[Diagnosis and treatment for myelodysplastic syndrome (MDS)].
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Aged↗
Biomedical subjects
Masamichi Sato
Publications and source records attributed to Masamichi Sato.
S-myotrophin promotes the hypertrophy of skeletal muscle of mice in vivo.
S-myotrophin is a newly discovered muscle growth factor. Effects of crude S-myotrophin injection on the growth and morphology of skeletal muscle of normal, ScN and mdx mice were investigated in the present study. Total dose of crude S-myotrophin was 100 microg (100 microg protein/ml x 50 microl x 20 times). In the case of normal mice (Sea:ddY), body weight and the weight of M. gluteus major of crude S-myotrophin injected mice was significantly heavier than that of control (PBS-injected) mice after 5 weeks' feeding. Antibody staining of laminin and dystrophin showed clear sarcolemmal and basement membrane structure surrounding each muscle fibre. The numbers of muscle fibres per 100 microm(2) was less in crude S-myotrophin-injected normal mice than in PBS-injected mice. Quite similar observations as in the case of normal mice were obtained in the case of ScN mice having heterogeneous gene of dystrophin. In the case of mdx mice, body weight and the weight of M. gluteus major of crude S-myotrophin injected mdx mice was significantly heavier than that of PBS-injected mdx mice. Antibody staining of laminin showed almost intact structure of the basement membrane containing laminin even in skeletal muscle of mdx mice subjected to crude S-myotrophin injection, while irregular and incompletely developed structure of muscle fibres or necrosis were observed in muscle fibres of PBS-injected mdx mice. In spite of crudeness of the preparation, the present animal experiments indicate that S-myotrophin has a strong growth promoting activity of muscle cells of normal and dystrophic mice.
Animals↗
Excessive zinc intake elevates systemic blood pressure levels in normotensive rats--potential role of superoxide-induced oxidative stress.
OBJECTIVES: The present study was designed to examine whether or not excessive Zn intake affects systemic blood pressure (BP) levels in a normotensive state. METHODS: Systolic BP (SBP) and mean arterial pressure (MAP) before and after administration of the nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME) or the exogenous superoxide scavenger, tempol and the activity of the endogenous superoxide scavenger, Cu/Zn-superoxide dismutase (SOD) and levels of endothelial type (e)NOS mRNA and protein in the thoracic aorta were analyzed in male Sprague-Dawley rats fed a standard diet containing 0.005% Zn or a high Zn diet containing 0.5% Zn for 8 weeks. RESULTS: SBP and MAP levels observed at the end of dietary conditioning were significantly elevated in rats fed a high Zn diet relative to rats fed a standard diet. Administration of L-NAME caused an increase in MAP levels in rats fed a standard and a high Zn diet, demonstrating the involvement of the vasodilator, nitric oxide (NO) in the regulation of systemic BP in the two groups of rats. However, the expression of eNOS mRNA and protein in the thoracic aorta was not significantly different between rats fed a standard and a high Zn diet. On the other hand, administration of tempol led to a decrease in MAP levels in rats fed a standard and a high Zn diet, indicating the participation of the oxygen free radical, superoxide in the modification of systemic BP in the two groups of rats. As reported recently, the mechanism involved is due likely to a decrease in the action of the vasodilator, NO through the formation of peroxynitrite based on the non-enzymatic reaction of superoxide and NO. In addition, tempol treatment dramatically restored MAP levels in rats fed a high Zn diet to levels comparable with those observed in rats fed a standard diet, indicating that an elevation in systemic BP levels seen in rats fed a high Zn versus a standard diet is presumably brought by a reduction in the action of the vasodilator, NO resulting from an increase in the action of superoxide. The activity of Cu/Zn-SOD in the thoracic aorta was significantly reduced in rats fed a high Zn diet relative to rats fed a standard diet, appearing to at least in part, play a role in an increase in the action of superoxide in the vessel wall of rats fed a high Zn diet. CONCLUSIONS: Excessive Zn intake may be a factor to elevate systemic BP levels in a normotensive state presumably through the oxidative stress caused by superoxide.
Animals↗
Dietary Zn deficiency does not influence systemic blood pressure and vascular nitric oxide signaling in normotensive rats.
Because zinc (Zn) is an important component for cell protection against certain oxygen species, it has been suggested that Zn deficiency impairs the potent oxidant defense capacity, which is constitutively provided in the vascular system. However, the influence of dietary Zn deficiency on systemic blood pressure and vascular system is controversial and unclear. We therefore examine the effect of dietary Zn deficiency on systemic blood pressure, a potent superoxide scavenger, aortic Cu/Zn superoxide dismutase (SOD) activity, a most representative synthase of the endothelium-derived relaxing factor, and aortic endothelial nitric oxide synthase (eNOS) expression. Furthermore, the direct effects of intravenous administration of NOS inhibitor, Nomega-nitro-L-arginine methyl ester (LNAME), and a SOD mimetic compound, tempol, in normotensives were tested in Wistar-Kyoto (WKY) rats. A Zn-deficient diet (4 wk) contributed to growth retardation, the decrease in thymus weight, and the lower levels of serum Zn compared with the standard diet group. However, no significant difference in conscious systolic and diastolic blood pressure was found in the Zn-deficiency group. The administration of L-NAME caused an increase in the mean arterial pressure (MAP) levels in the two groups of rats and the involvement of the vasodilator nitric oxide (NO) in the regulation of systemic BP in the normotensive state. On the other hand, administration of the superoxide scavenger, tempol, led to a decrease in MAP levels in the two groups of rats, indicating the participation of the oxygen free radical, superoxide, in the maintenance of the systemic BP in a normotensive state. There were no significant differences between the Zn-deficient diet group and the standard diet group in the normotensive state. eNOS expression and Cu/Zn SOD activity in the aorta were also intact in Zn-deficient normotensive rats. These findings suggest that the 4 wk of Zn deficiency was inadequate to alter systemic blood pressure and focal NO signaling in the normotensive state. Long-term Zn deficiency affects the neuronal, immune, and hematopoietic systems, which contribute to systemic and/or local circulation. However, Zn deficiency alone does not cause hypertension and local vascular dysfunction in the normotensive state.
Animals↗
[Effect of glycyrrhizin on anti-tuberculosis drug-induced hepatitis].
In cases in which hepatotoxicity developed during anti-tuberculosis chemotherapy, the rapid recovery of liver function is essential for the completion of the anti-tuberculosis chemotherapy protocol. Glycyrrhizin (Stronger Neo-Minophagen C: SNMC) is widely used in Japan for the treatment of patients with drug eruption or chronic hepatitis. However, a consensus on the clinical effects of glycyrrhizin for the treatment of anti-tuberculosis drug-induced hepatitis has not yet been reached. We studied 24 cases who showed abnormal liver function test results while undergoing anti-tuberculosis chemotherapy and who were treated with or without glycyrrhizin. We then compared recovery periods of liver function among both groups. The time required for liver function normalization in the patients who received glycyrrhizin (SNMC, 40 ml daily, intravenously) was 15.1 +/- 4.5 days and the time required for normalization in the non-glycyrrhizin group was 15.2 +/- 5.2 days. The difference was not significant and the fact indicated that glycyrrhizin is not useful for the treatment of anti-tuberculosis drug-induced hepatitis.
Adult↗
Decreased expression of brain nitric oxide synthase in macula densa cells and glomerular epithelial cells of rats with mercury chloride-induced acute renal failure.
To elucidate the mechanisms responsible for the development of HgCl(2)-induced acute renal failure (ARF), we examined the expression of brain type (b) nitric oxide synthase (NOS), which is involved in the generation of the vasodilator nitric oxide (NO), in the renal cortex of rats at 20 h after exposure to 7.5 mg/kg HgCl(2). Both blood urea nitrogen and serum creatinine were significantly increased in rats exposed to HgCl(2) relative to control rats, indicating the induction of ARF resulting from HgCl(2) exposure. Histopathological analysis demonstrated that, in addition to necrosis of proximal tubule epithelial cells, necrosis of macula densa cells and swelling of glomerular epithelial cells were observed in the renal cortex of rats with HgCl(2)-induced ARF. Consequently, the number of pars maculata segments was decreased by 42% in rats with HgCl(2)-induced ARF compared to control rats. The primary sites of bNOS mRNA and protein expression were macula densa cells and glomerular epithelial cells in the renal cortex of control rats and rats with HgCl(2)-induced ARF. The abundance of the bNOS mRNA and protein was significantly decreased in rats with HgCl(2)-induced ARF relative to control rats. These observations suggest that the production of the vasodilator NO derived from bNOS is decreased at the glomerulus level in the HgCl(2)-induced ARF setting. Thus, the reduction in bNOS expression may in part contribute to the progression of HgCl(2)-induced ARF through the deterioration of glomerular hemodynamics. In addition, the decrease in bNOS expression may be primarily the result of cell injury caused by the cytotoxic effect of HgCl(2).
Acute Kidney Injury↗
Increased renal vascular resistance in zinc-deficient rats: role of nitric oxide and superoxide.
1. Zinc deficiency (ZD) induces many kinds of pathological states. However, the effects of ZD on haemodynamics remain unclear. In the present study, we measured mean blood pressure (BP) and renal blood flow (RBF) under anaesthesia and calculated renal vascular resistance (RVR) from these parameters in rats maintained on a ZD diet (0.5 p.p.m. zinc) for 4 weeks. 2. Zinc deficiency did not change mean BP, but significantly reduced RBF and increased RVR (each P < 0.01). In addition, these effects of ZD were reversible. 3. Because Cu/Zn superoxide dismutase (SOD) is a zinc-containing enzyme and superoxide is a potent scavenger of nitric oxide (NO), a vasodilator, we hypothesized that one of the mechanisms by which ZD increases RVR is by decreasing NO bioavailability by the enhanced formation of superoxide due to low Cu/Zn SOD activity. To test this hypothesis, we observed the roles of NO and superoxide in the mechanism, after having confirmed the low activity of Cu/Zn SOD in the kidneys of ZD rats. 4. Administration of the SOD mimetic tempol (5 mg/kg per min) decreased RVR to a significantly greater extent in ZD rats compared with control, suggesting that superoxide was responsible for the mechanism. Low doses of the NO donor sodium nitroprusside (SNP; 2.0 micro g/kg per min, continuous) decreased RVR to a significantly smaller extent in ZD rats compared with control, whereas a high dose of SNP (0.75 mg/kg, bolus) decreased RVR to a significantly greater extent in ZD rats compared with control, suggesting that the mechanism includes an inhibition of NO activity in ZD, which is most likely to be a scavenging of NO by the activated superoxide. 5. In summary, ZD may increase RVR. The mechanism probably includes changes in NO and superoxide activities.
Animals↗
[Color Doppler ultrasonography].
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Blood Flow Velocity↗
[Internal pudendal arteriography].
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Alprostadil↗
[Erectile dysfunction in men under 39].
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Adolescent↗