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Volume 80 (1963)
- Issue 4 Pages 315-
- Issue 3 Pages 205-
- Issue 2 Pages 103-
- Issue 1 Pages 1-
Volume 80, Issue 2
Displaying 1-7 of 7 articles from this issue
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Takashi Miura1963 Volume 80 Issue 2 Pages 103-117
Published: July 25, 1963
Released on J-STAGE: November 28, 2008
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(“H” Disease-like Clinical Features without Indicanuria and Generalized Aminoaciduria): - A Probaby New Inborn Error of Tryptophan MetabolismKeiya Tada, Hisao Ito, Yoshiro Wada, Tsuneo Arakawa1963 Volume 80 Issue 2 Pages 118-134
Published: July 25, 1963
Released on J-STAGE: November 28, 2008
JOURNAL FREE ACCESSA case which was suggested to be a new inborn error of tryptophan metabolism was described. The patient, a 9 year-old girl, was characterized by dwarfism, mental defect, photosensitivity and gait disturbance like cerebellar ataxia. These symptoms and signs were clinically similar to those in H disease but definitely different from it in laboratory findings. Laboratory studies revealed that the patient excreted an excessive amounts of tryptophan without increase in indican or indoleacetic acid excretion. The tryptophan loading test exhibited that plasma level of tryptophan, following the loading, increased markedly and remained elevated longer accompanied with much increase in tryptophan and less increase in kynurenine in urine as compared with those in the controls. Basing upon the above-mentioned results, it was presumed that a biochemical lesion in the present disorder might lie in the conversion of tryptophan to kynurenine.View full abstractDownload PDF (2797K) -
Mizu Kojima, Masaru Amada1963 Volume 80 Issue 2 Pages 135-147
Published: July 25, 1963
Released on J-STAGE: November 28, 2008
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Report 14. Observations on the Appearance of Clinical Symptoms from the Standpoint of Hematopoietic Phases of the Bone Marrow and the Fields of Blood Defense Reaction, with Special Reference to theAkira Saito1963 Volume 80 Issue 2 Pages 148-167
Published: July 25, 1963
Released on J-STAGE: November 28, 2008
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Takeo Kuroyanagi, Masanobu Saito1963 Volume 80 Issue 2 Pages 168-174
Published: July 25, 1963
Released on J-STAGE: November 28, 2008
JOURNAL FREE ACCESSThe proliferative capacity of leukemic cells as reflected by their uptake of tritiated thymidine was determined in patients with AML and CML. The percentage of normal myeloblasts and myelocytes averaged 64.6% and 20%, respectively. The percentage of acute leukemic myeloblasts and myelocytes was markedly decreased, averaging 6.8% and 6.7%, respectively. The percentage of myeloblasts and myelocytes from CML was also decreased, averaging 8.7% and 7.8%, respectively. Interpretations about the total generation cycle derived from these results were discussed.View full abstractDownload PDF (986K) -
I. Effect of Normal BileTakashi Matsushiro1963 Volume 80 Issue 2 Pages 175-181
Published: July 25, 1963
Released on J-STAGE: November 28, 2008
JOURNAL FREE ACCESSUsing and assay system consisting of a bacterial β-glucuronidase preparation and phenolphthalein glucuronide, it was experimentally demonstrated that the bile, both the bladder bile and the choledochus bile, of patients without liver or biliary tract diseases had an inhibitory effect on the activity of bacterial β-glucuronidase.View full abstractDownload PDF (316K) -
Histometrical Studies of Renal Artery in Experimental Hypertension of RatsShigeru Ohyama1963 Volume 80 Issue 2 Pages 182-204
Published: July 25, 1963
Released on J-STAGE: November 28, 2008
JOURNAL FREE ACCESS1) Durable arterial hypertension could be induced in rats by unilateral application of silver clips on renal arteries. When the clamping was effective, blood pressure rose steadily, attained approximately its highest level in each case in 5 weeks and remained essentially at the same level to the 20th week after the operation. Severe arteriolar injuries were observed in renal arteries in cases with mean systolic blood pressure over 170 mm Hg.
2) Histometrical treatments of renal artery revealed a regular relation between anatomical radius R and corresponding medial thickness D in the form of D=aRb, a and b being constants.
3) Estimated D was calculated in each case from the above formula at R=100μ and was correlated to the mean systolic blood pressure P. The relation could be defined by D=uPw, u and w being constants. The value of w was 0.75±0.19, which indicated that the increase of medial thickness was about 68% corresponding to blood pressure elevation by 100% at R=100μ of rat's renal artery.
4) Because the value of w was a little smaller than 1, it was concluded that the adaptation of arterial muscular coat to blood pressure elevation was more or less imperfect in character, and finally a limit was inevitably reached where the equilibrium between blood pressure and arterial muscular coat was disturbed.
5) The incidence of arteriolar injuries was quantitatively expressed by an index of arteriolar lesions I, which was determined by the count of arterial lesions in a square centimeter of renal cortex in histological slides. The relation between I and P or between I and D was defined by an exponential Ip=IOPeαp or ID=IODeβD, respectively. The results demonstrated that arteriolar injuries, when they began to appear, increased so rapidly that they practically attaned the level of infinity within relatively narrow range of blood pressure elevation. The highest possible hlood pressure in rats was estimated to be about 230 mm Hg and the maximum medial hypertrophy was about 100% of the normal arterial muscular coat.
6) The development of arterial injuries in experimental hypertension was discussed in comparison to that in human hypertension. It was assumed that some process must precede histologically confirmable arterial lesions and lower the resistance of arterial wall, before renal artery succumbed to high blood pressure.View full abstractDownload PDF (4923K)
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