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Biomedical subjects

K Tanigawa

Publications and source records attributed to K Tanigawa.

At least 91 records · Page 5Linked to original sources
PubMed1995

Origins of nerve fibers containing nitric oxide synthase in the rat celiac-superior mesenteric ganglion.

The origin of nitric oxide synthase-containing nerve fibers in rat celiac-superior mesenteric ganglion was examined using retrograde tracing techniques combined with the immunofluorescence method. Fluoro-Gold was injected into the celiac-superior mesenteric ganglion. Neuronal cell bodies retrogradely labeled with Fluoro-Gold in the thoracic spinal cord, the dorsal root ganglia at the thoracic level, the nodose ganglion, and the intestine from the duodenum to the proximal colon were examined for nitric oxide synthase immunoreactivity. About 60% of sympathetic preganglionic neurons in the intermediolateral nucleus projecting to the celiac-superior mesenteric ganglion were immunoreactive for nitric oxide synthase, as were approximately 27% of nodose ganglion neurons and about 65% of dorsal root ganglion neurons projecting to the celiac-superior mesenteric ganglion. Neurons projecting to the celiac-superior mesenteric ganglion were found in the myenteric plexus of the small and large intestine. In the proximal colon, about 23% of such neurons were immunoreactive for nitric oxide synthase. However, in the small intestine, no immunoreactivity was found in these neurons.

Amino Acid Oxidoreductases↗
PubMed1995

Beta-cell function and replication in spontaneously hypertensive rats.

We examined beta-cell function and replication in spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY). Rats were subjected to 90% pancreatectomy (Px) or sham operation at the age of 8 weeks, and islet function and regeneration were examined 4 weeks after surgery. Plasma glucose levels were higher in SHR than in WKY (509 +/- 38 v 325 +/- 109 mg/dL, P < .0001) 1 week after Px and throughout the experimental period. Plasma glucose responses to intravenous injection of glucose (0.5 g/kg body weight) were not different in the sham-operated animals of the two strains, whereas plasma insulin responses were greater in SHR than in WKY. No insulin responses to glucose were observed in either strain of Px rats. The insulin content of the remnant equivalent (6.7 +/- 2.1 v 4.2 +/- 0.4 micrograms, P < .05) and whole pancreas (156.7 +/- 10.7 v 123.8 +/- 23.5 micrograms, P < .01) in sham-operated rats was greater in SHR than in WKY. However, insulin content was lower (P < .05) in Px-SHR (1.0 +/- 0.2 microgram) than in Px-WKY (3.9 +/- 1.7 micrograms). Histological examination showed that fibrotic degeneration of islets was much greater in Px-SHR than in Px-WKY. These data strongly suggest that the beta cells of SHR were more vulnerable to reduction of islet mass than those of WKY. Our data also suggest that hyperinsulinemia and/or insulin resistance in SHR has a deleterious effect on beta-cell replication.

Animals↗
PubMed1995

Effect of chronic vanadate administration in partially depancreatized rats.

The effects of vanadate on B-cell function and replication in rats after 90% partial pancreatectomy (Px) were compared with insulin therapy. At the age of 4 weeks, male Wistar rats were subjected to sham operation or Px. Vanadate (0.2 mg/ml) was given in drinking water for 3 weeks starting at 2 weeks after surgery. Regular insulin (2.4 units/day) was administered as a continuous subcutaneous infusion through an osmotic pump. Plasma glucose levels were significantly higher in the Px rats than in the sham rats from 1 week after surgery. Vanadate lowered plasma glucose levels to near normal values in the Px rats as early as 2 days. The effect was sustained throughout the experiment. The hypoglycemic effect of insulin was less than that of vanadate. During an i.p. glucose tolerance test, plasma glucose levels were decreased in the Px rats treated with vanadate or insulin, while plasma insulin levels were not affected. The insulin content in the Px rats treated with vanadate was significantly (P < 0.01) greater than in the insulin-treated Px rats. Histological examination showed fibrotic degeneration in the enlarged islets of Px rats, whereas the normal structure was retained in most islets of the Px rats treated with vanadate and insulin. In addition, B-cell areas within the islet were restored to normal levels not only in the insulin-treated Px rats but in the vanadate-treated Px rats. However, both vanadate and insulin failed to stimulate proliferative activity of the B-cells. These data suggest that vanadate is a new therapeutic option to ameliorate the diabetic state after Px.

Analysis of Variance↗
PubMed1995

Lack of effect of CS-045, a new antidiabetic agent, on insulin secretion in the remnant pancreas after 90% pancreatectomy in rats.

We assessed the effect of CS-045, a new hypoglycemic agent, on B-cell function in partially pancreatectomized rats. At the age of 4 weeks, male Wistar rats were subjected to 90% pancreatectomy (Px). For 2 weeks starting at 6 weeks after surgery the Px rats were treated with CS-045 (CS rats) mixed with chow pellets in a proportion of 0.2% (w/w). To compare the efficacy of CS-045 with that of insulin therapy, an osmotic pump was implanted to release insulin (1.2 units/day) into the intraperitoneal cavity of the Px rats (Is rats). Plasma glucose levels in the CS and Is rats were significantly lower than in the control Px rats; however, no marked improvement in plasma glucose or insulin levels was observed in glucose tolerance test (2 g/kg, i.p.) in the CS rats. Insulin secretion by the isolated perfused pancreas in response to 16.7 mM glucose showed a biphasic pattern, but was slightly reduced in the Px and CS rats compared with the Is rats. Insulin secretion induced by 19 mM arginine was unaffected by the treatment. The insulin content of the CS rats was significantly greater than in the Px and Is rats. Histological observations suggested regranulation of the pancreatic islets of the CS rats. B-cell areas within the islet were restored to normal levels in the Cs and Is rats. These findings indicate that the hypoglycemic effect of CS-045, which is not mediated by insulin secretion from the residual pancreas, prevents destruction of the islet.

Animals↗
PubMed1995

Effects of additives on irreversible inactivation of lysozyme at neutral pH and 100 degrees C.

The mechanism of irreversible inactivation of lysozyme at neutral pH at 100 degrees C, and effects of additives on the inactivation were investigated. The thermoinactivation of lysozyme at neutral pH was caused by intra- and intermolecular disulfide exchange and the production of irreversibly denatured lysozyme, which was destabilized by multiple chemical reactions other than disulfide exchange. In addition, independently, deamidation slightly affected the inactivation by causing a decrease of electrostatic interaction between positive charges of lysozyme and negative charges of the bacterial cell wall. As for the effects of additives on the inactivation, a small amount of copper ion suppressed intra- and intermolecular disulfide exchange by catalyzing air oxidation of heat-induced trace amounts of free thiols, and organic reagents (acetamide, ethanol, and glycerol) changed the mechanism of the inactivation to that under acidic conditions by shifting the pKa values of dissociable residues and also suppressed intermolecular disulfide exchange by decreasing hydrophobic interactions.

Acetamides↗
PubMed1995

Relationship between associations of NOR and chromosomal anomalies in the abnormal embryos of nonobese diabetic and STZ-diabetic mouse.

Associations of nucleolar organizing regions (NORs) in the postimplantation stage embryos of nonobese diabetic (NOD) mice, and diabetic ICR mice induced by streptozotocin (ST), were studied to investigate the possible cause of the numerical anomalies of the chromosomes in their abnormal embryos. The incidence of NOR associations in abnormal embryos from diabetic NOD (NOD-DM) and STZ-diabetic mice was 11.7 and 7.7%, respectively. This incidence was significantly higher than that (1.2%, p < 0.05) of normal embryos from ICR mice which were used as control. From the results analyzed cytogenetically it was suggested that the higher incidence of chromosomal numerical anomalies in the embryos from NOD-DM and STZ-diabetic mice were caused by the chromosomal nondisjunction induced by associations of NORs. Furthermore, it was suggested that NOD-DM embryos have a tendency to increase the associations of NOR in a diabetic condition together with other factors such as autoimmune disease, however a diabetic condition alone induced chromosomal anomalies. Regarding relationships between the incidence of associations of NOR and the types of malformed embryos, it was also clear that all of the abnormal embryos from NOD-DM and STZ-diabetic mice had a high incidence of associations of NOR, and that the incidence was not related to the types of congenital anomalies. Furthermore, in the mal-developed tissue of embryos from STZ-diabetic mice, many chromosomal anomalies were found (26.6%), and the incidence was similar to that of whole embryos (22.6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

A single missense mutation in codon 918 of the RET proto-oncogene in sporadic medullary thyroid carcinomas.

The RET proto-oncogene is expressed in human medullary thyroid carcinoma and pheochromocytoma. Recently germline mutations of the RET proto-oncogene were reported in four syndromes (MEN 2A, MEN 2B, familial medullary thyroid carcinoma and Hirschprung's disease) and somatic mutation was also found in sporadic medullary thyroid carcinoma. To determine the incidence of RET mutations in medullary thyroid carcinoma in Japan, we investigated 14 medullary thyroid carcinomas (comprising 1 case of MEN 2A, 1 case of MEN 2B, 2 cases of familial medullary thyroid carcinoma and 10 cases of sporadic). Tumors from all cases were screened by PCR-SSCP on exons 10 and 11. DNA sequencing on these exons was performed for the hereditary medullary thyroid carcinoma cases. The PCR products of exon 16 from tumor DNA were analyzed by means of Fok1 restriction enzyme digestion analysis and mutations confirmed by DNA sequencing. We found no structural abnormalities in either exon 10 or exon 11 in any of the cases examined, but in four of 10 sporadic cases we detected a common point mutation at codon 918 (ATG to ACG) in exon 16, where methionine was replaced with threonine. Our results support the theory that a point mutation of exon 16 of the RET proto-oncogene may be related to the oncogenesis of sporadic medullary thyroid carcinomas. However, further studies on the entire RET proto-oncogene are needed to clarify the relationship between its expression and thyroid tumorigenesis.

Base Sequence↗
PubMed1995

A study of effect of CS-045, a new antidiabetic drug, on hypertension in spontaneously hypertensive rat.

Several lines of evidence have suggested that insulin resistance may play an important role in the pathogenesis of hypertension. CS-045 is a new hypoglycemic drug by which improves insulin sensitivity in peripheral tissues. We assessed the effect of CS-045 on hypertension in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) as a control. At 20 weeks of age, the treatment with CS-045 was started by being mixed with chow pellets in the proportion of 0.2% (w/w) and continued for 6 weeks. Nonfasting plasma glucose levels were not changed in either strain of rats treated with CS-045, but plasma insulin levels decreased in SHR 4 and 5 weeks after the start of CS-045 therapy. Blood pressure increased with age in SHR without treatment, but CS-045 decreased blood pressure only 4 and 6 weeks after the treatment. These findings suggest that insulin resistance is not strongly associated with the pathogenesis of hypertension in SHR.

Animals↗
PubMed1995

Endoscopic polypectomy for pacemaker patients.

Endoscopic polypectomy using high frequency voltage is contraindicated in patients with cardiac pacemakers. Recently, highly advanced pacemakers have enabled us to perform endoscopic polypectomy on these patients by taking appropriate cautions. We successfully removed 10 colonic polyps and one gastric polyp in patients with pacemakers by endoscopic polypectomy. No complication and dysfunction of the pacemaker occurred before, during or after the polypectomy.

Aged↗
PubMed1995

[Congenital erythropoietic porphyria].

Congenital erythropoietic porphyria (CEP, Günther's disease) is an extremely rare autosomal recessive disease (There have been only 33 case reports in Japan to date.), characterized by mutilating cutaneous photosensitivity and abnormal haem synthesis in the bone marrow. Reduced activity of uroporphyrinogen III synthase (UROIIIS), the fourth enzyme of haem biosynthetic pathway causes this disease. Recent progresses of molecular biology enable us to analyze genetic defect at the molecular level of porphyrias. Also in CEP, it has been reported several reports of mutations of the UROIIIS gene since isolation of a full-length human cDNA encoding UROIIIS by Desnick et al. Here we report about epidemiology, signs and symptoms, laboratory findings and therapies of CEP.

Female↗
PubMed1995

Exon redefinition by a point mutation within exon 5 of the glucose-6-phosphatase gene is the major cause of glycogen storage disease type 1a in Japan.

Glycogen storage disease (GSD) type 1a (von Gierke disease) is an autosomal recessive disorder caused by a deficiency in microsomal glucose-6-phosphatase (G6Pase). We have identified a novel mutation in the G6Pase gene of a individual with GSD type 1a. The cDNA from the patient's liver revealed a 91-nt deletion in exon 5. The genomic DNA from the patient's white blood cells revealed no deletion or mutation at the splicing junction of intron 4 and exon 5. The 3' splicing occurred 91 bp from the 5' site of exon 5 (at position 732 in the coding region), causing a substitution of a single nucleotide (G to T) at position 727 in the coding region. Further confirmation of the missplicing was obtained by transient expression of allelic minigene constructs into animal cells. Another eight unrelated families of nine Japanese patients were all found to have this mutation. This mutation is a new type of splicing mutation in the G6Pase gene, and 91% of patients and carriers suffering from GSD1a in Japan are detectable with this splicing mutation.

Adult↗
PubMed1994

[Effective treatment with constant subcutaneous infusion of octreotide in a patient with acromegaly associated with diabetic pre-coma and diabetes insipidus].

A 58-year-old woman was admitted to our hospital for impaired consciousness, hyperglycemia and bitemporal hemianopsia. She was diagnosed as having NIDDM one year ago and was treated with diet and glibenclamide (1.25 mg/day) for 6 months. However, she stopped her medical treatment one month ago and then polydipsia and general fatigue were manifested. She was admitted to a hospital five days ago at which time hyperglycemia (405 mg/dl) and anemia (Hb8.0g/dl) were detected. She was transferred to our hospital for control of blood glucose and further examination of bitemporal hemianopsia. She showed typical acromegalic features including enlargement of the nose, lips and tongue, increased heel pad and acral growth. Conscious disturbance was cured by the infusion of saline and the administration of insulin. Endoscopy revealed an active gastric ulcer (A1). Endocrine data disclosed increased GH levels in plasma and urine, whereas plasma IGF-1 levels were low. Plasma GH paradoxically increased following the administration of TRH. A water deprivation test showed an impaired increase in urinary osmolarity, indicating partial central diabetes insipidus (DI). MRI with Gd-contrast revealed a macroadenoma which progressed toward suprasella. She was diagnosed as having acromegaly, partial DI and probable hyperosmolar hyperglycemic nonketotic diabetic pre-coma. Polyuria (5-101/day) due to partial DI was controlled by the administration of DDAVP (10 micrograms/day). The constant subcutaneous administration of octreotide (240 micrograms/day) resulted in normal plasma GH levels and a marked shrinkage of the pituitary tumor. The pituitary tumor was finally removed by the transsphenoidal approach following treatment with octreotide for 4 months. HE staining of the pituitary tumor showed atrophic and acidophilic cells surrounded by hyaloid connective tissue. After the surgery, plasma GH levels were normalized and complications were cured. In conclusion, this is a very rare case of acromegaly associated with diabetic pre-coma and partial DI, and effectively treated with constant subcutaneous infusion of octreotide.

Acromegaly↗
PubMed1994

Embryonic growth impaired by maternal hypoglycemia during early organogenesis in normal and diabetic rats.

The effect of maternal hypoglycemia on early organogenesis was studied in normal and diabetic rats. Female Wistar rats were made diabetic by an intravenous injection of streptozotocin (45 mg/kg) 2-3 weeks before conception. On day 9.5 or 10.5 of embryo development, both control and diabetic dams received saline or Actrapid human insulin (400 mU/rat) intraperitoneally after 19-h starvation. The fasting plasma glucose levels in diabetic dams decreased from approximately 23 to 8 mM. Hypoglycemia as low as 3.5 mM was maintained for 60 min in insulin-treated mother rats. Pregnancy was terminated on day 11.6 of embryo development. A significant growth retardation was found in diabetic embryos as compared with normal embryos. Maternal hypoglycemia lowered the DNA content in normal but not diabetic embryos, while the teratogenic effect of maternal hypoglycemia was not pronounced in either normal or diabetic embryos. These data may suggest that maternal hypoglycemia in vivo in early pregnancy influences the embryogenesis but not teratogenesis of rat embryos.

Animals↗
PubMed1994

Surgical treatment of hepatocellular carcinoma.

The effect of surgical treatment for hepatocellular carcinoma (HCC) was evaluated in 149 resected cases, 83.2% of which were associated with liver cirrhosis. The 3- and 5-year survival rates were 60.1% and 39.4%, respectively. The mortality rate was 4.1%. In patients aged over 70 years, liver cirrhosis was found in 53.3% of cases and the mortality rate was 6.7%. The 3- and 5-year survival rates were 50.8% and 33.9%, respectively. Factors that significantly affected survival for more than 5 years were a tumor size of less than 3 cm, Stage I disease, vp(-), IMo, and diploid type. The 5-year survival rate for patients with a single tumor of 3 cm or less was 54.2%, regardless of the surgical procedure. All 15 patients with a solitary tumor of 2 cm or less (Stage I, small liver tumor) were alive with a 5-year survival rate of 100%. The problem is the treatment of patients with a tumor measuring 3-5 cm in diameter and associated liver cirrhosis, because their prognosis after surgery is the worst. HrS (subsegmentectomy) is the minimal procedure of limited hepatectomy for these cases with postoperative multidisciplinary therapy.

Adult↗
PubMed1994

Phosphoinositide hydrolysis and insulin release in fetal rat islets.

The association between phosphoinositide hydrolysis and insulin release in fetal islets was investigated. Islets from 21.5-day-old fetal rats were cultured for 7 days in inositol-free RPMI 1640 containing 11.1 mM glucose and labeled with 20 microCi/ml [3H]inositol for the final 2 days. The labeled islets were then perifused under various conditions for 60 min. Glucose (16.7 mM) caused a modest increase in [3H] efflux from labeled islets, but there was a subsequent fall-off in [3H] efflux. Fetal islets showed the first phase of insulin release without the continued rising second phase. When islets were perifused with 5 mM LiCl, the glucose-induced efflux of [3H] was greatly reduced, whereas glucose-induced insulin release was not affected. A pronounced effect of LiCl was an increase in inositol monophosphate, indicating increased phospholipase C activity. Although marked release of [3H] from labeled islets occurred in the presence of 5 mM inositol, the decreases in radioactive inositol lipid and insulin release induced by glucose were not changed. These data suggest that the fall-off in the second phase of insulin release from fetal islets may be partly due to blunted phosphoinositide hydrolysis.

Animals↗
PubMed1994

Synergistic insulin release induced by glucose and carbachol is not associated with an increase in cytoplasmic free calcium levels.

Synergistic insulin release is observed in combination with muscarinic agonist and glucose. In order to define the role of changes in the cytoplasmic free Ca2+ level ([Ca2+]i), the effect of combination with carbachol and glucose on both phosphoinositide breakdown in rat pancreatic islets and [Ca2+]i dynamics in single fura 2-loaded B-cells was investigated. When the islets were prelabeled with myo-[2-3H]inositol, phosphoinositide breakdown was obtained and inositol trisphosphate levels were increased in the presence of carbachol (0.5 mM). Inositol trisphosphate levels induced by carbachol were further increased by co-stimulation with 16.7 mM glucose. [Ca2+]i in single-B-cells was increased by 16.7 mM glucose. A prompt, transient rise in [Ca2+]i was induced by carbachol. However, carbachol failed to augment the [Ca2+]i response in the presence of 16.7 mM glucose. These data suggest that a synergistic release of insulin occurs without an amplification of [Ca2+]i regardless of an increase in inositol trisphosphate.

Animals↗