[Relationship between phenotype and pathophysiology of dyslipoproteinemia].
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Biomedical subjects
Publications and source records attributed to N Takeuchi.
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Renal autotransplantation and ex vivo surgery in renal calculus disease are reviewed and their indications were discussed. In recent years, renal autotransplantation and ex vivo surgery have been applied in the management of renal calculus diseases. This technique has been believed to be a complete method for removing extensive renal calculi. However, this technique has some disadvantages such as technical difficulties and serious complications. Therefore, this technique should be indicated for cases carefully selected. At present, indications of this technique in the management of renal calculus disease are as follows; multiple or complicated calculi contained in a solitary kidney with narrow infundibla and dilated calices or in the kidney with history of previous surgery for calculus disease. This technique might not be chosen in those cases with perihilar inflammation, uncontrollable infection in the kidney or extensively damaged kidney (S-Cr 2.5 mg/dl, especially in solitary kidney).
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Diosgenin and beta-sitosterol (1% in diet) were administered to CRJ:CD-1 male mice for 15 days, in order to examine the changes in bile acid metabolism. There were some differences between diosgenin and beta-sitosterol in their effects on diet intake, liver weight, and plasma cholesterol level. However, both phytosterols caused no statistically significant changes in body weight gain, decreased cholesterol absorption to about one-third that observed in control mice, decreased liver cholesterol level, increased fecal excretion of cholesterol, and decreased fecal excretion of bile acids. Most of the increase in fecal excretion of cholesterol occurred 2 days after the start of feeding of phytosterols and gradually declined thereafter, but the levels on day 15 were nevertheless higher than those in the control mice. The fecal excretion of bile acids decreased progressively after the treatment with phytosterols. The decrease of bile acid derived from chenodeoxycholic acid was more predominant than the decrease of those derived from cholic acid, resulting in an increase of the cholic acid/chenodeoxycholic acid ratio. The biliary cholesterol, phospholipid, and bile acid mole % ratios and the lithogenic index were not changed, but the percentages of cholic acid and its related bile acids (the cholic acid group) to the total bile acids increased and those of the chenodeoxycholic acid group decreased after the treatments. The pool size of bile acids decreased in the mice given diosgenin but not in those given beta-sitosterol. Distribution of bile acids between the gallbladder and intestine was not altered by either phytosterol.(ABSTRACT TRUNCATED AT 250 WORDS)
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Primary adenocarcinoma arising at a colostomy or ileostomy site is very rare, and only three cases have been reported following surgical treatment of ulcerative colitis. A 38-year-old man who developed an adenocarcinoma originating at the site of a colonic stoma and producing a large fungating tumor mass in the surrounding abdominal wall is described. This occurred 19 years after Miles' operation for a carcinoma of the rectum.
The effects of aging on serum lipids, lipoproteins and apolipoprotein C subclasses in very low density lipoprotein (VLDL) were investigated in healthy male subjects aged from the 1st to the 9th decade. The serum cholesterol, phospholipid and triglyceride concentrations, the serum beta-lipoprotein concentration determined immunologically, and the beta-lipoprotein percentage determined by electrophoresis showed the lowest levels in the 2nd decade, increased gradually with age, attained the highest level in the 6th to 7th decade and slightly declined in the 9th decade. The VLDL-low density lipoprotein (LDL) cholesterol level changed almost in parallel with the serum total cholesterol level, but the HDL cholesterol level and the apolipoprotein A concentration remained almost constant showing no age-related change. The free cholesterol percentages in every lipoprotein fraction and the apolipoprotein content in LDL were higher in the subjects in the 6th and 7th decade than those in the 2nd to 3rd decade. The apo C II/C III ratio in VLDL increased with age. These data suggest that the ability to active lipoprotein lipase may not be impaired but the lecithin:cholesterol acyltransferase (LCAT) activity declines with age.
Effects of sodium ursodeoxycholate, hyodeoxycholate and dehydrocholate on serum and liver cholesterol levels, bile flow, biliary cholesterol, phospholipid and bile acid secretions, and fecal sterol and bile acid excretions were examined with Wistar strain male rats fed ordinary and 2% cholesterol supplemented diets. Dehydrocholate increased the liver cholesterol level, bile flow and biliary lipid secretion, but ursodeoxycholate and hyodeoxycholate did not. The serum cholesterol level was not changed by the treatments. Ursodeoxycholate and hyodeoxycholate increased their own secretion into the bile and decreased cholic acid secretion, while dehydrocholate increased deoxycholic acid and oxo bile acid secretion. Ursodeoxycholate increased but dehydrocholate decreased the fecal sterol excretion, and hyodeoxycholate caused no change. Dehydrocholate decreased the fecal coprostanol level. The total amounts of the fecal bile acids were similar in all the treated groups, but ursodeoxycholate increased lithocholic acid, alpha, beta- and omega-muricholic acids and ursodeoxycholic acid; hyodeoxycholate increased hyodeoxycholic acid, 3 alpha, 7 beta, 12 alpha-trihydroxy-5 beta-cholanoic acid and oxo bile acids; and dehydrocholate increased deoxycholic acid, cholic acid, omega-muricholic acid and oxo bile acids and decreased hyodeoxycholic acid. These data suggested that ursodeoxycholate was transformed into lithocholic and muricholic acids, and dehydrocholate into cholic and deoxycholic acids during the enterohepatic circulation, but hyodeoxycholate showed almost no change. Ursodeoxycholate and hyodeoxycholate caused neither accumulation of cholesterol in tissues nor increase in bile flow and biliary lipid secretion as well as chenodeoxycholate did. The biological effect of dehydrocholate was similar to that of cholate, and this was partially due to its conversion into cholic acid and deoxycholic acid.
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Effects of spinasterol and sitosterol on plasma and liver cholesterol levels and biliary and fecal sterol and bile acid excretions were examined with male mice. Both phytosterols were added to the diet at a 1% concentration and fed to mice for 15 days. Spinasterol increased the fecal cholesterol excretion and decreased the plasma and liver cholesterol levels, the bile acid pool size and the fecal bile acid excretion, especially those derived from chenodeoxycholic acid. Fecal coprostanol excretion remained unchanged. These changes were similar to those produced by sitosterol. These data led to the conclusions 1) that spinasterol, as well as sitosterol, inhibits cholesterol absorption, resulting in decreases of the plasma and liver cholesterol levels and 2) that when cholesterol absorption is inhibited, the synthesis of bile acids, especially that of chenodeoxycholic acid, decreases, suggesting that the dietary cholesterol is preferentially metabolized to chenodeoxycholic acid in mice.
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