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Biomedical subjects

J Yamauchi

Publications and source records attributed to J Yamauchi.

At least 109 records · Page 6Linked to original sources
PubMed1980

Thyrotropin releasing hormone (TRH): its widespread distribution in discrete hypothalamic nuclei and areas in rat brain.

The precise distribution of thyrotropin releasing hormone (TRH) in 23 discrete brain nuclei and areas of Wistar strain male rats was determined by specific radioimmunoassay. TRH was detected in most of these areas. The highest concentration was found in the median eminence (27.52 +/- 2.84 ng/mg protein). The arcuate nucleus (4.92 +/- 0.58 ng/mg protein), dorsomedial nucleus (4.77 +/- 0.59 ng/mg protein) and medial preoptic area (3.94 +/- 0.15 ng/mg protein) also contained a considerable concentration of TRH. However, no TRH was detected in cerebral cortex, cerebellar hemisphere, anterior pituitary or pineal body. The data indicated that TRH was widely distributed throughout the hypothalamus; in particular, high concentrations occure in relatively restricted areas: in the median eminence, arcuate nucleus, dorsomedial nucleus and medial preoptic area. These areas coincide well with the so-called "thyrotropic" area of the hypothalamus.

Animals↗
PubMed1978

Effect of glucagon on growth hormone secretion in rats.

Gentled rats injected subcutaneously with glucagon (20 microgram/100 g body weight) showed a significant decrease in plasma growth hormone (GH) at 15 min after glucagon injection. A subcutaneous injection of 50% glucose did not cause the early suppression as shown at 15 min after glucagon injection, but at 30 min after glucose injection a tendency to decrease in plasma GH was observed. In urethane anesthetized rats, a subcutaneous administration of glucagon (1 microgram or 10 microgram/100 g body weight) failed to elicit an increase in plasma GH. In vitro incubation of anterior pituitary fragments with glucagon failed to decrease the release of GH, suggesting that glucagon does not act directly on the anterior pituitary.

Anesthesia, General↗
PubMed1978

Chorio-meningo-encephalitis due to Listeria monocytogenes after renal transplantation.

A 35-year-old man, who underwent renal transplantation, died of meningo-encephalitis with symptoms of meningitis for only 8 days. The autopsy revealed marked chorio-meningo-encephalitis caused by Listeria monocytogenes. This report on listeriosis in renal transplant patients is the second in our country, where adult cases of listeriosis are rare. Recent knowledge about listeriosis in renal transplants is reviewed and discussed.

Adult↗
PubMed1977

Stimulatory effects of gamma-hydroxybutyric acid on growth hormone and prolactin release in humans.

A dose of 2.5 g of gamma-hydroxybutyric acid (GHB) was administered intravenously to 6 healthy male volunteers. A significant increase in plasma GH was observed at 30, 45, 60 and 90 min after injection. The plasma prolactin level increased significantly at 45 and 60 min after GHB injection. These responses were not found after the saline vehicle injection in the same subjects. It is conceivable that GHB could modify the release of serotonin from the nerve terminals and then stimulate the release of GH and prolactin.

Adult↗
PubMed1977

Effects of prostaglandin E1 and indomethacin on ACTH, prolactin, GH and LH from rat pituitary in vitro.

The effects of prostaglandin E1 (PGE1) and indomethacin (IDM) on the release of several pituitary hormones from the rat pituitary were investigated in vitro. An addition of 2 microng/ml of PGE1 to the medium elicited the release of growth hormone (GH) and prolactin, but not of adrenocorticotropin (ACTH) and luteinizing hormone (LH). Although the addition of 1 microng/ml of IDM alone resulted in no effect on the basal release of these hormones, IDM diminished the release of ACTH induced by crude rat hypothalamic extracts (HE) or lysine-8-vasopressin (LVP), and LH induced by HE or luteinizing hormone-releasing hormone (LH-RH). These findings implicate that a part of PGE1 action might be a direct one on the pituitary gland and PGE1 might release GH and prolactin, whereas IDM might have a direct action on the pituitary gland, and that blunt the release of these pituitary hormones induced by several stimuli.

Adrenocorticotropic Hormone↗
PubMed1975

[Comparison with growth hormone responses to various drugs or substances in patients with active acromegaly (author's transl)].

Growth hormone (GH) responses to L-dopa, 2-Br-alpha-ergocryptine (CB-154), thyrotropine-releasing hormone (TRH), luteinizing hormone-releasing hormone (LH-RH), glucagon and glucose were investigated in six patients with active acromegaly. The following results were obtained. 1) Subcutaneous injection of 1 mg glucagon caused a clear-cut decrease in plasma GH levels in 5 out of 6 active acromegalic patients at 30 minutes after the injection. In 2 out of 6 patients a rebound of plasma GH was observed. 2) In three out of six patients with active acromegaly, oral administration of 0.5 g L-dopa caused a significant suppression of plasma GH levels. 3) CB-154 (2.5mg) administered orally elicited a marked decrease in plasma GH levels in the same three patients who showed a significant suppressive GH reponse to L-dopa, and the inhibitory effect of CB-154 on GH secretion lasted for 6 hours. These patients who had a GH response to L-dopa or CB-154 were named "responders". 4) Intravenous administration of TRH resulted in a significant increase in plasma GH in 4 patients 3 of whom were responders and the other a non-responder. 5) Pretreatment with CB-154 did not modify the TRH-induced GH increase in all patients who had a positive response to TRH. 6) A significant increase in plasma GH was elicited by the intravenous injection of 100 mug LH-RH in 3 out of 6 patients with acromegaly. 7) When oral administration of CB-154 had been given 2 hours before LH-RH, the GH response to LH-RH was blunted in two of three patients who had a LH-RH-induced increase in plasma GH levels.

Acromegaly↗
PubMed1975

Suppression of serum growth hormone levels by glucagon in patients with active acromegaly.

One mg of glucagon was given subcutaneously to eight patients with active acromegaly. Seven out of eight patients had a rapid decrease in serum growth hormone (GH) levels at 30 min after the glucagon injection. In two out of seven patients a rebound increase in serum GH following the early GH reduction was observed. On the other hand, oral administration of 50 g glucose which caused a comparable increase in blood glucose to that after the glucagon injection elicited no early suppression in serum GH levels in the same patients. These data suggest that the inhibition of GH release induced by glucagon could not be related to the increase in blood glucose by glucagon.

Acromegaly↗
PubMed1975

Stimulation of lymphocytes of patients administered with a trypsin inhibitor, Trasylol (basic pancreatic trypsin inhibitor pharmaceutical), in vitro with BPTI and other several stimulants.

Distinguished lymphocytes stimulation was observed in vitro with one out of four patients received Trasylol therapy. The peak response of DNA synthesis was shown to occur at 100 mug/tube of basic pancreatic trypsin inhibitor (BPTI) itself, about 6 days after addition of BPTI. Reactivity (3H-thymidine incorporation) of lymphocytes of patients after the therapy, to specific antigen, ie., purified protein derivative (PPD) or Bordetella pertussis organisms in vitro, was markedly depressed. On the other hand, that to non-specific mitogen, phytohaemagglutinin-p of pokeweed mitogen, was a little reduced, or rather enhanced after the therapy. Conversly, lymphocytes of an originally tuberculin negative patient were lead to be stimulated with PPD in vitro, after skin test with PPD and Trasylol therapy. These various immune responses including drug-induced exanthemas of patients received the therapy, are discussed in this report, in comparison with immune responses of guinea pigs sensitized with BPTI, immune responses of animals in microorganism infections and the contrary immunological effects of Trasylol already reported.

Aprotinin↗