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Biomedical subjects

S Muto

Publications and source records attributed to S Muto.

At least 163 records · Page 9Linked to original sources

Polycythemia of end-stage renal failure: no inhibition of erythropoiesis by uremic serum and markedly increased serum erythropoietin level.

This report describes the case of a 50-year-old male with end-stage renal failure accompanied with congenital heart disease and polycythemia. After he had received continuous ambulatory peritoneal dialysis for 1 year, he still remained polycythemic and his serum erythropoietin titer, assayed using fetal mouse liver cells, was markedly increased. An inhibitory effect on erythropoiesis was not detected by this method. Bone marrow examination showed erythroid hyperplasia. These phenomena could be explained by an overproduction of erythropoietin by the remnant kidneys or extrarenal organs, such as the liver, in response to persisting hypoxia. The patient's bone marrow was still responsive to erythropoietin.

Erythropoiesis↗

A case of rhabdomyolysis in chronic renal failure.

Rhabdomyolysis can be induced by a variety of physical and chemical insults to skeletal muscle. Though there are only a few reports of myositis associated with viral diseases, and no reported cases of virus-induced rhabdomyolysis in uremic patients. Chronic uremic states have been known to potentiate a variety of metabolic and immunological abnormalities. Present case had an acute, progressive and fatal rhabdomyolysis which was thought to be induced by virus infection. A 43-year-old man had received hemodialysis therapy for 8 years. He suffered from an upper respiratory tract infection 11 days before admission. On admission, he was diagnosed as rhabdomyolysis with severe lactic acidosis and marked hyperkalemia. Although intensive care had been performed, he died of uncontrollable hyperkalemia (10.0 mEq/L) 2 days after admission. Maximum CPK and GOT levels were 105,200 and 56,800 mU/ml, respectively. Most probable cause of rhabdomyolysis was thought to be Parainfluenza type-3 infection, though histological examination failed to prove virus infection.

Adult↗

Biosynthesis and intracellular processing of carbonic anhydrase in Chlamydomonas reinhardtii.

Carbonic anhydrase (CA) of Chlamydomonas reinhardtii is a glycoprotein of 35 kDa which is localized outside the plasma membrane. The activity of CA was increased when the CO2 concentration during photoautotrophic growth was decreased to air level. After decreasing the CO2 concentration from 4% to 0.04%, several polypeptides including CA were induced continuously or transiently. To investigate the biosynthesis and intracellular processing of CA, the cells of wall-less mutant CW-15, which secretes CA into the culture medium, were pulse-labeled with radioactive arginine, chased, and radioactive proteins were immunoprecipitated with anti-CA serum. A 42-kDa polypeptide with isoelectric point (pI) of 7.1-7.3 was first synthesized. Within 5 min the molecular mass of this polypeptide was decreased to 35 kDa and it was then secreted into the culture medium within 30 min. This indicates that the former is the precursor form and the latter the mature form of CA. The primary translation product from poly(A)-rich RNA in a cell-free reticulocyte lysate system from a rabbit was a 38-kDa polypeptide. This was cotranslationally converted into the 42-kDa precursor in vitro in the presence of dog pancreatic microsomal membranes. As the 42-kDa precursor had a high affinity to concanavalin A, it was assumed to have a high-mannose-type oligosaccharide. The mature enzyme had a pI of 6.1-6.2 and was composed of more than two isoforms, which had a complex-type oligosaccharide with low affinity to concanavalin A. Chemical deglycosylation of the mature enzyme by trifluoromethanesulfonic acid indicated that the molecular mass of the polypeptide moiety was 32 kDa and the difference between this and the primary translation product suggests that cleavage of the polypeptide occurs during its biosynthesis.

Arginine↗

A simple and rapid method for the determination of macrophage activating factor involving a new type of apparatus suitable for the measurement of macrophage chemiluminescence.

A simple and rapid method for the determination of macrophage activating factor is described. A new type of apparatus suitable for the measurement of macrophage chemiluminescence was devised, and the effect of lymphokines on macrophage activities was studied by measuring phorbol myristate acetate-induced luminol-dependent chemiluminescence. An outstanding feature of the new apparatus is that the plastic dish used for the cell culture can be used as the vessel for the chemiluminescence reaction. When thioglycollate-elicited ICR mouse peritoneal macrophages were incubated with lymphokines, their ability to generate chemiluminescence increased rapidly, reaching a maximal level at about 4 h, and then it progressively decreased to the control level at 8 h. Although this increasing effect of lymphokines on macrophage chemiluminescence was short-lived, it could be seen at a relatively low concentration, at which lymphokine-mediated cytotoxic activity of macrophages was not observed.

Animals↗

Quantitative analysis of the early changes of hepatocyte nuclei after treating Syrian golden hamsters with di(2-ethylhexyl)phthalate.

Although the biological action of phthalates has been widely discussed there is little information on early cellular changes indicative for toxic or carcinogenic effects. To study subtle alterations in the cell morphology, we have by means of image processing evaluated the nuclei of hamster hepatocytes after treatment with di(2-ethylhexyl)phthalate given in single i.p. doses of 30, 300, and 3000 mg/kg. The results indicate that by using specially developed methods for analysis of images of cell nuclei and chromatin structure, it is possible to recognize changes eluding detection with usual light microscopy.

Animals↗

Image analysis of hepatocyte nuclei in assessing di(2-ethylhexyl)phthalate effects eluding detection by conventional microscopy.

The effect of di(2-ethylhexyl)phthalate (DEHP) administered in single intraperitoneal doses of 30, 300 and 3000 mg/kg in Syrian golden hamsters was studied by means of routine pathologic investigations, electron microscopy and image analysis. The morphological evaluations did not show apparent differences between the control and treated animals. Such differences, however, were recognized by using image analysis. They concerned morphology of the hepatocyte nuclei and were defined by quantitative parameters reflecting geometrical, optical and structural properties. Of importance for differentiating dose/effect relationships were features of chromatin structure. In order to describe those features we developed special algorithms capable of identifying and characterizing regions of condensed chromatin as subimages. These were distinguished by their size, shape and optical density and showed typical distributions within the nucleus. As our results demonstrate, image analysis methods permit detection of DEHP related pathology in animals which, as far as is evident from routine morphologic evaluations, belong to the no-effect experimental group.

Animals↗

[Effects of krestin (PSK) on drug-metabolizing enzymes with special reference to the activation of FT-207].

The effects of PSK on hepatic drug-metabolizing enzymes were investigated using Sarcoma 180-bearing and non-tumor-bearing ICR mice. PSK, an immunomodulator, has been commonly used in combination with tegafur for post-operative adjuvant chemotherapy. Tegafur is a typical masked compound transformed into 5-FU by the hepatic drug-metabolizing enzyme P-450. It has been reported that immunostimulants such as BCG and anaerobic Corynebacterium suppress the drug metabolism. PSK and Propionibacterium acnes were administered to mice inoculated s.c. with Sarcoma 180. It was demonstrated that Propionibacterium acnes had an effect of inhibiting these enzymatic activities, especially the amount of P-450 and cytochrome b5 and aminopyrine demethylation. On the other hand, PSK had no influence on the drug-metabolizing enzymes. Propionibacterium acnes was shown to decrease the 5-FU level in organs and sera of mice given FT-207 orally. By contrast, PSK showed no difference in 5-FU level compared to controls, indicating that PSK had no inhibitory effect on the activation of FT-207 by hepatic drug-metabolizing enzymes.

Aminopyrine↗

Dopaminergic inhibition of the action of vasopressin on the cortical collecting tubule.

The dopaminergic inhibition of the hydrosmotic effect of vasopressin was studied by in vitro perfusion of the cortical collecting tubule isolated from the rabbit kidney. Arginine vasopressin (AVP) 100 microU/ml increased hydrosmotic water permeability (Pf, 10(-3) cm/s) by 11.4 +/- 1.59. Although dopamine 10(-5) M added alone to the bath did not affect Pf, the combined administration of 10(-5) M dopamine and 100 microU/ml AVP reduced the hydrosmotic effect of AVP to to 2.37 +/- 0.34. This inhibitory effect of dopamine was reversed by the simultaneous addition of 10(-5) M metoclopramide, a D2-antagonist. These observations suggest that dopaminergic receptors also exist in the cortical collecting tubule. The dopaminergic inhibition of the hydrosmotic action of AVP may be at least in part responsible for the diuretic action of dopamine.

Animals↗

Hypergastrinemia and achlorhydria in chronic renal failure.

In 68 patients with chronic renal failure (CRF), 15 patients with duodenal ulcer and 15 normal subjects, basal plasma gastrin levels and basal and stimulated gastric acid secretion were measured. Two antisera were used: antiserum R2702 with specificity for human G34 and its N-terminal fragments [G34] and antiserum 2604 with specificity for the four main components of gastrin (total gastrin). Basal gastrin concentrations of both total gastrin and G34-like immunoreactivity (G34LI) were significantly higher in the CRF patients than in the other two groups, irrespective of dialysis. Total gastrin levels were not correlated with serum creatinine levels. Total gastrin levels were significantly decreased during hemodialysis, but G34LI levels showed no significant change. A small amount of total gastrin was detected in the dialysate by antiserum 2604. As to the postprandial gastrin release, in the first 30 min, the pattern of response in the patients with CRF was similar to that of the normal subjects, but the peak value was attained later, and the response was more rather prolonged. Gastric analysis showed a low basal acid out put and impaired acid secretion in response to secretagogue. It is concluded that (1) one of the predominant circulating forms of gastrin in CRF is G34LI, and (2) the hypergastrinemia in the CRF patients is probably due to reduced removal of gastrin by kidneys, increased gastrin production by impairment of the negative acid feedback mechanism induced by parietal cell dysfunction or reduced parietal cell sensitivity to gastrin by atrophic gastritis.

Achlorhydria↗