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Biomedical subjects

K Kosaka

Publications and source records attributed to K Kosaka.

At least 523 records · Page 29Linked to original sources
PubMed1975

Hexokinase isozyme pattern in CCl(4)-injured rat liver.

Activities of hexokinase isozymes in carbon tetrachloride (CCl(4))-injured rat liver were determined quantitatively by DEAE-cellulose column chromatography and compared with those of regenerating liver, fetal liver and ascites hepatoma cells (AH 130). The CCl(4)-injured liver revealed an isozyme distribution with predominant Types I, II and III (3.2, 8.8 and 6.8 times higher than the control values, respectively) and with undetectable activity of Type IV hexokinase (glucokinase). Although the isozyme pattern generally resembled that of fetal liver or hepatoma cells, the relatively high activity of hexokinase Type III in CCl(4) treatment characterizes the pattern of hexokinase isozyme in acue liver damage.

Animals↗
PubMed1975

Demonstration of anti-"a-component" antibody--a possible means to differentiate patients with auto-antibodies to endogenous insulin from insulin-treated patients.

The presence of anti-"a-component" antibody was examined in sera of 4 groups of patients with or without anti-insulin antibody, using 125I-a-component and the polyethylene glycol precipitation method. 125I-a-component crossreacted with insulin antibody. This cross-reactivity was abolished after preincubation of these sera with monocomponent insulin. The specificanti-"a-component" antibody could be estimated in this procedure. After preincubation with monocomponent insulin, significant binding of 125I-a-component was demonstrated in sera of most patients treated with ordinary commercial insulin, but not in sera of 2 hypoglycemic patients suspected of an insulin autoimmune syndrome. Some cases treated with commercial insulin for less than one year and all cases treated with monocomponent insulin for 7-10 months did not have significant anti-"a-component" antibody. The test for the presence of anti-"a-component" antibody is not definitive but if positive it differentiates "auto-antibodies" from the antibodies produced by injections of commercial insulin.

Animals↗
PubMed1975

Effect of splanchnic nerve stimulation on glucagon and insulin output in the dog.

In order to study the role of the sympathetic nerves in the regulation of glucagon and insulin secretion, the distal stump of the left splanchnic nerve was electrically stimulated at the diaphragmatic level in the anesthetized dog under bilateral ligation of the adrenal veins. During stimulation, plasma glucose concentration rose rapidly, and pancreatic vein plasma concentration of glucagon increased along with pancreatic vein blood flow, indicating a greater output of glucagon. Insulin output in pancreatic vein plasma was slowly elevated despite continued stimulation. Pretreatment with propranolol resulted in a decline of the basal output of both glucagon and insulin and in their marked initial fall at the onset of the stimulus. However, glucagon output still showed a vigorous increase during neural stimulation whereas insulin output remained totally suppressed, but showed a rebound rise after cessation of stimulation. Pretreatment with phentolamine evoked an enhancement in both basal output of insulin and its response to splanchnic stimulation, but did not exert any marked effect on glucagon output. Pretreatment with atropine inhibited the basal output of glucagon and insulin, but the response of insulin output to splanchnic stimulation was not suppressed, thus excluding the possibility that activation of aberrant parasympathetic nerve fibers located in the splanchnic nerve would be responsible for the delayed increase in insulin release. The present results indicate that glucagon secretion may be regulated by different receptor mechanisms from those involved in insulin release following sympathetic activation.

Animals↗
PubMed1975

Effect of beta and beta2 adrenoreceptor stimulants infused intrapancreatically on glucagon and insulin secretion.

L-Isoproterenol was infused at a dose of 20 pmol/kg/min for 10 min into the cranial pancreaticoduodenal artery in anesthetized dogs. Arterial plasma glucose, blood flow, and plasma concentrations of both glucagon and insulin in the cranial pancreaticoduodenal vein were significantly enhanced during the infusion, resulting in a greater increase of bihormonal output. Intrapancreatic pretreatment with propranolol abolished all of the isoproterenol-induced increases except for glucagon secretion which was suppressed only in part. Pretreatment with practolol, a specific receptor blocker of the beta1 type, did not exert any discernible inhibiting effect upon the isoproterenol-induced enhancement. Intrapancreatic infusion of trimetoquinol, a selective receptor stimulant of the beta2 type in some mammals, at an equimolar dose caused similar increases in plasma glucose, pancreatic venous blood flow, and bihormonal output when compared to those induced by isoproterenol. Pretreatment with a larger dose of propranolol totally abolished the trimetoquinol-induced enhancement of both glucagon and insulin secretion. Pretreatment with an isomolar dose of practolol, in contrast, did not show any suppressive effect on the parameters investigated. There was a dose-dependency in the bihormonal responses to trimetoquinol. Another beta2 receptor agonist, salbutamol, also significantly raised plasma glucose, pancreatic venous blood flothough to a lesser extent than did trimetoquinol. These results indicate that the adrenergic control over the function of the endocrine pancreas through beta adrenoreceptors may be mediated mainly via those of the beta2 type.

Adrenergic beta-Agonists↗
PubMed1975

Damaged DNA in lymphocytes of aplastic anemia.

The size of single-stranded DNA in lymphocytes in GO stage from 22 patients with acquired primary and secondary aplastic anemia was estimated by alkaline sucrose gradient centrifugation. The average size was 9.3 (+/-0.3) times 10(7) daltons. The lymphocytes of patients contained significantly more single-strand breaks in DNA, compared to those of normal persons. The difference in size of single-stranded DNA which had been present in nontransformed lymphocytes could also be observed in transformed lymphocytes. Some characteristic differences could be observed in the sedimentation patterns of single-stranded DNA in the lymphocytes of patients with aplastic anemia and those of normal persons. The single-strand breaks in DNA suggested that the repair processes were disturbed in the DNA molecules of circulating lymphocytes from patients with acquired primary and secondary aplastic anemia.

Anemia, Aplastic↗
PubMed1975

Microheterogeneity of rat alpha-fetoprotein.

A purified and homogeneous preparation of rat alpha-fetoprotein (AFP) was separated into two components, AFPa and AFPb, by polyacrylamide gel electrophoresis. These two components had a definite difference in electrostatic net charge and gave only a single band on sodium dodecyl sulfate-electrophoresis. Neuraminidase-treated AFP gave clearly separable, slower moving four to six and finally two components depending on the time of incubation with neuraminidase. The time-dependent conversion of each AFPa and AFPb into slower migrating components upon neuraminidase treatment was confirmed by re-electrophoresis of separated and similarly treated AFPa and AFPb.

Animals↗