[Quantitative analysis of disease activity by applying multiple regression analysis in patients with ulcerative colitis].
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Biomedical subjects
Publications and source records attributed to T Katsuki.
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Branched-chain keto acid dehydrogenase complex (BCKAD) was measured in lymphoid cells established from five patients with maple syrup urine disease (MSUD) and six control subjects. Two other MSUD lymphoid cell lines obtained from The Human Genetic Mutant Cell Repository were used as references. One day after subculture, the cells grew logarithmically up to 4-5 days. With this cell growth, BCKAD activity increased greatly in controls, but not in MSUD cells. The maximum BCKAD activity of MSUD cells was less than 7% and 13%-16% of the control in classic and variant types, respectively. Leucine added to culture medium at the concentration of 10-20 mM significantly inhibited cell growth in MSUD cells alone, and with increasing concentration and impaired enzyme activity in a cell line, the effect became more prominent. The effects of isoleucine and valine were mild and did not differ between control and MSUD cells.
We treated a patient with a jejunal diverticulum with a rare complication of iron deficiency anemia. The anemia was improved following resection of the diverticulum. It was revealed that the iron deficiency anemia was due to the malabsorption caused by the jejunal diverticulum.
Hepatic insulinase activity was studied in cirrhosis in an attempt to explain the hyperinsulinemia known to occur in this disease. Liver tissue was obtained during laparotomy in seven patients with cirrhosis of the liver and five patients without liver disease. Insulin degradation was significantly decreased in the cirrhotic liver at each time interval measured (p less than 0.05). Insulinase inhibitor activity was measured in the plasma of 12 patients with cirrhosis of the liver and six controls. There was no significant difference between the two groups. Decreased insulinase activity in cirrhosis may account, in part, for the hyperinsulinemia seen in this disease.
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A patient with membranous obstruction of the inferior vena cava (MOVC) who underwent portopulmonary shunting by splenopneumopexy 13 years before developed hepatocellular carcinoma (HCC). Postmortem studies revealed HCC in the bilateral lobes of the liver with cirrhosis and complete MOVC. There were numerous new vessel formations in the portion of the splenopneumopexy, which proved persistence of the patency. Clinically, postshunt encephalopathy, hepatic deterioration, and cardiac-respiratory dysfunction in the long-term follow-up period were not noticed. Factors that contributed to the occurrence of HCC are also discussed.
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To clarify the changes of vasoactive amines associated with acute hepatic failure, ammonia, tryptophan, serotonin (5-HT) and histamine in the blood and liver were studied in dogs (n = 22) of each three group of acute hepatic ischemia; occlusion of hepatic artery (controls), occlusion of hepatic artery and portal vein (THI), and portocaval shunt with THI (PCS + THI). These biochemical changes were studied in each group at six time intervals: Preocclusion, 15 and 30 minutes postocclusion, and 30, 60 and 120 minutes after release of occlusion. A rapid rise of blood ammonia levels was observed in groups of THI and PCS + THI after occlusion. Blood 5-HT increased in postocclusion of both controls and THI. However, a decrease of 5-HT was observed in PCS + THI. Hepatic 5-HT also increased after occlusion in THI and PCS + THI as compared with a decrease in controls. Plasma histamine rose significantly in all groups after the occlusion. These data demonstrated that the changes of vasoactive amines in hepatic ischemia and/or splanchnic pooling appeared to affect microcirculation of the liver and play a role of pathogenesis of hepatic failure after hepatic ischemia.
The conversion of 3,7-dihydroxy bile acids by anaerobic mixed cultures of intestinal microorganisms was studied in fecal samples from eight healthy adult males. Incubations using substrate chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA) were performed simultaneously in separate microbial suspensions from the same fecal samples. A time course study was done on four samples, chosen randomly from the eight. In the incubation of CDCA, substrate CDCA always decreased rapidly in amount; UDCA increased in amount, as did 3 beta, 7 beta-dihydroxy-5 beta-cholanoic acid (3 beta, 7 beta) and 3 beta, 7 alpha-dihydroxy-5 beta-cholanoic acid (3 beta, 7 alpha). In the incubation of UDCA, UDCA gradually decreased in amount; (3 beta, 7 beta), CDCA, and (3 beta, 7 alpha) increased gradually in amount. All reactions involved four epimers. After 48-72 hr UDCA was predominant and the reactions appeared to have reached equilibrium. In cultures from all eight samples, after 72-96 hr, a predominance of beta-hydroxy configurations at 7-position and alpha-hydroxy configurations at 3-position was observed. To compare these bile acid compositions to those in feces, an in vivo study using nine subjects was carried out. Concurrent with the collection of feces, transit time of food through the gut was measured. In samples from five subjects, in which amounts of lithocholic acid (LCA) was small, four 3,7-dihydroxy epimers were found. In samples from the other four, however, CDCA, the predominant epimer in bile, had apparently been converted to LCA by 7-dehydroxylation, and four epimers were not always found. In contrast to the incubation study, UDCA was not always the predominant 3,7-dihydroxy epimer in the fecal study. This may have been due to the transit times, which averaged 26.4 +/- 8.9 SD hr, being much shorter than the time it took for the incubation reactions to reach equilibrium.
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A 33-year-old male with diphasic dyskinesia was presented. He began to have difficulty with walking at the age of 27, and was diagnosed to have juvenile parkinsonism. For the past two years, L-dopa has been prescribed with good initial response. One year ago peripheral dopa decarboxylase inhibitor in combination with L-dopa was started, and he began to have involuntary movements. One hour after taking 2 tablets of EC dopa (L-dopa 100 mg + benserazide 25 mg), violent involuntary ballistic movements appeared in all four extremities which lasted for 15 minutes. For the following 50 minutes, his symptoms of parkinsonism markedly improved. The score of parkinsonism reduced by 58%, and he was able to walk. The plasma dopa level was increasing during this period. However, during decreasing period of plasma dopa concentration, he did not have end-of-dose dyskinesia. On the other hand, one hour after taking 500 mg of L-dopa involuntary choreic movements appeared in his right upper extremity for several minutes without any improvement of parkinsonism. Three hours and 20 minutes after taking L-dopa, he developed mild choreic movements for several minutes followed by marked improvement of parkinsonism for 30 minutes. The score of parkinsonism reduced by 79%. Thirty minutes later, he developed violent ballistic movements in all four extremities, lasting for 30 minutes followed by reappearance of parkinsonism. The concentration of plasma dopa was decreasing during this period.(ABSTRACT TRUNCATED AT 250 WORDS)
Sera from 34 children with recurrent parotitis were measured by indirect immunofluorescence technique for antibody levels to several Epstein-Barr virus (EBV) antigens. IgG antibodies to EBV-capsid antigen (VCA) and EBV-associated nuclear antigen, often at high titres, were found in 29 of these patients, of whom 20 also had IgA antibody to VCA. Antibody level to early antigen complex (R and D) rose in 19 patients, of whom 18 had antibody to the R component alone. The abnormal patterns of EBV antibodies persisted for 3-14 months during and after the illness in 8 patients. These observations suggest that EBV infection may be important in the pathogenesis of recurrent parotitis.
A case of systemic amyloidosis involving the gastrointestinal tract is presented. The initial manifestation of this case was mechanical obstruction. On laparotomy, a submucosal hematoma of the sigmoid colon which completely obliterated the lumen, was found. With intense medical treatment, the obstructed lumen became patent, but segmental ischemic colitis ensued. The terminal course of this case was complicated by chronic renal failure, upper gastrointestinal bleeding and coagulopathy. Pathological examination of the stomal specimen revealed massive amyloid deposits in the wall of the large intestine as well as other vital organs.
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The combined use of CoQ10 with adriamycin has been recommended for reduction of the cardiotoxicity that occurs during cancer chemotherapy. Vitamin B2-butyrate was also investigated in order to determine anti-oxidative effects on adriamycin cardiotoxicity. This vitamin analysis prevented enhanced lipid peroxidation and rectified the respiratory disorders of heart mitochondria induced by adriamycin, however, the deficiency of the CoQ10-pool was not rectified. The combined approach of using CoQ10 for rectifying the deficiency of this component and of using B2-butyrate for reducing lipid peroxidation was indicated for adriamycin cancer chemotherapy.
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The effect of teleocidin, a new, naturally occurring tumor promoter on induction of Epstein-Barr virus (EBV), was compared with that of a known tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Early antigen (EA) and/or capsid antigen (VCA) of EBV was induced in the EBV genome-carrying cell lines C-6 and P3HR-I cells by teleocidin, its effect being maximal at a concentration of 12.5 ng/ml. The production of infectious EBV from P3-HR-I cells was enhanced by teleocidin maximally at a concentration of 0.5 to 2.5 ng/ml. The outgrowth of EBV-transformed cells from peripheral lymphocytes of seropositive healthy donors was also enhanced by teleocidin at a concentration of 0.02 to 0.5 ng/ml. TPA tested simultaneously in all experiments exhibited the same activities as teleocidin, and was effective at similar concentrations. Teleocidin enhanced both EA and VCA synthesis in P3HR-I cells additively with n-butyrate, but not with TPA. This suggests that teleocidin and TPA have a common mechanism of action, although their chemical structures are different.