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Biomedical subjects

S Tarui

Publications and source records attributed to S Tarui.

At least 433 records · Page 24Linked to original sources
PubMed1980

Morphological changes of the liver in uremic patients treated with chronic hemodialysis--laparoscopic observations and light- and electron-microscopic studies.

In order to clarify morphological changes of the liver in the uremic state, 16 uremic patients treated with chronic hemodialysis were studied. Biopsy was performed in 14 cases under laparoscopic observation and in two on the occasion of renal transplantation. One uremic patients not being treated with dialysis was also studied for comparison. All biopsy specimens were examined by light and electron microscopy. The liver usually appeared mildly or moderately swollen under laparoscopic observations, which was considered at least partially due to the enlargement of the hepatocytes. All patients had hepatocytes with an Orcein-negative "ground glass" appearance, in which marked proliferation of smooth endoplasmic reticulum (SER) was found by electron microscopy. Since the patient not being on dialysis also had such hepatocytes, this finding may be characteristic of uremia. With electron microscopy, in addition to proliferation of SER, alteration of mitochondria and rough endoplasmic reticulum (RER) and an increase in cytoplasmic lipid droplets were observed. Hypertrophy of the Golgi apparatus containing electron-dense particles (VLDL) was often found in patients associated with hypertriglyceridemia. Amorphous electron-dense inclusions in microbodies were occasionally observed. Siderosis was observed in nine patients including three having parenchymal siderosis. With electron microscopy, various siderosomes were seen in the cytoplasm of hepatocytes in patients with parencymal siderosis. Conclusively, these histological and ultrastructral features of hepatocytes are rather associated with several metabolic abnormalities in uremia.

Adolescent↗
PubMed1980

Glycosidase activities in the liver and kidney of hereditary diabetic mice.

Hereditary diabetic mice (NSY) were inbred from original streptozotocin diabetic ICR mice for 8-9 generations using hyperglycemia as an index. The normoglycemic ICR mice were used as controls for the NSY line. The nonfasting blood sugar level of the NSY mice was 305 +/- 14 mg/100ml, while their immunoreactive insulin level was 30 +/- 4 microU/ml (the values of the controls were 165 +/- 12 mg/100 ml and 79 +/- 14 microU/ml, respectively). beta-N-Acetylglucosaminidase [EC 3.2.1.29], beta-galactosidase [EC 3.2.1.23], alpha-glucosidase [EC 3.2.1.21], and alpha-mannosidase [EC 3.2.1.24] activities were determined in the 1,000 X g supernatant of the liver and the kidney of control and streptozotocin diabetic ICR mice and their NSY line. In the kidneys of the insulinopenic NSY mice, the beta-galactosidase and alpha-mannosidase activities were significantly decreased. No significant changes were found in liver enzyme activities. Insulin treatment increased the kidney beta-galactosidase activity signficantly. The insulinopenic state, which caused a decrease in the glycosidase activities in the kidney, could induce retarded breakdown of glycoprotein.

Animals↗
PubMed1980

Specific modification of hepatic triglyceride lipase activity by ultracentrifugally separated serum lipoprotein fractions.

Hepatic triglyceride lipase (H-TGL) obtained from postheparin plasma is first stimulated and than progressively inhibited by addition of an increasing amount of serum. To solve the mechanism of this modification, serum fractions isolated by ultracentrifugation were added to the assay mixture and their effects on H-TGL activity were determined. We demonstrated that the addition of the d=1.21 bottom fraction together with HDL almost fully reproduces the effect of the whole serum.

Heparin↗
PubMed1980

Ethambutol neurophathy: clinical and electroneuromyographic studies.

Clinical features including changes in the peripheral nerve conduction were analzyed in 10 cases with ethambutol neuropathy. There were abnormalities in the visual field in seven and optic atrophy in five of 10 cases. Seven of 10 cases complained of numbness in the lower limbs. The age of onset and dose of ethambutol the patients continue to take after the occurrence of visual impairment were found to be important in determining the severity of neurological symptoms. A functional disturbance was more conspicuous in ethambutol neuropathy, particularly in the sensory system than in the motor system so far as the peripheral nerve conduction was serially examined. Some cases still had serious optic disturbances even about seven years after the onset of the disease and the presence of irreversible lesions was suspected.

Adolescent↗
PubMed1980

Peripheral nerve conduction function in patients treated with antituberculotic agents, with special reference to ethambutol and isoniazid.

The electrophysiological examination was made to clarify the effect of ethambutol on the peripheral nervous system in 39 patients at tuberculous sanatorium. Abnormalities in the sensory nerve action potential (toe-ankle) were observed in about 10 percent of the patients treated with ethambutol, and these patients were mostly elderly and/or received the high dose of ethambutol. The mixed nerve conduction velocity (ankle-knee) showed a significant decrease compared with healthy subjects. The conduction velocity tended to decrease in the high ethambutol dosage (200 gm or more) group compared with the low dosage (200 gm or less) group. The tendency for the conduction velocity to decrease was also observed in the 18 patients treated with isoniazid but the abnormalities were mild compared with the ethambutol.

Action Potentials↗
PubMed1980

Decrease in blood glucose and release of gut glucagon-like immunoreactive materials by bombesin infusion in the dog.

Synthetic bombesin (100 ng/min) was infused under pentobarbital anesthesia in normal dogs and in insulin deprived depancreatized dogs 4 days after surgery. The release of gut glucagon-like immunoreactive materials (gut GLI) calculated as the difference between the values measured using cross-reacting antiserum and a so-called pancreatic glucagon specific antiserum was markedly stimulated by bombesin infusion. Plasma glucagon immunoreactivity (GI) measured by pancreatic glucagon specific antiserum also showed a small increase, whereas plasma glucose decreased significantly with a transient rise in insulin. The plasma glucose level did not decrease in depancreatized dogs. Gut GLI response in the regional mesenteric vein to 5% glucose administered into the loop of the ileum was strongly augmented by bombesin infusion. It is concluded that (1) bombesin infusion decreased blood glucose level in normal dogs but not in depancreatized dogs. (2) Bombesin infusion markedly augmented the release of GLI from the intestine. (3) Bombesin also stimulated the release of glucagon which was probably of gastrointestinal origin. (4) Insulin release was stimulated transiently by bombesin infusion. Thus, a competition of gut GLI with glucagon at the glucagon receptor site may be an explanation of the reduction in blood glucose.

Animals↗
PubMed1980

Parallel dysfunctions of pancreatic A, B and PP cells in insulin dependent diabetes.

To test the possibility that insulitis might play an etiological role in the pathogenesis of insulin dependent diabetes, functions of 3 kinds of islet constituting cells (A, B and PP cells) were estimated by quantifying secretory responses of glucagon-, C-peptide-and pancreatic polypeptide-producing cells to hyperglycemia and hypoglycemia. In insulin dependent diabetes, all 3 hormonal responses were severely impaired to the same extent. On the other hand, 3 islet cell functions were uniformly but less severely impaired in insulin independent diabetics without a diabetic family history. These results suggest that A, B, and PP cells of islet of Langerhans are evenly destroyed in parallel fashion at least in insulin dependent diabetes and in some insulin independent diabetes, suggesting insulitis as a possible cause of these types of diabetes.

Blood Glucose↗
PubMed1980

Hereditary and acquired abnormalities in erythrocyte phosphofructokinase activity: the close association with altered 2,3-diphosphoglycerate levels.

Specific deficiency of erythrocyte phosphofructokinase (PFK) activity in Type VII glycogenosis presents a good model for the analysis of the relationship between 2,3 diphosphoglycerate (2,3 DPG) level and glycolysis in erythrocytes since glycolytic flow is partially blocked at the regulatory step. Enzymatic analyses of glycolytic intermediates of erythrocytes from a patient with Type VII glycogenosis demonstrated that 2,3 DPG is markedly decreased in parallel with fructose-1,6-phosphate (FDP). In acidosis including diabetic ketoacidosis and uremic acidosis a fall in 2,3 DPG is also associated with a marked reduction in FDP. On the other hand, in respiratory alkalosis glycolytic intermediates shift to the opposite direction and forward crossover at PFK step appears, being associated with an elevation of 2,3 DPG. These data indicate a close relationship between 2,3 DPG level and PFK activity in erythrocytes. At least in acidosis and alkalosis the alteration in 2,3 DPG level may well be explained by changes in PFK activity caused mainly through allosteric mechanism. In addition, twelve cases with hereditary PFK deficiency in muscle and erythrocytes reported in the world are reviewed and discussed briefly.

Alkalosis↗
PubMed1980

Specificities of antibody to acetylcholine receptor in rabbits with experimental myasthenia gravis.

The injection of acetylcholine receptor (AChR) purified from Narke electroplax japonica induced 'experimental autoimmune myasthenia gravis' (EAMG) in rabbits. Serial measurements of anti-AChR antibody titre using Narke AChR and rabbit AChR as antigen revealed that the intensity of myasthenia had a rather closer correlation with titre to Narke AChR than that to rabbit AChR. Antibody reacting to rabbit AChR was almost completely adsorbed out with torpedo receptor conjugated to agarose. Serum concentrations of antibody protein measured by affinity chromatography ranged from 54 to 896 microgram/ml serum and were well correlated with the intensity of myasthenia. The results suggested that in rabbits immunized with heterologous AChR the cross-reaction of anti-heterologous AChR antibody with rabbit AChR caused myasthenia rather than an immune response specific to rabbit AChR dose.

Acetylcholine↗
PubMed1980

Acetylcholine receptor in rabbit thymus: antigenic similarity between acetylcholine receptors of muscle and thymus.

This study was performed to examine the presence and immunological properties of acetylcholine receptor (AChR) in rabbit thymus. Binding of 125I-alpha Bungarotoxin (alpha BGT) to Triton extract from rabbit thymus was saturable (half saturation value: 10 X 10(-9) M) and occurred with at least two affinities, a high one with a dissociation constant of 1.1 X 10(-10)M and a low affinity one with a dissociation constant of 2 X 10(-9)M. The complex formation of 125I-alpha BGT-thymus extract was inhibited by both carbamylcholine and D-tubocurarine. These results indicate the existence of AChR in rabbit thymus. Antibody to AChR which was purified from experimental myasthenic rabbits with Narke AChR-affinity gel and labelled with 125I was used to identify the receptor antigenicity in rabbit thymus. Specific binding of 125I-antibody to thymic extract was demonstrated by the DEAE-paper disc assay. It is concluded from these results that AChRs with a similar antigenicity to that of skeletal muscle AChR exist in rabbit thymus. Our findings obtained in this study will support a hypothesis that the primary immunogen in myasthenia gravis may be AChR in thymus and an autoimmune reaction against AChR might be initiated within the thymus gland itself.

Acetylcholine↗