Aerosol particles at a high-altitude site on the Southeast Tibetan Plateau, China: Implications for pollution transport from South Asia

      Bulk aerosol samples were collected from 16 July 2008 to 26 July 2009 at Lulang, a high-altitude (>3300m above sea level) site on the southeast Tibetan Plateau (TP); objectives were to determine chemical characteristics of the aerosol and identify its major sources. We report aerosol (total suspended particulate, TSP) mass levels and the concentrations of selected elements, carbonaceous species, and water-soluble inorganic ions. Significant buildup of aerosol mass and chemical species (organic carbon, element carbon, nitrate, and sulfate) occurred during the premonsoon, while lower concentrations were observed during the monsoon. Seasonal variations in aerosol and chemical species were driven by precipitation scavenging and atmospheric circulation. Two kinds of high-aerosol episodes were observed: one was enriched with dust indicators (Fe and Ca2+), and the other was enhanced with organic and elemental carbon (OC and EC), SO42−, NO3−, and Fe. The TSP loadings during the latter were 3 to 6 times those on normal days. The greatest aerosol optical depths (National Centers for Environmental Protection/National Center for Atmospheric Research reanalysis) occurred upwind, in eastern India and Bangladesh, and trajectory analysis indicates that air pollutants were transported from the southwest. Northwesterly winds brought high levels of natural emissions (Fe, Ca2+) and low levels of pollutants (SO42−, NO3−, K+, and EC); this was consistent with high aerosol optical depths over the western deserts and Gobi. Our work provides evidence that both geological and pollution aerosols from surrounding regions impact the aerosol population of the TP

Austenite in Transformation-Induced Plasticity Steel Subjected to Multiple Isothermal Heat Treatments

The thermodynamic limit to the progress of the bainite reaction in steels containing a cementite inhibitor often leaves large quantities of thermally or mechanically unstable austenite. Such austenite is not effective in delaying the onset of plastic instabilities during the course of deformation. In such circumstances, it is useful to conduct isothermal transformation at a high temperature where the rate of reaction is relatively rapid, followed by a lower temperature step that permits more bainite to be generated. This in turn increases the stability of the refined austenite, which then transforms gently over a large range of strain during a tensile test. A significant corollary is that the two-step heat treatments are unnecessary in low-carbon steels, where the bainite reaction is able to proceed to a greater extent before reaching the thermodynamic limit. Furthermore, the two-step process can be counterproductive in low carbon steel, because the austenite content is reduced to a level below which it does not enhance the mechanical properties. Other circumstances in which multiple heat treatments are necessary are also discussed.The authors are grateful to POSCO for support through Steel Innovation Programme, and to the World Class University Programme of the National Research Foundation of Korea, Ministry of Education, Science and Technology, project number R32-2008-000-10147.This is the accepted manuscript version. The final published version is available from Springer at http://link.springer.com/article/10.1007%2Fs11661-014-2405-z

Variations in innate immune cell subtypes correlate with epigenetic clocks, inflammaging and health outcomes

Epigenetic clocks in blood have shown promise as tools to quantify biological age, displaying robust associations with morbidity and all-cause mortality. Whilst the effect of cell-type heterogeneity on epigenetic clock estimates has been explored, such studies have been limited to studying heterogeneity within the adaptive immune system. Much less is known about whether heterogeneity within the innate immune system can impact epigenetic clock estimates and their associations with health outcomes. Here, we apply a high-resolution DNAm reference panel of 19 immune cell-types, including young and adult monocyte, natural killer, and neutrophil subsets, demonstrating how shifts within these innate subtypes display associations with epigenetic clock acceleration, inflammaging, and all-cause mortality. The associations of monocyte heterogeneity with inflammation are further validated using transcriptomic and metabolomic data. Additionally, a non-negligible fraction of nucleated red blood cell-like cells in circulation is found to associate with inflammaging, markers of dysfunctional erythropoiesis, and is a major risk factor for all-cause mortality. These results extend findings obtained within the adaptive immune system to innate immune and erythrocyte-like cells, demonstrating how heterogeneity within these other blood cell compartments is also associated with inflammaging, epigenetic clocks, and health outcomes.Molecular Epidemiolog

Vascular Remodeling in Health and Disease

The term vascular remodeling is commonly used to define the structural changes in blood vessel geometry that occur in response to long-term physiologic alterations in blood flow or in response to vessel wall injury brought about by trauma or underlying cardiovascular diseases.1, 2, 3, 4 The process of remodeling, which begins as an adaptive response to long-term hemodynamic alterations such as elevated shear stress or increased intravascular pressure, may eventually become maladaptive, leading to impaired vascular function. The vascular endothelium, owing to its location lining the lumen of blood vessels, plays a pivotal role in regulation of all aspects of vascular function and homeostasis.5 Thus, not surprisingly, endothelial dysfunction has been recognized as the harbinger of all major cardiovascular diseases such as hypertension, atherosclerosis, and diabetes.6, 7, 8 The endothelium elaborates a variety of substances that influence vascular tone and protect the vessel wall against inflammatory cell adhesion, thrombus formation, and vascular cell proliferation.8, 9, 10 Among the primary biologic mediators emanating from the endothelium is nitric oxide (NO) and the arachidonic acid metabolite prostacyclin [prostaglandin I2 (PGI2)], which exert powerful vasodilatory, antiadhesive, and antiproliferative effects in the vessel wall