Folia Endocrinologica Japonica
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
Volume 39, Issue 1
Displaying 1-5 of 5 articles from this issue
  • Akito NOGUCHI, Seiya SATO, Hideo KURIHARA, Youichi OZEKI
    1963 Volume 39 Issue 1 Pages 7-10,1
    Published: April 20, 1963
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Attempts to extract a long-acting thyroid stimulator (LATS) in the serum from hyperthyroid patient, or at least to concentrate the activity of it, were performed by DEAE cellulose column chromatography.
    5 ml of serum containing LATS was placed on a 2 * 30 cm. column pached with DEAE cellulose which was equilibrated at pH 8.4 with 0.005 M Tris buffer. The elution was carried out by the step-wise method as shown in Fig. 1. Fractions of 6 ml. were collected at the rate of 30 ml per an hour.
    The activity of LATS was assayed by the Noguchi modification of McKenzie's method. The concentration of serum protein in each fraction was determined by Greenberg's method, and the paper electrophoresis was performed by the method which was reported by Mori et al.
    Fig. 1 shows a typical chromatogram of the LATS under these conditions. Four fractions were separated. A LATS was found in the first fraction, which contained about 34% (mean value) by weight of the original serum protein (Table 2). The most of thyrotropin was in the second fraction (Table 1). From this result, it is concluded that thyrotropin differed from LATS on the adsorption for DEAE cellulose. On the development of paper electrophpresis, it was observed that the greater part of protein in the first fraction was γ-gliblin.
    The clear separation of LATS from thyrotropin was not performed satisfactorily. However, it can be said, this method is useful to concentrate the activity of LATS in hyperthyroid serum.
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  • 2. Metabolism of I131-labeled L-diiodotyrosine in various thyroid diseases
    Tunesuke KUSAKABE
    1963 Volume 39 Issue 1 Pages 11-25,2
    Published: April 20, 1963
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Observations were made on the deiodination of I131-labeled L-diiodotyrosine (L-DIT I131) in 71 patients with various thyroid diseases. Of these patients 19 had simple goiter, 13 hyperthyroidism, 9 myxedema without goiter, 2 hypothyroidism with goiter, 5 cretinism with dysgenesis of the thyroid, 10 nodular goiter, 6 thyroid cyst, 3 thyroid cancer, 2 Hashimoto's struma, 1 Riedel's struma and 1 subacute thyroiditis.
    1. Simple goiter
    Thyroid tissues from the patients with simple goiter could deiodinate L-DIT I131 normally. All patients with simple goiter reported here had a normal rate of deiodination of administered L-DIT I131.
    2. Hyperthyroidism
    The iodotyrosine deiodinating activity of the thyroid in hyperthyroidism, though slightly higher than in simple goiter, was not significantly so. In the patients with hyperthyroidism, the rate of deiodination of administered L-DIT was similar to that in control subjects.
    3. Myxedema
    Many of the myxedematous subjects had a slow rate of deiodination of injected L-DIT I131 The percentage of labeled iodine which was present as L-DIT I131 in urine was distinctly higher in these patients than in control subjects. The percentage of the administered dose of L-DIT I131 which was excreted unchanged was higher in these patients than in any of the control subjects. This percentage was reduced by thyroid therapy. The results showed that these patients had a peripheral defect in deiodination of L-DIT I131, and that this defect was probably caused by hypothyroidism.
    On the other hand, some of the patients with myxedema had a normal rate of deiodination of administered L-DIT I131 This finding might suggest that myxedema itself does not cause a defect in peripheral deiodination.
    4. Hypothyroidism with goiter
    Thyroid tissues from the 2 patients with goitrous hypothyroidism could not deiodinate L-DIT I131 in vitro. In these patients, the rate of deiodination of injected L-DIT I131 persisted after thyroid therapy. Thyroid tissue from one of these left the L-DIT I131 unchanged after thyroid therapy. Thus, it seemed that these patients had a deiodination defect in the thyroid, but not in the periphery.
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  • 3. Defective deiodination of I131-labeled L-diiodotyrosine in patients with simple goiter
    Tunesuke KUSAKABE
    1963 Volume 39 Issue 1 Pages 26-36,4
    Published: April 20, 1963
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    A study was made of 10 patients with simple goiter and a defect in deiodination of diiodotyrosine.
    Six patients apparently had a defect both in thyroidal and in peripheral deiodination. All of them had an abnormally slow rate of deiodination of administered I131-labeled L-diiodotyrosine (L-DIT I131). In vitro studies of the thyroid glands from 3 of these 6 revealed defective deiodination. The other 3 were goitrous cousins of one of them, and presumably had a similar defect. The defective deiodination in these 6 patients persisted after thyroid therapy.
    The other 4 patients had a defect in peripheral deiodination. All of them had an abnormality of deiodination of administered L-DIT I131. Thyroid tissues from 3 of these 4 were tested in vitro, and the deiodinating activity was found to be normal. The fourth was a goitrous daughter of one of them. This defect in peripheral deiodination seemed to be somewhat corrected by thyroid therapy.
    Observations made on our patients suggest that a defect in deiodination of iodotyrosines in the periphery or throughout the body would supposedly produce simple goiter and that this defect is transmitted by a dominant and autosomal gene.
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  • Ryosaku KURODA
    1963 Volume 39 Issue 1 Pages 37-45,5
    Published: April 20, 1963
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Part II. Urinary antidiuretic hormone (ADH) and congestive heart failure.
    A clinical entity, congestive failue has been subjected to physiologic reinterpretation. This reinterpretation has been due for the most part to the fact that this entity is one involving a complex series of events occuring over a considerable period of time between the initiating factors and the final remarkable condition of the edematous state and there is no direct correlation between initiating factors and final condition.
    It is no doubt that the edema is a state of abnormal retention and distribution of Na and water in the decreased their excretion from kidney, therefore many investigators emphasized the role of the kidney in the development of congestive failure, and impaired glomerular filtration has been considered principal renal abnormality. Lately many peports has pointed out the abnormal function of the kidney tubules, and this in turn admitt the humoral factors which control the reabsorption of Na and water.
    As regard to the Na reabsorption aldosterone play an important role and evidence has shown that in congestive failure it's excretion is much greater than normal. On the other hand posterior pituitary antidiuretic hormone (ADH) is the potent water conservatory hormone and control water reabsoption in the kidney.
    In spite of many researchs, we are far from a final conclusion in regard to the role of posterior pituitary hormone. In the pervisous literature author has reported the reliable extraction and estimation method of this hormone from urine.
    Employing this method hospitalized valvular, congenital heart failure in various grade were used for the estimation of urinary antidiuretic hormone (ADH), and observed the changing pattern of ADH under the treatment of digitalis and diuretics. Secretion mechanism of ADH was examined by water load. Inactivation of ADH in the serum of congestive failure was compaired to liver cirrhosis and using portal vein constricted rabits.
    The conclusions thus obtained as follows.
    1) Urinary excretion of ADH in congestive heart failure were remarkably increased than the normal subject and as the grade of failure advance ADH increased.
    2) There was no direct correlation between the ADH excretion and the initial diuresis which was caused by the digitalis and diuretic therapy, but as the congestive failure improve urinaly ADH decreased.
    3) In contrast with normal subject no decrease or disappearance in urinary ADH was found after the administration of water in congestive failure. This in turn, proved
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  • 1963 Volume 39 Issue 1 Pages 46-71
    Published: April 20, 1963
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
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