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Biomedical subjects

M Kanai

Publications and source records attributed to M Kanai.

At least 271 records · Page 15Linked to original sources
PubMed1981

Biochemical characterization of Haemophilus species with the minitek differentiation system.

Characterization of 102 Haemophilus strains by the Minitek differentiation system (BBL Microbiology Systems, Cockeysville, Md.) was compared with that by the conventional method. The results obtained by the two methods were in good agreement (P less than 0.001; test of independence). Therefore, this system was found to be applicable for the identification of Haemophilus species in routine clinical bacteriology.

Bacteriological Techniques↗
PubMed1980

[A study of caerulein action on secretory cells, especially in the islets of Langerhans in the rat pancreas (author's transl)].

Although it is known that caerulein exerts an action on the secretory activity of the islets of Langerhans in the pancreas, the mechanism of this hormone has not yet been ascertained. The present investigation was undertaken to observe the ultramicroscopic changes of the pancreatic islets and the peripheral blood levels of insulin, glucagon, glucose and electrolites after caerulein administration. The animals were divided into four groups, and three were injected intraperitoneally with caerulein at 25 micrograms/kg, 2 micrograms/kg and 0.2 microgram/kg body weight, respectively. The fourth group served as the control. In the first group (25 micrograms caerulein), the endocrine cells of the pancreatic islets showed accelerated functioning immediately and up to about 2 hours after injection. Then these cells degenerated due to cytoplasmic edema and evidenced decreased secretory activity. In the second group (2 micrograms) depression in the secretory activity occurred for about 2 hours immediately after the injection, but there was no destruction of cells and they gradually recovered their functioning. The third group (0.2 microgram) displayed an acceleration of secretory activity immediately after the injection and then recovered to the normal state. There were some changes of electrolites in the peripheral blood in each of the three groups, suggesting that caerulein causes acceleration and depression of the secretory activities in the islets of Langerhans in the pancreas depending on the dosage. Moreover, the cell alterations may well depend on the changes of electrolites in the inner and outer atmospheres of the cells.

Animals↗
PubMed1980

Cholesterol alpha- and beta-epoxides as obligatory intermediates in the hepatic microsomal metabolism of cholesterol to cholestanetriol.

A high performance liquid chromatographic method for the good separation and direct determination of cholesterol alpha-epoxide (5,6 alpha-epoxy-5 alpha-cholestan-3 beta-ol) and beta-epoxide (5,6 beta-epoxy-5 beta-cholestan-3 beta-ol) was introduced to the study of microsomal lipid peroxidation-mediated oxygenation of the cholesterol double bond. In the presence of NADPH, FeSO4, and ADP, bovine liver microsomes converted [4-14C] cholesterol to the alpha-epoxide, beta-epoxide, and cholestanetriol (5 alpha-cholestane-3 beta,5,6 beta-triol) in the ratio 1.0:4.3:0.7. Obligatory intermidiacy of both cholesterol alpha- and beta-epoxides and essential role of microsomal cholesterol epoxide hydratease in the conversion of cholesterol to cholestanetriol were established by using the isotope trapping method as well as the cholesterol epoxide hydratase inhibitor, 5,6 alpha-imino-5 alpha-cholestan-3 beta-ol. Hepatic microsomal P-450 played no appreciable role in the epoxidation of cholesterol. Microsomal cholesterol epoxide hydratase was with no doubt found to differ in nature from microsomal xenobiotic epoxide hydratase. Microsomal hydrolysis of styrene oxide and safrole oxide (0.1 mM each) was almost completely inhibited by 3,3,3-trichloro-1-propene oxide (1 mM) but not by 5,6 alpha-imino-5 alpha-cholestan-3 beta-ol (1 mM). However, microsomal hydrolysis of both cholesterol alpha- and beta-epoxides was remarkably accelerated by 3,3,3-trichloro-1-propene oxide and inhibited by 5,6 alpha-imino-5 alpha-cholestan-3 beta-ol.

Animals↗
PubMed1980

Cholesterol diet increases plasma and liver concentrations of cholesterol epoxides and cholestanetriol.

Cholesterol alpha-epoxide (5, 6 alpha-epoxy-5-alpha-cholestan-3 beta-ol), cholesterol beta-epoxide (5, 6 beta-epoxy-5 beta-cholestan-3 beta-ol), and cholestanetriol (5 alpha-cholestane-3 beta, 5, 6 beta-triol) were isolated from plasma and liver of rabbits by high performance liquid chromatography and identified by gas-chromatography-mass spectrometry. The 5, 6-oxygenated cholestanols in the plasma and liver of rabbits fed for two months on a diet supplemented with cholesterol wee elevated to 2-5 times and 5-8 times for normal level, respectively. Among the 5, 6-oxy-generated steroids, the beta-epoxide existed at the highest level in tissues of both control and cholesterol-fed rabbits. The ratios of the beta-epoxide to the alpha-epoxide were 2-3 in all the examined biological specimens just as the previously demonstrated ones in the vitro lipid peroxidation-mediated reaction of cholesterol. These results strongly suggest that the epoxidation of the cholesterol double bond in the animal may be mediated by lipid peroxidation. The elevated 5, 6-oxygenated cholestanol levels on long term cholesterol feeding will be discussed in relation to a possible physiological role of cholestanetriol in regulation of tissue cholesterol levels.

Animals↗