Finite element analysis of tube drawing process with diameter expansion

This paper presents a tube drawing process with diameter expansion for producing a thin-walled tube effectively. In this proposed process, the tube was flared by a plug pushing into the tube, and then the tube was expanded by drawing the plug in the tube axial direction with chucking the flared tube edge. Optimum plug shape, such as the plug half angle and the corner radius, was investigated by a series of analyses using the finite element method (FEM) for improving the forming limit and the dimension accuracy. At first, a friction coefficient was determined to 0.3 by a comparison of the flaring limit between the analysis and the experiment of the tube flaring. As a result of the analyses in the drawing with the diameter expansion, the forming limit was high when the plug half angle was set to 18~30°. The thickness reduction ratio increased with an increase in the expansion ratio and the plug half angle. In addition, the overshoot, which is a difference between the plug diameter and the tube inner diameter after the drawing, was prevented by using the plug with the corner radius of 20 mm

Endothelial Progenitor Cells Dysfunction and Senescence: Contribution to Oxidative Stress

The identification of endothelial progenitor cells (EPCs) has led to a significant paradigm in the field of vascular biology and opened a door to the development of new therapeutic approaches. Based on the current evidence, it appears that EPCs may make both direct contribution to neovascularization and indirectly promote the angiogenic function of local endothelial cells via secretion of angiogenic factors. This concept of arterial wall repair mediated by bone marrow (BM)-derived EPCs provided an alternative to the local “response to injury hypothesis” for development of atherosclerotic inflammation. Increased oxidant stress has been proposed as a molecular mechanism for endothelial dysfunction, in part by reducing nitric oxide (NO) bioavailability. EPCs function may also be highly dependent on a well-controlled oxidant stress because EPCs NO bioavailability (which is highly sensitive to oxidant stress) is critical for their in vivo function. The critical question is whether oxidant damage directly leads to an impairment in EPCs function. It was revealed that activation of angiotensin II (Ang II) type 1 receptor stimulates nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase in the vascular endothelium and leads to production of reactive oxygen species. We observed that Ang II accelerates both BM- and peripheral blood (PB)-derived EPCs senescence by a gp91phox-mediated increase of oxidative stress, resulting in EPCs dysfunction. Consistently, both Ang II receptor 1 blockers (ARBs) and angiotensin converting enzyme (ACE) inhibitors have been reported to increase the number of EPCs in patients with cardiovascular disease. In this review, we describe current understanding of the contributions of oxidative stress in cardiovascular disease, focusing on the potential mechanisms of EPCs senescence

Diverse Roles of Macrophages in Atherosclerosis: From Inflammatory Biology to Biomarker Discovery

Cardiovascular disease, a leading cause of mortality in developed countries, is mainly caused by atherosclerosis, a chronic inflammatory disease. Macrophages, which differentiate from monocytes that are recruited from the blood, account for the majority of leukocytes in atherosclerotic plaques. Apoptosis and the suppressed clearance of apoptotic macrophages (efferocytosis) are associated with vulnerable plaques that are prone to rupture, leading to thrombosis. Based on the central functions of macrophages in atherogenesis, cytokines, chemokines, enzymes, or microRNAs related to or produced by macrophages have become important clinical prognostic or diagnostic biomarkers. This paper discusses the impact of monocyte-derived macrophages in early atherogenesis and advanced disease. The role and possible future development of macrophage inflammatory biomarkers are also described