Biomedical subjects
Publications and source records attributed to R Tanaka.
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Petuely's selective medium for Bifidobacterium was improved by addition of riboflavin, nucleic acid bases, pyruvic acid, and nalidixic acid. The modified medium, when examined under strictly anaerobic conditions for efficient isolation of Bifidobacterium from human fecal samples, exhibited selective and high viable counts that were close to those found on the usual nonselective medium.
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The effects of captopril administered intravenously in a dose of 1 mg/kg on systemic blood pressure (SBP), renal blood flow (RBF) and renal vascular resistance (RVR) were examined in pentobarbital anesthetized dogs. Untreated dogs were used in experiments in which the renal artery remained intact and others in which the renal artery was partially occluded (RAO). Captopril significantly decreased SBP, increased RBF and decreased RVR in untreated dogs. RAO induced an increase in arterial plasma renin activity and this increase was accompanied by an increase in RVR in the contralateral kidney and rise in SBP. During RAO, captopril induced qualitatively similar, but greater decreases in SBP and RVR of the contralateral kidney compared with those in the untreated dogs. These results suggest the vasodilator effect of captopril depends on the background level of angiotensin II and the enhanced effect would be expected under conditions such as RAO where circulating angiotensin II contributes to vascular tone.
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In order to ascertain whether insulin secretion is inhibited by insulin per se, the effect of exogenous rat insulin on basal and stimulated rat C-peptide reactivity (CPR) release was studied in the isolated perfused rat pancreas. The pancreas was perfused with a medium containing 20 or 200 ng/ml of rat insulin for a 20 min equilibration period and successively for a 25 to 30 min test period during which time glucose (300 mg/100 ml), tolbutamide (500 micrograms/ml), glucagon (500 ng/ml) or arginine (10 mM) was added as a secretagogue. The concentration of glucose in the basal medium was 60 mg/100 ml. Exogenous insulin did not significantly suppress the basal CPR secretion, nor did it cause a suppression of the peak value or incremental area of CPR while the pancreas was stimulated, but it rather augmented them. No inhibitory effect of exogenous insulin on the basal or stimulated CPR release was noticed in the present study.
To investigate the physiological role of glucagon in the maintenance of euglycemia, the effect of the neutralization of glucagon by an antiserum specific for glucagon on blood glucose and C-peptide immunoreactivity (CPR) levels was studied in the basal as well as in the hyperglucagonemic states caused by hypoglycemia or an intravenous infusion of arginine in rats. The antiserum employed in this study was raised in rabbits by subcutaneous injection as a conjugate of BSA and the C-terminal fragment of glucagon. Since the antiserum was found to contain 896 ng/ml of antibody-bound glucagon, the antigen-stripped glucagon antibody was prepared. Its affinity constant and binding capacity were 2.57 x 10(10) M-1 and 147 nM, respectively. After the administration of 1 ml of the antiserum in 24-hr-fasted rats, no free immuno reactive glucagon (IRG) was detected during the experiment for 60 min. Likewise, antiserum treatment prevented a rise in the plasma IRG level following an arginine infusion and insulin-induced hypoglycemia. Plasma CPR levels tended to be lower in antiserum-treated rats than in the control in any conditions covered by the present study. However, changes in blood glucose levels the both groups were comparable. These results demonstrate that in the presence of glucagon antibodies euglycemia can be maintained with a reduced supply of insulin.
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.
Carbaryl and dieldrin were accumulated mostly in the liver, and paraquat was accumulated in the kidney of normal diet (casein 24.5%) rats at 1 hr after the oral administration. At 5 hr after the administration, the concentration of carbaryl in liver or fat, and that of paraquat in kidney were markedly decreased. However, dieldrin in liver, kidney, lung, fat or others was signficantly increased at the same period. The absorption of paraquat from gastrointestinal tract was the least among the chemicals used. Biliary excretion of carbaryl was the highest and that of paraquat was the least by 5 hr after intravenous administration. The excretion ratio was about 100: 10: 1 for carbaryl, dieldrin and paraquat in normal diet rats. Biliary excretion of these chemicals was higher in high protein diet (casein 45%) rats and retention of the chemicals in tissue was higher in low protein diet (casein 5%) rats.
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Carcinoembryonic antigen (CEA) in plasma, cerebrospinal fluid (CSF), and tumor cyst fluid obtained from patients with a variety of intracranial tumors was determined by radioimmunoassay Slightly elevated levels of plasma CEA, ranging from 2.6 to 3.8 ng/ml, were noted in six (4%) of 161 patients with primary brain tumors: in three gliomas, two pineal tumors, and one acoustic neurinoma, respectively. On the other hand, 17 (37%) of 46 patients with metastatic brain tumors showed a definite elevation, and most of them had values higher than 5.0 ng/ml. Of 37 patients with primary brain tumors, only one with a pineal germinoma showed a significant elevation of CEA in CSF, whereas eight (44%) of 18 patients with metastatic brain tumors showed high values of CEA in CSF. All six patients with leptomeningeal carcinomatosis showed elevated CEA in CSF. Levels of CEA in tumor cyst fluid were determined in 17 patients with intracranial tumors, including 12 gliomas, two craniopharyngiomas, two metastatic tumors, and one meningioma; elevation of CEA in tumor fluid was noted in two craniopharyngiomas and one metastatic tumor. Sequential determination of CEA of plasma or CSF revealed that the CEA levels were well correlated with the activity of brain tumors. Consequently, the determination of CEA in plasma or CSF is valuable for the differential diagnosis between primary and metastatic brain tumors and for the management of CEA-producing tumors.
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The possible cause of the excessive increase in the number of polymorphonuclear leukocytes in the urine of patients suffering from urinary tract infections was investigated in regard to the chemotactic factor(s) for the leukocyte. We separated urinary protein fractions of 2 controls and 10 patients with urinary tract infections by gel filtration on a Sephadex G-50 column, and tested chemotactic activity in vitro by using Boyden's apparatus and in vivo by injecting the protein fractions into guinea pig skins. Chemotactic activity was found in the urinary protein fractions of 6 patients. The fractions of these 6 patients showed typical infiltration of polymorphonuclear leukocytes in the local tissue of guinea pigs. A high correlation was found between the activity and the leukocyte increase, although there was no relation between the type of infecting bacteria and chemotactic activity. The data suggest that the marked increase in the number of urinary leukocytes is attributable to the chemotactic factor(s) in the urine.