早稲田大学 · 工学
Murakami教授の研究室は、循環器疾患の発症メカニズムに焦点を当て、インスリン抵抗性やアディポネクチン、ナトリウムイオンチャネル、renin-angiotensinシステムの機能的役割を解明することを目的としています。特に高血圧や心不全における血管・心臓の代謝的・生理的変化、ならびに遺伝子発現制御の分子機構を、臨床的・実験的アプローチを融合して研究しています。また、血管生物学におけるkallikreインヒビター系の役割や、超合金材料の微細構造制御についても応用的研究を展開しています。
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Insulin resistance is one of the major risk factors associated with development of hypertension and atherosclerosis. Recent studies have shown that adiponectin, an adipocyte-derived hormone, may be involved in insulin resistance and development of atherosclerosis in diabetes patients. The aim of this study was to examine adiponectin levels in patients with essential hypertension to determine the relationships between adiponectin levels and insulin sensitivity and to examine the relationship of a
Tissue kallikrein cleaves kininogen substrate to produce vasoactive kinin peptides that have been implicated in the proliferation of vascular smooth muscle cells (VSMCs). To explore potential roles of the kallikrein-kinin system in vascular biology, we evaluated the effects of adenovirus-mediated human kallikrein gene delivery on the growth of primary cultured VSMCs and in balloon-injured rat artery in vivo. Kallikrein gene transfer into cultured rat VSMCs resulted in time-dependent secretion of
The effects of platinum group metals (PGMs) addition on microscopic characteristics of Ni-Al-PGM ternary and Ni-base single crystal superalloys were investigated. Several Ni-19at%Al-Xat% PGM (PGM: Ru, Rh, Pd, Ir and Pt) ternary alloys were prepared by arc-melting in order to understand the distribution of PGMs in y and y ' two phases. It is found from differential thermal analysis (DTA) that among PGMs, Ir and Ru increase the melting points whereas Pt and Pd decrease the melting points. These al
Because the renin-angiotensin system is activated in heart failure, we hypothesized that angiotensin II (ANG II) plays a role in altering baroreflex sensitivity in the setting of heart failure. Accordingly, we evaluated the baroreflex control of heart rate (HR) in conscious, chronically instrumented rabbits in the normal state and after the establishment of heart failure. Heart failure was induced by rapid ventricular pacing at a rate of 360-380 beats/min for an average of 14.5 +/- 1.4 days. The
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