Death in the United States, 2007.
ABSTRACT KEY FINDINGS: Data from the National Vital Statistics System, Mortality In 2007, the age-adjusted death rate for the United States reached a record low of 760.3 per 100,000 population. Life expectancy at birth reached a record high of 77.9 years. States in the southeast region have higher death rates than those in other regions of the country. In 2007, the five leading causes of death were heart disease, cancer, stroke, chronic lower respiratory diseases, and accidents. These accounted for over 64 percent of all deaths in the United States. White females have the longest life expectancy (80.7 years), followed by black females (77.0 years). The gap in life expectancy between white persons and black persons declined by 35 percent between 1989 and 2007. The race differential was 4.6 years in 2007.
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ABSTRACT: Worldwide, an estimated 200 million people have chronic kidney disease (CKD). In the United States, African Americans (AAs) have a four-fold excess risk of CKD compared to non-Hispanic white people and globally, people in the low-to-middle income countries of Asia and Sub-Saharan Africa have the highest rates of CKD. Annually, more than 500,000 individuals develop end-stage renal disease (or CKD stage 5) in Sub-Saharan Africa alone and the vast majority of these patients suffer premature mortality. The health care costs and economic burden of CKD are huge and not sustainable even in advanced Western countries. A recent discovery on the role of Apolipoprotein 1 (APOL1) G1 and G2 renal risk variants in AAs has a huge potential to unravel the etiology of CKD in both AA and other black populations. Under the National Institutes of Health (NIH)-sponsored Human Heredity and Health in Africa (H3Africa) initiative, a large prospective genetic study of CKD is being conducted in 8000 participants in four African countries (Ethiopia, Ghana, Kenya, and Nigeria; for a total population of 320 million). This and other basic research studies in the United States could potentially shed great insight into the genetics and biologic mechanisms involved in the excess predilection of Africans and AAs to CKD.Transactions of the American Clinical and Climatological Association 01/2014; 125:229-46.
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ABSTRACT: Familial hypercholesterolemia (FH) is a common autosomal codominant disease with a frequency of 1∶500 individuals in its heterozygous form. The genetic basis of FH is most commonly mutations within the LDLR gene. Assessing the pathogenicity of LDLR variants is particularly important to give a patient a definitive diagnosis of FH. Current studies of LDLR activity ex vivo are based on the analysis of 125I-labeled lipoproteins (reference method) or fluorescent-labelled LDL. The main purpose of this study was to compare the effectiveness of these two methods to assess LDLR functionality in order to validate a functional assay to analyse LDLR mutations. LDLR activity of different variants has been studied by flow cytometry using FITC-labelled LDL and compared with studies performed previously with 125I-labeled lipoproteins. Flow cytometry results are in full agreement with the data obtained by the 125I methodology. Additionally confocal microscopy allowed the assignment of different class mutation to the variants assayed. Use of fluorescence yielded similar results than 125I-labeled lipoproteins concerning LDLR activity determination, and also allows class mutation classification. The use of FITC-labelled LDL is easier in handling and disposal, cheaper than radioactivity and can be routinely performed by any group doing LDLR functional validations.PLoS ONE 11/2014; 9(11):e112677. DOI:10.1371/journal.pone.0112677 · 3.53 Impact Factor
Academic Emergency Medicine 05/2013; 20(5). DOI:10.1111/acem.12132 · 2.20 Impact Factor