-assessed ORRs were also consistent with those reported in study 046 (43% versus 29%).
Ixabepilone plus capecitabine was well tolerated in the phase 3 trials, with a manageable toxicity profile. The most common grade 3/4 adverse event in the combination-therapy arm was peripheral neuropathy, occurring in 23% and 24% of patients in trials 046 and 048, respectively, compared with 0% and 1% of patients in the capecitabine-monotherapy arms, respectively. Fatigue (9–12% versus 3%), myalgia (4–8% versus <1%), and asthenia (6-7% versus 1%) also occurred more frequently in the combination-therapy arm.
5. Ixabepilone in First-Line Therapy
5.1. Pooled Analysis from Trials 046 and 048
Post-adjuvant breast cancer patients who progress after anthracyclines and taxanes require effective first-line therapies for the treatment of their metastatic disease. This is of particular importance to patients whose tumors demonstrate primary resistance to anthracyclines and taxanes and for those whose anthracycline cumulative exposure is limited by cardiotoxicity. A predefined subgroup analysis of patients with TN breast cancer ()—based on the pooled analysis of trials 046 and 048 ()—showed that ixabepilone in combination with capecitabine significantly improved PFS (4.2 versus 1.7 months) and increased ORR (31% versus 15%) compared with capecitabine alone [31]. In another analysis from trials 046 and 048, a prespecified subset of post-adjuvant, rapidly relapsing patients (; patients relapsed less than 1 year after completing neoadjuvant/adjuvant therapy) were pooled to assess the efficacy and safety of ixabepilone in combination with capecitabine compared with capecitabine alone. Prespecification of the subset allowed patients to be followed prospectively and because both trials shared similar trial designs and patient populations, the individual subset data were pooled to increase the statistical power [39].
In patients who received first-line therapy, ixabepilone in combination with capecitabine improved median PFS by 2.8 months compared with capecitabine alone (HR = 0.58; 95% CI, 0.45–0.76; stratified log-rank ). Similarly, there was nearly a 2-fold increase in ORR of patients treated with ixabepilone in combination with capecitabine compared with capecitabine alone. Hematologic (i.e., neutropenia and febrile neutropenia) and nonhematologic toxicities (any peripheral neuropathy) associated with the combination were manageable and similar to those observed in the pooled overall population. Compared with capecitabine alone, ixabepilone plus capecitabine was an effective first-line treatment for post-adjuvant, rapidly progressing patients with clinically meaningful improvements in ORR and PFS [39].
5.2. Ixabepilone Combinations in MBC
5.2.1. Ixabepilone + Bevacizumab
Preliminary data from preclinical trials showed strong synergistic antitumor activity of ixabepilone in combination with bevacizumab [40]. Recently, a randomized phase 2 trial investigated this combination as first-line therapy for MBC by comparing a weekly ixabepilone-based regimen (16 mg/m2 weekly for 3 weeks, every 4 weeks, plus bevacizumab 10 mg/kg every 2 weeks; arm A []) and an every-3-week ixabepilone-based regimen (40 mg/m2 every 3 weeks plus bevacizumab 15 mg/kg every 3 weeks; arm B []). These experimental treatments were compared with a combination of paclitaxel and bevacizumab (90 mg/m2 weekly, plus bevacizumab at the same dose and schedule as arm A; arm C []) [41]. Final results showed that ORRs were not significantly different among the 3 arms (ORR of 48% [32.9–63.1]; 71% [55.7–83.6]; 63% [43.7–78.9] in arms A, B, C, resp.). Similarly, median PFS also did not show significant differences (9.6 months [6.1–11.7]; 11.9 months [8.7–14.7]; 13.5 months [10.0–18.2] in arms A, B, C, resp.) [41], suggesting that the every-3-week schedules of ixabepilone are as effective as paclitaxel when combined with bevacizumab. The most significant grade 3 or 4 treatment-related nonhematologic and hematologic adverse events included peripheral sensory neuropathy (18%, 24%, 25% in arms A, B, C, resp.) and neutropenia (16%, 60%, 22% in arms A, B, C, resp.); febrile neutropenia rates were ≤2.2% in all arms. Ixabepilone did not appear to exacerbate the toxicity profile of bevacizumab, as the rates of adverse events were similar to those observed with ixabepilone alone at these scheduled doses. Furthermore, the clinical efficacy and tolerability profile demonstrated with ixabepilone in combination with bevacizumab—weekly or every 3 weeks—was comparable to that observed in the phase 3 Eastern Cooperative Oncology Group (ECOG) 2100 trial of bevacizumab in combination with paclitaxel versus paclitaxel alone [42].
Although the phase 2 trial discussed herein assessed the effect of ixabepilone in combination with bevacizumab, it was the first to compare weekly ixabepilone to the approved every-3-week schedule. Final results from a comparative phase 2 trial of weekly (16 mg/m2) or every-3-week ixabepilone (40 mg/m2) for 176 patients with MBC suggested that both schedules have an acceptable safety profile [43]. The weekly versus every-3-week schedule produced ORR of 8% (95% CI, 2.5–16.8) versus 14% (95% CI, 6.9–24.1), respectively (); median OS of 13.4 months versus 15.0 months, respectively (); and median PFS of 2.8 months versus 5.1 months, respectively (). These results indicate a trend towards a longer median PFS with every-3-week, compared with weekly ixabepilone. However, the weekly schedule was better tolerated; grade 3/4 adverse events were reported in 28% of patients treated with the weekly schedule and in 69% of patients treated with the every-3-week schedule and included neuropathy (11% versus 20%) and neutropenia (7% versus 40%).
5.2.2. Ixabepilone + Trastuzumab + Carboplatin
Previous studies have shown that the addition of trastuzumab to chemotherapy improves the clinical efficacy profile of patients with MBC whose tumors demonstrate overexpression or amplification of HER2. In one study, the addition of trastuzumab to paclitaxel was associated with a significant improvement in ORR (38% versus 16%, ) [44, 45]. Likewise, in a phase 3 trial that evaluated the role of carboplatin as a treatment for HER2-positive MBC, the addition of carboplatin to weekly trastuzumab and paclitaxel (175 mg/m2 IV every 3 weeks) was associated with a significantly higher ORR (57% versus 36%, ) and extended PFS (10.7 months versus 7 months, ) [46, 47].
Phase 1/2 trials have previously established the efficacy of ixabepilone monotherapy (weekly and every 3 weeks) for patients with MBC [36, 44, 4651]. As part of combination therapy, phase 1 trials have demonstrated tolerability for ixabepilone in combination with carboplatin [44, 47, 52], and a phase 2 trial of ixabepilone in combination with trastuzumab demonstrated clinically meaningful results in patients with HER2-positive MBC [53]. As such, the ECOG conducted a phase 2 trial (E2103) of weekly ixabepilone in combination with carboplatin and trastuzumab as a first-line treatment for patients with HER2-positive MBC [44]. The primary endpoint of the trial was to determine if an ORR of at least 75% was attainable with the combination. A total of 59 patients were treated with weekly ixabepilone 15 mg/m2 IV and carboplatin (area under the curve = 2 IV on days 1, 8, and 15 of a 28-day cycle for a maximum of 6 cycles), plus weekly trastuzumab (4 mg/kg loading dose, then 2 mg/kg IV during chemotherapy, then 6 mg/kg IV every 3 weeks) until disease progression; 39 patients were centrally confirmed to overexpress HER2 (3+ by immunohistochemistry or gene amplification by fluorescent in situ hybridization).
For all patients treated, the ORR was 44% (95% CI, 31%–58%) and for those patients who had overexpressed or amplified HER2, ORRs were comparable (42%; 95% CI, 26%–58%). Treatment-related toxicities were found to be manageable and low-grade, with grade 3 to 4 neutropenia (49.1%) among the most severe of hematologic toxicities. Notably, there were no reports of febrile neutropenia. Nonhematologic treatment-related adverse events were predominantly mild, with fatigue (11.9%) and sensory neuropathy (6.8%) among the most common grade 3 toxicities. Only 1 patient (1.7%) experienced a grade 4 nonhematologic adverse event of thrombosis/embolism. Although clinically effective as a first-line therapy for HER2-positive MBC, the addition of ixabepilone to carboplatin and weekly trastuzumab did not meet the study primary endpoint. However, the regimen was well tolerated with an efficacy and toxicity profile consistent with that of paclitaxel in combination with carboplatin and trastuzumab.
6. Ixabepilone as a Neoadjuvant Therapy for Breast Cancer
With the availability and access to pretreatment biopsy, the neoadjuvant treatment setting offers the ideal opportunity to identify predictive biomarkers for novel therapeutics and identify single agents or combination regimens likely to impact prognosis. In fact, information regarding biomarkers obtained from tumor biopsies can be assessed and compared with the pathologic complete response in both breast and lymph nodes (pCR) or in the breast only (pCRB)—an endpoint strongly associated with disease-free and overall patient survival [5457]. Based on the encouraging data in MBC, it was deemed appropriate to evaluate the role of ixabepilone in primary disease by using the neoadjuvant model. A phase 2 trial—incorporating an expression analysis of genes identified from a prior clinical investigation as potentially associated with sensitivity/resistance to ixabepilone—evaluated ixabepilone in the neoadjuvant setting [54]. Among such genes was MAP-tau (Tau), a well characterized microtubule stabilizer that is responsible for the bundling, spacing, and assembly of microtubules. MAP-tau may compete for taxane binding sites and/or may be involved in the cooperative binding of paclitaxel to microtubules, therefore potentially having a role in taxanes resistance [5860].
A total of 161 patients with locally advanced breast cancer, defined as primary disease in the breast of ≥3 cm (T2-3), were treated with ixabepilone (40 mg/m2 IV over 3 hours every 3 weeks) for 4 or fewer cycles. Of the 161 patients, 42 (26%) had tumors that were TN. Ixabepilone demonstrated antitumor activity comparable with that reported in trials of other single agents in the neoadjuvant setting (pCRB= 18% and overall pCR = 17%). Moreover, the highest ORR, 46.1%, was observed in patients with aggressive ER-negative/HER2-positive tumors. These data suggest that ixabepilone may be particular effective in more aggressive cancer subtypes (Table 1). Results also confirmed that ER and tau expression are inversely related to pCRB and ixabepilone sensitivity, respectively, confirming what was previously observed in the preclinical setting. The majority of treatment-related toxicities were manageable and mild-to-moderate, with severe adverse events reported in nearly one-third of patients [54]. Grade 3 to 4 neuropathy occurred in ≤3% of patients, and sensory neuropathy was the most common. Grade 3 to 4 neutropenia was observed in 14% of patients and febrile neutropenia was reported in 1% of patients (Table 2). As a neoadjuvant therapy for breast cancer, ixabepilone provided clinically meaningful benefit and had an acceptable safety profile. Moreover, the use of gene expression assays permitted the identification of patients most likely to benefit from neoadjuvant ixabepilone treatment based on expression of the ER and tau biomarkers.
Table 1: Clinical efficacy of ixabepilone (ixa) as a monotherapy or in combination with a targeted agent and/or chemotherapy in the neoadjuvant and first-line breast cancer settings.
Table 2: Selected Grade 3 or 4 treatment-related adverse events in advanced, first-line, and neoadjuvant breast cancer settings.
7. Conclusions
The primary goal of treatment of metastatic disease is optimal palliation. The selection of the most appropriate treatment in this setting requires a careful evaluation of tumor characteristics (disease subtype and location) and patient-related factors (performance status and toxicity profile). In fact, the therapeutic index for various available agents should be considered in the selection of treatment to allow for a more personalized approach. This approach is particularly important to patients with a limited number of therapeutic options, such is the case with patients who have TN MBC. In large prospective clinical trials, ixabepilone has provided evidence of clinical benefit in this subtype and a manageable toxicity profile. Moreover, efficacy in taxane resistance models (β-tubulin overexpression) and the recent demonstration of the predictive value of tau expression in primary breast cancer tissue, for example, may possibly contribute to further refining the selection of patients who might benefit from ixabepilone as a single agent, or as part of combination therapy in primary and MBC. Future studies should explore the role of this drug in neoadjuvant setting either in combination with biological agents or with other cytotoxic agents to further assess the impact on patients’ outcome when used in earlier disease.
Acknowledgments
The author takes full responsibility for the content of this publication and confirms that it reflects his viewpoint and medical expertise. The author also wishes to acknowledge StemScientific, funded by Bristol-Myers Squibb, for providing writing and editorial support. Neither Bristol-Myers Squibb nor StemScientific influenced the content of the manuscript, nor did the author receive financial compensation for authoring the manuscript.
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25. P. Giannakakou, R. Gussio, E. Nogales et al., “A common pharmacophore for epothilone and taxanes: molecular basis for drug resistance conferred by tubulin mutations in human cancer cells,” Proceedings of the National Academy of Sciences of the United States of America, vol. 97, no. 6, pp. 2904–2909, 2000. View at Publisher · View at Google Scholar · View at Scopus
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29. F. Y. Lee, A. Camuso, S. Castenada, et al., “Preclinical studies of ixabepilone (BMS-247550) demonstrate optimal antitumor activity against both chemotherapy-sensitive and -resistant tumor types,” in Proceedings of the American Association of Cancer Research Annual Meeting, abstract 503, Washington, DC, USA, April 2006.
30. M. Jordan, H. Miller, L. Ni, et al., “The Pat-21 breast cancer model derived from a patient with primary taxol resistance recapitulates the phenotype of its origin, has altered beta-tubulin expression and is sensitive to ixabepilone,” in Proceedings of the American Association for Cancer Research Annual Meeting, abstract LB-280, Washington, DC, USA, April 2006.
31. E. A. Perez, T. Patel, and A. Moreno-Aspitia, “Efficacy of ixabepilone in ER/PR/HER2-negative (triple-negative) breast cancer,” Breast Cancer Research and Treatment, vol. 121, no. 2, pp. 261–271, 2010. View at Publisher · View at Google Scholar · View at Scopus
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33. E. Rivera, J. Lee, and A. Davies, “Clinical development of ixabepilone and other epothilones in patients with advanced solid tumors,” Oncologist, vol. 13, no. 12, pp. 1207–1223, 2008. View at Publisher · View at Google Scholar · View at Scopus
34. S. Goodin, M. P. Kane, and E. H. Rubin, “Epothilones: mechanism of action and biologic activity,” Journal of Clinical Oncology, vol. 22, no. 10, pp. 2015–2025, 2004. View at Publisher · View at Google Scholar · View at Scopus
35. Ixempra PI, IXEMPRA Kit (ixabepilone) for Injection, Full Prescribing Information, Bristol-Myers Squibb, 2010.
36. E. A. Perez, G. Lerzo, X. Pivot et al., “Efficacy and safety of ixabepilone (BMS-247550) in a phase II study of patients with advanced breast cancer resistant to an anthracycline, a taxane, and capecitabine,” Journal of Clinical Oncology, vol. 25, no. 23, pp. 3407–3414, 2007. View at Publisher · View at Google Scholar · View at Scopus
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38. E. S. Thomas, H. L. Gomez, R. K. Li et al., “Ixabepilone plus capecitabine for metastatic breast cancer progressing after anthracycline and taxane treatment,” Journal of Clinical Oncology, vol. 25, no. 33, pp. 5210–5217, 2007. View at Publisher · View at Google Scholar · View at Scopus
39. J. Jassem, L. Fein, M. Karwal et al., “Ixabepilone plus capecitabine in advanced breast cancer patients with early relapse after adjuvant anthracyclines and taxanes: a pooled subset analysis of two phase III studies,” Breast, vol. 21, no. 1, pp. 89–94, 2012. View at Publisher · View at Google Scholar
40. F. Y. Lee, K. L. Covello, S. Castaneda et al., “Synergistic antitumor activity of ixabepilone (BMS-247550)plus bevacizumab in multiple in vivo tumor models,” Clinical Cancer Research, vol. 14, no. 24, pp. 8123–8131, 2008. View at Publisher · View at Google Scholar · View at Scopus
41. H. S. Rugo, M. Campone, D. Amadori, et al., “Randomized phase II study of weekly versus every-3-week ixabepilone plus bevacizumab (ixa/bev) versus paclitaxel plus bevacizumab (pac/bev) as first-line therapy for metastatic breast cancer (MBC): final results,” Journal of Clinical Oncology, vol. 28, no. 15s, p. 1040, 2010.
42. K. Miller, M. Wang, J. Gralow et al., “Paclitaxel plus bevacizumab versus paclitaxel alone for metastatic breast cancer,” New England Journal of Medicine, vol. 357, no. 26, pp. 2666–2676, 2007. View at Publisher · View at Google Scholar · View at Scopus
43. J. W. Smith, S. J. Vukelja, A. C. Rabe, et al., “Final results of a phase II randomized trial of weekly or every-3-week ixabepilone in metastatic breast cancer (MBC),” in Proceedings of the Breast Cancer Symposium, Abstract 268, 2010.
44. S. Moulder, H. Li, M. Wang et al., “A phase II trial of trastuzumab plus weekly ixabepilone and carboplatin in patients with HER2-positive metastatic breast cancer: an Eastern Cooperative Oncology Group Trial,” Breast Cancer Research and Treatment, vol. 119, no. 3, pp. 663–671, 2010. View at Publisher · View at Google Scholar · View at Scopus
45. D. J. Slamon, B. Leyland-Jones, S. Shak et al., “Use of chemotherapy plus a monoclonal antibody against her2 for metastatic breast cancer that overexpresses HER2,” New England Journal of Medicine, vol. 344, no. 11, pp. 783–792, 2001. View at Publisher · View at Google Scholar · View at Scopus
46. N. Robert, B. Leyland-Jones, L. Asmar et al., “Randomized phase III study of trastuzumab, paclitaxel, and carboplatin compared with trastuzumab and paclitaxel in women with HER-2—overexpressing metastatic breast cancer,” Journal of Clinical Oncology, vol. 24, no. 18, pp. 2786–2792, 2006. View at Publisher · View at Google Scholar · View at Scopus
47. A. Awada, M. J. Piccart, S. F. Jones et al., “Phase i dose escalation study of weekly ixabepilone, an epothilone analog, in patients with advanced solid tumors who have failed standard therapy,” Cancer Chemotherapy and Pharmacology, vol. 63, no. 3, pp. 417–425, 2009. View at Publisher · View at Google Scholar · View at Scopus
48. N. Denduluri, J. A. Low, J. J. Lee et al., “Phase II trial of ixabepilone, an epothilone B analog, in patients with metastatic breast cancer previously untreated with taxanes,” Journal of Clinical Oncology, vol. 25, no. 23, pp. 3421–3427, 2007. View at Publisher · View at Google Scholar · View at Scopus
49. J. A. Low, S. B. Wedam, J. J. Lee et al., “Phase II clinical trial of ixabepilone (BMS-247550), an epothilone B analog, in metastatic and locally advanced breast cancer,” Journal of Clinical Oncology, vol. 23, no. 12, pp. 2726–2734, 2005. View at Publisher · View at Google Scholar · View at Scopus
50. H. Roché, L. Yelle, F. Cognetti et al., “Phase II clinical trial of ixabepilone (BMS-247550), an epothilone B analog, as first-line therapy in patients with metastatic breast cancer previously treated with anthracycline chemotherapy,” Journal of Clinical Oncology, vol. 25, no. 23, pp. 3415–3420, 2007. View at Publisher · View at Google Scholar · View at Scopus
51. E. Thomas, J. Tabernero, M. Fornier et al., “Phase II clinical trial of ixabepilone (BMS-247550), an epothilone B analog, in patients with taxane-resistant metastatic breast cancer,” Journal of Clinical Oncology, vol. 25, no. 23, pp. 3399–3406, 2007. View at Publisher · View at Google Scholar · View at Scopus
52. R. Plummer, P. Woll, D. Fyfe et al., “A phase i and pharmacokinetic study of lxabepilone in combination with carboplatin in patients with advanced solid malignancies,” Clinical Cancer Research, vol. 14, no. 24, pp. 8288–8294, 2008. View at Publisher · View at Google Scholar · View at Scopus
53. S. M. Tolaney, J. Najita, W. Chen, et al., “A phase II study of ixabepilone plus trastuzumab for metastatic HER2-positive breast cancer,” Cancer Research, vol. 69, abstract 3137, 2009.
54. J. Baselga, M. Zambetti, A. Llombart-Cussac et al., “Phase II genomics study of ixabepilone as neoadjuvant treatment for breast cancer,” Journal of Clinical Oncology, vol. 27, no. 4, pp. 526–534, 2009. View at Publisher · View at Google Scholar · View at Scopus
55. H. D. Bear, S. Anderson, R. E. Smith et al., “Sequential preoperative or postoperative docetaxel added to preoperative doxorubicin plus cyclophosphamide for operable breast cancer: national surgical adjuvant breast and bowel project protocol B-27,” Journal of Clinical Oncology, vol. 24, no. 13, pp. 2019–2027, 2006. View at Publisher · View at Google Scholar · View at Scopus
56. A. Wardley, “Capecitabine: expanding options for the treatment of patients with early or locally advanced breast cancer,” Oncologist, vol. 11, no. 1, pp. 20–26, 2006. View at Publisher · View at Google Scholar · View at Scopus
57. N. Wolmark, J. Wang, E. Mamounas, J. Bryant, and B. Fisher, “Preoperative chemotherapy in patients with operable breast cancer: nine-year results from National Surgical Adjuvant Breast and Bowel Project B-18,” Journal of the National Cancer Institute Monographs, no. 30, pp. 96–102, 2001. View at Scopus
58. K. J. Rosenberg, J. L. Ross, H. E. Feinstein, S. C. Feinstein, and J. Israelachvili, “Complementary dimerization of microtubule-associated tau protein: implications for microtubule bundling and tau-mediated pathogenesis,” Proceedings of the National Academy of Sciences of the United States of America, vol. 105, no. 21, pp. 7445–7450, 2008. View at Publisher · View at Google Scholar · View at Scopus
59. H. Felgner, R. Frank, J. Biernat et al., “Domains of neuronal microtubule-associated proteins and flexural rigidity of microtubules,” Journal of Cell Biology, vol. 138, no. 5, pp. 1067–1075, 1997. View at Publisher · View at Google Scholar · View at Scopus
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Physics307L:Schedule/Week 9 agenda
From OpenWetWare
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Contents
2010
• Possibly
• Weighted averages / discussion of maximum likelihood, weighted averages (this was later in the semester last year)
• Derivation of error propagation? (not that critical now, sorta interesting, related to last week)
• Discussion of shared notebooks / stress need to do own analysis
Last year
Continue linear fitting
Error propagation
Maximum likelihood
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Coverage Remainder Of Week Sporadic
Jul 24, 2006 • 9:28 pm | (0) by | Filed Under Blog Administration
My coverage this week will be sporadic at both this site and SEW. There has been a sudden need for me to be offline for this week. I have to be with family at this time. Everyone in my family is OK and well.
I am sorry for any inconvenience.
Previous story: SES San Jose '06 Party Thread
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CMD sent two reporters to track ALEC in Oklahoma
Click here to help support our future investigations.
HSBC Holdings
From SourceWatch
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HSBC Holdings Group
"Headquartered in London, HSBC is one of the largest banking and financial services organisations in the world. HSBC's international network comprises around 9,500 offices in 85 countries and territories in Europe, the Asia-Pacific region, the Americas, the Middle East and Africa." [1]
Contents
Board
Accessed September 2012: [2]
Directors (2009)
Accessed February 2009: [3]
Contact
Web: http://www.hsbc.com
Resources and articles
Related Sourcewatch articles
References
1. About, HSBC Holdings, accessed February 25, 2009.
2. HSBC Holdings Board, organizational web page, accessed September 20, 2012.
3. Directors, HSBC Holdings, accessed February 25, 2009.
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Person:Stephen Crabtree (1)
Watchers
Stephen B. Crabtree
b.1 MAR 1841 Ohio, United States
Facts and Events
Name Stephen B. Crabtree
Gender Male
Birth[3] 1 MAR 1841 Ohio, United States
Death[2][3] 24 JUN 1914 Jefferson, Jackson, Ohio, United States
Burial[3] Horeb Cemetery, Jefferson, Jackson, Ohio, United States
Civil War Service
Source: S1
Pension
Source: S2
• Application 883329; Certificate 612829
• Widow's Pension: Application 1031124, Certificate 782929
References
1. Foraker, J.B; H.A. Axline; and J.S. Robinson. Official roster of the soldiers of the state of Ohio in the War of the Rebellion, 1861-1866. (Akron [Ohio]: Werner Co., 1886-1895).
2. United States. Veterans Administration. Organization index to pension files of veterans who served between 1861 and 1900- [1917]. (Washington, District of Columbia: The National Archives, 1949).
3. 3.0 3.1 3.2 Ohio, United States. Death Certificate. (Ohio, United States).
cert. 34660 (1914)
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
1303.8 - Australian Capital Territory Business Indicators, Mar 2000
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 21/03/2000
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Provides a monthly summary of business-related statistics for the Australian Capital Territory, with national and other State comparisons. Includes population, Consumer Price Index, building approvals, housing finance, building commencements, established house price indexes, price indexes of building materials, engineering construction, retail turnover, labour force, job vacancies, industrial disputes, average weekly earnings, tourist accommodation, new motor vehicle registrations, wage and salary earners, wage cost index, private new capital expenditure, State accounts and business expectations. Also includes trend analysis, graphs and explanatory text. This publication is designed to be of assistance to business.
© Commonwealth of Australia 2013
Unless otherwise noted, content on this website is licensed under a Creative Commons Attribution 2.5 Australia Licence together with any terms, conditions and exclusions as set out in the website Copyright notice. For permission to do anything beyond the scope of this licence and copyright terms contact us.
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Australian Bureau of Statistics
Celebrating the International Year of Statistics 2013
ABS Home > Statistics > By Release Date
1301.0 - Year Book Australia, 2004
Previous ISSUE Released at 11:30 AM (CANBERRA TIME) 27/02/2004
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Contents >> Articles
This section contains the following subsection :
Articles contained in this issue
Articles contained in previous issues
Previous PageNext Page
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Source link: http://archive.mises.org/6284/lbj-would-be-proud/
LBJ Would Be Proud
February 20, 2007 by
of Bush’s $3 trillion budget for FY 2008, but why is the “conservative” Heritage Foundation praising the president for—are you ready—reining in entitlement costs? Concludes Brian Riedl:
The President deserves praise for beginning a long overdue examination of unsustainable entitlement costs. He makes strong proposals that take the first steps to rein in entitlement spending and set the stage for a serious discussion of these unaffordable programs.
Is it the Heritage Foundation or the Bush Foundation?
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Category:Debian
From NAS-Central Buffalo - The Linkstation Wiki
Revision as of 00:10, 23 July 2006 by Ramuk (Talk | contribs)
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from: http://www.debian.org/logos/
Debian Tutorials : Haven't upgraded to Debian yet? The PPC conversion method listed below is obsolete! You can now convert your PPC LinkStation to Debian by flashing it with the FreeLink Firmware!
Pages in category "Debian"
The following 97 pages are in this category, out of 97 total.
A
B
C
D
D cont.
E
F
G
H
I
J
K
L
M
N
P
R
S
T
U
V
W
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You are here: Home » Content
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Maybe Monad… My C# version
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kicks
Maybe Monad… My C# version (Unpublished)
Functional programming paradigms are increasingly important to all .NET developers. Monads are key concepts in functional languages. The maybe monad seen in some languages can be ported to C#. In this post, I detail the elements key to the maybe monad and the implementation decisions made when creating such a container.
Kicked By:
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2024-06-03T21:29:47.544Z
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2013-05-18T06:52:01.000Z
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x3w2z4uij23ioeoukk7hn22u4noswcmk
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"warc_filename": "<urn:uuid:1465fdc5-49a5-4e8c-8266-0d91c05df571>",
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United States Census 1840Edit This Page
From FamilySearch Wiki
Revision as of 15:55, 18 July 2008 by Mntvly5 (Talk | contribs)
Additional information may be found on the United States Census Portal page.
Contents
Content
1840 Census was taken beginning 1 June 1820, for eighteen months. The following information was recorded by the census taker:
Free white males under 5
Free Males 5-10
Free Males 10-15
Free Males 15-20
Free Males 20-30
Free Males 30-40
Free Males 40-50
Free Males 50-60
Free Males 60-70
Free Males 70-80
Free Males 80-90
Free Males 90-100
Free Males over 100
Free Females same as males
Slaves/free colored persons in age categories
Deaf, dumb, blind & aliens
Age of Rev. War pensioners
Mining; agriculture; commerce; manufacturing & trade; navigation of the ocean; navigation of canals, lakes & rivers; learned professions and
engineers; number in school; number in family over 21 who could not read & write; number insane
Information in the United States Population Census, 1790-2000: [***Internal Link - How?]
Value
The 1800 census can be used to:1
Identify locality
Distinguish target family from others of same name
Help determine family size
Locate possible relatives with same name
Identify neighbors
Identify slaveholders
Identify name variations
Free men of color listed as head of household
Slaves in age group by name of owner
Naturalization column may indicate length of residency in U.S. to find papers
Identify Pensioners leading to Rev. War information
Identify occupation
Identify education level
Identify insane leading to institution/guardianship records
1790-1840 searching tips: http://www.archives.gov/genealogy/census/1790-1840.html
Unique Features and Problems
1. Asked the age of Revolutionary war pensioners
2. Expanded occupational options
3. Lists the number of those in school
4. Lists the number of those over 21 who can read and write
5. Lists those who are insane
States Covered and Missing
• Alabama
• Arkansas
• Connecticut
• Delaware
• District of Columbia
• Georgia
• Illinois
• Indiana
• Kentucky
• Louisiana
• Maine
• Maryland
• Massachusetts
• Michigan
• Mississippi
• Missouri
• New Hampshire
• New Jersey
• New York
• North Carolina
• Ohio
• Pennsylvania
• Rhode Island
• South Carolina
• Tennessee
• Virginia
• Vermont
There are no states missing.
Territories
• Florida
• Iowa
• Oregon (also a part of Britain)
• Wisconsin
Web Sites
1790-1840 Info: http://www.census.gov/prod/2000pubs/cff-2.pdf
1790-1840 Search Tips: http://www.archives.gov/genealogy/census/1790-1840.html
Biographic Citations
1. Szucs, Loretto Dennis and Sandra Hargreaves Luebking. The Source: A Guide book to American Genealogy. 3rd ed. (Provo, UT: Ancestry, 2006.)
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