Poverty or income inequality as predictor of mortality: longitudinal cohort study.

OBJECTIVE: To determine the effect of inequality in income between communities independent of household income on individual all cause mortality in the United States. DESIGN: Longitudinal cohort study. SUBJECTS: A nationally representative sample of 14,407 people aged 25-74 years in the United States from the first national health and nutrition examination survey. SETTING: Subjects were followed from initial interview in 1971-5 until 1987. Complete follow up information was available for 92.2% of the sample. MAIN OUTCOME MEASURES: Relation between both household income and income inequality in community of residence and individual all cause mortality at follow up was examined with Cox proportional hazards survival analysis. RESULTS: Community income inequality showed a significant association with subsequent community mortality, and with individual mortality after adjustment for age, sex, and mean income in the community of residence. After adjustment for individual household income, however, the association with mortality was lost. CONCLUSIONS: In this nationally representative American sample, family income, but not community income inequality, independently predicts mortality. Previously reported ecological associations between income inequality and mortality may reflect confounding between individual family income and mortality.     

An imported thylakoid protein accumulates in the stroma when insertion into thylakoids is inhibited

The light-harvesting chlorophyll a/b protein (LHCP) is synthesized in the cytosol as a precursor (pLHCP) that is imported into chloroplasts and assembled into thylakoid membranes. Under appropriate conditions, either pLHCP or LHCP will integrate into isolated thylakoids. We have identified two situations that inhibit integration in this assay. Ionophores and uncouplers inhibited integration up to 70%. Carboxyl-terminal truncations of pLHCP also interfered with integration. A 22-residue truncation reduced integration to about 25% of control, whereas a 93 residue truncation completely abolished it. When pLHCP was imported into chloroplasts in the presence of uncouplers or when truncated forms of pLHCP were used, significant amounts of the imported proteins failed to insert into thylakoids and instead accumulated in the aqueous stroma. Accumulation of stromal LHCP occurred at uncoupler concentrations required to dissipate the trans-thylakoid proton electrochemical gradient and was enhanced at reduced levels of ATP. The latter effect may be a secondary consequence of a reduction in ATP-dependent degradation within the stroma. These results indicate that the stroma is an intermediate location in the LHCP assembly pathway and provide the first evidence for a soluble intermediate during biogenesis of a chloroplast membrane protein.     

A Model of Glutamate Neurotoxicity and Mechanisms of the Development of the Typical Pathological Process

Biophysics - A glutamate model of stroke was analyzed from the standpoint of the development of a typical pathological process that is thought to occur when major regulatory mechanisms are...