Folia Endocrinologica Japonica
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
Volume 46, Issue 5
Displaying 1-7 of 7 articles from this issue
  • Mitsuo NISHIKAWA
    1970 Volume 46 Issue 5 Pages 508-512,497
    Published: August 20, 1970
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    The first issue of FOLIA ENDOCRINOLOGICA JAPONICA was published in 1925 and association for the endocrine study was initiated, but the first annual meeting of this society was held on April 3, 1927, the president being Dr. Kanji Tsuji, Professor of Medicine of Kyoto University and a permanent organization was effected on that time. Since the foundation, the society has made a steady development, however, it was not before 1950 that the general concern to this society became urgent and the participants increased rapidly in number. At present the membership numbers over 2200.
    Looking around these forty-five years, there seems to be three distinct periods in this society. I. Period of Foundation (around 1927) -Independency of the endocrine society from the other related societies, in which interest in the endocrine glands had increased at a constantly accelerated pace by that time. II. Period of Expansion (after 1950) ?Al-though almost all scientific societies regained their activities with the end of the IInd World War, progress of steroid chemistry changed the scope of endocrinology and participants of this field increased markedly in this period. The society set up the Eastern and Western Branches in 1953, which have had respective meetings besides the annual meeting of the whole country. Furthermore, Diabetes Society was founded in 1958 and the independent activity started since then. Two national institutes for endocrine study were established during this period, the one in Gumma University (founded in 1951), the other in Tottori University (founded in 1966). And several periodicals for the study of endocrinology were published by some organs. Now three journals are being published periodically by this society, FOLIA ENDOCRINOLOGICA JAPONICA (since 1925, in Japanese), ENDOCRINOLOGIA JAPONICA (since 1954, in English) and PROCEEDINGS OF THE ANNUAL MEETING (since 1966, in English). III. Period of Richness (after 1960) -Recently peptide hormones have also become measurable and concrete data of most hormones have enabled us to know a more precise insight of the body. Now our members could stand in front of the general medicine with a more comprehensive knowledge of endocrinology.
    However, through checking up papers published in the meetings of the recent years, articles about pathologic physiology are overwhelmingly large and those about therapeutic field are found only in two or three percentage. Hereafter the vast knowledge on endocrinology should be applied to the therapeutic field and as this society, too, additional effort and time should be devoted to a therapeutic investigation. Finally many specialists on endocrinology have grown up by the long continuous effort of this society. On the other hand, with the progress in knowledge, the one specialized in one hormone, has become more difficult to understand the other hornmoes. And it is a problem of each researcher himself, but it should be taken into consideration by this society, too, in the arrangement of the annual meeting, -for instance, a coordinated effort on the part of the two societies should be essential between this and diabetes society. It would be desirable that the ex-cellent papers may be estimated properly by all members regardless of their fields and it is my belief that such an attitude of our members may become a greatest motive power for a further elevation of the level of this society.
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  • Glucocorticoids Therapy, Especially on the Results in the Cases of Alternative Day Treatment
    Kazuo KANEKO
    1970 Volume 46 Issue 5 Pages 513-525,499
    Published: August 20, 1970
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    This report presents the results on the study of the suppressive effects on the pituitary adrenocortical system by the administration of synthetic glucocorticoids concerning the period, doses and the method of administration, and the results of the clinical significance of the steroid alternative treatment.
    Plasma cortisol was measured by the following methods : extraction with chloroform, washing with alkaline solution and the fluorometry with H2O-CCl4 partition. Urinary 17-OHCS was measured by Silber-porter's method after hydrolyzing with β-glucuronidase.
    ACTH-test was performed by injecting 250 ug of β I-24 synthetic ACTH intramuscularyly, and another test by injecting 25 units of NE-ACTH by drip for 6 hours was adopted.
    On the SU-4885 test, the method of administration was 250 mg of metopirone every 2 hours for 24 hours.
    The results were summarized as follows :
    (1) The diurnal variation of plasma cortisol level in normal human adults was measured. The means and standard deviations were 11.0±3.9 ug/dl at 8.00 a.m., 9.0±3.2 ug/dl at 10.00 a.m., 5.6±2.6 ug/dl at 4 p.m, 4.7±1.7 ug/dl at 10.00 p.m., and 2.8±1.4, ug/dl at midnight, respectively. And they showed regular rhythm and reproducibility.
    (2) When 5 mg of hydrocortisone was administered to the normal adult at 0.00 a.m., the plasma cortisol level showed 5 to 10 ug/dl at 2.00 a.m., and a case with 10 mg of hydrocortisone showed 10 to 20 ug/dl, and at 8.00 a.m. the plasma cortisol level showed normal value in the former case, and decreased in the latter case. There was no suppression of cortisol secretion in the case with 2 mg × 4 of hydrocortisone. Therefore, it was observed that the plasma cortisol level was rather low at about 2.00 a.m., and this low level cortisol appeared in diurnal variation of human adult.
    (3) The suppression of cortisol secretion at the time of administration of 0.5 mg dexamethasone showed the least in the case administered at 8.00 a.m., and next in the case at 4.00 p.m., and the most in the case at 0.00 a.m. And there was a close corelation between the plasma cortisol level at 8.00 a.m., and the hours after administration of 1.5 mg of dexamethasone.
    The greater the doses of dexamethasone were, the more suppressed became the adrenal cortical function, and it took much time to return it to the normal level.
    (4) The steroids were administered at 8.00 a.m., every other day for a period of two weeks to two months, and then the plasma cortisol levels were measured at the time just before administering the steroids. There was observed a normal value in all cases in which 30 mg of prednisolone were administerd, in three out of five cases in which 40 mg of prednisolone were administered and decreased in both cases in which 60 mg of prednisolone were administered.
    On the rapid ACTH test, there were found normal changes in seven out of eleven cases in the group in which 30 to 40 mg of prednisolone were administered by the alternative day treatment.
    The standard ACTH test and the metopiron test were performed in the cases administered with 40 mg of prednisolone every other day for 45 days, and then no fluctuation was found in ACTH test, but significant suppressions were found in three out of four of metopiron tests.
    On comparing the alternative day treatment with every day treatment on the basis of the same doses, a decrease of about 50 % of suppression of adrenal gland function was found in the cases receiving the alternative day treatment.
    Less countenance change like Cushing's syndrome was found in the cases of alternative treatment, and that change was decreased markedly in the cases administered by the alternative day treatment changed from the every day treatment.
    As for the alternative treatment, it was found to be a useful treatment for following diseases : nephrotic syndrome, hepatitis, allergic disease,
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  • Toshikazu SAITO
    1970 Volume 46 Issue 5 Pages 526-533,501
    Published: August 20, 1970
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Plasma hypertonicity and hemorrhage cause release of antidiuretic hormone (ADH) from neurohypophysis. In order to elucidate the location of the pathways through which osmotic and hemorrhagic stimuli influence the neurohypophysis, hypertonic saline in-fusion and hemorrhage experiments were performed in dogs.
    Mongrel dogs of both sexes were used and the following seven groups of dogs were prepared.
    (1) Intact dogs : Experiments were performed under anesthesia with pentobarbital sodium.
    (2) Decorticated dogs : After craniotomy the telencephalon was removed by suction.
    (3) Decerebrated dogs : The transection of the midbrain was performed at the level of colliculus superior by suction.
    (4) Dogs with diencephalic islands : The telencephalon was removed and the transection of the midbrain was performed by suction.
    (5) Dogs with spinal cord sectioned : The spinal cord was sectioned at the level of C-1 by suction.
    (6) Dogs with cervical vagus nerves sectioned : The bilateral cervical vagus nerves were sectioned a few centimeters cephalad to the caudal cervical ganglion.
    (7) Dogs with abdominal vagus nerves sectioned : The abdominal vagus nerves (i.e. ventral and dorsal gastric nerve) were sectioned.
    The experiments on the intact dogs, decorticated dogs and dogs with cervical or abdominal vagus nerves sectioned were performed under pentobarbital sodium anesthesia. The decerebrated dogs, dogs with diencephalic islands and dogs with their spinal cord sectioned were not anesthetised during the experiments.
    In hemorrhage experiments each animal was allowed to bleed freely through an open cannula inserted into the femoral artery until the mean arterial blood pressure fell to a level below 50% of the initial value and less than 50 mmHg. The experiments of intravenous infusion of hypertonic saline were performed by infusing 2.5% saline at a speed of 0.25 ml/min/Kg B.W. for 45 minutes. The ADH titers in jugular vein plasma were measured by the method of Yoshida et al before and after the hemorrhage or infusion of saline.
    In intact dogs hemorrhage caused a marked increase in plasma ADH titer from 41.4 ±11.0 μU/ml to 360±74.6 μU/ml. Hemorrhage that was performed in the same way as that in the intact dogs caused an increase in plasma ADH level, from 26.9±9.0 μU/ml to 206±60.7 μU/ml in the decorticated dogs and from 28.1±7.5 μU/ml to 476±149 μU/ml in the spinal dogs. These increases are statistically highly significant. In two group of dogs whose midbrains were sectioned, i.e., the decerebrated dogs and the dogs with diencephalic islands, concentration of ADH did not increase significantly following hemorrhage.
    The dogs with abdominal vagus nerves sectioned also showed a marked increase in ADH levels in plasma in response to hemorrhage. Significant rises in ADH titers in plasma after hemorrhage were also observed in the dogs with cervical vagus nerves sectioned. However, these responses were markedly attenuated compared with those observed in the dogs with abdominal vagus nerves sectioned.
    The intravenous infusion of hypertonic saline in the intact dogs resulted in an increase in plasma ADH titer from 34.4±8.4 μU/ml to 72.2 ±12.3μU/ml. In the dogs with diencephalic islands the concentration of ADH rose from a control level 26.2±3.6 μU/ml concentration of ADH rose from a control level 26.2±3.6 μU/ml to 55.9±12.5, μU/ml after the hypertonic saline infusion. These increases in plasma ADH titers are statistically significant. There was no significant difference in the increment in plasma ADH titers between these two groups of dogs.
    These results suggested that isolated diencephalon could release ADH in response to an osmotic stimulus without nervous connection with the adjacent nervous system. On the contrary,
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  • Yutaka MATSUMOTO, Koichiro ISURUGI, Kenji KINOSHITA, Hisao TAKAYASU
    1970 Volume 46 Issue 5 Pages 534-538,503
    Published: August 20, 1970
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    A new synthetic corticotropin, DW-75 (D-Ser1-Nle4-Val251-25-Corticotropin), was applied in normal subjects for adrenocortical function test. 25 IU or 0.04 mg of DW-75 was administered by (1) 6 hr. I.V. infusion, (2) single I.V. injection, and (3) I.M. injection. Plasma cortisol was determined fluorimetrically in these subjects before and successively after the administration of the synthetic corticotropin.
    Urinary 17 OHCS and 17 KS were also studied. It was demonstrated that adrenal response was obtained maximally by the 6-hour-infusion method when observed by plasma corticsol level as well as urinary 17 OHCS exretion. In cases which received the single I.V. and I.M. injection, adrenal responses were less remarkable but plasma cortisol responded sufficiently enough to be used as a rapid stimulation test routinely.
    No side effects were observed throughout the study in any of the subjects. It is suggested that the preparation can be used also for treatment purposes.
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  • Report I. Estimation of Homovanillic Acid and Vanillylmandelic Acid in Urine
    Eiji TAKAHASHI
    1970 Volume 46 Issue 5 Pages 539-558,504
    Published: August 20, 1970
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Report I.Estimation of Homovanillic Acid and Vanillylmandelic Acid in Urine
    Homovanillic acid is the end product of dopamine and vanillylmandelic acid is that of noradrenaline and adrenaline. The major portion of these metabolites is excreted in the urine of normal subjects and the estimation of these is important in studying of the catecholamine metabolism. Especially, the simultaneous measurement of urinary homovanillic acid and vanillylmandelic acid excretion is a useful diagnostic procedure for neuro-genic tumors.
    For the estimation of homovanillic acid and vanillylmandelic acid, urinary phenolic acids were separated on the column chromatography of Amberlite CG-50 resin by the elution with 0.1 N acetic acid and the fractions of these two acids were obtained.
    Contaminations of these eluates were examined by the two dimensional paper chromatography. The homovanillic acid elute was contaminated with p-hydroxyphenylacetic acid, and the vanillylmandelic acid elute with p-hydroxymandelic acid. For the elimination of contaminating substances, homovanillic acid and vanillylmandelic acid were converted into 3-4-dihydroxyphenylacetic acid and 3-4-dihydroxymandelic acid, respectively, by the method of demethylation as described by Ruthven and associates. These catechol acids were absorbed on alumina, removed with acid and measured colorimetrically.
    In normal adults, the mean excretion of homovanillic acid was 4.93 ± 1.89 μg/mg creatinine and that of vanillylmandelic acid was 4.66 ± 1.62 μg/mg creatinine.
    It was found that this method for homovanillic acid and vanillylmandelic acid estimation was excellent in specificity and convenient in simultaneous estimation of these metabolites in the same urine samples.
    Report II. Catecholamine Metabolism in Neuroblastoma
    Catecholamine metabolism was studied in eight patients with neuroblastoma. The following results were obtained.
    1) The urinary excretion of homovanillic acid ranged from 296 to 22 μg/mg creatinine and that of vanillylmandelic acid ranged from 1175 to 7 μg/mg creatinine. The marked elevation in the urinary excretion of these two acids was found in all cases.
    2) The urinary excretions of dopamine and noradrenaline ranged from 10.552 to 0.987 μg/mg creatinine and 8.380 to 0.052 μg/mg creatinine, respectively, but those of adrenaline were within normal range or in trace.
    3) The tumor tissues and the metastatic liver tissues in four cases contained dopamine and noradrenaline in a high concentration but adrenaline could not be found.
    4) The activities of catechol-O-methyltransferase, a metabolizing enzyme of catecholamines and phenylethanolamine-N-methyltransferase, a synthesizing enzyme of adrenaline from noradrenaline, were assayed in two cases. The catechol-O-methyltransferase activity was detected in the tumor, but the phenylethanolamine-N-methyltransferase activity was not detected.
    The presence of dopamine and noradrenaline in the tumors, the increased urinary excretions of dopamine, noradrenaline, homovanillic acid and vanillylmandelic acid, and the presence of the catechol-O-methyltransferase activity in the tumor provide direct evidence of the existence of the dopa → dopamine → noradrenaline pathway in neuroblastoma.
    These observations strongly suggested that catecholamines, especialy dopamine and noradrenaline, which were synthesized in the tumor, might be metabolized into 3-methoxy-4-hydroxyphenyl compounds in it, at least by the mechanism of O-methylation. This possible mechanism might be supported by the fact that cystathionine is usually found in the urine of the patients with neuroblastoma because of abundant formations of s-adeno-sylmethionine from methionine and ATP for the O-methylation.
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  • Kishio F. ITOH
    1970 Volume 46 Issue 5 Pages 559-568,506
    Published: August 20, 1970
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    It is a well-known fact that thyroxine (T4) and 3, 5, 3′-triiodothyronine (T3) are bound to special serum proteins in the blood, called T4-binding proteins and T3-binding proteins. It seems generally accepted that there are at least three kinds of T4-binding proteins, which are T4-binding prealbumin (TBPA), T4-binding globulin (TBG) and albumin.
    Recently, several investigators, however, have suggested that T4 may be bound to another protein. With regard to T3-binding proteins only few works have been done. The present study was designed to demonstrate and identify these T4-and T3-binding proteins by utilizing various techniques.
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  • 1970 Volume 46 Issue 5 Pages 569-596
    Published: August 20, 1970
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
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