Publications

Food insecurity refers to the inability to afford enough food for an active, healthy life. Numerous studies have shown associations between food insecurity and adverse health outcomes among children. Studies of the health effects of food insecurity among adults are more limited and generally focus on the association between food insecurity and self-reported disease. We therefore examined the association between food insecurity and clinical evidence of diet-sensitive chronic disease, including hypertension, hyperlipidemia, and diabetes. Our population-based sample included 5094 poor adults aged 18-65 y participating in the NHANES (1999-2004 waves). We estimated the association between food insecurity (assessed by the Food Security Survey Module) and self-reported or laboratory/examination evidence of diet-sensitive chronic disease using Poisson regression. We adjusted the models to account for differences in age, gender, race, educational attainment, and income. Food insecurity was associated with self-reported hypertension [adjusted relative risk (ARR) 1.20; 95% CI, 1.04-1.38] and hyperlipidemia (ARR 1.30; 95% CI, 1.09-1.55), but not diabetes (ARR 1.19; 95% CI, 0.89-1.58). Food insecurity was associated with laboratory or examination evidence of hypertension (ARR 1.21; 95% CI, 1.04-1.41) and diabetes (ARR 1.48; 95% CI, 0.94-2.32). The association with laboratory evidence of diabetes did not reach significance in the fully adjusted model unless we used a stricter definition of food insecurity (ARR 2.42; 95% CI, 1.44-4.08). These data show that food insecurity is associated with cardiovascular risk factors. Health policy discussions should focus increased attention on ability to afford high-quality foods for adults with or at risk for chronic disease.

Standards-based, computable knowledge representations for eligibility criteria are increasingly needed to provide computer-based decision support for automated research participant screening, clinical evidence application, and clinical research knowledge management. We surveyed the literature and identified five aspects of eligibility criteria knowledge representation that contribute to the various research and clinical applications: the intended use of computable eligibility criteria, the classification of eligibility criteria, the expression language for representing eligibility rules, the encoding of eligibility concepts, and the modeling of patient data. We consider three of these aspects (expression language, codification of eligibility concepts, and patient data modeling) to be essential constructs of a formal knowledge representation for eligibility criteria. The requirements for each of the three knowledge constructs vary for different use cases, which therefore should inform the development and choice of the constructs toward cost-effective knowledge representation efforts. We discuss the implications of our findings for standardization efforts toward knowledge representation for sharable and computable eligibility criteria.

CONTEXT

Medical devices are common in clinical practice and have important effects on morbidity and mortality, yet there has not been a systematic examination of evidence used by the US Food and Drug Administration (FDA) for device approval.

OBJECTIVES

To study premarket approval (PMA)--the most stringent FDA review process--of cardiovascular devices and to characterize the type and strength of evidence on which it is based.

DATA SOURCES AND STUDY SELECTION

Systematic review of 78 summaries of safety and effectiveness data for 78 PMAs for high risk cardiovascular devices that received PMA between January 2000 and December 2007 [corrected].

DATA EXTRACTION

Examination of the methodological characteristics considered essential to minimize confounding and bias, as well as the primary end points of the 123 studies supporting the PMAs.

RESULTS

Thirty-three of 123 studies (27%) used to support recent FDA approval of cardiovascular devices were randomized and 17 of 123 (14%) were blinded. Fifty-one of 78 PMAs (65%) were based on a single study. One hundred eleven of 213 primary end points (52%) were compared with controls and 34 of 111 controls (31%) were retrospective. One hundred eighty-seven of 213 primary end points (88%) were surrogate measures and 122 of 157 (78%) had a discrepancy between the number of patients enrolled in the study and the number analyzed.

CONCLUSION

Premarket approval of cardiovascular devices by the FDA is often based on studies that lack adequate strength and may be prone to bias.

Pulmonary alveolar type I cells (TI cell) are very large (approximately 5400 microm(2) in surface area) squamous cells that cover more than 98% of the internal surface area of rodent lungs. In the past, TI cells were believed to serve only passive barrier functions, with no active functional properties in the lung. The fairly recent development of methods to isolate TI cells has permitted investigation of functions of this cell type for the first time. Resolvable by electron microscopy, TI cells contain microvilli and organelles typically associated with metabolic functions, such as mitochondria, abundant smooth and rough endoplasmic reticulum and Golgi apparatus. TI cells contain the molecular machinery necessary for ion transport and take up Na(+), K(+), and Cl(-), from which one can infer that it is likely that they play a role in ion and fluid transport in vivo. Because the abundance/microm(2) of highly selective Na(+) channels (HSC channels, consisting of all three ENaC subunits) is the same in TI and TII cells and because TI cells cover the majority of the lung internal surface, TI cells may play the major role in bulk transport of Na(+). In vitro, TI cells can proliferate and exhibit phenotypic plasticity, raising the question of whether this cell type may play a role in development and lung repair after injury. From gene expression analysis of TI cells, one can infer a variety of other possible functions for TI cells. The development of techniques to administer transgenes specifically to TI cells will permit direct study of this cell type in vivo.

Whether genetic factors account for differences in early kidney disease among blacks in a young healthy population is not well known. We evaluated the association of self-reported race and genetic African ancestry with elevated creatinine (> or =1.3 mg/dl for men, > or =1.1 mg/dl for women) among 3,113 black and white participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study, ages 38-50 years. We estimated individual African ancestry using 42 ancestry informative markers. Blacks were more likely to have elevated creatinine than whites, and this effect was more pronounced in men: adjusted odds ratio (AOR) for black versus white men = 7.03, 4.15-11.91; AOR for women = 2.40, 1.15-5.02. Higher African ancestry was independently associated with elevated creatinine among black men (AOR = 1.53,1.08-2.16 per SD increase in African ancestry), but not women. A graded increase in odds of elevated creatinine by African Ancestry was observed among black men compared with white men: AOR = 4.27 (2.26-10.06) for black men with 40-70% African ancestry; AOR = 8.09 (4.19-15.61) for black men with 70-80% African ancestry; AOR = 9.05 (4.81-17.02) for black men with >80% African ancestry. Genetic factors common to African ancestry may be associated with increased risk of early kidney dysfunction in a young, healthy population, particularly among black men.