Biomedical subjects
Publications and source records attributed to T Koide.
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Pituitary-gonadal functions were investigated by LH-RH test, HCG test and bilateral testicular biopsies in 5 boys with unilateral varicocele at various pubertal stages and the results were compared with those in the normal boys at puberty. The ages of the patients ranged from 12 to 18 years. With the progress of pubertal stage, both the basal value and response of serum FSH to LH-RH became higher as compared with normal boys. The basal value and response of serum LH showed no significant difference except for one case where higher values and no significant differences in the basal value and response of plasma testosterone to HCG stimulation were observed. The disturbance of spermatogenesis in the affected testis becomes prominent with the progress of puberty, while changes in the testis of opposite side were mild.
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Etiology of QT prolongation and T wave high voltage was studied in 90 chronic alcoholics in relation to history of alcoholism, blood chemical values, heart rate and QRS voltage with a technic of multiple regression analysis. Incidences of QT prolongation (22%), T wave high voltage in lead V2 (9%), hypopotassemia (23%), hypocalcemia (26%) and hypomagnesemia (28%) were high, despite these examinations were done after relatively long abstention period (35 days on average). Sinus tachycardia (19%) and QRS high voltage (SV1 + RV5 exceeding 4 mV, 41%) were also frequent. Unexpectedly, QT interval did not correlate to serum electrolytes, including calcium. Major factors associated with QT prolongation were sinus tachycardia, longer abstention period and larger amount of daily alcohol consumption. Although the reason of each association was not quite clear, alcoholic myocardial damage may be a cause of QT prolongation. Voltage of T wave in lead V2 was sensitive to serum potassium level, but the observed tendency of hypopotassemia acted to the direction against high voltage of T wave. The sole factor positively associated with high voltage of TV2 was high QRS voltage, which may be a manifestation of left ventricular hypertrophy.
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Long-term clinical effects of beta-blockers (propranolol in most cases) and calcium inhibitors (nifedipine in most cases) were studied in 16 patients with hypertrophic cardiomyopathy. On overall subjective symptoms, beta-blockers were effective in 50% of symptomatic patients, while calcium inhibitors were effective in only 33%. On angina pectoris, however, calcium inhibitors were superior to beta-blockers in our patients. Blood pressure decreased with each drug, and the decrease was significant with nifedipine. Otherwise there was no change in physical findings with either drug. Long-term (more than 6 months) use of beta-blockers resulted in an increase in cardiothoracic ratio on chest X-ray, a decrease in left ventricular ejection fraction on echocardiogram and more pronounced ST-T change on electrocardiogram. Prolonged use of nifedipine resulted in a slight decrease in cardiothoracic ratio, but no systematic change on echocardiogram and on electrocardiogram.
A simple human chorionic gonadotropin (hCG) test to measure Leydig cell function is described. Plasma testosterone was measured on two occasions, once before intramuscular injection of 10,000 IU of hCG and again four days later. Preliminary tests in 10 adult males showed a maximal increase in plasma testosterone between the third and fifth day that was confirmed in a further 20 normal subjects when measured once on the fourth day. Except for 2 patients with hypospermatogenesis, 24 showed a good response and the mean increase was comparable with that in normal males. Nineteen patients with Klinefelter's syndrome usually had lower basal levels and showed a poor response, with the exception of six patients in whom there were moderate but definite increases. Twelve patients with hypogonadotropic hypogonadism had basal testosterone concentrations below 1 ng/ml and eight responded poorly to hCG stimulation. However, four patients showed a moderate but definite response.
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We studied the inhibitory effect of urinary macromolecular substances (UMM), more than 10,000 mol. wt., on aggregation of calcium oxalate crystals in a crystal-seed system and a non-crystal-seed system. In both assay systems, UMM from non-stone-farmers showed a marked inhibitory activity on crystal aggregation, whereas UMM from recurrent stone-formers showed a weak inhibitory activity. The distinction between the two types of UMM was greater in the non-crystal-seed system. The macromolecular inhibitors seemed to be composed of proteins or protein-complexes inasmuch as approximately 70 to 90 per cent of the macromolecular inhibitory activity was destroyed by protein digestion with pronase. Urinary acid glycosaminoglycans, which have been considered possible inhibitors, played a small role in the inhibition of crystal aggregation.
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In histochemical studies it was shown that sulfated acid glycosaminoglycans (AGAGS) were produced and secreted into the tubular lumen in renal papilla, but not in the renal cortex of muddy stone forming kidney. There was no secretion of sulfated AGAGS in renal papilla histochemically during hydronephrosis before stone formation. On autoradiographic study with the use of 45Ca and 35S for labeling of sulfated AGAGS, we found that 45Ca accumulated in renal papilla of muddy stone forming kidney, but not in the other. 35S apparently accumulated into muddy stones. Measurement of calcium content of the renal papilla and cortex proved the results of autoradiographic studies, and measurement of uronic acid in the urine showed increased secretion of AGAGS in the urine from muddy stone forming kidney. From these results it was proposed that the sulfate AGAGS secreted in the urine could bind calcium crystals to each other amd make crystals aggregate massively.
Echocardiographic study was performed on the mitral valve echogram in cases with clinical as well as experimental acute myocardial infarction (AMI). The echocardiograms were recorded in 88 patients with AMI within 7 days from the onset. In 8 patients (9%), and abnormal monophasic triangular diastolic pattern of the mitral valve was observed. Among them, 6 were examined within 12 hours after the onset and the remainder 2 within 24 hours. In all 8, markedly prolonged isovolumic relaxation time (IRT) was present. Mitral valve motion, IRT and peak negative dp/dt of the left ventricle were examined in 5 mongrel dogs following obstruction of the main left coronary artery, one of which was followed up for next 24 hours. Following coronary occlusion, the IRT progressively prolonged from the control value of 20 msec to 130 msec (15 min), 130 msec (30 min), 140 msec (1 hr), 150 msec (6 hr) and 150 msec (24 hr), respectively. The respective values of peak negative dp/dt were 2,000, 800, 840, 840, and 620 mmHg/sec. The possible explanation for these changes was the impaired active relaxation of the left ventricle, resulting in a delayed opening (or at least the lack of usual diastolic opening) of the mitral value, which gave an abortive E-point or a markedly delayed D point. We conclude that the diastolic monophasic triangular pattern of the mitral valve echogram in a reflection of the prolonged left ventricular isovolumic relaxation, and an index of impaired left ventricular diastolic relaxation.
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The C-terminal amino acid sequences of human and of porcine antithrombin III have been determined as Gly-Arg-Val-Ala-Asn-Pro-Cys-Val-Lys and Gly-Arg-Val-Ala-Asn-Pro-Cys, respectively. These sequences are highly homologous with the C-terminal sequence of human alpha-1-proteinase inhibitor.