[A case of metastatic lung tumor showing multiple cavities].
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Biomedical subjects
Publications and source records attributed to H Mikami.
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Hereditary hypocomplementemia of the third component of complement (C3) was found in a strain of rabbits in which hereditary C8 alpha-gamma deficiency was also found. The serum C3 concentration, haemolytic C3 activity and total complement haemolytic activity (CH50) of these animals were, respectively, 6-12%, 8-13% and 27-37% of the normal levels. The haemolytic complement activity in the C3 hypocomplementemic (C3-hypo) rabbit serum was restored in a dose-dependent manner by the addition of purified rabbit C3. The levels of factor H and properdin and components C2 and C6 were in the normal range, and the levels of factors B and D and component C8 were higher than normal. The low level of serum C3 in C3-hypo rabbits was not due to C3 conversion, partial C3 antigenicity, presence of a C3 inhibitor or hypercatabolism of normal C3. Furthermore, no change in the ratio of C3 protein levels was observed between C3-hypo and normal rabbits, even after turpentine injection. In addition, the C8 alpha-gamma deficiency condition does not affect C3 activity and C3 catabolism in vivo. Mating tests showed that the C3 hypocomplementemia is transmitted as a simple autosomal co-dominant trait. C3-hypo rabbits have a lower survival at 3 months than normal rabbits. C3-hypo rabbit serum also has a lower bactericidal activity than normal rabbit serum. The PAGE under reducing conditions showed no difference in the molecular weights of C3 alpha and C3 beta chains between C3-hypo, heterozygous and normal animals.
The effects of chronic renal failure on the enzyme activity of pyruvate kinase and the mRNA level of this enzyme were studied in 7 out of 8 nephrectomized rats. The mRNA level was measured by RNA-DNA dot blot hybridization, using cloned pyruvate kinase cDNA as hybridized probe. Neither the activity of M1-type pyruvate kinase nor the level of this enzyme in rat gastrocnemius muscle was affected by chronic renal failure, whereas L-type pyruvate kinase enzyme activity in uremic rat liver was lower than that in control at both fasted and refed states. The levels of L-type pyruvate kinase mRNA were not different between two groups at the fasted state. Induction of L-type pyruvate kinase mRNA after high carbohydrate diet refeeding was suppressed proportionally to the severity of chronic renal failure, which was expressed by the serum creatinine concentrations (r = -.876, P less than .005). These results indicate that the suppression of L-type pyruvate kinase activity in uremia was partly reflected by the decreased accumulation of this enzyme mRNA. There was a significantly negative correlation between L-type pyruvate kinase mRNA levels and plasma glucagon/insulin ratios (r = -.719, P less than .05). Hyperglucagonemia in uremia might play a major role in this suppression.
Among the various biological effects of angiotensin II (AII), both pressor activity and aldosterone stimulation appear to be mediated by functionally different receptors. With this in mind, we compared pressor and aldosterone-stimulating activities of AII with those of triprolyl [(Pro)3] AII and pentasarcosyl [(Sar)5] AII. In conscious male Wistar rats (Pro)3 AII and (Sar)5 AII produced 48 and 46% of the pressor activity of AII. After intravenous infusion (conscious unrestrained rats, 125 pmol/kg/min for 30 min), plasma aldosterone concentrations were not significantly different from those of control rats which were infused with saline. However, when the rats were infused with AII (125 pmol/kg/min for 30 min), plasma aldosterone concentrations increased significantly (1,306 +/- 80 pg/ml). This study indicates that (Pro)3 AII and (Sar)5 AII may prove to be useful tools to elucidate biological actions of AII.
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A case of bilateral ureteral fibrosis is reported. The patient, a 32-year-old man, was admitted as a result of acute renal failure. Ultrasonography showed bilateral hydronephrosis, so that in-dwelling percutaneous nephrostomy tubes were immediately inserted in the bilateral kidneys. Since retrograde and antegrade pyelograms revealed bilateral midureteral stricture, idiopathic retroperitoneal fibrosis at first suspected, but no mass in the retroperitoneal space was found by a computed tomogram. An exploratory laparotomy showed no fibrous mass in the retroperitoneal space either, but that the wall of the ureter was thickened. Biopsy of the ureter led to a histological diagnosis of fibrosis. Since evidence of inflammation such as elevation of the erythrocyte sedimentation rate and cross-reacting protein was found, 50 mg of prednisolone has been administered every other day, with the result that inflammation is now under control. This report deals with specific ureteral fibrosis related to idiopathic systemic fibrosis and collagen disease.
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The role of peripheral resistance in volume loaded hypertension was examined by measuring changes in hemodynamic and humoral factors during dextran infusion for one hour, and for three hours after stopping the infusion in 30 anesthetized dogs. The mean blood pressure was elevated significantly (118%, p less than 0.01), accompanied by increased cardiac output (170%, p less than 0.01) during volume loading. In the recovery period, cardiac output returned to the basal level while the total peripheral resistance gradually increased (118%, p less than 0.01) contributing to the maintenance of high blood pressure (108%, p less than 0.01). There was no significant correlation between the hematocrit change and the increase in peripheral resistance in the recovery period. The levels of plasma norepinephrine, epinephrine, renin activity and vasopressin were suppressed by volume loading. These results demonstrated the importance of increase in peripheral resistance for maintaining high blood pressure in this acute volume excess model. The participation of the renin-angiotensin system, the sympathetic nervous system and vasopressin were all excluded and vascular structural changes were most unlikely to be involved in this acute experiment. It remains unknown whether this conversion is attributable to the summation of local autoregulation or to some other factors.
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A case with extra-adrenal pheochromocytoma, which was found by chance in the course of renovascular hypertension, is reported. The tumor was on the stenotic portion of the right renal artery. The results of examinations for pheochromocytoma were not conclusive, that is, inconsistent elevation of plasma catecholamines and urinary catecholamine excretion, equivocal results of pharmacological tests for pheochromocytoma, and negative results in [131I]metaiodobenzylguanidine scintigraphy. The stenosis of the right renal artery disappeared, the blood pressure was normalized by surgical resection of the tumor, and the extra-adrenal pheochromocytoma was finally diagnosed by pathohistological findings. Renovascular hypertension appeared to be the primary cause of this hypertension, judging from the significant decrease in blood pressure induced by an angiotensin II analog and a renal vein renin ratio of 7.3. Even in the case of obvious renovascular hypertension, the possibility of this unusual coexistence with pheochromocytoma should be considered.
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Accumulation of oxalate, resulting in high plasma levels, is a common finding in end-stage renal disease. We investigated plasma concentration and peritoneal clearance of oxalate in 14 patients on continuous ambulatory peritoneal dialysis. The plasma oxalate levels in these patients (30.2 +/- 11.2 mumol/l) were as high as those in hemodialysis patients before dialysis (31.9 +/- 11.1 mumol/l). There was a significant correlation between plasma oxalate and urea nitrogen appearance (UNA). Dietary protein seems to be an important oxalate source in these patients, because the UNA reflects protein intake in stable patients. The mean peritoneal oxalate clearance was 6.64 +/- 1.56 l/day, close to the creatinine clearance. These results suggest that the plasma oxalate levels in CAPD patients may be sufficiently high to induce calcium oxalate deposition, and that methods of increasing oxalate removal and reducing oxalate burden are necessary for CAPD patients.
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The oxygen consumption per kilogram of body weight was measured during walking at speeds of 3.0-6.0 km/hr on a tread-mill in twelve patients with spinal deformities, before and approximately two years after either an anterior surgical correction or a posterior surgical correction. The mean age was seventeen years. There were five male and seven female patients. There was no significant change in the pre-operative and the post-operative oxygen consumption per kilogram of body weight and respiratory rates. A significant increase was noted in the post-operative oxygen removal (VO2/VE) in both the anterior and posterior procedures groups. The post-operative improvement of pulmonary function was discussed.