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Biomedical subjects

Y Takamura

Publications and source records attributed to Y Takamura.

At least 91 records · Page 5Linked to original sources
PubMed1991

Restoration of circadian corticosterone rhythm in ventromedial hypothalamic lesioned rats.

The effects of ventromedial hypothalamic (VMH) lesions on the circadian periodicity of blood corticosterone were studied in female rats. The rats were kept on a 12-hour light/12-hour dark illumination regimen and fed ad libitum. Three, 10 and 12 weeks after the VMH lesions, the concentrations of blood corticosterone were measured every 4 h for 48 h in the same unanesthetized rats. Three weeks after the operation, the circadian rhythm in VMH-lesioned rats was disturbed and disappeared. The corticosterone levels at 03:00, 07:00, and 11:00 were significantly higher than those in sham-operated rats. 10 and 12 weeks after the operation, the circadian rhythm, however, was notable (p less than 0.05, p less than 0.05). The elevated mean corticosterone levels over 48 h at 3 weeks after the operation decreased at 10 and 12 weeks. The sham-operated rats showed a significant circadian rhythm at 3, 10 and 12 weeks after the operation (p less than 0.001 in each period) with a peak concentration at 19:00 and through at 07:00. These findings show that the corticosterone circadian rhythms which were disturbed in the dynamic phase after VMH lesions recovered in the static phase of obesity, suggesting that the ventromedial hypothalamus is not an essential biological clock of circadian corticosterone rhythm.

Animals↗
PubMed1991

[A case of paroxysmal cold hemoglobinuria (PCH) in the elderly found by severe anemia].

CASE: 69 year-old female. Two weeks before the admission, the patient had suffered from upper respiratory tract infection. Severe anemia was detected (Hb was 6.0 mg/dl) and she received a transfusion. Four days after the transfusion, she became icteric and was transferred to our hospital on Feb. 3, 1990 for evaluation of anemia. Laboratory data on admission are as follows; Hb 6.3 g/dl, reticulocytes 128%, total bilirubin 4.6 mg/dl, indirect bilirubin 3.4 mg/dl, urobilinogen in urine positive, WR negative, direct anti-globulin test positive, indirect of the test negative, and Donath-Landsteiner test positive (both direct and indirect). Her red blood cells were classified as P2-positive. From these findings, non-syphilitic PCH was diagnosed. She required bed rest and therapy to protect her from cold exposure. The hemoglobin recovered to 8.3 g/dl. The D-L test was positive for 9 months. This is a rare case of PCH because the patient fell ill in old age and PCH was found because of her severe anemia in spite of her unawareness of hemoglobinuria.

Aged↗
PubMed1990

Very-low-calorie diet-induced weight reduction reverses impaired growth hormone secretion response to growth hormone-releasing hormone, arginine, and L-dopa in obesity.

To determine whether impaired growth hormone (GH) secretion in obese subjects is a consequence of obesity or a pre-existing pituitary-hypothalamic disorder, we measured (1) plasma GH response to growth hormone-releasing hormone (GRH; 1 microgram/kg body weight [BW]), arginine (0.5 g/kg BW), and L-dopa (500 mg); and (2) plasma glucose, insulin, and free fatty acids (FFA) in obese subjects before and after weight reduction due to very-low-calorie diet therapy using Optifast (240 kcal/d for 8 to 12 weeks). Body weight and body mass index (BMI) values before and after weight reduction were 87.2 +/- 4.1 kg and 34.5 +/- 0.9 kg/m2, and 67.8 +/- 2.7 kg and 27.0 +/- 0.4 kg/m2, respectively. GH response to GRH, arginine, and L-dopa in obese subjects was markedly impaired before weight reduction, whereas significantly increased responses were noted after weight reduction (P less than .01). Impaired integrated GH response to GRH, arginine, and L-dopa in obese subjects was significantly restored after weight reduction (P less than .01). Plasma glucose levels did not change, while plasma insulin and FFA levels decreased significantly after weight reduction (P less than .01, P less than .05). There was no significant correlation between integrated GH response to these three stimuli and plasma levels of glucose, insulin, and FFA, respectively. The reversibility of GH response to all three stimuli after weight reduction suggests that impaired GH secretion is a consequence of obesity rather than a pre-existing pituitary-hypothalamic disorder.

Adolescent↗
PubMed1990

Amino acid sensors sensitive to alanine and leucine exist in the hepato-portal system in the rat.

We reported the existence of vagal arginine sensors in the liver which modulate arginine-induced pancreatic hormone secretion. The present study was carried out to examine the possible existence of other amino acid sensors such as L-alanine and L-leucine in the hepato-portal system in rats using an electrophysiological approach. Afferent discharges were recorded from fine filaments dissected from the peripheral cut end of the hepatic branch of the vagus nerve. Administration of 0.1, 1, and 10 mM L-alanine and L-leucine solution (0.1 ml) into the portal vein caused an increase in the discharge rate of hepatic vagal afferents in a dose-dependent manner. The results suggest the existence of vagal amino acid sensors which are sensitive to alanine and leucine in the hepato-portal system.

Alanine↗
PubMed1990

Modulation of arginine-induced insulin and glucagon secretion by the hepatic vagus nerve in the rat: effects of celiac vagotomy and administration of atropine.

We hypothesized the existence of vagal arginine sensors in the liver which modulate arginine-induced pancreatic hormone secretion. The present study was carried out to examine the efferent pathways and receptor mechanisms from arginine sensors using selective vagotomies and autonomic drugs on the secretion of insulin and glucagon after ip injection of L-arginine (1 g/kg BW) in rats in an unanesthetized and unrestrained state. Hepatic vagotomy (sectioning of the hepatic branch of the vagus nerve) enhanced both plasma insulin and glucagon concentrations after ip arginine more than those in sham-vagotomized (control) rats. The effect of hepatic vagotomy was blocked by adding celiac vagotomy (sectioning of the celiac branches of the vagus nerve) or by previous administration of atropine methyl nitrate (10 mg/kg BW), but not by phentolamine (1 mg/kg BW) or propranolol (2 mg/kg BW). Celiac vagotomy alone did not affect the plasma insulin concentration; however, it reduced the plasma glucagon concentration after ip arginine compared to that in sham-vagotomized rats. Administration of atropine alone did not affect plasma insulin or glucagon concentrations after ip arginine. These results suggest that celiac branches of the vagus nerve act as efferent pathways to the pancreas through a muscarinic receptor mechanism in the hepatic arginine sensor-mediated pancreatic neuroendocrine system. The physiological role of these hepatic sensors may be to prevent arginine-induced exaggerated pancreatic hormone secretion and maintain blood glucose homeostasis.

Animals↗
PubMed1990

Hyper-response of insulin release to arginine in streptozotocin-induced diabetic rats with hepatic vagotomy.

Vagal glucose receptor and arginine sensor have been found to exist in the liver of normal rats. The present study was designed to examine whether these sensory receptor systems function in streptozotocin-induced mildly diabetic rats. One week after streptozotocin injection (35 mg/kg body wt. iv), hepatic vagotomy and installation of a jugular vein catheter were performed. Three days after the surgery, intraperitoneal glucose (1 g/kg body wt.) or arginine (1 g/kg body wt.) stimulation was done with the rat in an unanesthetized and unrestrained state. Hepatic vagotomy significantly reduced glucose-induced insulin release with an increase in plasma glucose in control and diabetic rats. The rate of reduction of plasma insulin release was similar in the two groups. Hepatic vagotomy also significantly enhanced arginine-induced insulin release in both groups, but in control rats there was no change in the response to plasma glucose, while in diabetic rats there was a significant reduction. The rate of enhancement of plasma insulin release by hepatic vagotomy was significantly greater in diabetic than in control rats. The results indicate that streptozotocin-induced mildly diabetic rats have hyperfunction of the arginine sensor and normofunction of the glucose receptor and modulate insulin release through these receptor systems in the liver.

Animals↗
PubMed1990

Genetic control by I-A subregion in H-2 complex of incidence of streptozocin-induced autoimmune diabetes in mice.

An experimental autoimmune diabetes in mice characterized by delayed-onset hyperglycemia with lymphocytic infiltrations of the pancreatic islets can be induced by multiple administrations of low doses of streptozocin (STZ). We report on the influence of the MHC (H-2 complex) on this autoimmune diabetes by comparing the susceptibilities of various congenic and recombinant strains with a B10 background. In congenic strains, C57BL/10 (H-2b) and B10.BR (H-2k) mice showed a high incidence of diabetes, whereas B10.D2 (H-2d) and B10.S (H-2s) mice showed a low incidence. Therefore, we suggest that the H-2 complex influences diabetes susceptibility and that both b and k are high-susceptibility alleles, whereas d and s are low-susceptibility alleles. In recombinant strains, those with the same haplotypes on the K, E, S, and D subregions of the H-2 complex showed undefined (high and low) susceptibilities, indicating that the diabetes-susceptibility genes are located outside these loci. Strains possessing I-Ab or I-Ak gene products (C57BL/10, B10.BR, B10.TL, B10.A, and B10.A(2R] showed high incidences, whereas strains possessing I-Ad or I-As (B10.D2, B10.S, B10.S(7R), B10.S(9R), and B10.GD) showed low incidences. In addition, administration of anti-I-A monoclonal antibody prevented the manifestation of diabetes in STZ-administered mice. Passive transfer of STZ-administered T lymphocytes to mice given minute doses of STZ induced significant hyperglycemia. This successful transfer was only observed in H-2-compatible mice. Thus, we conclude that one gene coding for susceptibility to this experimental diabetes was located in the I-A subregion within the H-2 complex.

Animals↗
PubMed1990

[A case of pulmonary embolism with diabetes insipidus developed after removal of craniopharyngioma].

A case of pulmonary embolism associated with diabetes insipidus is reported in an 18-year-old male. The patient, who had been treated with DDAVP for diabetes insipidus and hydrocortisone for hypocorticism for two years after first operation for the removal of craniopharyngioma, was admitted with recurrence of that tumor. Diabetes insipidus immediately after second operation was controlled with intermittent drip infusion of a small amount of aqueous pitressin under monitorings of body weight hourly using a patient weighing system to keep the weight changes within +/- one kilogram. Serum and urine electrolytes levels, osmolarity, and free water clearance were also monitored every three hours to maintain water-electrolytes balances appropriately. Postoperative course had been uneventful except that CSF rhinorrhea occurred 7 days after operation. The patient was, then, kept in bed with horizontal plane to avoid further leakage of CSF. Two days later, he developed chest pain suddenly with tachypnea, tachycardia, and general cyanosis. The arterial-BGA showed PaO2 of 53.5mmHg and PaCO2 of 35.3mmHg in room air. The definite diagnosis of pulmonary embolism was made by technetium microaggregate lung perfusion scans and by pulmonary angiograms. The patient was treated with heparin, 15000IU/day, and urokinase, 720000IU/day. The symptoms due to pulmonary embolism had improved gradually within a couple of weeks. Recent articles have shown an unexpected high incidence of deep vein thrombosis and pulmonary embolism in neurosurgical patients associated with the elevation of blood coagulability. Brain tumors, especially suprasellar mass with hypothalamic dysfunction have been suggested to cause thromboembolic disorders frequently. The clinical course was described and factors causing pulmonary embolism on this patient was discussed.

Adolescent↗
PubMed1989

Dynamics of blood coagulation factor XIII in ulcerative colitis and preliminary study of the factor XIII concentrate.

Blood coagulation studies were performed in twenty patients with ulcerative colitis (UC). At the active stage of UC, a marked increase in platelet count and fibrinogen concentration, and a marked decrease in Factor XIII activity level were observed. At the active stage of UC, four patients were treated with Factor XIII concentrate leading to reduction of pain, bleeding and endoscopic findings.

Adult↗
PubMed1989

Development of a solid medium for growth and isolation of axenic microcystis strains (cyanobacteria).

Solid media on a base of B-12 or CB medium with agarose or agarose of low melting temperature were developed for the cultivation of Microcystis species. The media with 0.4% gel showed the highest number of CFU, and increasing the gel concentration resulted in a reduction of the number of CFU. There was no difference in the numbers of CFU between pour and spread plates made of the solid media. By using the solid media, 31 clones of Microcystis species were isolated from natural blooms in Lake Kasumigaura, and 5 axenic strains (1 of M. wesenbergii and 4 of M. aeruginosa) were established from the clones.

Journal Article↗
PubMed1989

[Clinical course of acute intracerebral hematoma which shows a fluid level presentation by X-ray CT].

Three cases of intracranial hematomas which showed a fluid level presentation and/or mixed density in the acute stage by X-ray CT were reported. Case 1 is a 7-year-old boy who had the epidural and intracerebral hematomas three hours after the traffic accident. During the course, intracerebral hematomas which showed a fluid-level presentation had grown both 6 and 17 hours after the episode. Case 2 is a 39-year-old female who had received an aortic valve replacement 20 years ago. She was diagnosed as cerebral infarction due to the occlusion of the right middle cerebral artery. Intracerebral hematomas with a fluid level presentation developed in the infarcted area 20 days after the embolectomy. Case 3 is a 67-year-old female who had a mild subarachnoid hemorrhage by the traffic accident. Intracerebral hematoma with mixed density developed 68 hours after the episode and it enlarged again 89 hours after the accident. All three cases showed the abnormalities in the coagulofibrinolytic activities during the hemorrhage and showed a growth of the hematomas. It should be noticed that the case which shows a mixed density and/or a fluid level presentation in the X-ray CT requires more intensive care in both neurosurgical and general management.

Acute Disease↗
PubMed1989

[Biliary excretion and clinical efficacy of T-3262 (tosufloxacin tosilate) administered in the treatment of cholecystitis].

T-3262 (tosufloxacin tosilate), a new oral pyridone carboxylic acid agent, was investigated for its biliary excretion and clinical efficacy and safety to evaluate its usefulness in the treatment of cholecystitis. T-3262 was administered to a total of 4 healthy volunteers for 2 days at a dose of 150 mg every 8 hours, and A-, B- or C-bile were collected using the MELTZER-LYON method at 10-11 hours after the final administration. Bile concentrations of T-3262 in 3 cases were 0.33-2.05 micrograms/ml (A-bile), 6.13-9.50 micrograms/ml (B-bile) and 1.11-2.70 micrograms/ml (C-bile). Thus, T-3262 levels in B-bile were 15-34 times higher than serum levels (0.28-0.41 micrograms/ml). Only a trace of serum concentration of T-3262 was detected in another case with the concentration in B-bile was 0.132 micrograms/ml. A total of 10 patients with cholecystitis were treated with T-3262 at a dose level of 150 mg per dose 3 times daily for 1 to 20 days. The clinical efficacy was excellent in 1 case, good in 5 cases and fair in 2 cases and unevaluable in 2 cases, thus the clinical efficacy rate was 75%. Bacteriologically, Klebsiella pneumoniae, Enterococcus faecalis and Haemophilus parahaemolyticus were isolated from biles of 3 patients before treatment. Upon the treatment, E. faecalis was eradicated and K. pneumoniae was unchanged. The fate of H. parahaemolyticus was not known because of examination was not done after treatment. Side effects were observed in 2 cases with diarrhea in 1 case and epigastric pain in another case. But those symptoms disappeared after cessation of administration of T-3262. Abnormal laboratory test values were not observed.

4-Quinolones↗
PubMed1988

Electrical stimulation of the suprachiasmatic nucleus of the hypothalamus causes hyperglycemia.

We have presented evidence suggesting that the suprachiasmatic nucleus (SCN) is involved in central regulation of glucose homeostasis. To elucidate this role of the SCN, we examined the effects of its electrical stimulation on glucose metabolism in male Wistar rats. During and shortly after this stimulation, we observed hyperglycemia associated with enhanced hyperglucagonemia but no immediate hyperinsulinemia. In addition, we detected significant increase in liver glycogen phosphorylase alpha activity and significant decrease in the liver glycogen content. These findings suggest that the SCN is important in control of glucose homeostasis through effects on glucagon and insulin secretions and liver glycogen metabolism.

Animals↗
PubMed1988

Changes in the intracellular concentration of acetyl-CoA and malonyl-CoA in relation to the carbon and energy metabolism of Escherichia coli K12.

Intracellular concentrations of acetyl-CoA and malonyl-CoA in Escherichia coli K12 were determined by a malonyl-CoA: acetyl-CoA cycling technique. Under aerobic growth conditions with glucose the acetyl-CoA and malonyl-CoA concentrations varied over a range of 0.05-1.5 nmol (mg dry wt)-1 (20-600 microM) and 0.01-0.23 nmol (mg dry wt)-1 (4-90 microM), respectively. The intracellular concentration of acetyl-CoA was highest in exponentially growing cells and it fell rapidly to less than 5% of the maximum level when the organism entered stationary phase after exhaustion of glucose. A linear relationship was observed between the intracellular concentration of total acyl-CoA and the logarithm of the concentration of glucose in the medium. Consequently, the acetyl-CoA/malonyl-CoA ratios also varied drastically, in a range of 0.6-41.7, under different conditions. Of several carbon sources tested, glucose was the most effective for promoting the synthesis of cellular acetyl-CoA. For cells grown on glycerol or acetate the maximum concentrations of total acyl-CoA were significantly lower. In cells incubated with citrate (not used as a carbon source by E. coli), the level was consistent with that in cells starved for exogenous carbon sources.

Acetyl Coenzyme A↗
PubMed1987

Insulin increases triglyceride secretion rate in rats in vivo.

To investigate whether insulin regulates triglyceride secretion from the liver in vivo, triglyceride secretion rate (TGSR) and serum insulin were measured in the following three experiments: in rats 12 weeks after ventromedial hypothalamic (VMH) lesions (Exp. 1), in rats 12 weeks after a high fat diet-feeding (Exp. 2), and in rats 10 days after streptozotocin treatment (65 mg/kg) (Exp. 3). Under hexobarbital anesthesia, overnight fasted rats were bled for measuring insulin and triglyceride. Rats were again bled 45 and 90 minutes after Triton WR 1339 (120 mg) injection, for measuring triglyceride. TGSR was calculated from serum triglyceride values measured before and after Triton injection. In Exp. 1, VMH obese rats had higher serum insulin concentrations and TGSR than control rats. There was a significantly positive correlation between serum insulin concentrations and TGSR in VMH lesioned rats alone (r = 0.939, P less than 0.001) and in VMH lesioned and control rats combined (r = 0.958, P less than 0.001). In Exp. 2, high fat diet-fed rats gained more weight than control rats, but they had the same levels of serum insulin concentrations and TGSR as those of control rats. In Exp. 3, streptozotocin treated rats had lower serum insulin concentrations and TGSR than control rats. There was a significantly positive correlation between serum insulin concentrations and TGSR in the two groups of rats combined (r = 0.680, P less than 0.05). From the results of these three sets of in vivo studies, we conclude that insulin increases TGSR in vivo.

Animals↗