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Y Shishiba

Publications and source records attributed to Y Shishiba.

At least 127 records · Page 7Linked to original sources
PubMed1975

[Specific and non-specific reaction of hemagglutination for the detection of anti-thyroglobulin antibody (author's transl)].

Tanned red cell hemagglutination has been widely accepted for use in the detection of anti-thyroglobulin antibodies. The interpretation, however, especially when the hemagglutination was observed at a low titer of serum dilution, has remained equivocal. In order to separate specific and non-specific hemagglutination, we tried to concentrate serum IgG to compare the hemagglutination titer at various concentrations of IgG. If the hemagglutination is specific for the presence of antithyroglobulin antibodies, the hemagglutination titer would increase as the IgG concentration rises. On the contrary, when the hemagglutination is non-specific and irrelevant to the presence of anti-thyroglobulin antibodies, the hemagglutination titer is expected not to increase while the IgG concentration rises. Based on this hypothesis, sera which showed various hemagglutination titer for anti-thyroglobulin antibodies were studied to examine the parallelism between hemagglutination titer and IgG concentration. IgG was concentrated with the method of ammonium sulfate precipitation. The grade of concentrate was examined by the IgG determination with the method of immunodiffusion technique employing the kit distributed by Behringwerke. The hemagglutination test was performed with the Boyden's method using the kit distributed by the Wellcome Company. The results showed that 4 out of 15 sera whose original hemagglutination titer was 1:3 failed to show increase in hemagglutination titer even at the 2 to 4 fold concentration of IgG. On the contrary, only 2 out of 26 sera whose hemagglutination titer was more than 1:6, failed to increase the titer at the IgG concentrate to the same degree. Thus, it is possible to conclude that the hemagglutination observed at 1:3 dilution of the serum is highly non-specific, while that observed at a serum dilution of more than 1:6 is thought to be specific.

Antibodies↗
PubMed1975

Lack of TRH-induced TSH secretion in a patient with Klinefelter's syndrome: a case report.

In a 41 year-old patient with Klinefelter's syndrome, a failure of TRH-induced TSH secretion was noticed. Low 131I-thyroid uptake, together with the elevation following exogenous TSH administration, indicates that the defective locus exists in the hypothalamus or pituitary resulting in an impaired secretion of TSH. Such a defect may underlie thyroid dysfunction often associated with Klinefelter's syndrome.

Adult↗
PubMed1975

Alteration of thyroidal responsiveness to TSH under the influence of circulating thyroid hormone: short feed-back regulatory effect.

In order to examine the hypothesis that the thyroidal responsiveness to TSH is under the influence of thyroid hormone, following the T3 injection to the mice, serum T3 concentrations and the response of thyroid tissue to a fixed dose of TSH in terms of intracellular colloid droplet formation was studied. The colloid droplets induced by TSH was significantly reduced when serum T3 was decreasing, while it was significantly increased when serum T3 was increasing. This results demonstrate for the first time the existence of short feed-back loop regulating intra-thyroidal function by circulating T3. To delineate the possible mechanism of action of T3, the thyroid gland of mouse whose serum T3 concentration was elevated by injecting 50 mug T3, was incubated with TSH in vitro. TSH-induced cyclic AMP generation was not inhibited at all but colloid droplet formation was significantly inhibited in the thyroid tissue of the animal whose serum T3 concentration was enormously high. Thus, it was demonstrated that the site at which T3 affects is beyond cylcic AMP generation but prior to endocytosis, being consistent with our previous results.

Animals↗
PubMed1975

Delayed equilibrium of pituitary triiodothyronine (T3) following an acute T3 administration.

To reconcile the knowledge on tissue T3 concentration with cellular metabolism regulatory mechanism of thyroid hormone secretion, the pattern of the change of tissue T3 concentration following an acute administration of T3 was studied in mice. Basal T3 concentration in serum, liver, brain and pituitary was 61, 173, 198 and 1630ng/100g, respectively. After 0.5 mug T3 dose, T3 concentration in serum and liver reached the maximum level 1 to 3 hrs following the administration and decreased exponetially thereafter, thus, maintaining almost constant tissue/plasma T3 ratio. In contrast, T3 increase in brain or pituitary was far delayed, not until 7 to 12 hrs following T3 injection, and then decreased parallel to that in serum. Furthermore, the magnitude of increase in pituitary T3 was limited when compared to that in liver. Thus, tissue/plasma T3 ratio in pituitary decreased markedly after the dose of T3. This finding suggests the possibility that there is blood-brain barrier or blood-tissue barrier for the transport of T3 in pituitary or brain, resulting in delayed equilibrium with that in serum. These results may also explain the delay of inhibition of TRH-induced TSH release after single dose of T3 as recently reported by Azizi et al. (1975).

Animals↗
PubMed1975

Effect of triiodothyronine or iodide on the thyroidal secretion in vitro: Inhibition of TSH- and dibutyryl-cyclic-AMP induced endocytosis.

T3 or iodide, at the concentration of 10- minus 3M, inhibits TSH- or dibutyryl-cyclic AMP-induced thyroidal intracellular colloid droplet formation, while leaving the TSH-induced increase in cyclic AMP levels intact. The effect of T3 appeared not to be mediated through the iodide derived from deiodination of T3. Those results clearly demonstrate that T3 or iodide acts at the point beyond cyclic AMP generation and prior tothe formation of intracellular colloid droplets. This is also the site at which microtubule active reagents exert their influence. Whether T3 or iodide fits this category or acts in as yet undetermined manner remains to be established.

Animals↗
PubMed1974

[Endocrine myopathy].

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Endocrine System Diseases↗