Biomedical subjects

T Nogimori

Publications and source records attributed to T Nogimori.

At least 37 records · Page 2Linked to original sources

PubMed1997

Effects of gamma-butyric acid on the release of thyrotropin-releasing hormone from the rat retina in vitro.

Effects of gamma-butyric acid (GABA) on the release of thyrotropin-releasing hormone (TRH) from the rat retina in vitro were studied. The rat retina was incubated in medium 199 (pH 7.4) with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid (medium). The amount of TRH release into the medium was measured by radioimmunoassay. The TRH release from the rat retina was inhibited significantly in a dose-related manner with the addition of GABA, but not with bicuculline. The inhibitory effect of GABA on TRH release from the retina was blocked by adding bicuculline to the medium. The findings suggest that the GABAergic system inhibits TRH release from the rat retina in vitro.

Animals↗

PubMed1997

DISTRIBUTION OF SOMATOSTATIN RECEPTOR TYPE 3 IN THE RAT: IMMUNOHISTOCHEMICAL STUDY.

Somatostatin receptor type 3 (SSTR-3) was identified immunohistochemically in the rat tissues using specific anti-SSTR-3 serum which was raised in New Zealand white rabbits immunized with a conjugate of synthetic SSTR-3 peptide (28-41) with bovine serum albumin. Immunohistochemical analysis was performed by avidin-biotin complex method. SSTR-3 immunoreactivity was visualized in the central nervous system, anterior pituitary, gastric and duodenal mucosa, Auerbach's and Meissner's nervous branch of gastrointestinal tract, adrenal medulla, testis and pancreas. Significant staining was detected in neural perikarya, axons and dendrites. When using antiserum preincubated with synthetic SSTR-3 peptide (28-41) or rat anterior pituitary homogenate which contains SSTR-3 peptide, no significant stain of the anterior pituitary or neurons in the hypothalamus was detected. These findings suggest that SSTR-3 is widely distributed and that this method is valuable in studying the distribution of SSTR-3 in rats.

Journal Article↗

PubMed1997

Organ distribution of iodide transporter (symporter) in the rat: immunohistochemical study.

Iodide transporter/symporter (NIS) was identified immunohistochemically in rat tissues using specific antipeptide serum. Anti-NIS serum was raised in New Zealand white rabbits immunized with a conjugate of synthetic NIS peptide (39-53) with bovine serum albumin. Immunohistochemical analysis was performed by avidine-biotin complex method. NIS immunoreactivity was visualized in the thyroid gland, gastric and small intestine mucosa, anterior pituitary, adrenal medulla, pancreatic islets, kidney, chorioid plexus and several brain and spinal cord nuclei. When using antiserum preincubated with synthetic NIS peptide (39-53) or rat thyroid homogenate containing NIS, no significant stain of the thyroid gland was detected. These findings suggest that NIS is widely distributed and that the method used is suitable for studying the distribution of NIS in rats.

Journal Article↗

PubMed1996

Effects of serotonin on the release of thyrotropin-releasing hormone from the rat retina in vitro.

Effects of serotonin on the release of thyrotropin-releasing hormone (TRH) from the rat retina were studied in vitro. The retina was incubated in medium 199 (pH 7.4) with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid (medium) for 20 min. The amount of TRH release into the medium was measured by radioimmunoassay. The TRH release from the rat retina was inhibited significantly in a dose-related manner with the addition of serotonin and enhanced with cyproheptadine. The inhibitory effect of serotonin on TRH release from the retina was blocked with the addition of cyproheptadine. The elution profile of methanol extract of the rat retina was identical to that of synthetic TRH. The findings suggest that the serotonergic system inhibits TRH release from the rat retina in vitro.

Animals↗

PubMed1996

Distribution of somatostatin receptor type 2 in the rat: immunohistochemical study.

Somatostatin receptor type 2 (SSTR-2) was identified immunohistochemically in the rat tissues using specific antipeptide antiserum raised in New Zealand white rabbits immunized with a conjugate of synthetic SSTR-2 peptide (31-41) with bovine serum albumin. Immunohistochemical analysis was performed by avidin-biotin complex method. SSTR-2 immunoreactivity was visualized in the central nervous system and anterior pituitary thus supporting previous investigations of SSTR-2 distribution using in vitro autoradiographic ligand binding. Significant stain was detected in neural perikarya, axons and dendrites as well as in many cells of retina, adrenal medulla, gastric and duodenal mucosa, Auerbach's nervous branch and Meíssner's nervous branch of the stomach, small intestine and colon. When using antiserum preincubated with synthetic SSTR-2 peptide (31- 41) or rat anterior pituitary homogenate which contains SSTR-2 peptide, no significant stain of the anterior pituitary or neurons in the hypothalamus was detected. These findings suggest that SSTR-2 is widely distributed and that the method used is valuable in studying the distribution of SSTR-2 in rats.

Journal Article↗

PubMed1996

Effect of anti-TRH-receptor antibody on corticosterone release from rat adrenal gland in vitro.

The effect of anti-thyrotropin-releasing hormone (TRH) receptor antibody on corticosterone release from the rat adrenal gland in vitro was studied. The adrenal glands were incubated in medium 199 with 1.0 mg/ml bacitracin (pH 7.4, medium) for 20 min and the release of corticosterone into the medium was measured by radioimmunoassay. TRH inhibited corticosterone release from the adrenal gland in a dose-related manner. The inhibitory effect of TRH on corticosterone release from the adrenal gland was prevented by the addition of anti-TRH-receptor antibody. The present findings suggest that TRH inhibits corticosterone release from the adrenal gland in vitro and its effect is mediated via TRH receptor.

Journal Article↗

PubMed1995

Distribution of thyrotropin releasing hormone receptor in rats: an immunohistochemical study.

Thyrotropin releasing hormone (TRH) receptor was identified immunohistochemically in the rat tissues using anti-peptide antiserum. Anti-TRH receptor antiserum was raised in New Zealand white rabbits immunized with a conjugate of synthetic TRH-receptor peptide (15-28) to bovine serum albumin. Immunohistochemical analysis was performed by the avidin-biotin complex method. TRH-receptor immunoreactivity was visualized in the central nervous system and anterior pituitary thus supporting previous investigations of TRH receptor distribution using in vitro autoradiographic ligand binding. Significant stain was detected in neural perikarya, axons and dendrites as well as in many cells of the retina, adrenal medulla, stomach mucosa, Auerbach's nervous branch and Mysner's nervous branch of the stomach, small intestine and colon. When using antiserum preincubated with synthetic TRH-receptor peptide (15-28) or rat anterior pituitary homogenate which contains TRH-receptor peptide, no significant stain of the anterior pituitary cells or neurons in the hypothalamus was detected. These findings suggest that TRH-receptor is widely distributed and that this method is valuable in studying the distribution of TRH-receptor in rats.

Journal Article↗

PubMed1995

Distribution of somatostatin receptor type 1 in the rat. An immunohistochemical study.

Somatostatin receptor type 1 (SSTR-1) was identified immunohistochemically in the rat tissues using anti-peptide antiserum. Anti-somatostatin receptor antiserum was raised in New Zealand white rabbits immunized with a conjugate of synthetic SSTR-1 peptide (41-52) with bovine serum albumin. Immunohistochemical analysis was performed by the ABC method. SSTR-1 immunoreactivity was visualized in the central nervous system, anterior pituitary, mucosa of stomach and duodenum, Auerbach's nervous branch and Mysner's nervous branch of gastrointestinal tract and pancreas. Significant staining was detected in neural perikarya, axon and dendrite. When using antiserum preincubated with synthetic SSTR-1 peptide (41-52) or rat anterior pituitary homogenated which contains SSTR-1, no significantly stained anterior pituitary cells or neurons in the hypothalamus were detected. These findings suggest that SSTR-1 is widely distributed and that this method is valuable in studying the distribution of somatostatin receptor in rats.

Journal Article↗

PubMed1994

Effects of hypophysectomy on TRH and its related peptides concentrations in various rat organs.

The effects of hypophysectomy on thyrotropin releasing hormone (TRH), TRH-glycine (TRH-Gly) and pre-pro-TRH (178-199) concentrations in the rat hypothalamus, cerebrum, cerebellum, brain stem, stomach and retina were studied 7 days after the operation. The hypophysectomized rats were administered a single i.p. injection of T4 (500 micrograms/kg), T3 (100 micrograms/kg) or bovine TSH (1.25 IU/kg), and 5 rats of each subgroup were decapitated at 4 hours later. After hypophysectomy, TRH-Gly and pre-pro-TRH (178-199) concentrations in the hypothalamus increased significantly and TRH concentrations decreased after hypophysectomy. After the injection of T4, T3, TRH or TSH TRH-Gly and pre-pro-TRH (178-199) concentration in the hypothalamus of hypophysectomized rats decreased significantly, while that of TRH significantly increased. No changes in TRH, TRH-Gly and pre-pro-TRH (178-199) concentration in other tissues were observed after hypophysectomy or hormone treatment. The findings suggest that hypophysectomy stimulated TRH synthesis and release in the hypothalamus, that TRH, TSH, T3 and T4 regulate hypothalamic TRH levels, and that pro-TRH synthesis in the tissues except the hypothalamus may not be regulated by thyroid hormone.

Animals↗

PubMed1993

Deregulated production of interleukin-4 (IL4) in autoimmune thyroid disease assayed with a new radioimmunoassay.

A sensitive, reproducible and specific radioimmunoassay for human interleukin-4 (IL4) has been developed. Using 125I-labeled IL4 and polyclonal rabbit antisera raised against recombinant human IL4, a competitive inhibition assay was developed which could detect 5 pg/ml of human IL4. Other interleukins, growth factors, hormones, peptides and lectins did not affect the assay. IL4 was measured in supernatants of culture media of stimulated human peripheral blood mononuclear cells (PBMC). Kinetics of IL4 production in PHA-stimulated PBMC from seven normal subjects revealed that the peak levels of IL4 were seen at 24 h and then declined. Peak IL4 levels in PHA stimulation of PBMC from untreated patients with autoimmune thyroid diseases (Graves' disease and chronic thyroiditis) were significantly higher than normal controls. However, after treatment, IL4 production decreased to normal. The present study demonstrates the usefulness of quantitating human IL4 produced by PBMC and that there exists a deregulated production of IL4 in autoimmune thyroid diseases.

Antibody Specificity↗

PubMed1993

In vivo stimulation of thyroid hormone release by rabbit antibodies with thyroid stimulating activity raised against the mutated receptor peptide TSH-R-HIS17.

The present study was designed to examine whether thyroid stimulating antibodies (TSAb) against the mutated or non-mutated peptide of human TSH receptor stimulates release of thyroid hormones in mice in vivo. We generated antibodies against mutated TSH receptor peptide TSH-R-HIS17 and non-mutated TSH receptor peptide TSH-R-ASP17 immunizing the peptides to rabbits. We isolated immunoglobulin G (IgG) from these antibodies and injected iv into male ddy mice. Control mice were injected iv with bTSH or TSAb-negative normal rabbit IgG. Serum T3 and T4 concentrations were elevated after the administration of bTSH in a dose-dependent manner. Serum T3 and T4 concentrations were significantly elevated after the injection of IgG from the rabbit antibodies with TSAb activity produced against TSH-R-HIS17. However serum T3 and T4 remained within normal levels after the injection of IgG from the rabbit antibodies without TSAb activity toward TSH-R-ASP17. The present data offer in vivo support of the IgG with TSAb activity interaction with the TSH receptor of the thyroid and raise the possibility that TSAb against mutated human TSH receptor peptide might be contributed to induce thyroid hyperfunction.

Amino Acid Sequence↗

PubMed1993

Effects of immunoneutralization of endogenous opioid peptides on the hypothalamic-pituitary-thyroid axis in rats.

Effects of opioid peptide antisera treatment on the secretion of thyrotropin (TSH) and thyrotropin-releasing hormone (TRH) in rats were studied. Anti-beta-endorphin antiserum, anti-methionine-enkephalin antiserum, or antidynorphin antiserum was injected intraperitoneally and the rats were serially decapitated. TRH levels in the hypothalamus along with plasma TRH, TSH and thyroid hormone levels were measured by individual radioimmunoassay. TRH contents in the hypothalamus decreased significantly after opioid peptide antisera treatment, while its plasma levels tended to decrease, but not significantly. Plasma TSH levels increased significantly after opioid peptide antisera injection. Plasma TRH and TSH level responses to cold as well as plasma TSH level response to TRH were enhanced with treatment of antisera to these peptides. Plasma 3,3',5-triiodothyronine levels increased significantly after treatment of antisera to these peptides. From these findings it is concluded that the treatment of opioid peptide antisera stimulates TRH and TSH secretion in rats.

Animals↗

PubMed1993

Pituitary resistance to thyroid hormone associated with a base mutation in the hormone-binding domain of the human 3,5,3'-triiodothyronine receptor-beta.

Point mutations in the human T3 receptor-beta (TR beta) gene causing single amino acid substitutions have been identified in several different kindreds with generalized resistance to thyroid hormone. Until now, no study has been reported on the TR gene in cases of pituitary resistance (PRTH). In the present study, we analyzed the TR beta gene in a 30-yr-old Japanese female with PRTH. She exhibited clinical features of hyperthyroidism, elevated serum thyroid hormone levels accompanied by inappropriately increased secretion of TSH, mildly elevated basal metabolic rate, and increased urinary excretion of hydroxyproline. No pituitary tumor was detected. DNA fragments of exons 3-8 of the genomic TR beta gene were generated by the polymerase chain reaction and analyzed by a single stranded conformation polymorphism method. Exon 7 of the patient's TR beta gene showed an abnormal band, suggesting the existence of mutation(s). By subcloning and sequencing the DNA, a point mutation was identified in one allele at nucleotide 1297 (C to T), which altered the 333rd amino acid, arginine, to tryptophan. Neither of her apparently normal parents had any mutations of the TR beta gene. In vitro translation products of the mutant TR beta gene showed remarkably decreased T3-binding activity (Ka, 2.1 x 10(8) M-1; normal TR beta Ka, 1.1 x 10(10) M-1). Since the molecular defect detected in a patient with PRTH is similar to that seen in subjects with generalized resistance to thyroid hormone, both types of the syndrome may represent a continuous spectrum of the same etiological defect with variable tissue resistance to thyroid hormone.

Adult↗

PubMed1993

Deregulated production of interleukin-8 (IL-8) in autoimmune thyroid disease studied by newly developed IL-8 radioimmunoassay.

We have developed a sensitive, reproducible and specific radioimmunoassay for human interleukin-8 (IL-8). Using 125I-labelled IL-8 and polyclonal rabbit antisera raised against recombinant human IL-8, a competitive inhibition assay was developed which could detect 5 pg/ml of human IL-8. Other interleukins, growth factors, hormones, peptides and lectins did not affect the assay. IL-8 measured in supernatants of culture media of stimulated human peripheral blood mononuclear cells (PBMC). Kinetics of IL-8 production in SAC-stimulated PBMC from seven normal subjects revealed that the production of IL-8 was detectable within 12 h and reached a plateau at 24 h. IL-8 levels in SAC-stimulation of PBMC from untreated patients with autoimmune thyroid diseases (Graves' disease and chronic thyroiditis) were significantly higher than in normal controls. However, after treatment, IL-8 production decreased to normal. The present study demonstrates the usefulness of quantitating human IL-8 produced by PBMC and the presence of a deregulated production of IL-8 in autoimmune thyroid diseases.

Antibody Specificity↗

PubMed1993

Effects of dexamethasone on TRH, TRH-glycine and pre-pro-TRH (178-199) levels in various rat organs.

The effect of dexamethasone administration on the concentration of thyrotropin releasing hormone (TRH) and pre-pro-TRH connecting peptides TRH-glycine (TRH-Gly), and pre-pro-TRH (178-199) in various rat organs was studied. Three groups of 35 rats each were injected dexamethasone (Group A: 25 micrograms/100 g; Group B: 500 micrograms/100 g) or saline (Group C: control). The subgroups of 7 rats each were decapitated at 1, 2, 3, 4 and 24 h after the injection and the levels of TRH-Gly, pre-pro-TRH (178-199) and TRH in the hypothalamus, cerebrum, cerebellum and brain stem, stomach, retina were estimated by specific radioimmunoassays. The level of TRH-Gly and pre-pro-TRH (178-199) in the hypothalamus decreased significantly in groups A and B at 1-4 hours after the injection, and then returned to pretreatment levels at 24 h after the injection. In contrast, TRH levels in the hypothalamus increased significantly in groups A and B at 1-4 h after the injection. The TRH-Gly, pre-pro-TRH (178-199) and TRH levels in other organs showed no changes after dexamethasone injection. From these findings it is concluded that dexamethasone inhibits the synthesis and secretion of TRH and the maturation of pro-TRH in the hypothalamus, while its effects on other organs is different from the hypothalamus.

Animals↗

PubMed1993

Production of bioactive rabbit antibodies against the mutated receptor peptide TSH-R-HIS17 and detection of hypertriiodothyroninemia in the rabbit.

We produced rabbit antibodies against mutated thyrotropin (TSH) receptor peptide TSH-R-HIS17 in comparison with non-mutated TSH receptor peptide TSH-R-ASP17. All the antibodies raised against TSH-R-HIS17 showed thyroid stimulating antibody (TSAb), thyroid stimulation blocking antibody (TSBAb) and/or TSH binding inhibiting immunoglobulin (TBII) activities and also those serum T3 levels were all in thyrotoxic levels associated with TSAb activities. However, all the antibodies raised against TSH-R-ASP17 had no activities of TSAb, TSBAb and/or TBII and those serum T3 levels were all within normal range. The data suggest that the mutation in the TSH receptor gene may have a possible relevance for the pathogenesis of Graves' disease.

Amino Acid Sequence↗

PubMed1992

Effects of acetylcholine on the release of thyrotropin-releasing hormone from the rat retina in vitro.

Effects of acetylcholine on the release of thyrotropin-releasing hormone (TRH) from the rat retina were studied in vitro. The retina was incubated in medium 199 (pH 7.4) with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid (medium) for 20 min. The amount of TRH release into the medium was measured by radioimmunoassay. The TRH release from the rat retina was enhanced significantly in a dose-related manner with the addition of acetylcholine and inhibited with addition of atropine. The stimulatory effect of acetylcholine on TRH release from the retina was blocked with the addition of atropine. The elution profile of methanol-extract of the rat retina was identical to that of synthetic TRH. The findings suggest that the cholinergic system stimulates TRH release from the rat stomach in vitro.

Acetylcholine↗

PubMed1992

Effects of dopamine on the release of thyrotropin-releasing hormone from the rat retina in vitro.

The effects of dopamine on the release of thyrotropin-releasing hormone (TRH) from the rat retina in vitro were studied. The rat retina was incubated in the medium 199 (pH 7.4) with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid. The amount of TRH release into the medium was measured by radioimmunoassay. The TRH release from the rat retina was inhibited significantly in a dose-related manner with the addition of dopamine, but not with pimozide. The inhibitory effects of dopamine on TRH release from the rat retina were blocked with an addition of pimozide to the medium. The elution profile of methanol-extracted rat retina on sephadex G-10 was identical to that of synthetic TRH. From these findings it is concluded that the dopaminergic system inhibits TRH release from the rat retina in vitro.

Analysis of Variance↗