older men with HI or DSI had a greater risk of dying from any cause and particularly cardiovascular causes within a median 5-year follow-up. Women with hearing impairment had a non-significantly elevated risk. Vision impairment alone was not associated with increased mortality.

Objective To investigate the incidence and progression of age related m acular degeneration (AMD) and associated risk factors. Design Population-based prospective cohort study. Participants 2868 participants from the Age Gene/Environment Susceptibility-Reykjavik Study with retinal data at baseline and five-year follow-up. Methods Digital macular photographs were graded for presence of AMD. Participants completed a questionnaire and extensive clinical battery. Biomarkers were assessed. Risk factors for AMD were analyzed using multivariate regression analysis with odds ratios (ORs) and 95% confidence intervals (CIs). Main outcome measures AMD, defined as early or late. Results Among 2196 participants free of AMD at baseline, 14.9% developed incident AMD. In multivariate models, incident AMD was significantly associated with age (OR per year 1.14 (95% CI 1.11, 1.17)), current smoking (OR 2.07 (1.38, 3.11)), former smoking (OR 1.36 (1.04, 1.79)), plasma high-density lipoprotein (HDL) cholesterol level (OR 1.62 per mmol/L (1.19, 2.22)), and body mass index (BMI) (OR 1.04 per kg/m2 (1.01, 1.07)). Among 563 participants with early AMD at baseline, 22.7% progressed to late AMD (11.0% pure geographic atrophy (GA) and 11.7% exudative AMD). In multivariate analyses, age was significantly associated with progression to GA (OR 1.14 (1.07, 1.21)) and exudative AMD (OR 1.08 (1.01, 1.14)). Adjusting for age, female sex was associated with exudative AMD (OR 2.10 (1.10, 3.98)) and plasma HDL cholesterol with GA (OR 2.03 per mmol/L (1.02, 4.05)). Conclusion By age 85 years, 57.4% of participants had signs of AMD. Age, smoking, plasma HDL cholesterol, BMI and female sex are associated with AMD. Elevated HDL cholesterol is associated with GA development.

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Bacterial exotoxins and endotoxins both stimulate proinflammatory mediators but the contribution of each individual toxin in the release of mediators causing lethal shock is incompletely understood. This study examines the cytokine response and lethality of mice exposed to varying doses of staphylococcal enterotoxin B (SEB) or lipopolysaccharide (LPS) and their combinations. In vivo, SEB alone induced moderate levels of IL-2 and MCP-1 and all mice survived even with a high dose of SEB (100 μg/mouse). LPS (80 μg/mouse) caused 48% lethality and induced high levels of IL-6 and MCP-1. SEB induced low levels of TNFα, IL-1, IFNγ, MIP-2, and LPS synergized with SEB in the expression of these cytokines and that of IL-6 and MCP-1. Importantly, the synergistic action of SEB and LPS resulted in lethal shock and hypothermia. ANOVA of cytokine levels by survival status of SEB-plus-LPS groups revealed significantly higher levels of TNFα, IL-6, MIP-2, and MCP-1 in nonsurvivors measured at 8 hours. Significantly higher levels of IFNγ and IL-2 were observed at 21 hours in nonsurvivors of toxic shock compared to those in survivors. Overall, synergistic action of SEB and LPS resulted in higher and prolonged levels of these key cytokines leading to toxic shock.