Research on lightning transient distribution characteristics of cable-stayed bridges

Bridges are usually located at the junction of land and water, where the surrounding area is open terrain, making them to be easily damaged by lightning strikes. The quantitative analysis of lightning transient characteristics and the impulse effect on bridges can provide scientific data to support the lightning protection design for bridges. In this study, a single-tower cable-stayed bridge is taken as a representative case. The CDEGS (Current Distribution Electromagnetic Interference Grounding and Soil Structure Analysis) software is used to establish a three-dimensional simulation model of the bridge. With this model, the magnetic field, step voltage, and lightning current distribution on the tower top, stay cables, and bridge deck under the most severe direct lightning strike scenario typical for cable-stayed structures are simulated. The results are as follows: (1) when the stay cables are struck by lightning, the peak of the magnetic field intensity is highest at the location of electronic information equipment, followed by that at the top of the tower, and the lowest at the bridge deck. The peak step voltage at the ground below the bridge is the largest when lightning strikes the cable, and that is the smallest when lightning strikes the bridge deck. (2) The magnitude distribution of the lightning current on the stay cables is related to the strike location, the distance between the strike point and the grounding system, and the length of the stay cables. When the stay cables are closer to the grounding system and the length is shorter, the lightning current that flows through them is larger. (3) The magnitude distribution of the lightning current on the grounding system is associated with the location of the strike and the position of the grounding system. The closer the grounding system is to the strike point, the larger the amplitude of the lightning current on the grounding system. The grounding system positioned in the middle significantly reduces the lightning current due to the shielding effect. The grounding system located at the edge shows minimal variation in the time domain characteristics of the lightning current, resulting in less reduction of the initial steepness of the lightning wave. However, the grounding system at the middle position experiences a significant increase in the temporal characteristics of lightning current, reducing the hazards caused by the steepness of the original lightning wave

Risk of cardiac-related death in astrocytoma patients treated with chemotherapy: A competing risk analysis using the SEER database

PurposeTo explore the impact of chemotherapy on the risk of cardiac-related death in astrocytoma patients.MethodsWe retrospectively evaluated astrocytoma patients diagnosed between 1,975 and 2016 in the Surveillance, Epidemiology, and End Results (SEER) database. Using Cox proportional hazards models, we compared the risks of cardiac-related death between a chemotherapy group and non-chemotherapy group. Competing-risks regression analyses were used to evaluate the difference in cardiac-related death. Also, propensity score matching (PSM) was employed to reduce confounding bias. The robustness of these findings was evaluated by sensitivity analysis, and E values were calculated.ResultsA total of 14,834 patients diagnosed with astrocytoma were included. Chemotherapy (HR = 0.625, 95%CI: 0.444–0.881) was associated with cardiac-related death in univariate Cox regression analysis. Chemotherapy was an independent prognostic factor for a lower risk of cardiac-related death before (HR = 0.579, 95%CI: 0.409–0.82, P = 0.002) and after PSM (HR = 0.550, 95%CI: 0.367–0.823 P = 0.004). Sensitivity analysis determined that the E-value of chemotherapy was 2.848 and 3.038 before and after PSM.ConclusionsChemotherapy did not increase the risk of cardiac-related death in astrocytoma patients. This study highlights that cardio–oncology teams should provide comprehensive care and long-term monitoring for cancer patients, especially those with an increased risk of cardiovascular disease

GW29-e1129 Clinical Outcomes Associated with Medical Management versus Coronary Intervention in Patients with Acute Coronary Syndrome

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Pore pressures induced by piezocone penetration

The excess pore water pressures (u) induced by piezocone penetration and their dissipation around the cone have been investigated by laboratory model tests and theoretical/numerical analyses. Based on the test results, a method for predicting the cone penetration induced distribution of u has been proposed. By numerical analysis using the predicted initial distribution of u it has been demonstrated that dissipation of the pore water pressure measured at the shoulder of the cone (u2-type cone) is a two-dimensional (horizontal radial and vertical) process. By comparing the simulated and laboratory-measured 2D dissipation curves, a back-fitted coefficient of consolidation in the horizontal direction (ch) can be obtained. It has also been shown that a published method for estimating ch from measured non-standard dissipation curves (in which u2 increases initially and then reduces) results in values of ch that agree well with values of ch deduced from the 2D analysis.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

VDR Agonist Prevents Diabetic Endothelial Dysfunction through Inhibition of Prolyl Isomerase-1-Mediated Mitochondrial Oxidative Stress and Inflammation

Background and aim. Upregulation of prolyl isomerase-1 (Pin1) protein expression and activity was associated with the pathogenesis of diabetic vasculopathy through induction of endothelial oxidative stress and inflammation. Moreover, VDR agonist protects against high glucose-induced endothelial apoptosis through the inhibition of oxidative stress. We aimed to explore the effects of the VDR agonist on diabetes-associated endothelial dysfunction and the role of Pin1 in this process. Methods. Streptozocin-induced diabetic mice were randomly treated with vehicle, VDR agonist (10 μg/kg/d, i.g., twice a week), or Pin1 inhibitor, Juglone (1 mg/kg/d, i.p., every other day), for eight weeks. In parallel, human umbilical vein endothelial cells (HUVECs) exposed to high-glucose condition were treated with 1,25-dihydroxyvitamin D3 and Juglone or vehicle for 72 hours. Organ chamber experiments were performed to assess endothelium-dependent relaxation to acetylcholine. Circulatory levels of Pin1, SOD, MDA, IL-1β, IL-6, and NO in diabetic mice, Pin1 protein expression and activity, subcellular distribution of p66Shc, and NF-κB p65 in high glucose-cultured HUVECs were determined. Results. Both VDR agonist and Juglone significantly improved diabetes-associated endothelial dysfunction and reduced high glucose-induced endothelial apoptosis. Mechanistically, the circulatory levels of SOD and NO were increased compared with those of vehicle-treated diabetic mice. Additionally, Pin1 protein expression and activity, p66Shc mitochondrial translocation, and NF-κB p65 in high glucose-cultured HUVECs were also inhibited by VDR agonist and Juglone. Knockdown of VDR abolished the inhibitory effects of VDR agonist on high glucose-induced upregulation of Pin1 protein expression and activity. Conclusions. VDR agonist prevents diabetic endothelial dysfunction through inhibition of Pin1-mediated mitochondrial oxidative stress and inflammation

Cardiovascular outcomes of β‐blocker—calcium channel blocker initial dual therapy vs. other initial dual therapies in Chinese patients with hypertension: A real‐world retrospective study

Abstract This retrospective study compared cardiovascular (CV) outcomes between initial β‐blocker (BB) + calcium channel blocker (CCB) dual therapy (“B + C”) and other initial dual therapies in Chinese newly diagnosed hypertensive patients. In this study, all patients in a regional electronic database with newly diagnosed hypertension from January 01, 2012 to December 31, 2016 who received any initial optimal dual therapy recommended by the Chinese hypertension guideline were included. 1:2 propensity score matching (PSM) was used to balance baseline characteristics between patients receiving B + C and patients receiving other initial dual therapies (“Others”). The primary outcome was major adverse cardiovascular events (MACE) that occurred from January 01, 2012 to December 31, 2017, consisting of non‐fatal stroke, non‐fatal myocardial infarction (MI), non‐fatal chronic heart failure (CHF), and all‐cause death. Cox proportional hazard models were used to compare these CV outcomes in the 2 matched cohorts. After the PSM, 6227 patients receiving B + C and 12 454 patients receiving Others were included. Compared to patients receiving Others, patients receiving B + C had a significantly lower risk of MACE (hazard ratio [HR] 0.85; 95% confidential interval [CI] 0.78–0.92; p < .001), non‐fatal stroke (HR 0.89; 95% CI 0.81–0.98; p = .018) and non‐fatal CHF (HR 0.74; 95% CI 0.63–0.86; p < .0001). Additionally, differences in risks of non‐fatal MI and all‐cause death between the 2 treatment cohorts were not statistically significant. In conclusion, BB + CCB initial dual therapy was associated with a lower risk of MACE, stroke, and CHF than other optimal initial dual therapies recommended by the Chinese hypertension guideline in Chinese newly diagnosed hypertensive patients

Anti-Diabetic Atherosclerosis by Inhibiting High Glucose-Induced Vascular Smooth Muscle Cell Proliferation via Pin1/BRD4 Pathway

Background and purpose. Vascular smooth muscle cells (VSMC) proliferation and migration is the important pathological process of diabetic atherosclerosis. Bromine domain protein 4 (BRD4) is involved in cell proliferation and inflammatory disease. Pin1 enhances BRD4 stability and its transcriptional activity. This study aimed to explore the possible mechanism of Pin1/BRD4 in diabetic atherosclerosis. Methods. Diabetic Apoe-/- mice induced by streptozotocin were treated with vehicle, the Pin1 inhibitor juglone, or the BRD4 inhibitor JQ1 for 3 weeks. VSMCs were pretreated with juglone, JQ1, or vehicle for 45 min, and then exposed to high glucose for 48 h. Hematoxylin–eosin staining was performed to assess atherosclerotic plaques of the thoracic aorta. Western blotting was used to detect expression levels of Pin1, BRD4, cyclin D1, and matrix metalloproteinase-9 (MMP-9) in the thoracic aorta and VSMCs. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell assay were used to measure proliferation and migration of VSMCs. Results. Juglone and JQ1 significantly improved atherosclerosis of diabetic Apoe-/- mice and reduced high glucose-induced VSMC proliferation and migration. Cyclin D1 and MMP-9 levels in the thoracic aorta were lower in diabetic Apoe-/- mice treated with juglone and JQ1 compared with vehicle-treated diabetic Apoe-/- mice. Additionally, BRD4 protein expression in high glucose-induced VSMCs was inhibited by juglone and JQ1. Upregulation of Pin1 expression by transduction of the Pin1 plasmid vector promoted BRD4 expression induced by high glucose, and stimulated proliferation and migration of VSMCs. Conclusions. Inhibition of Pin1/BRD4 pathway may improve diabetic atherosclerosis by inhibiting proliferation and migration of VSMCs

RXR agonists inhibit high-glucose-induced oxidative stress by repressing PKC activity in human endothelial cells

Activation of retinoid X receptor (RYR) is known to exert antiatherogenic effects. However, the underlying mechanism remains unclear. In this study.. we examined the effects of the RXR agonists 9-cis-retinoic acid and SR11237 on high-glucose-induced oxidative stress in human endothelial cells. Our results demonstrated that high-glucose-induced oxidative stress in human umbilical vein endothelial cells (HUVECs) was mainly mediated through its activation of the Nox4, gp91(phox), and p22(phox) components of nicotinamide adenine dinucleotide phosphate oxidase. Treatment of endothelial cells with RXR agonists resulted in significant inhibition of high-glucose-induced oxidative stress and expression of Nox4, gp91(phox), and P22(phox). The effect of RXR agonists was due to their inhibition of Rac-1 activation. Furthermore, RXR agonists rapidly inhibited high-glucose-induced activation of protein kinase C (PKC), an upstream activator of Rac-1. To study whether the rapid inhibitory effects of RXR agonists were mediated by RXR, we examined the effect of RXR downregulation by RXR siRNA. Our results showed that expression of RXR siRNA largely abrogated the effects of RXR agonists, suggesting the requirement of RXR expression. Interestingly, RXR alpha, which was diffusely distributed in HUVECs, accumulated mainly in the nucleus upon high glucose exposure. Treatment of cells with RXR agonists prevented the effect of high glucose. Thus, RXR ligands rapidly inhibit high-glucose-induced oxidative stress by antagonizing high-glucose-induced PKC activation, and cytoplasmic RXR alpha is implicated in this regulation. (C) 2007 Elsevier Inc. All rights reserved

Activation of AHR by ITE improves cardiac remodelling and function in rats after myocardial infarction

Abstract Aims Left ventricular remodelling subsequent to myocardial infarction (MI) constitutes a pivotal underlying cause of heart failure. Intervention with the nontoxic endogenous aryl hydrocarbon receptor (AHR) agonist 2‐(1′H‐indole‐3′‐carbonyl)‐thiazole‐4‐carboxylic acid methyl ester (ITE) in the acute phase of MI has been shown to ameliorate cardiac function, but its role in the chronic phase remains obscured. This study explores the beneficial role of ITE in delaying the progression of heart failure in the chronic phase of MI. Methods and results MI rats established by ligating the left anterior descending coronary artery were treated with the indicated concentration of the AHR agonist ITE or vehicle alone. Echocardiography was performed to determine cardiac structure and function; myocardial morphology and fibrosis were observed by haematoxylin and eosin and Masson's trichrome staining; serum biochemical indices, BNP, and inflammatory cytokine levels were detected by enzyme‐linked immunosorbent assay; F4/80+iNOS+M1 macrophages and F4/80+CD206+M2 macrophages were detected by immunofluorescence; the terminal deoxynucleotidyl transferase‐mediated dUTP nick end labelling assay was used to detect the apoptosis of cardiomyocytes; ultrastructural changes in myocardial tissue were observed by transmission electron microscopy; and Cyp1a1, Akt, P‐Akt, p70S6K, P‐p70S6K, Bcl‐2, Bax, caspase‐3, and cleaved caspase‐3 protein levels were determined via Western blotting. We found that therapy with the AHR agonist ITE rescued cardiac remodelling and dysfunction in rats with MI and attenuated myocardial fibrosis, inflammation, and mitochondrial damage. Further studies confirmed that ITE dose‐dependently improved myocardial cell apoptosis after MI, as demonstrated by reduced levels of the apoptosis‐related proteins cleaved caspase‐3 and Bax but increased expression levels of Bcl‐2. These effects were attributed to ITE‐induced activation of AHR receptors, leading to the down‐regulation of Akt and p70S6K phosphorylation. Conclusions The AHR agonist ITE alleviates cardiomyocyte apoptosis through the Akt/p70S6K signalling pathway, thereby rescuing left ventricular adverse remodelling and cardiac dysfunction after MI

Evaluation of the genetic diversity of Asian peach accessions using a selected set of SSR markers

A total of 94 peach accessions from the Zhejiang province of China were analyzed using 34 polymorphic single-locus simple sequence repeat (SSR) markers. Genetic distance analysis divided the accessions into two major clusters, one with mainly local accessions from the Fenghua region. Preselected lines from some crosses were exclusively clustered with the local ones, possibly related to maintaining the taste quality of the fruit. The number of alleles per locus at most loci was two or three, with an average of 2.85. The value of observed heterozygosity varied from 0.05 to 0.84 (average of 0.48). Diversity within the introduced accessions was higher than that of the Fenghua local accessions. Of the accessions analyzed in this study, 94% were individually identified. Those that could not be differentiated were all derived from the ‘Yulu’ cultivar, being either mutations or of identical origin. Our results suggest that Fenghua accessions are derived from limited parental materials and inbreeding over a long period of time. They will be useful for breeders to better manage their pre-breeding materials and choice of parents for further crossings.This study has been carried out with financial support from the Natural Science Foundation of China (30771496), the Science and Technology Department of Zhejiang Province (2007C22068) and Ningbo (2006C100029).Peer reviewe