[A case of mitochondrial encephalomyopathy with myoclonic attacks, hyper-lactic-pyruvic acidemia, and decreased activities of complex II and cytochrome c oxidase].
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Biomedical subjects
Publications and source records attributed to M Shoji.
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12-O-Tetradecanoylphorbol-13-acetate (TPA) induced decreases in the catalytic activity and immunoreactivity of protein kinase C (PK-C) in the soluble fraction, accompanied by increases in their activities in the particulate fraction, of a human myeloid leukemia cell line KG-1. TPA also caused a similar down-regulation and translocation of PK-C in KG-1a, a cloned subline shown to be resistant to the differentiating effect of TPA. The activity levels of enzyme in the soluble and particulate fractions from KG-1 cells, however, were about three times higher than those from KG-1a cells. Immunocytochemical studies showed that, when KG-1 cells were treated with 10 nM TPA for 30 min, PK-C was translocated to the plasma membrane in the adherent subpopulation of cells, whereas the enzyme remained largely in the cytoplasm and perinuclear area of the nonadherent cells. TPA, in contrast, caused a PK-C translocation primarily to the perinuclear region in KG-1a cells. Phosphorylation patterns of PK-C substrate proteins in the two cell lines were similar, except that phosphorylation of the Mr 33,000 and 97,000 proteins were predominant in KG-1 and KG-1a cells, respectively. The present findings showed existence of certain differential effects of TPA on the PK-C system in the two leukemia cell lines, suggesting a molecular basis for the selective resistance of KG-1a cells to the differentiating action of TPA.
Human myeloid leukemia KG-1 cells are induced to differentiate to macrophage-like cells by tumor-promoting phorbol esters, such as 12-O-tetradecanoylphorbol-13-acetate (TPA). Cells from the cloned subline, KG-1a, unlike the parental line, are resistant to the differentiating effect of TPA. In the present studies, we investigated in these cells protein phosphorylation stimulated by various protein kinase C activators, including 1-oleoyl-2-acetylglycerol in the presence of the diacylglycerol kinase inhibitor R59022, TPA, mezerein, and bryostatin. All the agents stimulated, to a greater extent and with a higher potency, phosphorylation of several proteins in KG-1 cells than in KG-1a cells. On the other hand, these agents markedly stimulated phosphorylation of other proteins in KG-1a cells compared to that in KG-1 cells. The findings indicated that the actions of the diacylglycerol, 1-oleoyl-2-acetylglycerol, and the non-metabolizable activators (TPA, mezerein, and bryostatin) were very similar but not fully equivalent; and that KG-1a cells exhibited altered (increased or decreased) phosphorylation patterns, perhaps related to the TPA resistance characteristic of this subline of cells.
The general pharmacological properties of musk were studied. After the application of musk, inhibition of acetic acid-induced writhing, hemolytic effect and excitation of spontaneous uterine motility of rats, inhibition of spontaneous motility in isolated ileum of rabbits, and anti-inflammatory effects and potentiation of beta-adrenergic action in isolated preparations of guinea pig trachea were observed. These effects were not observed after application of muscone or allantoin, constituents of musk.
1. The pharmacological properties of a water extract of the Zizyphus seed (HO2) and that of the Zizyphus seed containing drug (HO1) were studied. 2. After oral or intraduodenal administration of 3 g/kg of HO1 or HO2, the hypnotic effects induced by hexobarbital-Na (38 mg/kg, i.p.) and diazepam-induced sleep in mice were potentiated. 3. After oral or intraduodenal administration of 3 g/kg of HO1 or HO2, gastric juice secretion and ulcers induced by water immersion stress, histamine and reserpine in rats were inhibited.
A quantitative bioassay for the detection and quantification of atrial natriuretic polypeptides (ANPs) was developed in a pentobarbital-anesthetized rat. Ten percent mannitol in 0.9% saline was infused to achieve stable diuresis. The conductivity of the urine, urine flow, and blood pressure were continuously recorded. A bolus injection of synthetic alpha-human atrial natriuretic polypeptide (alpha-hANP) elicited dose-dependent increases in the urine conductivity, sodium excretion, and urine volume. Changes in the urine conductivity correlated significantly with the increase in sodium excretion. By use of changes in urine conductivity, biological ANP activity of crude rat atrial extract was determined. Atrial contents of ANP in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were 25.5 +/- 1.2 microgram per atrium (n = 4) and 25.1 +/- 0.8 (n = 5) in euhydration. They were increased to 27.0 +/- 1.1 micrograms (n = 4) and 29.3 +/- 1.3 (n = 5, P less than 0.05), after 5-day water deprivation, respectively. This assay procedure provides a good tool for rapid and quantitative determination of ANPs.
To study responses of methionine enkephalin-like substance (MELS) and vasopressin (AVP) to hemorrhage, plasma MELS, AVP, and catecholamine levels and mean arterial blood pressure (MAP) and central venous pressure (CVP) were investigated in intact and adrenalectomized dogs (n = 34) under pentobarbital anesthesia. Plasma MELS increased significantly following a hemorrhage-induced rise in plasma epinephrine in intact dogs (n = 6). Plasma AVP rose concomitantly with a fall in CVP before MAP fell, but the subsequent fall in MAP was accompanied by a further elevation in plasma AVP concentration. In nonhemorrhaged control dogs (n = 6) these parameters did not change during the experiment. In adrenalectomized dogs (n = 6) the hemorrhage-induced increase in plasma MELS and AVP was significantly attenuated despite similar decreases in MAP as in intact dogs. In sham-operated dogs (n = 10) changes in these parameters were similar to those in intact dogs. The differences between plasma MELS in the superior vena cava and thoracic aorta did not change during hemorrhage in intact dogs (n = 6), but the differences in plasma AVP rose significantly, indicating a release of the hormone from the head. These results indicate that MELS release elicited by hemorrhage may largely arise from the adrenal gland and not the brain. Adrenalectomy attenuated AVP response to hemorrhagic hypotension.
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In order to assess the effects of centrally administered atrial natriuretic peptide (ANP) on renal water and electrolytes handling, arterial blood pressure, plasma vasopressin, renin activity, aldosterone, and ANP concentrations, synthetic alpha-human ANP (alpha-hANP) was administered intracerebroventricularly at a dose of 2.6 pmol.kg-1.min-1 for 30 min in pentobarbital-anaesthetized dogs (N = 6). In the control study (N = 6), artificial cerebrospinal fluid was infused. Intracerebroventricular administration of alpha-hANP increased significantly urine flow from 178 +/- 37 to 303 +/- 43 microliter/min (mean +/- SEM), sodium excretion from 27.3 +/- 8.9 to 54.4 +/- 10.5, mumol/min, potassium excretion from 16.1 +/- 3.7 to 24.0 +/- 5.1 mumol/min, and osmolar and negative free water clearances, accompanied by a significant rise in renal blood flow from 77.0 +/- 14.6 to 94.9 +/- 16.9 ml/min. Whereas glomerular filtration rate fell significantly, blood pressure and heart rate did not change. Plasma ANP, aldosterone, and PRA did not change significantly during the experiment, but plasma AVP were slightly but significantly decreased from 52 +/- 11 to 34 +/- 6 nmol/l. On the other hand, these parameters showed no changes in the control study, except a significant fall in glomerular filtration rate and a significant rise in PRA. Thus, it has been confirmed that ANP centrally brings about diuresis, natriuresis, and kaliuresis via some unknown mechanisms independent of the release of these hormones.
In order to study the effect of atrial tachycardia on the release of atrial natriuretic peptide (ANP), AVP, and methionine enkephalin (M-Enk), plasma concentrations of these peptides in the right ventricle were determined in patients with various arrhythmias (N = 10) during cardiac catheterization and incremental atrial pacing. Each pacing (100 per min, the maximum rate for 1:1 atrioventricular conduction, and 200 per min) lasted 4 to 5 min. Plasma ANP was significantly increased from 53.1 +/- 12.2 in the resting condition to 168.9 +/- 59.9 pmol/l at a pacing rate of 200 beats per min (P less than 0.05); plasma AVP tended to decrease, but not significantly, and plasma M-Enk did not change at all. Pulse pressure in the right atrium (PPRA) and mean right atrial pressure (MRAP) tended to increase during the pacing, and at the rate of 200 beats per min PPRA was significantly higher than at the rate of 100 beats per min. Mean arterial blood pressure, plasma osmolality, and plasma sodium and potassium concentrations did not change significantly. There were significant correlations between plasma ANP and PPRA, MRAP and heart rate. These results indicate that atrial pacing stimulates ANP release with a rise in right atrial pressure, but does not influence M-Enk and AVP releases.
The environmental radioactivity caused by the reactor accident at Chernobyl' was investigated from May 7 to May 31 of 1986 in Toyama. Measurement of radioactivities in airborne particles, rain water, drinking water, milk, and mugwort are carried out by gamma-ray spectrometry (pure Ge detector; ORTEC GMX-23195). Ten different nuclides (103Ru, 106Ru, 131I, 132Te-I, 134Cs, 136Cs, 137Cs, 140Ba-La) are identified from samples of airborne particles. In the air samples, a maximum radioactivity concentration of each nuclide is observed on 13th May 1986. The time of the reactor shut-down and the flux of thermal neutron at the reactor were calculated from 131I/132I and 137Cs/134Cs ratio. The exposure dose in Toyama by this accident is given as follows: internal exposure; [thyroid] adult-59 microSv, child-140 microSv, baby-130 microSv, [total body] adult-0.2 microSv, child, baby-0.4 microSv, external exposure; 7 microSv, effective dose equivalent; adult-9 microSv, child-12 Sv, baby-11 microSv.
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Recently, the number of women who participate in strenuous exercise has increased significantly. The relationship between delayed menarche and early onset of sports training, and increased incidence of menstrual dysfunction related to athletic activity had led to increased interest. Five basketball players who are among the best players in Japan were subjected to an investigation of endocrinological responses effected by 60 minutes continuous exercise cycle ergometer. The VO2max value was previously examined. Then, the level of load during exercise was established at 60% VO2max in this study. The serum level of estradiol increased significantly in the luteal phase but not so significantly in the follicular phase. Progesterone did not show a significant change during exercise. FSH increased slightly in both phases. However, LH showed a slight increase in the follicular phase and a slight decrease in the luteal phase. On the other hand, prolactin showed a continuous significant increase during exercise in both phases. These data suggested that strenuous daily training leads to a frequent significant increase in prolactin in athletic women and this frequent increase in prolactin may be one of the major factors causing menstrual dysfunction in athletic women. The specialized physician should be more concerned about the managing of athletes who are suffering from menstrual dysfunction.
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Fourteen goat fetuses were totally sustained in water by extracorporeal perfusion using a membrane oxygenator. The two groups which underwent perfusion methods may be described as follows: One was an A-V bypass through umbilical vessels which has been reported previously, and the other was a new method, a V-A bypass through cervical vessels. Ten fetuses were perfused by an A-V bypass and the longest survival time was 9 hours. Three fetuses suddenly died shortly after perfusion was started. Four fetuses were perfused by a V-A bypass and the longest survival time was 27 hours. Cardiovascular dynamics were stable from the beginning of perfusion. Autopsy revealed hepatomegaly and bloody ascites in A-V bypassed fetuses but not in the fetuses perfused by a V-A bypass. The A-V bypass through umbilical vessels resembles physiological fetal circulation, and the cannulation technique is not difficult but it needs strict control, especially in the early stages of perfusion. A V-A bypass through cervical vessels doesn't seem to be close to a physiological perfusion for fetuses and the cannulation technique is difficult. But the cardiovascular dynamics are stable, so they are employed for clinical uses in neonatal ECMO. The V-A bypass method seems to be an adequate technique for managing extremely premature fetuses in water.