城轨地铁用车轴强度计算分析

为了保证某城轨地铁车辆的行车安全,对其车轴强度进行了分析。参照标准EN13103中的材料力学计算方法,选取该车轴的7个截面,计算出各截面的合力矩、应力以及安全系数。结果表明,车轴危险截面位于轮座与刹车盘座圆弧过渡处和刹车盘座与轴身圆弧过渡处,且最大计算应力小于许用应力,满足车轴强度设计要求。     

一种新的动态权重更新相关反馈方法*

提出了正负相关图像所占比例与特征值的标准方差相结合来调整对应权值的方法.为了避免相关反馈的权值调整陷入局部最优状态,引入一个干扰因子,使权值跳出局部最优区域.结果表明了该方法的优越性.     

Confocal Blood Flow Videomicroscopy of Thrombus Formation over Human Arteries and Local Targeting of P2X7

Atherothrombosis exposes vascular components to blood. Currently, new antithrombotic therapies are emerging. Herein we investigated thrombogenesis of human arteries with/without atherosclerosis, and the interaction of coagulation and vascular components, we and explored the anti-thrombogenic efficacy of blockade of the P2X purinoceptor 7 (P2X7). A confocal blood flow videomicroscopy system was performed on cryosections of internal mammary artery (IMA) or carotid plaque (CPL) determining/localizing platelets and fibrin. Blood from healthy donors elicited thrombi over arterial layers. Confocal microscopy associated thrombus with tissue presence of collagen type I, laminin, fibrin(ogen) and tissue factor (TF). The addition of antibodies blocking TF (aTF) or factor XI (aFXI) to blood significantly reduced fibrin deposition, variable platelet aggregation and aTF + aFXI almost abolished thrombus formation, showing synergy between coagulation pathways. A scarce effect of aTF over sub-endothelial regions, more abundant in tissue TF and bundles of laminin and collagen type I than deep intima, may suggest tissue thrombogenicity as molecular structure-related. Consistently with TF-related vascular function and expression of P2X7, the sections from CPL but not IMA tissue cultures pre-treated with the P2X7 antagonist A740003 demonstrated poor thrombogenesis in flow experiments. These data hint to local targeting studies on P2X7 modulation for atherothrombosis prevention/therapy.     

TNFα-Induced LDL Cholesterol Accumulation Involve Elevated LDLR Cell Surface Levels and SR-B1 Downregulation in Human Arterial Endothelial Cells

Excess lipid droplets are frequently observed in arterial endothelial cells at sites of advanced atherosclerotic plaques. Here, the role of tumor necrosis factor alpha (TNFα) in modulating the low-density lipoprotein (LDL) content in confluent primary human aortic endothelial cells (pHAECs) was investigated. TNFα promoted an up to 2 folds increase in cellular cholesterol, which was resistant to ACAT inhibition. The cholesterol increase was associated with increased ¹²⁵I-LDL surface binding. Using the non-hydrolysable label, Dil, TNFα could induce a massive increase in Dil-LDL by over 200 folds. The elevated intracellular Dil-LDL was blocked with excess unlabeled LDL and PCSK9, but not oxidized LDL (oxLDL), or apolipoprotein (apoE) depletion. Moreover, the TNFα-induced increase of LDL-derived lipids was elevated through lysosome inhibition. Using specific LDLR antibody, the Dil-LDL accumulation was reduced by over 99%. The effects of TNFα included an LDLR cell surface increase of 138%, and very large increases in ICAM-1 total and surface proteins, respectively. In contrast, that of scavenger receptor B1 (SR-B1) was reduced. Additionally, LDLR antibody bound rapidly in TNFα-treated cells by about 30 folds, inducing a migrating shift in the LDLR protein. The effect of TNFα on Dil-LDL accumulation was inhibited by the antioxidant tetramethythiourea (TMTU) dose-dependently, but not by inhibitors against NF-κB, stress kinases, ASK1, JNK, p38, or apoptosis caspases. Grown on Transwell inserts, TNFα did not enhance apical to basolateral LDL cholesterol or Dil release. It is concluded that TNFα promotes LDLR functions through combined increase at the cell surface and SR-B1 downregulation.     

The “Angiogenic Switch” and Functional Resources in Cyclic Sports Athletes

Regular physical activity in cyclic sports can influence the so-called “angiogenic switch”, which is considered as an imbalance between proangiogenic and anti-angiogenic molecules. Disruption of the synthesis of angiogenic molecules can be caused by local changes in tissues under the influence of excessive physical exertion and its consequences, such as chronic oxidative stress and associated hypoxia, metabolic acidosis, sports injuries, etc. A review of publications on signaling pathways that activate and inhibit angiogenesis in skeletal muscles, myocardium, lung, and nervous tissue under the influence of intense physical activity in cyclic sports. Materials: We searched PubMed, SCOPUS, Web of Science, Google Scholar, Clinical keys, and e-LIBRARY databases for full-text articles published from 2000 to 2020, using keywords and their combinations. Results: An important aspect of adaptation to training loads in cyclic sports is an increase in the number of capillaries in muscle fibers, which improves the metabolism of skeletal muscles and myocardium, as well as nervous and lung tissue. Recent studies have shown that myocardial endothelial cells not only respond to hemodynamic forces and paracrine signals from neighboring cells, but also take an active part in heart remodeling processes, stimulating the growth and contractility of cardiomyocytes or the production of extracellular matrix proteins in myofibroblasts. As myocardial vascularization plays a central role in the transition from adaptive heart hypertrophy to heart failure, further study of the signaling mechanisms involved in the regulation of angiogenesis in the myocardium is important in sports practice. The study of the “angiogenic switch” problem in the cerebrovascular and cardiovascular systems allows us to claim that the formation of new vessels is mediated by a complex interaction of all growth factors. Although the lungs are one of the limiting systems of the body in cyclic sports, their response to high-intensity loads and other environmental stresses is often overlooked. Airway epithelial cells are the predominant source of several growth factors throughout lung organogenesis and appear to be critical for normal alveolarization, rapid alveolar proliferation, and normal vascular development. There are many controversial questions about the role of growth factors in the physiology and pathology of the lungs. The presented review has demonstrated that when doing sports, it is necessary to give a careful consideration to the possible positive and negative effects of growth factors on muscles, myocardium, lung tissue, and brain. Primarily, the “angiogenic switch” is important in aerobic sports (long distance running). Conclusions: Angiogenesis is a physiological process of the formation of new blood capillaries, which play an important role in the functioning of skeletal muscles, myocardium, lung, and nervous tissue in athletes. Violation of the “angiogenic switch” as a balance between proangiogenic and anti-angiogenic molecules can lead to a decrease in the functional resources of the nervous, musculoskeletal, cardiovascular, and respiratory systems in athletes and, as a consequence, to a decrease in sports performance.     

CREEP CRACK PROPAGATION IN CONVENTIONAL CAST AND DIRECTIONALLY SOLIDIFIED SUPERALLOY RENE 80

The creep crack propagation in superalloy René80 of two different microstructures,i.e.,equiaxed grain structure by conventional casting and columnar grain by directionalsolidification,was investigated under static load at 1123 K.The creep crack growth rate,da/dt,seems to be correlated with the stress intensity factor,K.The creep crack growth ratein the directionally solidified alloy is lower than that in the conventional cast alloy,owing tothe elimination of transverse grain boundaries.The effect of microstructure on creep crackpropagation has also been discussed.     

IN-SITU OBSERVATION OF CRACK TIP DEFORMATION IN A DUPLEX STAINLESS STEEL

The development of dislocation structures in the plastic zone ahead of a crack tip has been in-vestigated in a duplex stainless steel during in-situ deformation experiments in a scanningtransmission electron microscope.It was found that the dislocation distribution wassignificantly different in the ferrite and in the austenite.In the ferrite grains,the dislocationsemitted by the crack tip may cross-slip out of the original slip planes and form a broad plasticzone.However,in the austenite,the dislocation free zone is small and the dislocations emittedby the crack pile up in its slip plane.The selection of slip systems at the crack tip depends onthe crack tip Schmid factors in both phases.But after large deformation,the selection of thesecond slip systems at the craek tip in austenite does not depend on the Schmid factors.     

磁性纤维随机混合媒质等效电磁参数的计算

为计及强散射偶极子间的相互作用,引入参量εh和μh,利用广义多重散射理论及MATLAB计算机软件对在2 GHz～18 GHz频率下的体积占空比为8%的铁纤维随机混合媒质等效磁导率的实验值进行曲线的拟合,导出了耦合系数εh和μh,并在此基础上,对体积占空比分别为30%和20%的铁纤维随机混合媒质等效磁导率进行了计算,计算结果与实验吻合良好.