Biomedical subjects
Publications and source records attributed to T Kawabe.
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Excavated bones (rib) obtained from 50 sites in Japan were measured by ICP atomic emission spectrometry and atomic absorption spectrometry for concentration of 19 elements, including Al, B, Ca, Cd, Cr, Co, Cu, Fe, K, Mg, Mn, Na, Ni, P, Pb, Sr, Ti, V and Zn. One hundred and forty-one specimens were classified into five groups according to Japanese prehistoric and historic eras (Jomon, Yayoi, Kofun, Kamakura and Muromachi, and Edo). The elements, with concentrations which showed no significant change with era were Al, B and Cr. Average concentrations of Ca were in the range 2-2.5 X 10(-1) g g-1 and those of P ranged from 1.1 to 1.3 X 10(-1) g g-1, indicating a well-preserved bone mineral matrix. The Ca/P ratio (mol/mol) was lowest in the Edo group--1.48 as compared with 1.54-1.66 in the other groups. Among the elements which showed changes with era were Pb, Fe, Co and Mn, all of which showed remarkably elevated concentrations in the Edo group. In addition to this unique elemental composition of Edo bones, samples from the Kofun era showed a completely different composition from those of other periods, i.e. they had the highest concentrations of Cd, Zn and Mg, and the lowest concentrations of Cu, K, Ni and Sr. The cause of the elevated Pb concentration in Edo bones is discussed in relation to human activities which may have led to environmental Pb pollution.
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A 57-year-old male, who had been suffered from hypertension and diabetes mellitus for 10 years, was admitted to the hospital because of thirst, lassitude and muscle wasting. On admission, his urinary excretion of 17-OHCS and plasma cortisol levels were elevated without diurnal variations. Plasma ACTH levels were found to be very low with repeated determinations. Dexamethasone suppression test, 2 mg 4 times a day orally for 2 days, showed no changes in plasma cortisol levels and only a mild reduction in urinary 17-OHCS excretion. Estimation of urinary catecholamines showed an increase only in norepinephrine. Abdominal computerized tomography and radionuclide scanning of adrenal glands with 131I-adosterol demonstrated a well-defined adrenal mass in the left side without apparent changes in the right side. 131I-metaiodobenzylguanidine scintigraphy was negative. At surgery, his left adrenal medulla was found to be hypertrophic in addition to the cortical tumor. The left adrenal gland was also removed. After surgery, excretion of urinary catecholamines fell to nearly the normal range and he was discharged without insulin and antihypertensive drugs. Microscopically, the cortical tumor is an adenoma consisting of lipid laden cells and eosinophilic compact cells. Medullary cells were distinctly hyperplastic in appearance and many of the cells were extensively vacuolated, suggesting an active functional status. The present report describes a patient with Cushing's syndrome who showed increased urinary catecholamine excretion due to the possible coexistence of adrenal medullary hyperplasia. As far as we know, this is the first case of Cushing's syndrome with this abnormality.
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A fluorometric liquid chromatographic method was developed for measurements of unconjugated oestradiol and oestriol in the serum of pregnant women. The serum samples are injected directly into the apparatus and pass to a pretreatment column, where oestrogens are adsorbed while hydrophilic components such as proteins and carbohydrates are not. The oestrogens then pass into a separation column containing a new type of polymer gel. The mobile phase consists of an acetonitrile-water mixture, and separation is achieved by a reversed-phase mechanism. The eluent is monitored for fluorescence. Data on the reproducibility and recovery by this method and the correlation of values with those obtained by radioimmunoassay are reported. Results on the increases of oestradiol and oestriol in the serum during pregnancy are also reported.
Fetal pancreatic islets (21.5 days old) were cultured in RPMI 1640 containing either 2.8 or 11.1 mM glucose for 7 days. After the 7-day culture period, islets cultured in 2.8 mM glucose demonstrated a minimal first phase of insulin secretion in response to acute glucose stimulation, whereas islets cultured in 11.1 mM glucose demonstrated a biphasic insulin secretory pattern. Islets cultured in 11.1 mM glucose initiated insulin secretion at 4.4 +/- 0.1 mM glucose and plateaued at 11.6 mM glucose when exposed to a linear gradient. In addition, culture in 11.1 mM glucose increased DNA content (P less than 0.01) and [3H]thymidine incorporation (P less than 0.05) in fetal islets. However, ultrastructural morphometric analysis indicated that the actual number of beta-cells within islets cultured in either 2.8 or 11.1 mM glucose did not increase. The insulin contents of islets cultured in 2.8 and 11.1 mM glucose were 0.46 +/- 0.06 and 1.14 +/- 0.10 mU/islet, respectively. During subsequent glucose stimulation, islets cultured in 2.8 and 11.1 mM glucose released 3% and 5.6% of their total insulin content, respectively. Ultrastructural morphometric analysis indicated that 11.1 mM glucose stimulated an increase in the volume of individual beta-cells, i.e. hypertrophy. The hypertrophy of beta-cells within islets cultured in 11.1 mM glucose resulted in a concomitant increase in islet volume. Finally, the hypertrophy of beta-cells within islets cultured in 11.1 mM glucose was a result of increased volumes of mitochondria, secretory granules, and, to the greatest extent, endoplasmic reticulum. These findings indicate that glucose is a potent factor in the maturation of cultured fetal rat islets.
The value of creatinine height index (CHI), defined as milligrams of 24-h urinary excretion of creatinine divided by height in centimeters, was investigated on 21 healthy Japanese adults engaged in sedentary work. The average values were 10.58 in males and 6.68 in females. High partial correlation coefficients controlling sex were found among CHI, weight, fat-free mass, arm muscle area (AMA) and 24-h urinary excretion of creatinine. These indices had high loadings in the first factor of body size by principal component analysis. Regression of CHI on AMA differed in the intercept (i.e. the level of CHI at corresponding AMA) but not in the slope, from that studied under low-creatine diet in the U.S.A. Correcting AMA using arm bone area for Japanese and CHI with dietary factor, the relation between CHI and AMA in this study seemed to be in good agreement with that found in the U.S.A.
To study the effects of growth hormone (GH) on the in vitro maturation of fetal islets, the fetal islets were cultured for 7 days in RPMI 1640 containing 10% fetal bovine serum and 11.1 mM glucose with or without GH. Culture with 1 microgram/ml of bovine GH increased the DNA content of the islets and [3H]thymidine incorporation into DNA confirming results of other investigators. In addition, however, the insulin secretory dynamics and ultrastructural morphometrics were investigated. It was found that GH-treated islets demonstrated increased insulin release during acute glucose stimulation when expressed as microunits per islet per minute. However, when insulin release during acute glucose stimulation was expressed as microunits per microgram of DNA per minute to compensate for the increased DNA content of GH-treated islets, no change in insulin release was observed compared to control islets. When GH-treated islets were perifused with a linear glucose gradient, the insulin secretory response was suppressed as indicated by changes in the threshold level, plateau level, and half-maximal response. Ultrastructural morphometric data showed that the average beta-cell volume in control and GH-treated islets was the same, eliminating the possibility that beta-cell hypertrophy occurred. Similarly, the nuclear volumes of the beta cells in control and GH-treated islets remained unchanged. This finding coupled with the observed increased DNA content and [3H]thymidine incorporation suggests that GH functions by increasing cell multiplication within the islets and not by inducing polyploidy. Finally, the volumes of cytoplasmic organelles in control and GH-treated islets were the same indicating that cytodifferentiation did not occur.
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The direct effects of growth hormone (GH) on the endocrine pancreas were studied in isolated islets of rats. To study GH-induced insulin release, islets were incubated in RPMI 1640 medium containing 1 or 10 micrograms/ml of bovine GH for 120 minutes. Islets incubated in the absence of GH served as controls. During the incubation, GH significantly increased the insulin concentration in the medium. To study the effect of GH on subsequent glucose-induced insulin release, islets were preincubated with GH; then the islets were transferred to perifusion chambers and after a 30-minute stabilization period with 2.8 mM glucose, the islets were stimulated by addition of 16.7 mM glucose for 60 minutes. These perifusions were performed in the absence of GH. Glucose-induced insulin release from control and GH-pretreated islets peaked at five minutes during the first phase (0-8 minutes) and plateaued at 25 minutes during the second phase (9-60 minutes). Preincubation with GH (1 microgram/ml) did not change baseline or first phase release, but significantly suppressed the second phase of insulin release. When islets were preincubated with 10 micrograms/ml of GH, both phases of glucose-induced insulin release were suppressed; the total amount of insulin released by GH-pretreated islets was suppressed by 36.6% during the subsequent glucose stimulation period. These data indicate that GH stimulates insulin release by itself (GH-induced insulin release) but inhibits subsequent glucose-induced insulin release in a dose-dependent manner.
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This report dealt with a rapidly growing ball thrombus floating in the left atrium in a case with mitral stenosis detected by serial two-dimensional echocardiography and confirmed at operation. A 45-year-old female was admitted to our hospital on January 7, 1982 because of dyspnea, orthopnea and fever. On admission she had typical auscultatory signs of mitral stenosis, and her chest roentgenogram revealed slight pulmonary venous congestion and marked left atrial enlargement. Laboratory findings including complete blood counts, coagulation studies and blood chemistry were normal except a positive CRP test. Two-dimensional echocardiography performed on January 8 revealed a tight mitral stenosis with the mitral orifice area of about 0.9 cm2, and a floating ball thrombus in the left atrium, which was 2.5 X 3 cm in size. Fuzzy echoes flowing slowly around the thrombus were also observed. Intravenous administration of heparin was started immediately. In the next morning (January 9), the two-dimensional echocardiography was reexamined, which revealed a markedly growing thrombus which became 4 X 4 cm in size. Several hours after the reexamination mitral valve replacement was performed. The removed thrombus was 5.5 X 7 cm in size and consisted of three laminated structures. This finding was consistent with the echocardiographic observations. Coagulation studies made just before operation showed increased coagulability. Increased stagnation of blood in the left atrium due to heart failure and a transient increase of blood cell aggregation and coagulability induced by preceding infection might be responsible for the genesis of such a thrombus.