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Biomedical subjects

K Ejiri

Publications and source records attributed to K Ejiri.

At least 73 records · Page 4Linked to original sources
PubMed1984

Production of monoclonal antibodies to islet cell surface antigens using hybridization of spleen lymphocytes from non-obese diabetic mice.

Non-obese diabetic mice display a syndrome with dramatic clinical and pathological features similar to those of Type 1 (insulin-dependent) diabetes in man. Circulating autoantibodies to the surface of islet cells were demonstrated in some of these mice by a protein A radioligand assay. To produce monoclonal antibodies to islet cell surface antigens, therefore, we took the spleens of non-obese diabetic mice, transferred the spleen cells into non-immunized recipient mice, which were made immunologically incompetent by a large dose of X-irradiation, and then fused their lymphocytes with FO mouse myeloma cells. After screening the resultant hybrids, one stable hybridoma (3A4) that produced a monoclonal antibody (IgG1) specifically bound to the surface of islet cells was obtained. The purified monoclonal antibody was bound to the surface of transplantable Syrian golden hamster insulinoma cells sevenfold more than control antibody. Adsorption of the antibody on mouse spleen lymphocytes or thymocytes resulted in only a slight decrease in 125I-protein A binding to insulinoma cells. This antibody also reacted with the surface of mouse and rat islet cells, but not with that of rat spleen cells or hepatocytes. A spectrophotometric assay for peroxidase activity demonstrated that six times more peroxidase bound to insulinoma cells incubated with the antibody than to cells treated with control antibody. Furthermore, this antibody could be visually detected in the immunoenzymatic labelling of the surface of insulinoma cells. In summary, we have developed a novel method of producing monoclonal antibodies to the surface of islet cells for probing into the pathogenesis of Type 1 diabetes.

Animals↗
PubMed1984

[Developmental changes in taurine and other sulfur-containing amino acid concentrations in fetal and neonatal rats].

The concentrations of taurine and other sulfur-containing amino acids in the fetal, neonatal and maternal liver, placenta, and whole fetal body between the 15th day of gestation and the 14th day after birth were determined using an automatic amino acid analyzer. In the fetal liver and placenta, the taurine concentration was the highest among all ninhydrin positive compounds. In these tissues the concentration of taurine increased significantly with the number of gestational days. Moreover, the total amount of taurine per fetus increased markedly up to term after the 15th day of gestation, and reached almost the same value as the total amount for adult rat liver. A striking difference in the changes in taurine concentrations during gestation between the fetal and maternal rat liver was observed: In contrast to the increase in the fetal liver, a significant decrease in the maternal liver was observed near term. But in these organs, no significant change in methionine, cystathionine and cysteine concentrations was observed during the perinatal period. These results suggest that taurine is supplied to the developing rat fetus from the maternal liver throughout gestation.

Animals↗
PubMed1983

Cardiac beat-to-beat variation as an indicator of neuropathy and the frequency of its abnormality in diabetes mellitus.

The cardiac beat-to-beat variation and the maximum constriction velocity and acceleration of the pupillary light reflex have been considered indices of parasympathetic neuropathy. The abnormality of these indices was evaluated in 191 non-diabetics and 151 diabetics. The cardiac beat-to-beat variation decreased gradually with age in non-diabetics as well as diabetics. It was small in diabetics compared to non-diabetics in corresponding age group between 10 and 59 years. In diabetics it was still smaller in the presence of peripheral neuropathy than in its absence. The overall prevalence of this abnormality was 30.1% in diabetics but only 3.0% in non-diabetics. In diabetics it rose to 40.0, 42.6 and 52.2% in the presence of motor, sensory and motor plus sensory nerve neuropathy, respectively. In 63 diabetics examined for both cardiac beat-to-beat variation and pupillary light reflex, no statistical difference was observed between the frequency of these abnormalities. These observations indicate an extremely high prevalence of abnormality in autonomic nerve function in diabetics especially in the presence of abnormality in autonomic nerve function in diabetics especially in the presence of other types of neuropathy, so that diabetics with peripheral neuropathy should be carefully examined for autonomic neuropathy and vice versa. Besides, the measurement of the cardiac beat-to-beat variation is similar in sensitivity in the detection of neuropathy to the measurement of pupillary light reflex.

Adolescent↗
PubMed1982

Modulation of somatostatin release by endogenous glucagon and insulin: physiological relationship between A, B and D cells in rat pancreatic islets.

In order to understand the physiological role of endogenous insulin or glucagon in somatostatin release, isolated rat pancreatic islets were treated with antiinsulin or antiglucagon antiserum in the presence of physiological amounts of glucose. The release of somatostatin was unchanged by treatment with antiinsulin antiserum which neutralized insulin released by 3.3, 8.3 and 16.7 mM of glucose. However, somatostatin release after treatment with antiglucagon antiserum was much reduced at all concentrations of glucose when compared with the release from control serum. Exogenous rat insulin (0.11, 1.11 micrograms/ml) had no effect, but exogenous glucagon (1, 5 micrograms/ml) resulted in a significant increase. Somatostatin release was stimulated by glucose, but the effect was insignificant. These results clearly indicate the physiological role of endogenous glucagon in the modulation of somatostatin release from the islets of Langerhans. Furthermore, the physiological relationship between A, B and D cells may be mediated through the paracrine mechanism.

Animals↗
PubMed1982

Protection by nicotinamide against streptozotocin-induced reduction in pancreatic TRH.

The concentration of thyrotrophin-releasing hormone (TRH) immunoreactivity was determined in pancreatic islets and acini in the rat. In addition, time-course changes in TRH in response to an iv injection of streptozotocin (65 mg/kg body weight) with or without nicotinamide (500 mg/kg body weight) were examined in the whole pancreas. Furthermore, pancreatic TRH was measured in diabetic rats treated with insulin for 3 weeks. The TRH concentration in rat islets was 42-fold higher than in exocrine glands, indicating that the majority of pancreatic TRH is of islet origin. The mean concentration of pancreatic TRH decreased to 60 and 65% of the respective control values at 4 and 7 h after administration of streptozotocin, respectively. AT 24 h, it fell to 10% of control values without significant changes in TRH levels in the hypothalamus and gastrointestinal tract. In contrast, no significant change in pancreatic TRH was noted in rats given combined treatment with streptozotocin and nicotinamide. The injection of streptozotocin alone resulted in severe hypoglycaemia at 7 h and hyperglycaemia at 24 h, whereas neither resulted from the combined treatment. Insulin therapy had no influence on the decreased TRH concentrations in the diabetic pancreas. These results suggest that TRH may be localized to the B cells of pancreatic islets, and that the marked reduction in TRH in diabetic pancreases is not a metabolic consequence of insulin deficiency.

Animals↗
PubMed1980

Role of glucagon and somatostatin in insulin release.

The role of endogenous glucagon and somatostatin in insulin release was studied. Islets isolated from adult rats were incubated for 60 min in 3.3, 8,3 and 16.7 mM glucose with anti-glucagon antiserum (AGA) or anti-somatostatin antiserum (ASA) which was produced in rabbits. For the control experiments the antiserum was replaced by normal rabbit serum (NRS). Insulin release from islets treated with AGA was suppressed in 3.3 and 8.3 mM glucose as compared to islets treated with NRS, while insulin release was not affected in 16.7 mM glucose. On the other hand, insulin release from islets treated with ASA was enhanced in 3.3 and 8.3 mM glucose as compared to that from islets treated with NRS, whereas in 16.7 mM glucose it was not different from the control. These observations indicate that endogenous glucagon and somatostatin play a physiological role in the regulation of insulin release, but their regulation of insulin release is deranged at non-physiologically high glucose concentrations.

Animals↗
PubMed1980

[Studies on entero hepatic circulation of urea nitrogen in pregnant rat (author's transl)].

The purpose of this paper is to investigate the specific metabolism of the protein and amino acid during pregnancy from a standpoint of urea nitrogen recycling hydrolyzed by intestinal bacterial urease of pregnant rat. For this purpose, the activity of urease of the intestinal flora, and L-glutamate dehydrogenase (GDH) in liver mitochondria, the concentration of free ammonia and urea in the intestinal tract, portal vein and right ventricle of the rat were discussed. The results were: 1) The activity of urease moderately increased during pregnancy with the peak on 19th gestational day. 2) The concentration of free ammonia in the intestinal tract elevated slightly, and markedly elevated in portal vein, but seemed to be no specific change in right ventricle. The peak showed on 19th gestational day. 3) The activity of GDH increased markedly during pregnancy, and the protein synthesis was thought to be accelerated. 4) Urea concentration in intestinal tract and blood stream seemed somewhat increased. This results revealed that the urea recycling system and protein synthesis accelerated during pregnancy because of high urease and GDH activity. This phenomenon adapted the pregnant to nutrient of the fetus for growing and development, and introduced a new concept of maternal-fetal unit of nutrition, especially in protein metabolism.

Ammonia↗
PubMed1980

Fetal activity determination and neosynephrine test for evaluation of fetal well-being in high risk pregnancies.

At the special outpatient clinic for high risk pregnancies, a total of 197 patients were evaluated with fetal activity acceleration determination (FAD) as a non stress test. FAD was done on 197 patients, of these there were 8 fetal distress (4.7%) and 3 low Apgar scores (1 minute Apgar score less than 6) (1.8%) of 169 positive FAD, on the other hand, 14 fetal distress (50%) and 10 low Apgar scores (35.7%) of 28 negative FAD. Neosynephrine Test was performed in 62 cases as a stress test and the correlation between these two tests was evaluated. In 51 instances FAD was positive and the simultaneous Neosynephrine Test was normal. In 2 cases of negative FAD with positive Neosynephrine Test, there were 2 fetal distress (100%) and 2 low Apgar scores (100%). All the two tests are reliable for fetal evaluation in high risk pregnancies, because FAD and Neosynephrine Test are less time consuming and have fewer contraindications. It is concluded that the combination of these two tests are the most useful screening methods for fetal evaluation in high risk pregnancies.

Evaluation Studies as Topic↗