Air quality changes during the COVID-19 in YRD region are analyzed. • The WRF-CAMx modelling system is applied to investigate impact of lowered human activities on air quality changes. • Sources of the residual pollution are figured out for policy implications for future air pollution control.

Diabetic nephropathy is a major cause of end-stage kidney disease, and overactivity of the endocannabinoid/cannabinoid 1 receptor (CB 1 R) system contributes to diabetes and its complications. Zucker diabetic fatty (ZDF) rats develop type 2 diabetic nephropathy with albuminuria, reduced glomerular filtration, activation of the reninangiotensin system (RAS), oxidative/nitrative stress, podocyte loss, and increased CB 1 R expression in glomeruli. Peripheral CB 1 R blockade initiated in the prediabetic stage prevented these changes or reversed them when animals with fully developed diabetic nephropathy were treated. Treatment of diabetic ZDF rats with losartan, an angiotensin II receptor-1 (Agtr1) antagonist, attenuated the development of nephropathy and down-regulated renal cortical CB 1 R expression, without affecting the marked hyperglycemia. In cultured human podocytes, CB 1 R and desmin gene expression were increased and podocin and nephrin content were decreased by either the CB 1 R agonist arachydonoyl-2′-chloroethylamide, angiotensin II, or high glucose, and the effects of all three were antagonized by CB 1 R blockade or siRNA-mediated knockdown of CNR1 (the cannabinoid type 1 receptor gene). We conclude that increased CB 1 R signaling in podocytes contributes to the development of diabetic nephropathy and represents a common pathway through which both hyperglycemia and increased RAS activity exert their deleterious effects, highlighting the therapeutic potential of peripheral CB 1 R blockade.iabetic nephropathy, a highly prevalent and serious complication of both type 1 and type 2 diabetes mellitus and a leading cause of renal failure, is characterized by albuminuria, decreased glomerular filtration rate (GFR), mesangial expansion, thickening of the glomerular basement membrane, and glomerular sclerosis (1). Multiple mechanisms have been implicated in the development of diabetic nephropathy, including activation of the renin-angiotensin system (RAS) (2), increase in oxidative (3) and nitrosative/nitrative stress (4), as well as an increase in local inflammation (5).The endocannabinoid system plays a well-documented role in obesity and its metabolic complications, including insulin resistance and type 2 diabetes (T2DM). Globally acting cannabinoid 1 receptor (CB 1 R) antagonists/inverse agonists improve obesity-related insulin resistance, dyslipidemia, fatty liver, and β-cell loss, and attenuate obesity-related inflammatory changes both in preclinical models of diet-induced or genetic obesity and in clinical trials in overweight subjects with metabolic syndrome (reviewed in refs. 6 and 7). Global CB 1 R blockade also has beneficial effects in mouse models of type 1 and type 2 diabetic nephropathy (8-11). However, the therapeutic development of this class of compounds has been halted because of adverse neuropsychiatric side effects in a small proportion of treated subjects (12). Recent studies in rodent models have demonstrated that peripherally restricted CB 1 R antagonists are as effective as globally acti...

E ndothelial cells (ECs) play an essential role in the modulation of vascular homeostasis. During aging and specifically during the development of atherosclerosis, ECs are exposed to various damaging stimuli and are thereby prone to injury.1 Rapid endothelial recovery, or re-endothelialization, correlates with diminished plaque formation. 2 Likewise, coronary intervention-induced vascular injury requires an Background-ADAMTS-7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, was recently identified to be significantly associated genomewide with coronary artery disease. However, the mechanisms that link ADAMTS-7 and coronary artery disease risk remain elusive. We have previously demonstrated that ADAMTS-7 promotes vascular smooth muscle cell migration and postinjury neointima formation via degradation of a matrix protein cartilage oligomeric matrix protein. Because delayed endothelium repair renders neointima and atherosclerosis plaque formation after vessel injury, we examined whether ADAMTS-7 also inhibits re-endothelialization. Methods and Results-Wire injury of the carotid artery and Evans blue staining were performed in Adamts7-/-and wild-type mice. Adamts-7 deficiency greatly promoted re-endothelialization at 3, 5, and 7 days after injury. Consequently, Adamts-7 deficiency substantially ameliorated neointima formation in mice at days 14 and 28 after injury in comparison with the wild type. In vitro studies further indicated that ADAMTS-7 inhibited both endothelial cell proliferation and migration. Surprisingly, cartilage oligomeric matrix protein deficiency did not affect endothelial cell proliferation/migration and re-endothelialization in mice. In a further examination of other potential vascular substrates of ADAMTS-7, a labelfree liquid chromatography-tandem mass spectrometry secretome analysis revealed thrombospondin-1 as a potential ADAMTS-7 target. The subsequent studies showed that ADAMTS-7 was directly associated with thrombospondin-1 by its C terminus and degraded thrombospondin-1 in vivo and in vitro. The inhibitory effect of ADAMTS-7 on postinjury endothelium recovery was circumvented in Tsp1 -/-mice. Conclusions-Our study revealed a novel mechanism by which ADAMTS-7 affects neointima formation. Thus, ADAMTS-7 is a promising treatment target for postinjury vascular intima hyperplasia. potentially because they inhibit not only vascular smooth muscle cell (VSMC) proliferation/migration, but also reendothelialization. 6,7 Therefore, new strategies that aim to promote endothelial recovery, and simultaneously inhibit VSMC activation, as well, are needed for the effective prevention and treatment of atherosclerosis and postinjury restenosis.Metalloproteinases are critical in vascular wall remodeling through matrix or nonmatrix degradation. 8 Recently, we described ADAMTS-7, a member of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, in the mediation of VSMC migration and the promotion of neointima formation following ar...

Securing the sensitive data stored and accessed from mobile devices makes user authentication a problem of paramount importance. The tension between security and usability renders however the task of user authentication on mobile devices a challenging task. This paper introduces FAST (Fingergestures Authentication System using Touchscreen), a novel touchscreen based authentication approach on mobile devices. Besides extracting touch data from touchscreen equipped smartphones, FAST complements and validates this data using a digital sensor glove that we have built using off-the-shelf components. FAST leverages state-of-the-art classification algorithms to provide transparent and continuous mobile system protection. A notable feature is FAST 's continuous, user transparent postlogin authentication. We use touch data collected from 40 users to show that FAST achieves a False Accept Rate (FAR) of 4.66% and False Reject Rate of 0.13% for the continuous post-login user authentication. The low FAR and FRR values indicate that FAST provides excellent post-login access security, without disturbing the honest mobile users.

A bdominal aortic aneurysm (AAA), characterized by chronic aortic wall inflammation and destructive connective tissue remodeling, is one of the leading causes of sudden death in aging men (>55 years).1 Despite the current progress of surgical invasive repair or medical treatment, we lack a strategy to predict AAA rupture or to delay its progression. Epidemiological studies have identified several risk factors associated with AAA, including aging, male sex, smoking, and hypertension.1-3 However, the cause of AAA remains far from being fully elucidated. In This Issue, see p 1249Homocysteine (Hcy) is a sulfur-containing nonconstitutive amino acid derived from the essential amino acid methionine. The upper limit of the normal range for circulating Hcy is approximately 15 μmol/L, whereas a sex difference has been found, with approximately 10% to 15% higher levels in men versus women. Compelling evidence suggests that hyperhomocysteinemia (HHcy) is a strong independent risk factor of coronary heart disease and stroke in human.