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Biomedical subjects

Y Hirose

Publications and source records attributed to Y Hirose.

At least 307 records · Page 17Linked to original sources
PubMed1986

Thyrotropin-releasing hormone and insulin in chemically induced pancreatic islet cell tumors in rats.

Thyrotropin-releasing hormone (TRH) and insulin were measured by radioimmunoassay in acetic-acid extracts of 19 pancreatic islet cell tumors induced by streptozotocin and nicotinamide in rats. In addition, gel filtration properties of TRH-immunoreactivity and immunoreactive insulin (IRI) were examined in 5 and 14 tumors, respectively. TRH was demonstrated in 10 of 19 tumors, with a mean of 166 +/- 47 (SEM) pg/mg wet weight, whereas the concentration was less than 3 pg/mg wet weight in the other tumors. In contrast, all tumors contained IRI, with a mean of 11.0 +/- 1.6 micrograms/mg wet weight. Ten tumors in which TRH was demonstrated contained more IRI than those in which TRH was not detected (13.1 +/- 1.8 vs 6.5 +/- 1.7 micrograms/mg wet weight, P less than 0.02). After gel filtration, all TRH immunoreactivity was eluted at the same place as synthetic TRH in the 5 tumors. In addition, gel filtration elutes showed essentially the same pattern of IRI in the 14 tumors, with 3 peaks. The predominant IRI peak comigrated with marker insulin (95.7 +/- 0.8%), another prominent peak occurred coincident with proinsulin standard (3.3 +/- 0.5%), a third peak was present in the void volume (0.28 +/- 0.04%). These distributions of IRI were similar to those in extracts of normal pancreases. The present studies demonstrate TRH immunoreactivity in pancreatic islet cell tumors induced by streptozotocin and nicotinamide in rats. Chemically induced insulinomas can serve as a model for insulin storage which is analogous to islet B cells.

Adenoma, Islet Cell↗
PubMed1986

Serum monoclonal IgM undetectable by cellulose acetate membrane electrophoresis in four patients with B cell malignant lymphoma.

A small amount of monoclonal IgM was demonstrated in the serum of four B cell malignant lymphoma patients in whom electrophoretically homogeneous protein bands were not detected by either cellulose acetate membrane electrophoresis or immunoelectrophoresis. By using anti-idiotypic (Id) antisera prepared against serum IgM, the M proteins were detected and identified as the products of malignant cells. These findings suggest that the use of more sensitive technics than the usual serum electrophoresis shows that the incidence of M proteins in B cell malignant lymphomas is higher than has been previously reported.

Adult↗
PubMed1986

Reversible down-regulation of liver cyclo(His-Pro) binding sites by cyclo(His-Pro) administration to mice.

Intraperitoneal injections of histidyl-proline diketopiperazine [cyclo(His-Pro), 15 mg/kg/day] to mice for 3 days caused a significant loss of cyclo(His-Pro) binding sites in the liver. This loss depended on the decrease in the number of binding sites and not on the change in affinity. The cyclo(His-Pro)-mediated loss was reversible, and the specific binding returned to the original level within 3 days of the cessation of cyclo(His-Pro). These results suggest that cyclo(His-Pro) participates in regulating its own binding sites in the liver.

Animals↗
PubMed1985

Properties of histidyl-proline diketopiperazine [cyclo(His-Pro)] binding sites in rat liver.

Characteristics of cyclo(His-Pro) binding sites in the rat liver were studied using 3H-labeled cyclo(His-Pro). Scatchard analysis suggested that the rat liver membrane had a single binding site with an apparent dissociation constant (Kd) of 7 X 10(-8) M. Pretreatment of membrane preparations with soybean trypsin inhibitor increased cyclo(His-Pro) binding, and the binding activity was sensitive to trypsin and phospholipase A digestion, suggesting that protein and phospholipid moieties are essential for cyclo(His-Pro) binding. Thiol reagents reduced binding activity, suggesting that the thiol group might be an important constituent of the cyclo(His-Pro) binding site. Cross-reactivities of TRH, TRH analogues, L-His and L-Pro were very low (0.2-9%). These findings indicate that specific binding sites for cyclo(His-Pro) in the rat liver have similar properties to the receptors for other polypeptides.

Animals↗
PubMed1985

Involvement of thyrotropin-releasing hormone (TRH) neural system of the brain in pentylenetetrazol-induced seizures.

In order to study the relationship between pentylenetetrazol (PTZ)-induced seizures and the thyrotropin-releasing hormone (TRH) neural system, immunoreactive TRH (IR-TRH) and TRH receptor binding activity were determined in discrete regions of the rat brain before as well as 40 s (immediately before seizures), 150 s (during seizures) and 24 h after an intraperitoneal injection of PTZ (75 mg/kg). IR-TRH markedly increased in the septum 40 and 150 s after the injection, and also in the hippocampus and the thalamus-midbrain region 40 and 150 s after the injection, respectively. However, no significant changes were observed in the TRH receptor binding before, during or after the seizures, suggesting that the increased IR-TRH was not released into the synaptic cleft. This speculation was supported by the dose-dependent inhibition of PTZ-induced generalized seizures by the pre-treatment with TRH or its analogue DN-1417 into the cerebral ventricle.

Animals↗
PubMed1985

Monoclonal gammopathies in Japanese patients with Sjögren's syndrome.

We report 10 Japanese patients with Sjögren's syndrome (SS) who developed monoclonal gammopathies (MG). One was of the IgG class, five of IgA, three of IgM, and one of IgG/IgM. The monoclonality of 7 of 10 M proteins was studied using antiidiotypic (Id) antibodies against M proteins. Four (three IgA and one IgM) of 10 M proteins had rheumatoid factor (RF) activity. Hemagglutination inhibition tests and enzyme-linked immunosorbent assays (ELISA) showed that the RF activity was inhibited by anti-Id antibodies in all four monoclonal RFs. In two patients examined, many cells infiltrating into the salivary glands were stained with anti-Id antibodies. Our review of 19 Japanese SS patients with MG revealed that the non-IgM class predominated (13/19). This contrasts with 19 reported non-Japanese SS patients, among whom 14 were IgM. In both Japanese and non-Japanese patients there was a higher incidence of MG in primary than in secondary SS. The difference in the dominant heavy-chain class may reflect a difference in the genetic factors affecting B cell differentiation in immunologically disordered states.

Adult↗
PubMed1985

Effects of ketamine on the dynorphin levels and the ethylketocyclazocine (EKC) receptor binding in discrete regions of rat brains.

Intraperitoneal (ip) injection of ketamine increased the concentration of dynorphin in the cortex of rat brain, while decreased it in the septal area. The affinity of ethylketocyclazocine (EKC) receptor binding was decreased in the cortex, but increased in the septal area after pretreating the rats with ketamine. This suggests that the dynorphin neuronal system is stimulated in the cortex and suppressed in the septal area by ketamine. In other 5 brain areas, ketamine had no effect on neither dynorphin concentration nor EKC receptor binding. As dynorphin was reported to produce seizure and spike discharge in the cortex while suppressed the hippocampal EEG of rat brain, it is likely that the dynorphin neuronal system may play at least a part in ketamine induced electrophysiological changes in the brain.

Animals↗
PubMed1985

Up-regulation of thyrotropin-releasing hormone (TRH) receptors in rat spinal cord after codepletion of serotonin and TRH.

Immunohistochemical evidence indicates the coexistence of serotonin and TRH in many raphe neurons. We examined the biochemical changes in TRH receptors after destruction of the serotonergic pathways by 5,7-dihydroxytryptamine (5,7-DHT). 2 weeks after an intracerebroventricular injection of 5,7-DHT, rats were killed, and specific brain regions were dissected on ice. Serotonin levels in the CNS of lesioned rats was reduced by 50-85% in all regions, with the highest reduction in the spinal cord and hippocampus. Immunoreactive TRH was reduced in the spinal cord by 70%, but other brain regions contained normal levels of TRH. TRH receptor binding was increased by 40% in the spinal cord of lesioned rats, but appeared unchanged in rostral brain regions in which no decrease in TRH content was detected. Scatchard plots of TRH receptor binding in the spinal cord indicated that the increased binding after 5,7-DHT administration reflected an increased receptor number. These findings suggest that biochemical up-regulation of TRH receptors occurs in the spinal cord following depletion of TRH.

5,7-Dihydroxytryptamine↗
PubMed1985

Effects of tris(hydroxymethyl)aminomethane on biosynthesis and release of insulin in the pancreatic Langerhans islets.

Tris(hydroxymethyl)aminomethane (Tris) has been shown to inhibit selectively the Golgi apparatus and Golgi-endoplasmic reticulum-lysosomal system (GERL system) of several kinds of cells including pancreatic B cells. This study was designed to assess the effect of Tris on insulin, glucagon and somatostatin release and insulin synthesis in pancreatic B cells by using isolated rat pancreatic islets. Tris suppressed glucose-induced insulin release, whereas it did not affect the glucagon and somatostatin release. Furthermore, the incorporation of [3H]leucine into the insulin fraction was suppressed by 10 mM Tris, but the sum of the radioactivity of both proinsulin and insulin fraction were not influenced. The present study suggests that the Golgi apparatus and GERL system may play a role in insulin secretion and biosynthesis in pancreatic B cells.

Animals↗
PubMed1985

Effects of calcium hopantenate on neurotransmitter receptors in the rat brain.

Effects of calcium hopantenate (HOPA) on neurotransmitter and neuropeptide receptors in the central nervous system (CNS) were investigated. In the radioreceptor assay (RRA), HOPA inhibited the [3H]-gamma-aminobutylic acid (GABA) receptor binding in a dose-dependent manner with a cross-reactive potency of 0.2%. On the other hand, radiolabeled ligand binding to CNS receptors in the benzodiazepine (BDZ)-, muscarinic cholinergic (mACh)-, methionine-enkephalin (ENK)- and thyrotropin releasing hormone (TRH)-RRA systems was not inhibited even by the addition of HOPA up to 100 microM. Repeated injection of HOPA (250 mg/kg/day for 7 consecutive days) increased GABA receptor binding by 53% in the cerebral cortex, while GABA binding in the rest of the forebrain did not change. The increased GABA receptor binding in the cerebral cortex of HOPA treated rats was due to the increased affinity of the binding sites. BDZ-, mACh-, ENK- and TRH-receptor bindings were not affected in either the cerebral cortex or the rest of the forebrain by repeated injection of HOPA. These results suggest that at least a part of the therapeutic efficacy of HOPA is due to sensitization of the GABA receptor in the cerebral cortex.

Animals↗
PubMed1985

Effects of pentazocine and concomitant clonidine on opioid receptors in the rat brain.

The changes in opioid receptors (Op-R) caused by repeated administration of pentazocine and the effect of concomitant clonidine were investigated. Binding of [3H] naloxone was markedly decreased in the absence of Na+, but was increased in the presence of Na+ in the diencephalon-mesencephalon of chronic pentazocine-treated rats. No significant changes were observed in the cerebral cortex of pentazocine-treated rats. The pentazocine-induced changes in Op-R were abolished by the concurrent use of clonidine, an alpha-adrenergic agonist, which has been shown to relieve the withdrawal symptoms of morphine. This result indicated that the behavioral action of clonidine can also be observed at the Op-R level.

Animals↗
PubMed1985

B cell malignant lymphoma in a patient with progressive systemic sclerosis and Sjögren's syndrome. Report of a case and review of the literature.

We report a patient with progressive systemic sclerosis (PSS) and Sjogren's syndrome (SS) who developed B cell malignant lymphoma 11 and 10 years after the onset of signs of PSS and SS, respectively. As her lymphoma developed, autoantibodies such as rheumatoid factor and antinuclear antibody disappeared from the serum, the lupus erythematosus test yielded negative results and her immunoglobulin levels declined. A good response to chemotherapy was obtained but she died of acute interstitial pneumonitis. Postmortem examination revealed marked diffuse interstitial fibrosis of the lungs.

B-Lymphocytes↗
PubMed1985

A simple quantitative bradykinesia test in MPTP-treated mice.

A neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which produces pathological changes similar to human idiopathic Parkinson's disease in animals, was injected in mice for biochemical and pharmacological studies. The dopamine concentration showed a marked decrease (-75%) in the striatum 1-2 weeks after the injection of MPTP (30 mg/kg i.p. twice a day for 5 days; a total dose, 300 mg/kg) but no changes or only slight decreases in other brain regions. The norepinephrine concentration also decreased to half the preadministration level in the striatum. These changes closely resembled those observed in the brain of parkinsonian patients. An examination for evaluating bradykinesia of MPTP-treated mice (pole test) devised by the author revealed that bradykinesia was alleviated dose-dependently by injection of L-DOPA. These results suggested that MPTP-treated mice are a useful experimental model for the study of parkinsonism, and that the pole test using these animals is of value in the screening of anti-parkinsonian agents.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

Effects of bencyclane on concussion following head injury in mice.

Bencyclane showed a dose-dependent anti-concussive effect with a duration of at least 60 minutes in an experimental model of concussion induced by head injury. This long-lasting effect cannot be explained only by the changes in the serum level of the agent or the increase in brain circulation due to its vasodilative action, both of which are of much shorter durations. Our findings suggest that bencyclane causes alterations in brain metabolism, which is partly responsible for reduction in the duration of the experimental concussion.

Animals↗