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Volume 42, Issue 8
Displaying 1-11 of 11 articles from this issue
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1966 Volume 42 Issue 8 Pages 841
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
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Masaji INOUE, Motozo KO1966 Volume 42 Issue 8 Pages 842-843
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESS1) The first dialysis of the homogenate is necessary to the increase of the nondialyzable ACh-like substance in the homogenate containing exogenous ACh, as illustrated in the previous report and experiment A of this report. That increase would be the results of the decrease of K ion after the first dialysis of the homogenate, because K ion can release ACh from combined ACh.
2) It is inferred from the results of experiment A that a part of exogenous ACh added to the homogenate would be combined with depot protein. On the other hand, a part of such exogenous ACh would also be combined with receptor protein.
3) It is supposed from the results of experiment B that oxytocin could accelerate the binding of exogenous ACh with depot protein and receptor protein in the homogenate.View full abstractDownload PDF (200K) -
Kiyotaka UCHIYAMA1966 Volume 42 Issue 8 Pages 844-845
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSThe 127I suppression test was carried out in 63 healthy persons and 87 patients with hyperthyroidism. Thyroidal iodine uptake was measured in the various concentrations of blood iodine, and the effects of TSH and antithyroid drugs on the thyroidal iodine uptake were observed by this method.
In order to clarify the mechanism of recovery from hyperthyroidism, TSH test and triiodothyronine suppression test were carried out throughout the antithyroid drug therapy in patients with hyperthyroidism. The thyroidal 131I uptake increase after the administration of TSH was slight or none in untreated 29 patients with hyperthyroidism. On the contrary, thyroidal 131I uptake decrease after administration of TSH was observed in 11 cases among 40 patients with hyperthyroidism.
By tracing daily variation of thyroidal 131I uptake, inhibitions of thyroidal 131I uptake were observed during the administration of antithyroid drug, and rebound phenomena of thyroidal 121I uptake were observed after the interruption of administration. In these cases, thyroidal a 131I uptake decrease after the administration of TSH was observed.
After normalization of thyroidal function tests, B.M.R., P.B.I. with the administration of antithyroid drug, the treatment should be continued for more than 1-2 years. The TSH test in some of these cases, very remarkably increased in thyroidal 131I uptake (34.6 ± 9.0 in the mean) were observed by the TSH test. Those were named “over respose group”.
The TSH test for this group was followed up for 5 years, which had much the same value for healthy persons.
T3 suppression tests were carried out in 12 healthy persons and 42 patients with hyperthyroidism. Suppression of thyroidal 131I uptake after administration of triiodothyronine was not observed in the untreated 12 patients with hyperthyroidism, but thyroidal 131I uptake was remarkably suppressed in 11 cases of 17 patients who had been in remission with antithyroid drugs therapy, so that feed-back relation of pituitary thyroid axis might be recovered previous to the healing of hyperthyroidism.
Thyroid reserve action capacity gradually diminished, and triiodothronine suppression test for the cured group had much the same value as healthy persons.
The result of antithyroid drug treatment was investigated in 100 patients with hyperthyroidism between 3 and 5 years after discontinuance of treatment, and the relationship of sex, age, degree of goiter, exophthalmos, duration of antithyroid drugs, and total doses, as well as the results of treatment, were reported. Twenty-four hrs. thyroidal 131I uptake for 41 cases of this cured group showed under 40%, and recoveries of their feed-back relation were recognized in TSH test and triiodothyronine suppression test.View full abstractDownload PDF (137K) -
Norisuke HOUKI1966 Volume 42 Issue 8 Pages 846-847
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSThe metabolism of two synthetic progestins, 6α-methyl-17α-acetoxy-progesterone (MAP) and 6-dehydro-retroprogesterone (DHRP), was investigated in human subjects. Compounds were administered in doses of 100 mg. per day to patients who had undergone extensive radical hysterectomy with salpingo-oophorectomia bilateralis for uterine cancer. Single oral administration of 3H-DHRP in a dose of 5 mg. was also carried out in two cases. During the experiments, betha-methasone (3 mg./day) was given orally to these patients in order to suppress endogenous steroid excretion.
Throughout the experiments, urine samples were collected every 24 hours and stored in a deep freezer without preservatives. The urine was analysed as soon as possible. The methods of hydrolysis and extraction are listed in Fig. 1.
The crude extracts were adsorbed on alumina and eluted successively with each 100 ml of benzene, 0.1, 0.3, 0.5, 1.0, 5.0 and 30.0% methanol in benzene and then with methanol. In the isolation of MAP metabolites, column chromatography was omitted from the procedure. The radioactivities were determined on a Tri-Carb Liquid Scintillation Spectrometer. Radioactive peaks thus obtained were chromatographed on papers in modified Bush B5, Ba and B3 systems. Radioactive peaks or UV absorbing areas were eluted with methanol and further characterized with the aid of the following procedures. 1) INAH reaction. 2) Zimmermann reaction. 3) Acetylation. 4) Saponification. 5) Oxidation. 6) Dehydration. 7) UV absorption. 8) Sulfuric acid chromogen spectrum. 9) Porter-Silber reaction.
Results and Discussion.
1) 6β, 17α, 21-trihydroxy-6α-methyl-progesterone was identified as a main metabolite of MAP (Fig. 6).
2) It was suspected that 6β-hydroxylation and 21-hydroxylation of MAP took place in vivo in an organ other than the adrenal, probably at the liver.
3) 20α-hydroxy-9β 10α-pregna-4, 6-diene-3-one was isolated and identified in the glucuronide fraction of urine as a single major metabolite of orally administered DHRP. (Fig. 15. 17.)
4) Increasing urinary excretion of tritium was observed during the first 5 hours after administration of 3H-DHRP in an estrogen primed rabbit. On the other hand, simultaneous administration of 4-14C-progesterone to the same animal resulted in maximum urinary excretion of 14C within 2 hours (Fig. 23).
5) The recovery of radioactivities from the first 6 days urine after administration of 3H-DHRP was culculated as being about 20% (Fig. 7).
6) The radioactivities found in glucuronide fraction were accounted for 75% of the total administered doses, 8-13% in free fraction, 3-9% in sulfate fraction, and 10% in unextractable fraction. (Table 1.)
7) The other urinary metabolites of DHRP also retained the 4, 6-dien-3-one structure, but no further critical analysis of the structure could be made.
8) These experimental data suggested that the reduced reduction of Δ4-3-ketone system in vivo of these synthetic progestins led them into the other metabolic pathways from that of progesterone.View full abstractDownload PDF (146K) -
Part 1. Thyroid autoantibodies in various thyroid disordersMasao HARA1966 Volume 42 Issue 8 Pages 848
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSThe sera of subjects with and without thyroid disease were tested for the presence of circulating antibodies against thyroid extracts by precipitation test, tanned red-cell hemagglutination technic and microsomal compliment fixation test.
The thyroglobulin antibodies (demonstrated by tanned red-cell hemagglutination technics) were detected with the highest frequency in patients with chronic thyroiditis. In 26 patients studied, 21 had these antibodies in the serum.
By the precipitation test, the thyroid autoantibodies were detected only in patients with chronic thyroiditis, in 5 among 26 cases.
By the tanned red-cell hemagglutination technics, auto-antibodies could be rarely demonstrated in subjects without thyroid deseases. Among 196 cases of non thyroideal diseases, thyroglobulin antibody was detected in 14.
In 29 of 60 hypothyroidism cases of various causes, and in 8 of 15 thyroid cancer, this antibody was detected.
Among 153 patients with hyperthyroidism, thyroglobulin antibody was demonstrated in 49.0% and microsomal compliment fixation antibody in 52.8%.
On the other hand, the finding in 126 diffuse simple goiter, in 73 nodular simple goiter and in 16 subacute thyroiditis did not differ essentially from those in the non thyroideal diseases.
Biopsy studies showed a correlation between the presence of thyroid antibody and the inflammative histological changes in the gland, but this correlation was not absolute.
In hyperthyroidism there was poor correlation between microsomal compliment fixation antibody and thyroglobulin antibody detected by the tanned red-cell hemagglutination technics or between these thyroid autoantibodies and clinical pictures such as age, sex, the weight of thyroid, exophthalmos, thyroid function tests and thyroid stimulating hormone or long-acting thyroid stimulator in sera, while autoantibodies were found in higher incidence in the long-standing cases.
Thyroglobulin antibody was slightly reduced by treatment with I-triiodothyronine or glucocorticoid in chronic thyroiditis. The decrease of thyroglobulin autoantibody titer was not always accompanied by the reduction of the gland with the treatment.
Thyroglobulin antibody was also found with higher titer in untreated myxedema than in cases treated with I-triiodothyronine or dessicated thyroid for various periods.View full abstractDownload PDF (118K) -
1966 Volume 42 Issue 8 Pages 849-879
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
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[in Japanese], [in Japanese]1966 Volume 42 Issue 8 Pages 880-883
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
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[in Japanese]1966 Volume 42 Issue 8 Pages 884-899
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
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[in Japanese]1966 Volume 42 Issue 8 Pages 900-917
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
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[in Japanese]1966 Volume 42 Issue 8 Pages 918-933
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
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1966 Volume 42 Issue 8 Pages 934-940
Published: November 20, 1966
Released on J-STAGE: September 24, 2012
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