Biomedical subjects

K Chihara

Publications and source records attributed to K Chihara.

At least 253 records · Page 14Linked to original sources

PubMed1992

Apparent cleavage of the retinal nerve fiber layer in asymptomatic eyes with high myopia.

The appearance of the retinal nerve fiber layer was studied in one eye of 203 normal Asians (59 with high myopia greater than or equal to -5 D, and 144 with emmetropia or hyperopia). "Cleavage" of the retinal nerve fiber layer was observed in 3 of these 59 highly myopic eyes, but there was no significant damage to either the retinal pigment epithelium or the choroid. In contrast, no cleavage was observed in the other 144 emmetropic or hyperopic eyes. High myopia (P = 0.0237, Fisher's exact test) was a significant risk factor for "cleavage" development in the retinal nerve fiber layer. The occurrence of a defect (nerve fiber loss) in the retinal nerve fiber layer in severe myopia (5/59, 8%) was also greater than that in either emmetropia or hyperopia (2/144, 1%; P = 0.0229). These results indicate that subtle changes can occur in the appearance of the retinal nerve fiber layer of the eye in some patients with asymptomatic myopia.

Adult↗

PubMed1992

The expression of parathyroid hormone-related protein (PTHrP) in normal parathyroid: histochemistry and in situ hybridization.

The expression and localization of parathyroid hormone-related protein (PTHrP), a major factor responsible for humoral hypercalcemia of malignancy (HHM), was investigated in 14 cases of surgically resected normal parathyroid glands. For light microscopic immunohistochemistry, formalin-fixed and paraffin-embedded specimens were stained with avidin-biotin-peroxidase complex (ABC) using the anti-PTHrP monoclonal antibody (MoAb), 4B3. Four percent paraformaldehyde (PFA)-fixed and OCT compound-embedded specimens were used for pre-embedded immunoelectron microscopy. For in situ hybridization, 4% PFA-fixed, frozen sections were studied using a bromodeoxyuridine (BrdU)-labeled PTHrP cDNA probe. Immunohistochemically, 12 of the 14 cases were positive for PTHrP, which was observed mainly in the oxyphil and transitional oxyphil cells. The chief and clear cells, on the other hand, were faintly positive. Electron microscopically, secretory granules positive for PTHrP were observed in cells containing abundant mitochondria. Consistent with the PTHrP immunoreactivity, transcripts of PTHrP were observed also in the oxyphilic cells by in situ hybridization. Thus the production and secretion of PTHrP was shown by the oxyphil cell lineage in the normal parathyroid glands.

Histocytochemistry↗

PubMed1992

Acute changes in growth hormone-releasing hormone secretion after injection of BIM 23014, a long acting somatostatin analog, in rams.

BIM 23014 is a somatostatin analog displaying an increased biological half life due to resistance to enzymatic degradation. This peptide inhibits GH release directly at the level of pituitary somatotrophs. In addition, an action of BIM 23014 at the level of the hypothalamus is possible since somatostatinergic fibers and receptors have been identified on GH-RH neurons. To evaluate the effect of BIM 23014 on GH-RH secretion, hypophysial portal blood (HPB) was continuously collected in conscious sheep. Twelve rams (40-45 kg, 9-month-old) with chronically implanted perihypophysial cannulae were i.v. injected with BIM 23014 (1 mg) or saline. HPB and jugular blood were collected for 3-5 hours before and after the injection for the determinations of GH-RH and GH concentrations respectively. The acute injection of BIM 23014 induced a rapid decrease of plasma GH within the first two hours. Simultaneously, GH-RH in HPB decreased significantly. After reaching a nadir, GH concentrations increased to values greater than baseline. A similar rebound in GH-RH levels in HPB was also observed. These data indicate that BIM 23014 acts at the level of GH-RH hypothalamic neurons, in addition to its well-know effect on the pituitary gland.

Animals↗

PubMed1992

Repeated administration of antidepressant drugs reduces regional somatostatin concentrations in rat brain.

A possible role for somatostatin in affective disorders is suggested by its low concentration in cerebrospinal fluid of patients with depression. Therefore, we studied the regional effects of antidepressant drugs and antimanic agents on somatostatin concentrations in rat brain. Repeated, but not acute, administration of clomipramine, a specific serotonin uptake inhibitor, caused a highly significant, widespread reduction in somatostatin levels. Somatostatin content was similarly reduced in the hypothalamus, and midbrain and thalamus following repeated administration of zimelidine, another specific serotonin uptake inhibitor. Repeated administration of either imipramine, maprotiline, mianserin, carbamazepine or zotepine were without effect on somatostatin levels. These results suggest that somatostatin in the brain might be involved in therapeutic effects of some of antidepressant drugs.

Animals↗

PubMed1992

[Two cases of pericardial diverticulum].

Two cases of resection of pericardial diverticulum are reported. The lesion was located in the right upper mediastinum in case 1 (66-year-old woman) and at the right anterior cardio-phrenic angle in case 2 (20-year-old woman). In case 1, the shape of the lesion varied on fluoroscopic observation when the position of the patient was changed, and in case 2, ICG instilled into the lesion operation diffused into the pericardial cavity. These procedures seemed to be useful in the diagnosis of pericardial diverticulum, differentiating it from pericardial cyst.

Adult↗

PubMed1991

Neuropeptide regulation of feeding in dogs.

Norepinephrine and four families of neuropeptides, namely, neuropeptide Y (NPY), opioid peptides, galanin, and growth hormone-releasing factor (GRH), have been shown to stimulate feeding after central administration. Because these studies were mainly done on laboratory rats, the present study was designed to ascertain the central stimulators of feeding in dogs. We have shown that porcine and human pancreatic polypeptides (PPs), when administered into the third cerebral ventricle (intracerebroventricularly), increased food and water intake of satiated animals but that the COOH-terminal fragments [hPP-(18-36) and hPP-(23-36)] did not do so at the same molar dose (11.9 nmol). The kappa-opioid receptor agonist dynorphin (A-(1-17) also stimulated food and water intake, whereas alpha-neoendorphin and Met-enkephalin did not. These results suggest the structural specificity of PPs and dynorphin peptides for stimulating feeding. Surprisingly, neither intracerebroventricular injections of NPY and peptide YY nor intracerebroventricular pretreatment with anti-hNPY gamma-globulin modulated feeding, stressing the species differences in the feeding response to exogenous substances and the underlying physiology. Intracerebroventricular injections of norepinephrine, GRH, galanin, and pancreastatin also failed to increase food intake, although most substances tended to or did increase water intake. These results suggest that neuropeptides play a role in a species-specific way in modulating appetite regulation.

Animals↗

PubMed1991

Intranasal administration of His-D-Trp-Ala-Trp-D-Phe-LysNH2 (growth hormone releasing peptide) increased plasma growth hormone and insulin-like growth factor-I levels in normal men.

The effects of intranasal and iv administration of His-D-Trp-Ala-Trp-D-Phe-LysNH2 (GHRP) on plasma GH, PRL, LH, FSH, TSH, cortisol, insulin, IGF-I as well as GHRH-like immunoreactivity (LI) levels were examined in 6 healthy male subjects. An iv bolus injection of GHRP(1 micrograms/kg BW) caused a remarkable increase in plasma GH levels with a mean (+/- SE) peak of 54.9 +/- 4.2-micrograms/L. In addition an intranasal administration of GHRP resulted in a significant, dose-related increase in plasma GH with peaks of 39.6 +/- 15.3 micrograms/L at a dose of 30 micrograms/kg BW, 14.1 +/- 5.0 micrograms/L at 15 micrograms/kg BW and 7.5 +/- 5.7 micrograms/L at 5 microgram/kg BW. Plasma PRL and cortisol levels were slightly but significantly increased after iv administration of GHRP, whereas GHRP totally failed to affect plasma TSH, LH, FSH, insulin, blood sugar and GHRH-LI levels. Seven consecutive, intranasal administrations of 15 micrograms/kg BW GHRP every 8h were well tolerated in all subjects examined. During this treatment, GH responsiveness to GHRP was not attenuated by desensitization and plasma IGF-I was increased from 94.5 +/- 5.8 micrograms/L before GHRP to 125.8 +/- 6.0 micrograms/L after repeated GHRP administration. These findings indicate that intranasal administration of GHRP stimulates GH secretion and consequently enhances IGF-I production in normal subjects. If GHRP is demonstrated to be beneficial in the treatment of some patients with GH deficiency, the intranasal route of administration may be more useful than the painful injection because a prolonged period is required for the treatment.

Administration, Intranasal↗

PubMed1991

Suckling stimulates the expression of vasoactive intestinal polypeptide gene in rats.

The effect of suckling on vasoactive intestinal polypeptide (VIP) gene expression in the hypothalami was studied during the postpartum period in rats. Female rats were divided into two groups immediately after delivery. In one group, a mother was housed with 8 pups, and in the other, without any pups. The former group was named S(+) and the latter S(-). On days 0, 3, 6, 9 and 12 after delivery, the mothers were killed by decapitation. Hypothalamic VIP mRNA was measured by RNA dot hybridization. Although the VIP mRNA level showed no significant change after delivery in the S(-) group, VIP mRNA in the S(+) group on days 6, 9 and 12 increased to 1.6, 3.5 and 2.1 times higher than the level observed on day 0, respectively. These results suggest that suckling induces the synthesis of VIP after 6 postpartum days.

Actins↗

PubMed1991

[The role of surgeon in treatment of chronic respiratory failure after pulmonary tuberculosis operations].

We analyzed pulmonary functions and rib cage-phrenic motions on 296 cases of chronic empyema patients who had surgical treatment. Pulmonary functions were better preserved in patients with a single step than in those with multi-step operations, and in those who had more than five operations the impairment was inevitable. Both %VC and rib cage-phrenic motions improved by decortication, and by air-plombage, but in those who developed multi-rib fractures after the latter procedure, ipsilateral chest wall motion almost disappeared. Since some restriction of rib cage-phrenic motion is inevitable after the surgery, we have developed a cuirass respirator which can synchronize with the respiration to assist the movement of the chest wall. The results attained so far are satisfactory.

Aged↗

PubMed1991

[Preservation and improvement of chest wall function].

Anterolateral multiple rib fractures near xiphoid process impaired mechanical linkage which resists distortion between pulmonary (upper) and abdominal (lower) rib cage resulting in flail chest. Repair of fractured ribs with ceramic pins improved phase shift between the diaphragm and the rib cage and the amplitude of the injured rib cage motion, and decreased rib cage distortion. Asymmetrical motion of lower rib and upper abdomen which suggested impairment of the diaphragm action on the abdominal rib cage was found in three patients whose emphysematous bullae were located in the middle and lower lung fields, and disappeared after bullectomy. To control the pressure in the pleural cavity after pneumonectomy from excessive negative pressure to atmospheric pressure with SF6 improved pulmonary function. Chest wall function can be preserved on the basis of functional anatomy and physiology of the chest wall.

Humans↗

PubMed1990

Immunohistochemical evidence for synaptic connections between neuropeptide Y-containing axons and periventricular somatostatin neurons in the anterior hypothalamus in rats.

By employing a pre-embedding double immunolabeling technique, we examined light and electron microscopically synaptic associations between neuropeptide Y (NPY)-containing axons and somatostatin (SRIH)-containing neurons in the anterior periventricular area (APV) of the rat hypothalamus. For light microscopy, the immunoreactions for NPY and SRIH were visualized with silver-gold and diaminobenzidine (DAB), respectively, and the reverse labeling was used for electron microscopy. Light microscopy disclosed many brown SRIH perikarya surrounded by several black beads of NPY fibers in the APV. In electron microscopy, immunoreactive SRIH neurons revealed silver-gold particles scattered throughout the cytoplasm and accumulated in the Golgi area and the secretory granules. SRIH perikarya and dendritic processes indicated synaptic associations with DAB-labeled NPY fiber terminals and immunonegative fibers. NPY presynaptic terminals possessed numerous small clear vesicles and a few dense core vesicles; vesicular membranes and cores were labeled with DAB chromogen. Both the pre- and postsynaptic membranes were thickened equally to be a symmetric synapse. These findings suggest that NPY neurons are involved in the regulation of growth hormone secretion from the pituitary by affecting periventricular SRIH neurons.

Animals↗

PubMed1990

Vasopressin-deficient paraventricular magnocellular neurons of homozygous Brattleboro rats synthesize neuropeptide Y.

Immunohistochemical study was carried out to determine whether neuropeptide Y (NPY), which was only found in certain experimental procedures in arginine vasopressin (AVP)-containing neurons of the magnocellular paraventricular nucleus, might also be synthesized in AVP-deficient homozygous Brattleboro (BB) rats. After an intraventricular colchicine administration, NPY was found in many AVP-deficient non-oxytocinergic magnocellular neurons of the paraventricular and supraoptic nuclei in BB rats, but not in suprachiasmatic nucleus neurons. The results suggest that the NPY synthesis is a phenotype of magnocellular non-oxytocinergic neurosecretory neurons and occurs independently from the synthesis of AVP.

Animals↗

PubMed1990

Morphological evidence for neuronal regulation of luteinizing hormone-releasing hormone-containing neurons by neuropeptide Y in the rat septo-preoptic area.

Using a preembedding double immunolabeling technique, synaptic contacts were found between luteinizing hormone-releasing hormone (LHRH)-containing neurons and neuropeptide Y-containing axonal fibers in the rat septo-preoptic area. In demonstrating LHRH neurons, we used mainly an antiserum generated against rat gonadotrophic hormone-releasing hormone-associated peptide. Although many diaminobenzidine-labeled neuropeptide Y-containing fibers were seen around silver-gold-labeled LHRH cell bodies, synapses with synaptic membrane specialization were scarce. The fiber terminals usually contained many small clear vesicles and some large cored vesicles. The synapses were characterized with the presynaptic accumulation of the small clear vesicles and symmetric thickenings of the synaptic membranes.

Animals↗

PubMed1990

Brain neuropeptide Y in the control of adrenocorticotropic hormone secretion in the dog.

An immunoneutralization technique with specific antibodies was used to explore the role of endogenous neuropeptide Y (NPY) in the adrenocorticotropic hormone (ACTH) release after hypoglycemic stress in the dog. Dogs received injections of rabbit antihuman NPY gamma-globulin (anti-NPY) or normal gamma-globulin (NGG) into the third cerebral ventricle, which was followed by i.v. injection of insulin. Hypoglycemia of a 40% fall in systemic glucose levels occurred in anti-NPY-treated dogs as well as NGG-treated animals. An intraventricular administration of anti-NPY significantly inhibited the ACTH and cortisol release to hypoglycemia, but had no effect on the pancreatic polypeptide (PP) response. These findings suggest involvement by endogenous NPY in the ACTH secretion induced by hypoglycemia.

Adrenocorticotropic Hormone↗

PubMed1990

Intragranular co-storage of neuropeptide Y and arginine vasopressin in the paraventricular magnocellular neurons of the rat hypothalamus.

Certain populations of arginine vasopressin (AVP) neurons in the magnocellular paraventricular nucleus became immunoreactive for neuropeptide Y (NPY) when rats were treated with colchicine or monosodium glutamate (MSG). The co-storage of these peptides was examined by employing a post-embedding electron-microscopic immunohistochemistry technique using gold-labeled antibodies to the two peptides. In colchicine-treated rats, the neuronal perikarya contained numerous secretory granules showing co-storage of the two peptides. The cells of the MSG-treated rats were characterized by having well-developed Golgi bodies with the granular structures also co-storing the two peptides, although the secretory granules in the perikarya were rather fewer than in the colchicine-treated rats. It is concluded that the destruction of the arcuate nucleus by MSG-treatment may potentiate the synthesis of NPY in AVP neurons, the synthesis of which is latent in intact animals.

Animals↗

PubMed1990

Galanin stimulates immunoreactive growth hormone-releasing factor secretion from rat hypothalamic slices perifused in vitro.

The effect of galanin (GAL) on the release of GH-releasing factor (GRF) and somatostatin (SRIF) was examined in an in vitro perifusion system of rat hypothalamic slices. GAL at doses of 10(-7) and 10(-6)M stimulated the release of immunoreactive GRF while it failed to affect SRIF release. Therefore, in vivo stimulation of GH release by GAL may be explained in part by the GRF-releasing effect of this peptide.

Animals↗

PubMed1990

Effect of haloperidol on immunoreactive neuropeptide Y in rat cerebral cortex and basal ganglia.

To clarify the dopaminergic regulation of neuropeptide Y (NPY) neurons, the effect of haloperidol on NPY in basal ganglia and the cerebral cortex of the rat brain was investigated by sensitive radioimmunoassay and immunocytochemistry using antiserum against rat NPY. After repeated intraperitoneal injections of haloperidol (5 mg/kg) for 6 days, the content of immunoreactive NPY was significantly decreased in the caudate-putamen, but significantly increased in the lateral prefrontal cortex. After treatment for 21 days, the content of immunoreactive NPY in the caudate-putamen remained significantly low, but the extent of change in the lateral prefrontal cortex diminished. In the medial prefrontal cortex, piriform cortex, parietal cortex and nucleus accumbens, no significant changes were found after treatment for either 6 or 21 days. These findings were compatible with those obtained by immunocytochemistry using the same antiserum: an increase of immunoreactive fibers and terminals in the lateral prefrontal cortex and their decrease in the caudate-putamen. However, in the nucleus accumbens the density of immunoreactive fibers and terminals was decreased in the rostral portion, but not in the caudal portion after haloperidol treatment for 6 and 21 days. These findings suggest that dopaminergic afferents region-specifically regulate dopamine-sensitive NPY neurons in the rat brain.

Animals↗

PubMed1990

Calcitonin gene-related peptide and induction of hyperglycemia in conscious rats in vivo.

The effect of calcitonin gene-related peptide (CGRP) on glucose metabolism was investigated in conscious and unrestrained rats in vivo. Intravenous injection of rat CGRP (5.67 and 0.567 nmol/kg) caused a significant, dose-dependent increase in plasma glucose concentration and a simultaneous dose-dependent increase in plasma insulin level. In contrast, plasma glucagon level was not changed. On the other hand, intravenous infusion of CGRP (46.6 pmol.kg-1.min-1) decreased tolerance to intragastric administration of glucose (IGGTT). Plasma insulin response to IGGTT, however, was not affected by CGRP infusion. Moreover, although intravenous injection of CGRP (5.67 nmol/kg) elicited a significant increase in plasma epinephrine and norepinephrine concentrations, concomitant administration of epinephrine and norepinephrine, inducing a more prominent rise in plasma catecholamines than those induced by CGRP, affected neither plasma glucose nor insulin levels. Finally, plasma insulin levels obtained by simulating CGRP-induced changes in plasma glucose or glucose plus catecholamine levels by infusion of glucose or glucose plus catecholamines were not different from those induced by CGRP injection. These results suggest that CGRP has a hyperglycemic action that is not mediated by sympathetic outflow in conscious rats, and inhibition of insulin secretion, if any, does not play a major role in this hyperglycemic action of CGRP. We have demonstrated specific CGRP receptors linked to adenylate cyclase activation in rat liver plasma membranes; this hyperglycemic effect of CGRP in vivo may be partly due to its direct action on the liver.

Animals↗