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Biomedical subjects

N Nihei

Publications and source records attributed to N Nihei.

At least 37 records · Page 2Linked to original sources
PubMed1984

Abnormal lymphocyte function precedes hyperglycaemia in mice treated with multiple low doses of streptozotocin.

To investigate early immunological disturbances at the onset of diabetes, lymphocyte function and islet cell surface antibodies were studied in streptozotocin-treated C57BL/10 and B10.BR mice. In C57BL/10 mice, streptozotocin given in multiple low doses depressed lymphoblastic transformation to phytohaemagglutinin and pokeweed mitogen, but not to concanavalin A on day 6 after the first administration. On day 20, the transformation remained suppressed with phytohaemagglutinin, but recovered to the control level with pokeweed mitogen. In the early phase after treatment, the islet cell surface antibodies were elevated and then declined. Single high dose administration depressed responses to phytohaemagglutinin with no detectable islet cell surface antibodies. In B10.BR mice transformations to pokeweed mitogen and concanavalin A were suppressed in the early phase. The strain of mice may be a factor to be considered. Thus, it was suggested that the deterioration of immunological function with the formation of islet cell surface antibodies preceded the onset of hyperglycaemia in mice treated with multiple low doses of streptozotocin.

Animals↗
PubMed1983

Response of plasma somatostatin-like immunoreactivity (SLI) to a 75 g oral glucose tolerance test in normal subjects and patients with impaired glucose tolerance.

To study the role of somatostatin in the pathophysiology of glucose intolerance in man, plasma somatostatin-like immunoreactivity (SLI) was measured in 8 normal subjects, 6 patients with insulin dependent diabetes mellitus (IDDM), 13 with non-insulin dependent diabetes mellitus (NIDDM), and 9 with hyperthyroidism, by extraction of plasma SLI and radioimmunoassay. The extraction method gave a recovery rate for synthetic somatostatin-14 and somatostatin-28 of 72 +/- 6 and 55 +/- 7%, respectively. No SLI corresponding to somatostatin-28 in human peripheral blood was observed. Incubation of somatostatin-28 in plasma gave a rapid decrease of immunoreactivity, and no conversion to somatostatin-14 was observed. It is speculated that SLI extracted with acid-acetone mainly represents a molecular weight similar to somatostatin-14. After oral administration of glucose (75 g), a clear and sustained rise in plasma SLI was seen in normal subjects from an initial value (+/- SEM) of 29.9 +/- 5.4 pg/ml to a peak value, at 60 min of 93.4 +/- 15.5 pg/ml. The increase of plasma SLI after 75 g glucose was also observed in IDDM and NIDDM. The peak level of SLI was significantly less than that for normal subjects. The extraction of plasma SLI with acetic acid and acetone gave reproducible results and showed a fluctuation of SLI with glucose concentration.

Adult↗
PubMed1980

Blood level and brain distribution of thyrotropin-releasing hormone (TRH) determined by radioimmunoassay after intravenous administration in rats.

The blood level and brain distribution of immunoreactive TRH after intravenous administration of TRH tartrate monohydrate (TRH-T) were investigated by radioimmunoassay in rats. Optimal condition for complete inactivation of TRH-degradative enzymes in brain by a microwave irradiation was found to be a 5kW power for 1.5 seconds. The endogenous TRH was present at the highest concentration in the hypothalamus, followed by the brain stem and thalamus, and was the lowest in the cerebral cortex including hippocampus and cerebellum. The time-course of TRH blood levels following administration of TRH-T at 0.5, 5 and 25 mg/kg fitted to a two compartment open model, and the half-lives in beta-phase increased dose-dependently. The administered TRH was incorporated rapidly from blood into whole brain, and the peak brain level corresponding to 0.108--0.166% of the total dose administered was attained 1 min after the administration. The brain TRH was eliminated with a half-life of about 3 min. The administered TRH was distributed throughout the brain, at the highest concentration in the hypothalamus, followed by the brain stem, cerebellum, thalamus and cerebral cortex. TRH tended to be eliminated most rapidly from the cerebellum.

Animals↗
PubMed1979

[Changes of plasma levels of TRH and its target hormones by two hour constant intravenous infusion of TRH tartrate in man (author's transl)].

Constant iv infusion of TRH tartrate for 2 hours was administered to normal men in a dosage of 0.5 (n=4), 1.0 (n=2) and 2 (n=4) mg/120 minutes. Measurements at every 15 minutes were performed for plasma levels of TRH, TSH, Thyroxine (T4) and Triiodothyronine (T3) by radioimmunoassay. Plasma levels of TRH increased promptly and stayed at the same levels until the end of the infusion. The Mean Clearance Rate (MRC), Half-life and Volume of Distribution of TRH were respectively, 4.62 +/- 0.53 L/min. (M +/- SE), 17.8 +/- 3.8 minutes and 112 +/- 15 L in the 0.5 mg administered group and 6.38 +/- 2.50 L/min., 9.0 +/- 1.4 minutes and 82 +/- 30 L in the 2 mg administered group. Plasma levels of TRH increased in two phases, and increments of plasma TSH were dose dependable to the dosage of TRH. Plasma levels of T4 increased gradually in the course of TRH infusion and stayed at high levels even in the withdrawal phase of TRH. Plasma levels of T3 increased markedly during and after the TRH infusion in the 0.5 mg administered group, while increments of plasma T3 were minute in the 2 mg administered group. From the above data, it is suggested that the amount of TRH production in man, which is much more than has previously been reported, may indicate the existence of an extrahypothalamic synthesis of TRH in man.

Adult↗
PubMed1978

The effect of L-DOPA administration on thyrotropin (TSH) and thyrotropin releasing hormone (TRH) levels in serum in primary or pituitary hypothyroidism.

The effect of acute administration of L-DOPA on TSH and TRH levels in serum was studied in primary or pituitary hypothyroidism. TRH levels in serum fell and then returned to initial levels after L-DOPA administration in primary or pituitary hypothyroidism. TSH levels in serum fell and then returned to initial levels after L-DOPA administration in primary hypothyroidism. T4 and T3 levels in serum did not change after L-DOPA administration in primary or pituitary hypothyroidism. These data suggested that L-DOPA might act directly to hypothalamus.

Humans↗
PubMed1976

[The effect of various amines on TRH contents in rat brain (author's transl)].

To study the effect of vatious amines on TRH contents in rat brain, various amines or inhibitor of synthesis of amines were injected into rat through i.v. or i.p.. Rats were decapitated and brain was frozen in dry ice and aceton. TRH contents in hypothalamus(H), cerebrum(C) and cerebellum and brain stem (C and S) were measured by TRH radioimmunoassay. TRH contents in normal rats were 3.9+/-0.5ng in H, 2.6+/-0.5NG IN C and 1.6+/-0.3ng in C and S. TRH contents in all parts of brain were increased in L-DOPA treated group and did not change in T3 or T4 treated group. TRH contents in all parts of brain were decreased in alpha-methyl-DOPA, alpha-methyl-para-tyrosine, fusaric acid and 5-HTP treated groups. In D,L-p-chlorophenylalanine treated group TRH contents in brain were increased only in hypothalamus. In L-DOPA or 5-HTP treated group with T4 or T3 preadministration, TRH contents in all parts of brain were same levels of L-DOPA or 5-HTP treated group. The above data suggested the TRH contents in rat brain were increased with increase of dopamine level in rat brain and decreased with increase of serotonine level or decrease of noradrenaline level in rat brain and inhibitory effect of T4 or T3 on TRH release might be mediated through dopaminergic and serotonergic mechanism.

5-Hydroxytryptophan↗
PubMed1976

Radioimmunoassay of thyrotrophin releasing hormone in human serum and its clinical application.

A radioimmunoassay for thyrotrophin releasing hormone (TRH) in human serum is described. Inactivation of TRH immunoreactivity by serum is prevented by a mixture of 8-hydroxyquinoline sulphate and Tween 20. This persisted for a long period and at the concentration used in this study did not affect the TRH value. The TRH was extracted from serum with methanol. The results of the recovery experiment, dilution curve of high TRH serum, intra-assay reproducibility and inter-assay variation were quite satisfactory. The lowest detectable amount in this system was 5.0 pg/ml. Immunoreactive TRH levels in the serum were less than 60 pg/ml in normal subjects, were below the limit of detectability in hyperthyroid patients, were 40 to 400 pg/ml in primary hypothyroid patients, were 100 to 600 pg/ml in pituitary hypothyroid patients and below the limit of detectability in hypothalamic hypothyroid patients. In primary hypothyroidism, immunoreactive TRH concentrations in the serum fell to in the normal range during thyroxine substitution. In most cases of hyperthyroidism, immunoreactive TRH concentrations in the serum increased to 5.0 pg/ml or more during antithyroid drug treatment, but in a few cases the level remained below the limit of detectability even though thyroid hormone levels were in the normal range. The above data suggest that this assay system would be a useful tool to study the role of TRH in the hypothalamo-pituitary-thyroid axis.

Antibodies↗