世界核电设备与结构将长期面临的一个问题--微动损伤

核电设备至仍面临许多不易解决的问题,经过对核电和结构部件多例事故的分析可知,核电设备中微动是不可避免的现象,核能工程中的相当一部分结构损伤事故与和微动损伤有着直接的关系;在反应力集中,腐蚀部位,微动又是许多核电设备提前损伤失效的直接原因。     

Long COVID: Association of Functional Autoantibodies against G-Protein-Coupled Receptors with an Impaired Retinal Microcirculation

Long COVID (LC) describes the clinical phenotype of symptoms after infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Diagnostic and therapeutic options are limited, as the pathomechanism of LC is elusive. As the number of acute SARS-CoV-2 infections was and is large, LC will be a challenge for the healthcare system. Previous studies revealed an impaired blood flow, the formation of microclots, and autoimmune mechanisms as potential factors in this complex interplay. Since functionally active autoantibodies against G-protein-coupled receptors (GPCR-AAbs) were observed in patients after SARS-CoV-2 infection, this study aimed to correlate the appearance of GPCR-AAbs with capillary microcirculation. The seropositivity of GPCR-AAbs was measured by an established cardiomyocyte bioassay in 42 patients with LC and 6 controls. Retinal microcirculation was measured by OCT–angiography and quantified as macula and peripapillary vessel density (VD) by the Erlangen-Angio Tool. A statistical analysis yielded impaired VD in patients with LC compared to the controls, which was accentuated in female persons. A significant decrease in macula and peripapillary VD for AAbs targeting adrenergic β2-receptor, MAS-receptor angiotensin-II-type-1 receptor, and adrenergic α1-receptor were observed. The present study might suggest that a seropositivity of GPCR-AAbs can be linked to an impaired retinal capillary microcirculation, potentially mirroring the systemic microcirculation with consecutive clinical symptoms.     

Pituitary Tumor-Transforming Gene 1/Delta like Non-Canonical Notch Ligand 1 Signaling in Chronic Liver Diseases

The management of chronic liver diseases (CLDs) remains a challenge, and identifying effective treatments is a major unmet medical need. In the current review we focus on the pituitary tumor transforming gene (PTTG1)/delta like non-canonical notch ligand 1 (DLK1) axis as a potential therapeutic target to attenuate the progression of these pathological conditions. PTTG1 is a proto-oncogene involved in proliferation and metabolism. PTTG1 expression has been related to inflammation, angiogenesis, and fibrogenesis in cancer and experimental fibrosis. On the other hand, DLK1 has been identified as one of the most abundantly expressed PTTG1 targets in adipose tissue and has shown to contribute to hepatic fibrosis by promoting the activation of hepatic stellate cells. Here, we extensively analyze the increasing amount of information pointing to the PTTG1/DLK1 signaling pathway as an important player in the regulation of these disturbances. These data prompted us to hypothesize that activation of the PTTG1/DLK1 axis is a key factor upregulating the tissue remodeling mechanisms characteristic of CLDs. Therefore, disruption of this signaling pathway could be useful in the therapeutic management of CLDs.     

基于IGBT芯片疲劳机理的关断时间可靠性模型

基于绝缘栅双极型晶体管(IGBT)芯片疲劳机理,提出采用关断时间对IGBT健康状态进行监控的可靠性评估方法。采用理论分析与解析描述相结合的方法,建立了IGBT关断电流下降时间模型,进而通过研究IGBT关断时间特征量疲劳机理,建立了IGBT关断时间可靠性评估模型。仿真和实验验证了该模型的正确性与准确性。通过该模型可对IGBT的健康状况进行准确评估。     

锅炉水冷壁管横向裂纹故障机理分析

根据国产 Ｈ Ｇ２００８ 控制循环锅炉和 Ｓ Ｇ１０００ 直流锅炉水冷壁壁温测定结果和炉管受力分析,探讨了锅炉水冷壁管横向裂纹性及造成炉管破的的机理,并分析了产生横向裂纹故障的主要原因。     

荧光灯闪烁和视疲劳关系的实验研究

本研究在模拟教室、家庭阅读环境及 VDT环境三种场景下 ,测试被试在不同闪烁频率光源下进行单词查找、数字校对、光栅圈、兰道环等视觉作业的速度及正确率 ,并对他们的主观感受进行调查。结果直流荧光灯下 ,视觉功效高 ,说明降低荧光灯闪烁可减轻视觉疲劳程度     

350MW超临界直流锅炉水冷壁H型鳍片开裂失效分析

采用宏观形貌分析、化学成分分析、显微组织分析和数值模拟等方法对某电厂350MW超临界直流锅炉水冷壁H型鳍片开裂原因进行分析。分析结果表明,该锅炉水冷壁H型鳍片开裂的主要原因是鳍片较宽且厚度设计过小,致使鳍片不能被有效冷却而造成严重老化和脱碳,在交变热应力的作用下产生热疲劳而开裂。通过分析计算,确定了鳍片的合理厚度供参考。     

长期高温高压氢暴露对Cr-Mo钢断裂韧性和裂纹行为的影响

选用Cr-Mo钢经400℃,20 MPa,10⁴ h氢暴露后进行拉伸、断裂韧性和疲劳试验.结果表明:Cr-Mo钢已经发生了氢腐蚀,氢蚀使Cr-Mo钢强度、塑性和断裂韧性均有所降低,也使断裂机制由韧窝型转变为解理脆性.氢蚀使疲劳裂纹扩展行为也发生了变化,疲劳裂纹扩展速率增加,ΔK_th降低.Cr-Mo钢氢蚀后,随应力比增加,疲劳裂纹扩展门槛值大幅度降低.     

叉车门架断裂原因分析

采用化学成分分析、力学性能测试、金相检验以及断口分析等方法对某叉车门架断裂的原因进行了分析。结果表明:由于在门架焊缝收弧部位存在凹坑缺陷和裂纹,形成缺口效应,产生缺口应力集中,加之门架的不对称工作应力的作用,最终造成门架发生了疲劳断裂失效。