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Biomedical subjects

H Kodama

Publications and source records attributed to H Kodama.

At least 559 records · Page 31Linked to original sources

Cystathionine accumulation in various regions of brain of DL-propargylglycine-treated rats.

The contents of cystathionine and taurine, as well as cystathionine beta-synthase activity in various regions of the brains of normal and DL-propargylglycine-treated rats, were measured. The content of cystathionine in each region of brain increased gradually from 0.5 mg to 20 mg/200 g body weight in relation to the dose of DL-propargylglycine. Cystathionine was found to be unevenly distributed in brains of both normal and DL-propargylglycine-treated rats. On the other hand, the activity of cystathionine beta-synthase was evenly distributed in various regions of normal rat brain, and was unaltered following treatment of rats with DL-propargylglycine. The concentration of taurine was similarly unaffected by DL-propargylglycine injection.

Alkynes↗

Regional distribution of rat growth hormone releasing factor-like immunoreactivity in rat hypothalamus.

A heterologous RIA for rat GH-releasing factor (rGRF) was established using synthetic rGRF-(1-43)OH for both standard reference and radioiodination with the antiserum produced against human GRF-(1-44) NH2. The regional distribution of rGRF-like immunoreactivity (LI) in rat hypothalamus was examined according to the Palkovits microdissection method and compared with that of somatostatin (SRIF)-LI. Both rGRF- and SRIF-LI contents (mean +/- SE; nanograms per mg protein) were highest in the median eminence (rGRF, 32.28 +/- 11.42; SRIF, 109.9 +/- 19.2) and next most abundant in the arcuate nucleus (rGRF, 3.50 +/- 0.47; SRIF, 12.88 +/- 0.60). Only a small amount of rGRF-LI was found in the ventromedial (1.41 +/- 0.51) and dorsomedial (1.16 +/- 0.15) nuclei and the anterior hypothalamic area (1.29 +/- 0.42), whereas rGRF-LI was not detected in the other nuclei of the hypothalamus. A considerable amount of SRIF-LI was contained in the periventricular, ventromedial, and paraventricular nuclei and the anterior hypothalamic area, in accordance with other reports. Gel filtration chromatography revealed that hypothalamic extracts contained a major peak of rGRF-LI corresponding to rGRF-(1-43)OH and two peaks of SRIF-LI equivalent to SRIF-(1-28) and SRIF-(1-14), respectively. These findings indicate that rGRF-LI is localized in the median eminence and arcuate nucleus in the rat and that rGRF-, SRIF-(1-28)-, and SRIF-(1-14)-LI are present in a 1:2.10:6.29 ratio on a molar basis.

Animals↗

Inhibitory effect of [Asu1,7]-eel calcitonin on growth hormone-secretion in conscious, freely moving, male rats.

The effect of [Asu1,7]-eel calcitonin (ECT), which is an equipotent analog of eel calcitonin (CT), on GH secretion was investigated in freely moving conscious male rats. Pulsatile GH secretion was completely inhibited by iv injection of ECT (2.5 micrograms/rat). The mean 6-h plasma GH levels, 9.54 +/- 2.34 ng/ml (mean +/- SEM) in ECT-treated rats, were significantly lower than those in saline-treated rats (69.9 +/- 9.4 ng/ml, P less than 0.001). In order to examine the action of ECT on the central nervous system, 25 ng ECT dissolved in 10 microliters saline were injected into the lateral ventricle of conscious male rats. The bursts of GH secretion were completely abolished by this dose of intraventricularly (ivt) injected ECT. The mean 6-h GH levels 5.8 +/- 0.8 ng/ml, were also significantly lower than those in control rats (35.8 +/- 6.6 ng/ml, P less than 0.01). Serum Ca levels did not change after the ivt injection of 25 ng ECT but fell significantly after the iv injection of 2.5 micrograms ECT. In order to clarify the inhibitory mechanism of GH secretion by ECT, the effect of ECT on the release of GH elicited by prostaglandin E1 (PGE1), a well-known GH secretagogue acting directly on the pituitary, was examined in vivo as well as in vitro. Both ivt (2.5, 25, or 250 ng/10 microliters X rat) and iv (2.5 or 25 micrograms/rat) injections of ECT caused a significant and dose-dependent suppression of PGE1-induced GH rises in conscious rats. In contrast, 10(-8) to 10(-7) M ECT failed to affect the baseline secretion of GH and its release by 5 X 10(-6) M PGE1 from rat anterior pituitary tissues perifused in vitro. These findings suggest that ECT suppresses GH secretion in the rat, at least in part, through the central nervous system.

Alprostadil↗

Augmentation by propranolol of growth hormone-releasing hormone-(1-44)-NH2-induced growth hormone release in normal short and normal children.

The effect of a 90-min iv infusion of propranolol, a beta-adrenergic antagonist (0.2 mg/kg BW), on basal plasma GH levels and the GH responses to an iv bolus injection of GH-releasing hormone-(1-44)-NH2 (GHRH; 1 microgram/kg BW) was examined in 10 prepubertal children (6 short but otherwise normal and 4 normal). The iv injection of GHRH resulted in significant increases in plasma GH, comparable to those after either insulin-induced hypoglycemia or arginine infusion. Only a small and inconsistent increase in plasma GH levels occurred during the iv infusion of propranolol, whereas simultaneous administration of propranolol with GHRH caused marked enhancement of GHRH-induced GH release in all subjects. The difference between the plasma GH response to GHRH given with propranolol and the response to GHRH given with 0.9% saline was significantly greater than that between the plasma GH level after propranolol and that after 0.9% saline infusion without GHRH injections. There was no difference in plasma GH responses to GHRH, propranolol, or both in the normal short children or normal children. These findings indicate that beta-adrenergic blockade potentiates GHRH-induced GH secretion in prepubertal children.

Child↗

Real-time sonography of palpable breast masses.

In order to evaluate the clinical usefulness of an electronic real-time linear array scanner in breast diseases, ultrasonography was performed in 148 cases of histologically confirmed palpable breast masses. The real-time images were observed on a television monitor while moving the hand-held transducer probes over the masses. It took only a few minutes to examine and diagnose a palpable mass. Among 45 carcinomas, 39 lesions were correctly diagnosed, four lesions were not detected by ultrasound and two were misdiagnosed as fibroadenomas. On the other hand, ten benign lesions were falsely diagnosed as breast cancers: seven mastopathies (including four sclerosing adenosis), two fibroadenomas and one abscess. The sensitivity and specificity for diagnosing breast cancer were 0.87 and 0.90 respectively. Real-time sonography is a simple, time-saving and useful tool for examining palpable breast masses. However, it should be realised that some breast cancers are difficult to image and differentiate from benign lesions.

Adenofibroma↗

Effect of [Asu1,7]eel calcitonin on prolactin release in normal subjects and patients with prolactinoma.

The effect of [Asu1,7]eel calcitonin (ECT), an equipotent analogue of eel CT, on prolactin (Prl) secretion was examined in 12 healthy male subjects and in 6 patients with prolactinoma. In healthy subjects, ECT (0.5 microgram/kg body weight . h) or saline was infused for 2 h and TRH was injected iv as a bolus of 500 micrograms at 1 h of ECT or saline administration. ECT did not affect basal Prl levels during 1 h of infusion. TRH caused a significant increase of plasma Prl with peak values of 75.2 +/- 11.6 ng/ml in ECT-infused subjects, which did not differ from those infused with saline (68.5 +/- 8.3 ng/ml). Next, an iv bolus injection of regular insulin (0.1 U/kg body weight) was followed by an infusion of ECT or saline alone. Plasma Prl peaks after hypoglycaemic stress were significantly lower in ECT-infused subjects than those in saline-injected controls (ECT, 16.5 +/- 3.1 vs 33.5 +/- 9.6 ng/ml, P less than 0.05). In patients with prolactinoma, basal levels of plasma Prl ranging from 42.0-4130 ng/ml failed to change during iv infusion of ECT. Moreover, ECT (10(-9) - 10(-6)M) did not affect Prl release from prolactinoma tissues perifused in vitro. These findings suggest that ECT may not act directly on the pituitary to modify Prl release. Rather, peripherally administered ECT appears to suppress Prl release via the central nervous system.

Adenoma↗

Effect of various catecholamine antagonists on prolactin secretion in conscious male rabbits.

To clarify physiological roles of catecholaminergic systems in the control of rabbit prolactin (PRL) release, the effect of various catecholamine receptor antagonists on plasma PRL levels was examined in conscious, freely moving male rabbits. An intravenous (iv) injection of yohimbin (2.5 mg/kg body wt), an alpha 2-adrenoreceptor antagonist, but not prazosin (2 mg/kg body wt), an alpha 1-adrenergic receptor antagonist, resulted in a significant elevation of plasma PRL. Conversely, propranolol (2.5 mg/kg body wt, iv), a nonselective beta-adrenoreceptor antagonist, and metoprolol (2.6 mg/kg body wt, iv), a beta 1-adrenergic antagonist, slightly but significantly suppressed basal levels of plasma PRL. On the other hand, haloperidol (0.5 mg/kg body wt, iv), pimozide (0.3 mg/kg body wt, iv), sulpiride (5 mg/kg body wt, iv), chlorpromazine (3 mg/kg body wt, iv), and YM-09151-2 (0.2 mg/kg body wt, iv), all dopamine receptor antagonists caused a significant increase in plasma PRL. These results suggest that dopaminergic and alpha 2-adrenergic mechanisms exert a tonic inhibitory role and beta-adrenergic mechanisms, probably beta 1, a tonic stimulatory role in the regulation of PRL release in the rabbit.

Animals↗

Comparison of the major histocompatibility antigen on Marek's disease-derived cell lines detected by membrane fluorescent antibody, cytotoxicity, and lymphoagglutination tests.

The reactivity of 13 antisera specific for the major histocompatibility antigen (MHA) of the B complex against cells in 6 cell lines (MDCC-JP1, JP2, HP1, HP2, RP1, and MSB1), derived from Marek's disease (MD) lymphoma, was compared by using membrane fluorescent antibody, cytotoxicity, and lymphoagglutination tests. The membrane fluorescent antibody test was found to be the most sensitive method for detecting the MHA of the B complex on the MD cell lines. After absorption of these antisera with the homologous erythrocytes, the reactivities of the absorbed sera to the homologous erythrocytes and the MD line cells were reduced or lost altogether. However, after absorbing the antisera reactive for MD cell lines with the respective cell line, the reactivities of the absorbed sera to the line cells were not detected at all when examined by the above tests. However, the reactivities of these absorbed sera to the homologous erythrocytes could still be observed when examined by a hemagglutination test. These results indicate that the antisera contain at least two kinds of antibody (against Class I and Class IV antigens), and the three different tests used here are detecting the Class I antigens of MHA on the MD line cells.

Agglutination Tests↗

[Reevaluation of the histological classification of breast cancer--a presentation of a new histological classification considering the relationship between scirrhous tendency and postoperative prognosis].

The present study was designed to evaluate the correlation between the histology and the prognosis of the patients with breast cancer. In this study, 1271 cases with breast cancer were retrospectively studied and an attempt of a new histological classification was presented, which was intended to reflect the prognosis more exactly than the ordinarily used classification by Japan Mammary Cancer Society. Japan Mammary Cancer Society classifies infiltrating carcinoma into 3 types; papillotubular, medullary tubular and scirrhous carcinoma. In this study, when scirrhous interstitial infiltration was observed in papillotubular or medullary tubular carcinoma, even if scirrhous tendency was observed only in small part, the patients' prognosis was as poor as scirrhous carcinoma. The prognosis of common type of infiltrating carcinoma with scirrhous tendency corresponded to that of one grade advanced stage without scirrhous tendency. Considering these results and clinical usefulness, common type of infiltrating carcinoma should be classified to 2 types, namely with or without scirrhous tendency in order to reflect the prognosis and to correspond to WHO classification.

Adenocarcinoma, Scirrhous↗

Effect of L-propargylglycine on metabolism of sulfur-containing amino acids in pregnant rats and their fetuses.

Cystathionine accumulated in several tissues of dams and fetuses by a single intraperitoneal administration of L-proparglyglycine to pregnant rats. Cystathionine in the liver of dams reached its maximal level at about 15 hrs after L-proparglyglycine injection (10 mg/300g), while that in the kidney and brain of dams, and in the liver, kidney, and brain of fetuses reached a maximum at about 21 hrs. The content of cystine in the liver of fetuses decreased gradually in proportion to the amount of L-proparglyglycine administered. Cystathionine gamma-lyase activity in the liver of dams and fetuses decreased to about 2-4% of that of control rats at 15 hrs after L-proparglyglycine injection, and that in the kidney and pancreas of dams to about 10-20% of that of control rats. On the other hand, cystathionine beta-synthase activity did not show significant changes from that of control rats.

Alkynes↗

Enzymatic production of S-(2-hydroxy-2-carboxyethyl)homocysteine.

The monodeamination product of L-cystathionine, S-(2-oxo-2-carboxyethyl)homocysteine is enzymatically reduced by human and hog L-lactate dehydrogenase to S-(2 hydroxy-2-carboxyhethyl)homocysteine which has been found in the urine of cystathioninuric patients. Km values are 6.6 mM and 13 mM for human and hog enzymes respectively. The reaction is not complete at alkaline pH values because of cyclization of the ketoacid into a 1,4 thiazepine derivative ring. By a coupled enzymatic system of L-amino acid oxidase and L-lactate dehydrogenase S-(2-hydroxy-2-carboxyethyl)homocysteine is also formed from L-cystathionine.

Animals↗

Improvement of the anoxia-induced mitochondrial dysfunction by membrane modulation.

The mitochondrial dysfunction induced by anoxia in vitro was improved with chlorpromazine, cepharanthine, bromophenacyl bromide, and mepacrine without affecting phospholipid or adenine nucleotide metabolisms. The drugs inhibited lipid peroxidation by Fe2+, mitochondrial disruption by Ca2+, and membrane perturbation by lysolecithin, and retained the activity to control H+ permeability across mitochondrial membranes. The drugs appeared to preserve the functions by acting to suppress the development of membrane deterioration which may have resided in the deenergization of mitochondria in the absence of oxygen.

Acetophenones↗

Stimulatory effect of peptide histidine isoleucine amide 1-27 on prolactin release in the rat.

Intravenous injection of pure peptide histidine isoleucine amide 1-27 (PHI) resulted in a prompt and significant increase of plasma prolactin (PRL) in conscious freely-moving male rats. Using a perifusion system of rat anterior pituitary tissues in vitro, effluent PRL levels were also increased by 10(-8)-10(-7) M PHI. A PRL releasing potency of PHI was almost similar with that of vasoactive intestinal polypeptide (VIP) or TRH both in vivo and in vitro. Coupled with the recent immunocytochemical studies showing the dense network of PHI immunoreactive fibers around the hypophysial portal vessels, PHI might be another candidate for PRL releasing factor.

Animals↗