Dynamics of Race, Culture and Key Indicators of Health in the Nation's 100 Largest Cities and Their Suburbs

Profiles the 2000 status of, and changes since 1990, in rates of health and health-related measures to identify patterns in race/ethnicity, foreign-born status, language use, poverty, income, low birth weight, teen births, prenatal care, and tuberculosis

Video Manipulation Techniques for the Protection of Privacy in Remote Presence Systems

Systems that give control of a mobile robot to a remote user raise privacy concerns about what the remote user can see and do through the robot. We aim to preserve some of that privacy by manipulating the video data that the remote user sees. Through two user studies, we explore the effectiveness of different video manipulation techniques at providing different types of privacy. We simultaneously examine task performance in the presence of privacy protection. In the first study, participants were asked to watch a video captured by a robot exploring an office environment and to complete a series of observational tasks under differing video manipulation conditions. Our results show that using manipulations of the video stream can lead to fewer privacy violations for different privacy types. Through a second user study, it was demonstrated that these privacy-protecting techniques were effective without diminishing the task performance of the remote user.Comment: 14 pages, 8 figure

Immobility, inheritance and plasticity of shape of the yeast nucleus

<p>Abstract</p> <p>Background</p> <p>Since <it>S. cerevisiae </it>undergoes closed mitosis, the nuclear envelope of the daughter nucleus is continuous with that of the maternal nucleus at anaphase. Nevertheless, several constitutents of the maternal nucleus are not present in the daughter nucleus. The present study aims to identify proteins which impact the shape of the yeast nucleus and to learn whether modifications of shape are passed on to the next mitotic generation. The Esc1p protein of <it>S. cerevisiae </it>localizes to the periphery of the nucleoplasm, can anchor chromatin, and has been implicated in targeted silencing both at telomeres and at HMR.</p> <p>Results</p> <p>Upon increased Esc1p expression, cell division continues and dramatic elaborations of the nuclear envelope extend into the cytoplasm. These "escapades" include nuclear pores and associate with the nucleolus, but exclude chromatin. Escapades are not inherited by daughter nuclei. This exclusion reflects their relative immobility, which we document in studies of prezygotes. Moreover, excess Esc1p affects the levels of multiple transcripts, not all of which originate at telomere-proximal loci. Unlike Esc1p and the colocalizing protein, Mlp1p, overexpression of selected proteins of the inner nuclear membrane is toxic.</p> <p>Conclusion</p> <p>Esc1p is the first non-membrane protein of the nuclear periphery which – like proteins of the nuclear lamina of higher eukaryotes – can modify the shape of the yeast nucleus. The elaborations of the nuclear envelope ("escapades") which appear upon induction of excess Esc1p are not inherited during mitotic growth. The lack of inheritance of such components could help sustain cell growth when parental nuclei have acquired potentially deleterious characteristics.</p

Refined localization of the asparagine synthetase gene (ASNS) to chromosome 7, region q21.3, and characterization of the somatic cell hybrid line 4AF/106/K015

We have mapped the asparagine synthetase gene (ASNS) to 7q21.3 by fluorescence in situ hybridization. While this study refined the localization of the gene, it also revealed a rearrangement in a somatic cell hybrid line which was used in previous ASNS mapping. Using additional probes from other regions of human chromosome 7, we showed that this cell line (4AF/106/KO15) contained a rearranged chromosome 7 in which a segment of the long arm was apparently duplicated and inserted into the short arm. Caution should be used therefore when interpreting data obtained from this cell line for gene mapping studies.published_or_final_versio

Implications of the Patient Protection and Affordable Care Act for Health Inequities

To assess implications , opportunities, and challenges of health care reform for improving the health and health care of racially and ethnically diverse populations

PATIENT PROTECTION AND AFFORDABLE CARE ACT OF 2010: Advancing Health Equity for Racially and Ethnically Diverse Populations

Racial/ethnic disparities in health and health care in the United States are persistent and well documented. Communities of color fare far worse than their white counterparts across a range of health indicators: life expectancy, infant mortality, prevalence of chronic diseases, self-rated health status, insurance coverage, and many others.1 As the nation’s population continues to become increasingly diverse—people of color are projected to comprise 54% of the U.S. population by 2050 and more than half of U.S. children by 20232— these disparities are likely to grow if left unaddressed. Recent health care reform legislation, while not a panacea for eliminating health disparities, off ers an important fi rst step and an unprecedented opportunity to improve health equity in the United States. Reforming the nation’s health care system was President Obama’s top domestic priority when he was sworn into offi ce in January 2009. Th e road to reform was complex and unoffi cially started in summer of 2009 when House and Senate committees began to draft legislation. On November 7, 2009, the House of Representatives passed its health care reform proposal, Th e Aff ordable Health Choices Act of 2009 (H.R. 3962). On December 24, 2009, the Senate passed its own proposal for health care reform, Th e Patient Protection and Aff ordable Care Act (H.R. 3590)*, which was a merged version of the Senate Finance Committee’s America’s Health Future Act (S.1796) and the Senate Committee on Health, Education, Labor, and Pensions’ Aff ordable Health Choices Act (S. 1697).† Eff orts to reconcile diff erences between the Senate and House bills were stymied by the death of Senator Edward Kennedy (D-MA), a lifelong proponent of health care reform and critical force in securing a proposal’s passage in the Senate. Faced with limited options and expecting that a compromise bill could not get Senate support, the House passed the Senate’s proposal and Th e Patient Protection and Aff ordable Care Act (ACA) was signed into law by President Obama on March 23, 2010 (Pub. L. No. 111-148).‡ On March 30, 2010, the ACA was amended by Th e Health Care and Education Reconciliation Act of 2010 (H.R. 4872). According to Congressional Budget Offi ce (CBO) estimates, the ACA, as reconciled by H.R. 4872, will reduce the defi cit by $143 billion over the next decade and decrease the number of non-elderly uninsured by 32 million, leaving 23 million uninsured— approximately one-third of whom would be undocumented immigrants.3 Th is report provides a comprehensive review of general and specifi c ACA provisions with the potential to signifi cantly improve health and health care for millions of diverse populations and their communities. Th e narrative that follows identifi es these provisions, discusses why they are important, and considers challenges that may lie ahead in implementing them. We have organized this presentation in three major sections. Th e next section discusses provisions that explicitly address health disparities, such as those concerning data collection by race/ethnicity, workforce diversity, cultural competence, health disparities research, health disparities initiatives in prevention, and health equity in health insurance reform, and discusses their implications for racially and ethnically diverse communities. Section III describes general provisions, including health insurance reforms, access to care, quality improvement, cost containment, public health and social determinants of health, all of which are likely to have major implications for diverse communities. An accompanying appendix identifi es these provisions, provides a timetable and, where identifi ed in the legislation, the federal agencies responsible for implementation, as well as allocations as of June 30, 2010. Section IV discusses issues that will be critical in realizing the full potential of health care reform and highlights questions and directions for the future, particularly in context of important priorities for reducing racial/ethnic health disparities that were left unaddressed

Emergency Department Initiatives to Improve the Public Health *

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71985/1/j.1553-2712.1998.tb02827.x.pd

Clinical–pathologic significance of cancer stem cell marker expression in familial breast cancers

Human breast cancer cells with a CD44(+)/CD24(−/low) or ALDH1+ phenotype have been demonstrated to be enriched for cancer stem cells (CSCs) using in vitro and in vivo techniques. The aim of this study was to determine the association between CD44(+)/CD24(−/low) and ALDH1 expression with clinical–pathologic tumor characteristics, tumor molecular subtype, and survival in a well characterized collection of familial breast cancer cases. 364 familial breast cancers from the Ontario Familial Breast Cancer Registry (58 BRCA1-associated, 64 BRCA2-associated, and 242 familial non-BRCA1/2 cancers) were studied. Each tumor had a centralized pathology review performed. TMA sections of all tumors were analyzed for the expression of ER, PR, HER2, CK5, CK14, EGFR, CD44, CD24, and ALDH1. The Chi square test or Fisher’s exact test was used to analyze the marker associations with clinical–pathologic tumor variables, molecular subtype and genetic subtype. Analyses of the association of overall survival (OS) with marker status were conducted using Kaplan–Meier plots and log-rank tests. The CD44(+)/CD24(−/low) and ALDH1+ phenotypes were identified in 16% and 15% of the familial breast cancer cases, respectively, and associated with high-tumor grade, a high-mitotic count, and component features of the medullary type of breast cancer. CD44(+)/CD24(−/low) and ALDH1 expression in this series were further associated with the basal-like molecular subtype and the CD44(+)/CD24(−/low) phenotype was independently associated with BRCA1 mutational status. The currently accepted breast CSCs markers are present in a minority of familial breast cancers. Whereas the presence of these markers is correlated with several poor prognostic features and the basal-like subtype of breast cancer, they do not predict OS

Hypermethylation of CpG islands in the mouse asparagine synthetase gene: relationship to asparaginase sensitivity in lymphoma cells. Partial methylation in normal cells

We have sequenced the promoter region of the murine asparagine synthetase gene and examined its methylation profile in the CpG islands of L-asparaginase-sensitive 6C3HED cells (asparagine auxotrophs) and resistant variants (prototrophs). In the former, complete methylation of the CpG island is correlated with failure of expression of mRNA: cells of the latter possess both methylated and unmethylated alleles, as do cells of the intrinsically asparagine-independent lines L1210 and EL4. A similar phenomenon was seen in normal splenic cells of adult mice. This was age related: no methylation was found in weanlings, but up to 45% of gene copies in animals 18 weeks or older were methylated. It was also tissue related, with methylation occurring rarely in liver cells. The relationship of these changes to oncogenesis is considered. http://www.bjcancer.com © 2001 Cancer Research Campaignhttp://www.bjcancer.co