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Biomedical subjects

M Kadowaki

Publications and source records attributed to M Kadowaki.

At least 91 records · Page 5Linked to original sources
PubMed1978

Age-related changes in cholesterol and bile acid metabolism in rats.

Age-related changes in serum and liver cholesterol, phospholipid and triglyceride levels, serum lipoproteins, biliary secretion of cholesterol, phospholipid and bile acids, and fecal excretion of sterols and bile acids were examined in Sprague-Dawley and Wistar strain male rats, 7 to 106 weeks in age. Serum and liver lipid levels increased with age in both strains but the liver phospholipid level remained unchanged. The proportion of serum alpha-lipoprotein increases and that of beta- and prebeta-lipoproteins slightly decreased. Cholesterol and phospholipids in low density lipoprotein and cholesterol in high density lipoprotein fractions also increased with age. Bile flow and biliary secretion of cholesterol and bile acids decreased in aged rats, but when they were expressed in terms of units per rat they were almost constant without regard to age. Pool size, synthesis, secretion, and turnover frequency of bile acids also did not change when they were expressed per rat, though 7-week-old rats showed a low value for turnover frequency. Biliary secretion of phospholipid, however, increased in aged rats. Biliary secretion of chenodeoxycholic and alpha-muricholic acids decreased but that of cholic and hyodeoxycholic acids increased. Daily excretion of feces and fecal neutral sterols decreases in aged rats but the excretion of bile acids remained constant regardless of age. The ratio of coprostanol and cholesterol in the total sterols was not affected. Fecal lithocholic, beta-muricholic and P10 (probably omega-muricholic) acids were decreased with age but the other bile acid components were not changed or were slightly increased.

Aging↗
PubMed1977

Dextran derivatives in single and combination chemotherapy against transplantable mouse ascites and solid tumors.

Dextran, a typical homopolysaccharide without antitumor activity, was modified by palmitoylation and/or phosphorylation to yield three derivatives: palmitoyldextran phosphate, dextran phosphate, and palmitoyldextran. Of these compounds, only palmitoyldextran phosphate showed growth-inhibitory activity against Ehrlich solid tumor in mice. In combination therapy with mitomycin C, bleomycin, cyclophosphamide, and 5-fluorouracil, palmitoyldextran phosphate manifested strong synergistic effects against both Sarcoma 180 ascites and L1210 leukemic tumors. The compound is not directly cytocidal against Sarcoma 180 ascites tumor, but it appears to act via activation of peritoneal macrophage. The antitumor activity of palmitoyldextran phosphate apparently is mainly due to immunological host-mediated mechanisms.

Animals↗
PubMed1976

Effects of synthetic progestational steroids on liver and serum lipids in rats.

Effects of norethisterone (NT) purified norethisterone (pure NT), norethynodrel (NE), medroxyprogesterone acetate (MAP), chlormadinone acetate (CMA) and desoxycorticosterone acetate (DOCA) on serum and liver lipid levels and serum lipoproteins were examined in both intact and estradiol-treated male rats. NT and NE caused a decrease in serum cholesterol and phospholipid levels, an increase in liver cholesterol level, no significant change in triglyceride levels of both serum and liver, with a significant change in serum lipoprotein patterns; a decreased in alpha- and beta-lipoproteins and a marked increase in pre beta-lipoprotein. Pure NT decreased serum cholesterol without causing any change in lipoprotein pattern. MAP, CMA and DOCA causee almost no effect on lipid levels in serum and liver, but CMA and DOCA increased alpha-lipoprotein and decreased beta- and pre beta-lipoproteins. An acute treatment with estradiol caused a decrease in alpha- and beta-lipoproteins and an increase in pre beta-lipoprotein with a decrease in serum lipid levels and an increase in liver lipids. By contrary, a chronic treatment with a marked hypercholesterolemia. This increase of alpha-lipoprotein in estradiol-treated rats was prevented by NT and NE, not affected or rather decreased by MAP but further increased with CMA and DOCA. These data suggest that the effects of synthetic progestational steroids on lipids are classified into two groups, 19-nortestosterone derivatives and 17alpha-hydroxyprogesterone derivatives including DOCA. The former caused a decrease in serum lipid levels with an increase of pre beta-lipoprotein and adecrease of alpha-lipoprotein. The latter caused almost no change or a slight increase in serum lipid levels with a decrease in pre beta-lipoprotein and an increase in alpha-lipoprotein, though it was not found in MAP.

Animals↗