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tion of active fire points. However, this preliminary study represents the first systematic investigation of WSOC deposition in southeastern TP. Further robust in-situ field investigations and laboratory measurements are urgently necessary to improve our understanding of the transfer process and optical property of WSOC.More frequent and intense periods of extreme heat (heatwaves) represent the most direct challenge to human health posed by climate change. Older adults are particularly vulnerable, especially those with common age-associated chronic health conditions (e.g., cardiovascular disease, hypertension, obesity, type 2 diabetes, chronic kidney disease). In parallel, the global population is aging and age-associated disease rates are on the rise. Impairments in the physiological responses tasked with maintaining homeostasis during heat exposure have long been thought to contribute to increased risk of health disorders in older adults during heatwaves. As such, a comprehensive overview of the provisional links between age-related physiological dysfunction and elevated risk of heat-related injury in older adults would be of great value to healthcare officials and policy makers concerned with protecting heat-vulnerable sectors of the population from the adverse health impacts of heatwaves. In this narrative review, we therefore summarize our current understanding of the physiological mechanisms by which aging impairs the regulation of body temperature, hemodynamic stability and hydration status. We then examine how these impairments may contribute to acute pathophysiological events common during heatwaves (e.g., heatstroke, major adverse cardiovascular events, acute kidney injury) and discuss how age-associated chronic health conditions may exacerbate those impairments. Finally, we briefly consider the importance of physiological research in the development of climate-health programs aimed at protecting heat-vulnerable individuals.The Target of Rapamycin (TOR) protein kinase plays a pivotal role in metabolism and gene expression, which enables cell proliferation, growth and development. Lipopolysaccharides (LPS) are a class of complex glycolipids present in the cell surface of Gram-negative bacteria and mediate plant-bacteria interactions. In this study, we examined whether LPS from Azospirillum brasilense Sp245 affect Arabidopsis thaliana growth via a mechanism involving TOR. A. thaliana plants were treated with LPS and plant growth and development were analyzed in mature plants. Morphological and molecular changes as well as TOR expression and activity were analyzed in root tissues. LPS increased total fresh weight, root length and TORGUS expression in the root meristem. Phosphorylation of S6k protein, a downstream target of TOR, increased following LPS treatment, which correlated with increased or decreased expression of CycB1;1GUS protein upon treatment with LPS or TOR inhibitor AZD-8055, respectively. Long term LPS treatment further increased the rosette size as well as the number of stems and siliques per plant, indicating an overall phytostimulant effect for these signaling molecules. Taken together, the results suggest that A. brasilense LPS play probiotic roles in plants influencing TOR-mediated processes.

Although coronary artery calcium (CAC) density has been associated with plaque stability, pathological evidence is lacking. We investigated the relationship between coronary computed tomography (CCT)-derived CAC density and multiple calcified and high-risk plaque (HRP) characteristics using optical coherence tomography (OCT).

We analyzed 83 plaques from 33 stable angina patients who underwent both CCT and OCT. CAC density was measured at calcium plaques with ≥90 Hounsfield units (HU) and ≥130 HU using custom CT software. The correlation between median CAC density and OCT-derived calcium size (thickness and area) was assessed. To investigate whether median CAC densities measured at the 90 HU threshold were associated with plaque vulnerability, OCT-derived plaque characteristics and HRP characteristics were compared between the low (90-129 HU), intermediate (130-199 HU) and high (≥200 HU) CAC HU groups.

Median CAC densities at 130 HU were moderately associated with calcium thickness (R=0.573, p<0.001) and area (R=0.560, p<0.001). Similar results were observed at 90 HU (thickness, R=0.615, p<0.001; area, R=0.612, p<0.001). Among groups with low, intermediate and high HU levels, calcium thickness (0.42±0.14mm, 0.60±0.17mm and 0.77±0.19mm, respectively; p<0.001) and area (0.55±0.29mm

, 1.20±0.58mm

and 1.78±0.87mm

, respectively; p<0.001) were significantly greater in the high HU group. BI-3406 HRP characteristics, however, did not differ among the three groups.

OCT-derived calcium size, but not HRP characteristics, were associated with CAC density, suggesting that CAC density is driven mainly by calcified plaque size but not local plaque vulnerability.

OCT-derived calcium size, but not HRP characteristics, were associated with CAC density, suggesting that CAC density is driven mainly by calcified plaque size but not local plaque vulnerability.

Coronary artery disease (CAD) arises from the interaction of genetic and environmental factors. Although genome-wide association studies (GWAS) have identified multiple risk loci and single nucleotide polymorphisms (SNPs) associated with risk of CAD, they are predominantly located in non-coding or intergenic regions and their mechanisms of effect are largely unknown. Accordingly, our objective was to develop a data-driven informatics pipeline to understand complex CAD risk loci, and to apply this to a poorly understood cluster of SNPs in the vicinity of ZEB2.

We developed a unique informatics pipeline leveraging a multi-tissue CAD genetics-of-gene-expression dataset, GWAS datasets, and other resources. The pipeline first dissected SNP locations and their linkage disequilibrium relationships, and progressed through analyses of tissue-specific expression quantitative trait loci, and then gene-gene, gene-phenotype, SNP-phenotype relationships. The pipeline concluded by exploring CAD-relevant gene regulatory networks (GRNs).