[Cementation using my methods].
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Biomedical subjects
Publications and source records attributed to T Yasui.
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Angiotensin I-converting enzyme (ACE) is present in human amniotic fluid. We characterized the enzyme by both its antigenic and enzymatic properties. Using a specific direct radioimmunoassay, ACE was quantified and characterized in each of the 19 samples tested. Mean level was 136 +/- 83 ng/ml. Amniotic ACE completely crossreacted, like that in plasma and kidney, with antibodies raised against the lung enzyme. ACE activity in amniotic fluid averaged 8.7 +/- 5.6 microU/ml using Hip-His-Leu as substrate and was significantly correlated with ACE antigen levels. ACE was not associated with the cells or the free intracellular organelles in amniotic fluid, and the enzyme was present in soluble form. Angiotensinase activity and high levels of kininase activity were found in amniotic fluid. Inhibition studies with captopril and anti-human ACE antibodies suggest that angiotensinases and kininases other than ACE were also present. Because renin, mostly in inactive form, and angiotensinogen were also found in these amniotic fluids, it appears that a complete, although not fully activated, renin angiotensin system is present in amniotic fluid and fetal membranes during pregnancy.
Angiotensin I-converting enzyme (ACE) is found in human amniotic fluid and foetal membranes taken during Caesarean sections at term. ACE contents are higher in the chorion than in the amnion. Cells cultured from chorion contain ACE together with renin. Chorionic ACE was inhibited by captopril and by an excess of anti-ACE immuneserum. It is concluded that extravascular ACE is present in the uteroplacental complex during pregnancy.
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In this paper the author reported an operative approach for ossification of the posterior longitudinal ligament (OPLL) of the lower cervical and upper thoracic vertebrae. There are two types of surgery for OPLL, namely, posterior and anterior approaches. As a rule, we utilize an anterior approach for OPLL. Recently we performed a modified sternum-splitting approach in surgery for OPLL in the cervico-thoracic junction. In the original trans-sternal approach introduced by Cauchoix, the sternum is split from the suprasternal notch to the xiphoid process. We cut the manubrium only. However, a satisfactory exposure of the cervico-thoracic vertebrae down to the third thoracic level was obtained. After reaching the anterior surface of the cervico-thoracic vertebrae, the central portion of the vertebral body and the ossified lesion between the lower one third of the C7 vertebral body and the upper one third of the Th3 vertebral body were removed with an air-drill under an operating microscope. The longitudinal bone defect of the vertebral bodies was filled with a bone graft obtained from the iliac bone. Removal of the ossified lesion in the cervico-thoracic junction can be performed safely by utilizing the modified sternum-splitting approach. This approach can be applied also to endarterectomies at the origins of the vertebral arteries and the right subclavian artery.
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Angiotensin I converting enzyme levels were determined in 18 healthy males using either a direct radioimmunoassay or the enzymatic assay described by Cushman and Cheung (Biochem Pharmac 1971, 20: 1637-48). Mean levels in recumbent position were 2.47 +/- 0.68 pmol ml-1 by radioimmunoassay and 28.1 +/- 6.7 mU ml-1 by enzymatic assay. An excellent correlation (r = 0.86, P less than 0.001) was found between the results obtained with both methods of measurement. The ratio of enzyme activity to immunoreactive angiotensin I converting enzyme levels in plasma was 75.3 +/- 9.5 U mg-1, a value identical to that obtained for the purified enzyme (84 U mg-1). Plasma angiotensin I converting enzyme is immunologically identical to that from the kidney and lung. Comparison of plasma angiotensin I converting enzyme levels in supine and recumbent subjects revealed no effect of posture.
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Direct renal effects of angiotensin I converting enzyme inhibitors (CEIs), captopril, SA446 and MK421, were examined in isolated rat kidneys perfused with a renin-substrate-free medium. Among three CEIs, only captopril induced a significant natriuresis, whereas SA446 and MK421 did not. UKV, renal vascular resistance and creatinine clearance were not affected by any of these CEIs. Renin release from perfused rat kidneys were not influenced by CEIs under the present experimental conditions. These results suggest that among three different types of CEIs, only captopril possesses natriuretic action in the isolated perfused rat kidney and that this action may be independent of its inhibitory action on angiotensin converting enzyme. It is also suggested that these three CEIs themselves do not have a direct effect on the renal vascular bed.
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Direct effects of captopril on renal function were examined in isolated perfused rat kidneys. Captopril induced a significant increase in urinary volume and urinary sodium excretion (1.8- and 1.7-fold, respectively; both p less than 0.005), whereas urinary potassium excretion and renovascular resistance were not significantly changed. Because the perfusion medium lacks angiotensinogen, kininogen and aldosterone, the natriuretic action in perfused kidneys may not be related to its inhibitory action on angiotensin I converting enzyme or kininase II. Because the natriuresis was not accompanied by changes in renovascular resistance, it is suggested that captopril possesses a direct natriuretic action and that this property may partly explain the mechanism of captopril-induced natriuresis clinically observed.
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