Search PubMed⌕ Search

Biomedical subjects

M Kurata

Publications and source records attributed to M Kurata.

133 records · Page 8Linked to original sources
PubMedDate not supplied

Suppression of T lymphocyte proliferation by peritoneal macrophages in chickens.

The mechanism of the suppression of lymphocyte proliferation by peritoneal macrophages (MPs) in chickens and the presence of a suppressive substance in the culture supernatant of MPs were studied. The results showed that gelatin- and peptone-induced peritoneal MPs had an inhibitory accessory function against blastogenesis of mitogen-stimulated splenic lymphocytes and that resident peritoneal MPs had an enhanced accessory function. The suppressive factor produced by gelatin-induced peritoneal MPs is a protein having a pI of 3.6 and a molecular weight of 64,000 and it is physically and chemically a relatively stable substance. Moreover, it has no cytotoxic effect against lymphocytes and it was verified that the suppressor in the culture supernatant of MPs was not prostaglandin E2 or alpha-acid glycoprotein.

Animals↗
PubMedDate not supplied

Glutathione regeneration in calcium-loaded erythrocytes: a possible relationship among calcium accumulation, ATP decrement and oxidative damage.

Glutathione (GSH) regeneration was studied in rabbit erythrocytes which were loaded with calcium using ionophore A23187. Calcium-loading induced by A23187 and various concentrations of CaCl2 caused a dose-dependent depression in red cell GSH regeneration. The lowered GSH regeneration was mainly due to reduction of ATP level. In an experiment using haemolysate, the effect of calcium per se was negligible, while magnesium strongly affected GSH regeneration by controlling the rate of hexokinase reaction. These results indicate a possibility that cation perturbation, metabolic decay and oxidative damage are all interrelated in the erythrocyte aging process.

Adenosine Triphosphate↗
PubMedDate not supplied

Cerivastatin induces carotid artery plaque stabilization independently of cholesterol lowering in patients with hypercholesterolaemia.

To prevent cardiovascular events in hyperlipidaemic patients, plaque stabilization by inhibition of localized inflammatory reactions in the blood vessels is important in addition to cholesterol lowering. Cerivastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor (statin), has more potent enzyme-inhibitory effects than other statins and has also been reported in vitro to inhibit, at low concentrations, various inflammatory reactions due to plaque instability. Cerivastatin was therefore administered over 12 months to five patients with hypercholesterolaemia and atherosclerotic plaque diagnosed by ultrasonography of the carotid artery, and changes in the plaque composition were determined. The mean cholesterol level decreased over the study period, although not significantly. However, the mean percentage of fibrous matrix of the plaque increased significantly from a mean of 11.2 +/- 7.7% at study entry to 18.3 +/- 5.9% at the end of the study. Additionally, the mean maximum plaque height was significantly reduced from 3.7 +/- 0.9 mm to 3.0 +/- 0.7 mm. These results indicate that cerivastatin induces plaque stability independently of cholesterol lowering.

Aged↗
PubMedDate not supplied

The effect of low-density lipoprotein apheresis on plasma thrombomodulating factors.

The authors have investigated the effects of double-membrane filtration with hollow fiber membranes made of different artificial materials and low-density lipoprotein (LDL)-adsorbent dextran sulfate cellulose (DS) columns on coagulation-related proteins and complement components to evaluate their hemocompatibility. All membrane filters showed similar sieving effects, which depended upon the molecular weights of the proteins. In the double-membrane filtration system, free protein S, protein C, antithrombin III, and alpha 1-antitrypsin were returned to the intracorporeal circulation, whereas alpha 2-macroglobulin and fibrinogen were almost completely removed from the circulation; C4b-binding protein (C4BP)-protein S complexes were also trapped by the second membrane, and in some instances were even blocked by the first membrane, if it was made of material that activated the classic pathway of the complement system. The DS column adsorbed C4BP-protein S complex, but free protein S was almost completely recovered in the eluate.

Antithrombin III↗