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Biomedical subjects

M Hatano

Publications and source records attributed to M Hatano.

At least 181 records · Page 10Linked to original sources

[Study of hard mineralized tissues effect of calcium-deficient diets with and without cholecalciferol supplementation on the incisor dentine of rats].

It has been known that both tooth and bone have an apatite structure similar to that of mineral hydroxyapatite. The apatite crystal in living tissues of tooth and bone generally is constructed from submicrocrystals and has many impurities. It seems that chemical and physical aspects of resistance of hard tissues depend on the diet. Consequently, the matrix of organic, free radicals in X-ray irradiated hard tissues were studied by means of electron spin resonance (ESR). The effects of calcium-deficient diets with and without cholecalciferol supplementation on the incisor dentine of rats were examined by the rate of decay of organic, free fadicals in X-ray irradiated incisor dentine of rats. The crystal size of incisor dentine became smaller in case of calcium contained diet.

Animals↗

[Changes in complement breakdown products and terminal complement complex in patients with acute glomerulonephritis].

In this study we examined the role of the complement system in acute glomerulonephritis (AGN). Breakdown products of complements (iC3b, C4d and Bb) and Terminal complement complex (TCC, SC5b-9 complex) in plasma samples were measured by ELISA. The microassay plates were coated with monoclonal antibodies which bind specifically to human iC3b, C4d, Bb and SC5b-9 complex. This assay accurately quantitates small amounts of in vivo complement activation. The plasma samples were drawn from patients with AGN and other glomerulonephritis. There were some patients with various glomerulonephritis whose plasma iC3b, C4d and Bb concentrations were higher than those in normal human. However specificity was not found. The ratios iC3b/C3 and C4d/C4 were increased in the early stages of AGN, but plasma Bb concentrations revealed no significant changes. Plasma SC5b-9 complex concentrations were increased in the early stages of AGN. C3c, C3d, C4d and SC5b-9 were found to be localised in the glomeruli of those AGN patients. It is suggestive that in these cases of AGN (especially case 2) complement activation is predominantly mediated through the classical pathway and TCC is formed by this activation. This complement activation in the blood and the renal tissue is presumed to be involved in the initiation and progression of AGN.

Acute Disease↗

Treatment of secondary hyperparathyroidism in patients on maintenance hemodialysis.

The effects of CaCO3 were investigated in 7 patients undergoing maintenance hemodialysis who had been treated with 1 microgram/day 1 alpha (OH)D3 and 2 g/day Al(OH)3. CaCO3 (3 g/day) was administered instead of Al(OH)3. The levels of serum total calcium and ionized calcium were significantly increased, the level of C-terminal parathyroid hormone was appreciably decreased and the levels of serum aluminum in all patients were reduced. There were no significant changes in the levels of serum phosphate, calcium x phosphate product, alkaline phosphatase, calcitonin, magnesium and bicarbonate. It is concluded that 3 g/day CaCO3 is equivalent to 2 g/day Al(OH)3 in terms of its phosphate-binding effect, and the prescription of CaCO3 together with 1 alpha (OH)D3 ameliorates secondary hyperparathyroidism.

Adult↗

[Significance of "overshoot" elevation of ejection fraction in early recovery period after exercise in patients with coronary artery disease].

To investigate the relationship between "overshoot" elevation of left ventricular (LV) ejection fraction (EF) in the early recovery period after exercise and myocardial ischemia, LV function was measured in 5 healthy volunteers and 47 pts with coronary artery disease (CAD) using supine ergometer. EF at rest (EFRE), at peak exercise (EFEX), at peak of overshoot (EFOS) and time from cessation of exercise to peak of overshoot (T-OS) were measured using an ambulatory LV function monitor system with a high sensitive CdTe detector. The patients were classified into 3 groups according to EF depression (EFRE-EFEX) by exercise, i.e., D1 (EF decreases less than 5%): 15 pts, D2 (EF decreases 5-10%): 12 pts, D3 (EF decreases greater than or equal to 10%): 20 pts. Degree of overshoot which shows difference in EF between rest and peak of overshoot was 23.8 +/- 2.13% (mean +/- SD) in the normal group, 11.72 +/- 5.12% in D1, 9.56 +/- 6.51 in D2 and 6.12 +/- 4.15% in D3, respectively. T-OS was 1.4 +/- 0.48 in the normal group, 2.8 +/- 0.54 in D1, 4.5 +/- 2.36 in D2 and 5.6 +/- 1.93 min in D3, respectively. We conclude that left ventricular dysfunction was proportionally related to time-lapse from cessation of exercise to peak of overshoot while inversely related to degree of overshoot.

Adult↗

Effect of antimacrophage serum on the proliferation of glomerular cells in nephrotoxic serum nephritis in the rat.

To evaluate the effect of a rabbit anti-rat macrophage serum (AMS) on glomerular cells in vivo, glomeruli were isolated from an accelerated autologous form of nephrotoxic serum nephritis (NTSN) in rats and grown in tissue culture. The prominent feature of the glomerular outgrowth of the glomeruli in the NTSN was the presence of large numbers of type III (macrophages) cells, which were not present in cultured normal glomeruli. In addition, there were significantly greater numbers of type II (mesangial) cells in culture from the NTSN rats as compared with glomeruli from normal rats though the numbers of type I (epithelial) cells were the same. The administration of AMS prevented the outgrowth of macrophages and reduced the number of mesangial cells in the outgrowth of glomeruli from the NTSN rats. The AMS-treated rats showed profound reduction in proteinuria. Light micrographs showed only minor histologic lesion in the AMS-treated rats. These findings suggest that AMS may be applicable to the modulation of the proliferative response seen in NTSN.

Animals↗

[Limitation of myocardial infarct size by polyethylene glycol-conjugated superoxide dismutase in a canine model of 90 min coronary occlusion followed by 4 days of reperfusion].

The role of oxygen free radicals in the genesis of myocardial reperfusion injury is supported by the studies with superoxide dismutase (SOD) which provides protection against the extention of myocardial injury. However, the efficacy of SOD may be of limited value due to its short plasma half-life of 5-6 min. Conjugation of SOD to polyethylene glycol (PEG-SOD) increases the half-life to greater than 30 hours. Forty-two male, mongrel anesthetized dogs were subjected to occlusion of left circumflex coronary artery for 90 min followed by 4 days of reperfusion. Dogs were randomized to receive either PEG-SOD (1,000 U/kg) or PEG-Albumin via left atrium, starting 15 min before reperfusion and ending simultaneously with reperfusion, and were sacrificed 4 days later. The hearts were stained by ex vivo dual perfusion technique for the determination of myocardial infarct size. Infarct size expressed as a percent of area-at-risk in PEG-SOD (n = 13) and PEG-Albumin (n = 13) treated dogs differed significantly between groups: 29.2 +/- 1.6% vs 44.2 +/- 2.6%, respectively (p less than 0.01) with no observed difference in the size of area-at-risk: 46.0 +/- 1.6% vs 44.4 +/- 1.4% (n.s.). Hemodynamic parameters between groups did not differ during coronary artery occlusion and could not account for the effect of PEG-SOD on infarct size. Collateral blood flows to the inner 2/3 of the ischemic myocardium for both groups did not differ. Plasma SOD activity in PEG-SOD group initially exceeded 20 U/kg and sustained significantly for 4 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

C3 nephritic factor and C4 nephritic factor in the serum of two patients with hypocomplementaemic membranoproliferative glomerulonephritis.

Both C3 nephritic factor (C3NeF) and C4 nephritic factor (C4NeF) were found in the serum of two patients with hypocomplementaemic membranoproliferative glomerulonephritis type 1 (H-MPGN type 1). Both stabilizing activities were associated with the IgG fraction. The serum levels of C3 and C5 were quite low, whereas the levels of early components and control proteins were in the normal range.

Adolescent↗

[A case of sarcoidosis associated with membranous nephropathy].

A 59-year-old woman was admitted to the hospital with a complaint of right visual disturbance. At admission, she had proteinuria and microscopic hematuria. The pulmonary X-ray showed bilateral hilar lymphadenopathy (BHL) but tuberculin test were negative. Also, bronchoalveolar lavage (BAL) and renal biopsy were performed. Bronchoalveolar lavage fluid (BALF) contained a high percentage of OKT 4 positive cells. In renal biopsy, light microscopic study showed thickening glomerular basement membrane (GBM) with tubulo-interstitial legion. Immuno-fluorescent study revealed granular deposits of IgG along glomerular capillary wall. Electron microscopic study showed subepithelial electron dense deposits of GBM, which are characteristic for membranous nephropathy (MN). It is well known that both sarcoidosis and MN are associated with immunological abnormality. This case might be significant for the study of pathogenesis of sarcoidosis.

Female↗

[Activation of complement by hemodialysis membrane].

Incubation of normal human serum with hemodialysis membranes in vitro resulted in conversion of C3 which was detected by crossed immunoelectrophoresis. In addition, formation of C3d was also observed, as was detected by double-decker rocket immunoelectrophoresis. Furthermore, breakdown products of complement (iC3b, C4d & Bb) in plasma samples were measured by ELISA. The microassay plates were coated with monoclonal antibodies which bind specifically to human iC3b, C4d and Bb, respectively, while the plasma samples were drawn from five polycystic kidney patients during initial hemodialysis. As a result, the iC3b and Bb levels in plasma were seen to increase during hemodialysis but the C4d levels revealed no significant changes. It was also observed that the Bb levels in patients undergoing hemodialysis were significantly higher than those in various renal and collagen diseases. Terminal complement complex (TCC) was not present in detectable amounts in normal human serum when measured by ELISA. However, incubation of normal human serum with hemodialysis membranes in vitro resulted in detection of TCC. TCC was present in the same plasma samples drawned from the five polycystic kidney patients during initial hemodialysis. It is suggestive that activation of complement by hemodialysis membrane is predominantly mediated through the alternative pathway and products such as TCC and anaphylatoxin are formed by this activation.

Complement Activation↗

Production of interleukin 1 in glomerular cell cultures from rats with nephrotoxic serum nephritis.

To investigate the role of cytokines in the pathogenesis of experimental glomerulonephritis (GN), we examined interleukin 1 (IL-1) activity in isolated glomeruli of rats with an accelerated autologous form of nephrotoxic serum nephritis (NTSN). Glomeruli were isolated and explanted in tissue culture. The prominent feature of the glomerular outgrowth of the glomeruli in the NTSN was the presence of large numbers of type III cells (macrophages). In addition, there were significantly greater numbers of type II (mesangial) cells in culture from the NTSN rats as compared with glomeruli from normal rats, though the numbers of type I (epithelial) cells were the same. IL-1 bioactivity was significantly higher in culture supernatants generated by glomeruli isolated from NTSN animals versus normal animals early in the course of the disease. When glomerular culture supernatants and purified IL-1 were pre-incubated with an anti-IL-1 beta antibody, a parallel decrease of the biological activity was found, suggesting that the biologically active binding sites of the culture supernatants and monocyte-produced IL-1 share some common structure. The administration of a rabbit anti-rat macrophage serum (AMS) prevented the outgrowths of type III cells (macrophages) and type II (mesangial) cells and reduced the production of IL-1 activity in the NTSN rats. In this experimental model IL-1 synthesis, probably by multiple cell types, is present early in the disease process and perhaps may be an important mediator of glomerular immune injury.

Animals↗

[Effects of cimetidine on plasma concentration of catecholamine and baroreflex control of heart rate in anesthetized humans].

To clarify the mechanism of cardiovascular depression by cimetidine, we studied the effects of intravenous cimetidine on the plasma catecholamine concentration and baroreflex control of heart rate in man before and during enflurane-nitrous oxide anesthesia. Baroreflex control of heart rate was assessed by raising the arterial pressure by phenylephrine. Before anesthesia, 200 mg cimetidine decreased plasma epinephrine concentration (E) from 135 +/- 48 (s.e.) pg.ml-1 at baseline to 91 +/- 35 pg.ml-1 5 min after administration, but there were no significant changes in the norepinephrine concentration (NE), slope of pressor response, systolic blood pressure (SBP) or heart rate (HR). In anesthetized patients, baseline values of E, NE and slope were all significantly decreased as compared to those without anesthesia. However, cimetidine administered during anesthesia decreased both SBP and HR, by 19 +/- 5 mmHg and 9 +/- 6 beats.min-1, respectively, without further decrease of plasma catecholamine or slope by cimetidine than those at baseline. We conclude that inhibition by cimetidine of cardiovascular system during anesthesia is not due to further depression of baroreflex or plasma catecholamine concentration.

Anesthesia, Inhalation↗

Influence of 1 alpha-hydroxy vitamin D3 (0.25 micrograms/day) and calcium carbonate on patients with chronic renal failure at the predialytic stage.

The influence of a small amount of 1 alpha (OH)D3 on patients with chronic renal failure at the predialytic stage (CRFPS patients) receiving CaCO3 was investigated. 7 patients given CaCO3 (3 g/day) were administered 1 alpha (OH)D3 (0.25 micrograms/day) over a period of 12 weeks. 2 patients were eliminated from the study because of obvious deterioration of renal function. The others revealed no significant changes in levels of serum creatinine, adjusted calcium, phosphate, calcium x phosphate product, alkaline phosphatase, C-terminal parathyroid hormone, pH and bicarbonate. Our results indicated that even 0.25 micrograms/day 1 alpha (OH)D3 should not be prescribed to CRFPS patients given 3 g/day CaCO3. We recommend a little sole use of CaCO3 in CRFPS patients, paying attention to any exacerbation of renal function due to a rise in serum calcium concentration, when therapy for secondary hyperparathyroidism is required.

Aged↗

[A study on the effects of a Mg-deficient diet on blood pressure and various hormonal systems in Wistar rats and spontaneously hypertensive rats].

The influence of a Mg-deficient diet on blood pressure and various hormonal systems was examined in Wistar rats (WR) and spontaneously hypertensive rats (SHR). The WR and SHR were individually divided into 2 groups. The Mg-deficient diet was given to one group, and a Mg-containing diet was given to the other group for 3 weeks. During this experimental period, the body weight, blood pressure, urine volume, blood and urinary electrolytes, plasma steroid hormones, plasma renin activity (PRA), and urinary hormones [kinin, prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and noradrenaline] were examined. Although no significant difference in body weight was observed between the Mg-deficient and Mg-containing diet groups in either the WR or SHR (because the experiments were performed in a pair-fed fashion in both kinds of rat), the blood pressure was increased in the Mg-containing diet group but was unchanged in the Mg-deficient diet group. As regards changes in electrolytes, a decreased urinary excretion of Mg and significantly increased urinary excretion of P were observed in the Mg-deficient diet group in both the WR and SHR. Furthermore, decreased levels of serum Mg and P and increased levels of serum Ca were also noted. In the WR group, the urinary excretion of noradrenaline was significantly increased in the Mg-deficient diet group as compared to the Mg-containing diet group. However, the change was reversed in the SHR group. The plasma steroid hormones and PRA were both significantly low in the Mg-deficient diet group in both the WR and SHR. The urinary excretions of PGE2, 6-keto-PGF1 alpha, and kinin showed no significant differences between the two diet groups. The above results indicate that blood pressure is not affected by the Mg-deficient diet in either the WR or SHR, and the possible participation of the sympathetic nervous system in the mechanism of control of blood pressure may differ somewhat between the WR and SHR. In addition, Mg ion was found to play an important role in the biosynthesis of renin and steroid hormones but to have no such significant role in the urinary excretions of kinin, PGE2, and 6-keto-PGF1 alpha.

Animals↗

Site-directed mutageneses of rat liver cytochrome P-450d: axial ligand and heme incorporation.

By oligonucleotide-directed mutageneses, 13 substitutions of amino acids at the carboxy-terminal region of rat liver cytochrome P-450d were done as follows: (A) Phe-449----Tyr; (B) Gly-450----Ser; (C) Leu-451----Ser; (D) Gly-452----Glu; (E) Lys-453----Glu; (F) Arg-454----Leu; (G) Arg-455----Gly; (H) Cys-456----Tyr; (I) Cys-456----His; (J) Ile-457----Ser; (K) Gly-458----Glu; (L) Glu-459----Ala; (M) Ile-460----Ser. The CO-bound reduced forms of the wild type and mutants B-G, J, L, and M gave Soret peaks at 448 nm. The CO complex of mutant A gave a Soret peak at 445 nm. The intensities of the CO-bound forms of mutants A, C, D, and J were very small compared with that of the wild-type complex. The CO-reduced forms of mutants H, I, and K did not give a Soret peak around 450 nm at all. The 448-nm peak of mutant F was unstable and quickly disappeared with the concomitant appearance of a peak at 420 nm.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗

[Influence of spironolactone on urinary prostaglandin E2 and kinin excretions in spontaneously hypertensive rats].

Spironolactone was administered to spontaneously hypertensive rats (SHRs) in order to examine the urinary excretions of prostaglandin E2 (PGE2) and kinin. Thirteen SHRs were divided into 2 groups, and 0.1 ml of sesame oil was administered to one of 2 groups (spironolactone-untreated group) (n = 6) and 20 mg of spironolactone in 0.1 ml of sesame oil was administered to the other group (spironolactone-treated group) (n = 7) by the subcutaneous route for 10 days in succession, followed by the determination of body weight, blood pressure, urine volume, excretion levels of Na, K, kinin and PGE2 in 24-hour urine. Blood samples were drawn after these animals were killed by decapitation for determining plasma renin activity (PRA). In consequence, decreased blood pressure and increased urinary Na excretion were observed in the spironolactone-treated group. On the other hand, PGE2 excretion level in 24-hour urine markedly decreased immediately after administration of spironolactone (p less than 0.05) and was maintained at lower levels up to the end of experiment. However, 24-hour urinary kinin levels showed similar changes in the spironolactone-treated group and the untreated group with no significant difference between the two groups. These results indicate that spironolactone has a suppressive effect on urinary PGE2 excretion, the activity of which is not mediated by kinin production in the kidneys but produced by a direct action of spironolactone itself.

Animals↗