[Histochemical demonstration of the carbonic anhydrase in the gastric surface epithelium of the human (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Kamada.
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The lipoperoxide level in the liver as well as serum in chronic alcoholics was measured. Of patients with chronic hepatitis, alcoholic patients had a significantly higher level of hepatic lipoperoxide than non alcoholic patients. The hepatic lipoperoxide level was correlated with serum lipoperoxide level. Chronic alcoholics with high level of serum glutamic-oxaloacetic transaminase (S-GOT) showed a higher serum lipoperoxide level than alcoholics with the low S-GOT level. After 2 weeks' abstinence the high serum level of lipoperoxide decreased remarkedly, which was associated with improvement in liver function test. These results suggest the involvement of lipid peroxidation in alcohol induced liver damage.
Hemoperfusion and rate of O2 uptake in the livers in vivo following ethanol ingestion were measured by reflectance spectrophotometry. Pressurization on the liver in situ above the sinusoidal blood pressure caused complete blocking of blood flow, followed by spectral changes due to transition from hepatic normoxia to anoxia. Analyses of such spectra provided informations as to the rate of O2 consumption in situ and the redox level of cytochrome c (+cl)) in the mitochondrial respiratory chain. The rate of O2 consumption thus calculated remained constant until the apparent O2-saturation of hemoglobin in situ decreased to less than 10% of the total of hemoglobin. In parallel with the decrease of the rate of O2 consumption, the apparent reduction level of cytochrome c (+Cl) increased. It was shown in fed rats that the ethanol ingestion (1 g/kg) stimulated O2 uptake in the liver by 29% which initially caused a decrease in O2-saturation of hemoglobin, followed by an increase in blood supply to the liver. Thus, the ethanol consumption resulted in an increase in hepatic oxidative metabolism, possibly leading to hepatic hypoxia and liver damage.
Scintiphotosplenoportography (SSP) was performed in 190 instances in 161 patients. No significant complications, such as severe pain or splenic haemorrhage, were encountered in any of the patients studied. Flow patterns of SSP were classified into nine groups according to the direction of collateral flow. Hepatopetal collateral flow was frequently observed in pancreatic cancer. In portal hypertension, cephalic collateral flow was more frequently observed than caudal flow. In detecting oesophageal varices, both SSP and endoscopy were performed in 81 patients. In four out of 46 patients with cephalic flow, oesophageal varices could not be observed by endoscopy. Conversely, in three out of 44 patients with oesophageal varices, SSP failed to show cephalic flow. The combined use of SSP and endoscopy would therefore provide more useful information in the management of patients with portal hypertension.
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Significantly higher levels of erythrocyte membrane microviscosity (MV) [n-: 5.22 +/- 0.17 (4.70--5.92), mean +/- SD (range), poise, N = 67, P less than 0.005] measured by fluorescence depolarization using 1,6-diphenyl-1,3,5-hexatriene as a fluorescent probe were found in diabetic patients when compared with normal controls [5.05 +/- 0.15 (4.70--5.29), N = 22]. No significant differences in MV existed between males and females, nor was MV significantly correlated with diabetic age, duration of diabetes, plasma cholesterol, cholesterol/phsopholipid ratios, and plasma lecithin:cholesterol acyltransferase activities. No significant difference in MV was observed between groups with or without diabetic retinopathy. There was, however, significantly higher MV [5.29 +/- 0.19 (5.00--5.92), N = 20, P less than 0.05] in the group with fasting blood glucose (FBG) greater than or equal to 140 mg/dl than that [5.19 +/- 0.15 (4.70--5.46), N = 47] in the group with FBG less than 140 mg/dl. The changes in erythrocyte membrane MV presented in this study appear to be related to the current metabolic control of diabetic patients and are considered to be one of the factors responsible for the reduced erythrocyte deformability in diabetes.
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