Exposure to tricyclic antidepressants is associated with an increased risk of incident CHD events in a population-based study

Purpose The purpose of this study was to assess the association between antidepressant use and incident coronary heart disease (CHD) events in a sample of individuals without known baseline heart disease. Participants and methods We studied a group of 970 randomly selected community-dwelling adults in the 1995 Nova Scotia Health Survey, who were followed for up to 10 years. Antidepressant usage was classified according to class. Primary outcomes were acute coronary syndrome hospitalizations or cardiac death, determined by centralized, standardized ratings. Results During a follow-up period of 10 years, there were 147 incident CHD events (139 acute coronary syndromes and 8 cardiac deaths) during the 8129 person-years of observation (incidence rate=18.1 events/1000 person-years). In a model controlling for age, sex, Framingham risk score, time to last annual exam, aspirin exposure, and depressive symptoms, an increased risk of CHD events was associated with tricyclic antidepressant exposure (adjusted hazard ratio, 2.10; 95% confidence interval, 1.09–4.06; p =0.027). Conclusion In this prospective population-based study, exposure to tricyclic antidepressants was associated with higher risk of first CHD events

Endothelial cell activation, reduced endothelial cell reparative capacity, and impaired endothelial-dependent vasodilation after anger provocation

The experience of anger increases the acute and long-term risks of incident cardiovascular disease (CVD) events [1] and [2]. The mechanism(s) whereby anger is associated with increased CVD risk remains to be fully characterized. One promising candidate mechanism is endothelial dysfunction. Endothelial dysfunction, as evidenced by impaired endothelial-dependent vasodilation, is an early pathogenic process underlying atherosclerosis development and CVD onset. More recent investigations have elucidated the cellular pathways underlying endothelial dysfunction. Endothelial cell (EC) injury can be assessed by measuring circulating levels of EC-derived microparticles (EMPs), which are phospholipid rich, submicron particles derived and released from the membranes of activated or apoptotic ECs [3]. In addition, the discovery of circulating, bone marrow-derived endothelial progenitor cells (EPCs) capable of EC repair and regeneration [4] suggests that endothelial function represents a balance between ongoing injury and repair. We previously reported that anger provocation acutely impairs arterial vasomotion in apparently healthy individuals [5]. We conducted a study to examine the acute effects of anger provocation not only on arterial vasodilation but also on levels of EMPs and bone marrow-derived EPCs. To our knowledge, this is the first report concerning the adverse effects of anger provocation on cellular pathways underlying EC health

US Cosmic Visions: New Ideas in Dark Matter 2017: Community Report

This white paper summarizes the workshop "U.S. Cosmic Visions: New Ideas in Dark Matter" held at University of Maryland on March 23-25, 2017.Comment: 102 pages + reference

An index to assess the health and benefits of the global ocean

The ocean plays a critical role in supporting human well-being, from providing food, livelihoods and recreational opportunities to regulating the global climate. Sustainable management aimed at maintaining the flow of a broad range of benefits from the ocean requires a comprehensive and quantitative method to measure and monitor the health of coupled human–ocean systems. We created an index comprising ten diverse public goals for a healthy coupled human–ocean system and calculated the index for every coastal country. Globally, the overall index score was 60 out of 100 (range 36–86), with developed countries generally performing better than developing countries, but with notable exceptions. Only 5% of countries scored higher than 70, whereas 32% scored lower than 50. The index provides a powerful tool to raise public awareness, direct resource management, improve policy and prioritize scientific research.This is the publisher’s final pdf. The published article is copyrighted by the Nature Publishing Group and can be found at: http://www.nature.com/nature/index.htm

Mouse genomic variation and its effect on phenotypes and gene regulation

We report genome sequences of 17 inbred strains of laboratory mice and identify almost ten times more variants than previously known. We use these genomes to explore the phylogenetic history of the laboratory mouse and to examine the functional consequences of allele-specific variation on transcript abundance, revealing that at least 12% of transcripts show a significant tissue-specific expression bias. By identifying candidate functional variants at 718 quantitative trait loci we show that the molecular nature of functional variants and their position relative to genes vary according to the effect size of the locus. These sequences provide a starting point for a new era in the functional analysis of a key model organism