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Biomedical subjects

M Itakura

Publications and source records attributed to M Itakura.

At least 199 records · Page 11Linked to original sources
PubMed1982

Paradoxical response to parathyroid hormone of renal handling of phosphate in hyperparathyroid rats.

The effect of PTH given as a bolus on renal handling of phosphate in rats was studied by a perfusion balance study method. In vitamin D-fed rats, iv PTH as a bolus (10 USP units) elicited a phosphaturic response and an increase in urinary cAMP, whether or not the rats were thyroparathyroidectomized. When given to thyroparathyroidectomized rats receiving continuous infusion of PTH (2.5 USP units/h) for 16 h, PTH led to a paradoxical decline of phosphate clearance in spite of an increase in urinary cAMP. Vitamin D-deficient intact rats also showed this paradoxical response. Vitamin D-deficient thyroparathyroidectomized rats showed an ordinary phosphaturic response. When PTH had been supplied continuously (2.5 USP units/h) to these rats, the PTH bolus again produced the paradoxical response. Phosphate supplementation did not restore the phosphaturic response. (Bu)2cAMP infusion reproduced the paradoxical effect in vitamin D-fed, thyroparathyroidectomized rats receiving continuous infusion of PTH. These data indicate that a long-lasting excess of circulating PTH alters the nature of the response of the kidney to an iv bolus of PTH, so that PTH leads to a paradoxical decline of phosphate clearance, and that the mechanism responsible for the paradox may lie in a step (or steps) subsequent to cAMP production.

Animals↗
PubMed1981

A clinical evaluation of serum alpha-1-antichymotrypsin levels in liver disease and cancers.

The serum levels of alpha-1-antichymotrypsin (ACT) were studied in 168 patients with various liver diseases and cancers in conjunction with other liver function tests, serum sialic acid, AFP and CEA. The ACT levels in acute viral hepatitis and chronic hepatitis were not significantly altered compared with the normal level (220 +/- 40 microgram/ml), although the level was slightly increased or decreased temporarily during the acute phase of the former. In liver cirrhosis, the mean level was significantly lower than the normal in spite of the absence of signs of hepatic decompensation (168 +/- 51 microgram/ml, p less than 0.001). In contrast to cirrhosis, the levels were increased to various extents in 65% of cases with hepatoma, in spite of the association of liver cirrhosis in the majority of them. Much higher levels were observed in all cases of metastatic liver cancers and cancers of the pancreas and the biliary tract. The elevations were observed even in cases without the increase of AFP or CEA. Both in cirrhosis and cancers, ACT levels were not correlated with any of serum bilirubin and serum enzyme activities, but were positively correlated with the levels of plasma fibrinogen and serum sialic acid. The measurement of serum ACT level can be taken advantage of for the diagnosis and monitoring of liver cirrhosis and liver cancers, particularly of hepatoma without AFP elevation.

Blood Sedimentation↗
PubMed1981

Basis for the control of purine biosynthesis by purine ribonucleotides.

An animal model was used to determine the basis for the increase in purine biosynthesis that results from hepatic depletion of purine nucleotides, such as seen in patients with type I glycogen storage disease or following fructose administration. Mice were injected intravenously with glucose or fructose, 2.5 mg/g of body weight, and the animals were killed at 0, 3, and 30 min following carbohydrate infusion. Fructose, but not glucose, administration led to a threefold increase in [14C]glycine incorporation into hepatic purine nucleotides documenting an increase in the rate of purine biosynthesis in the liver of fructose-treated animals. In the fructose, but not the glucose-treated animals, there was a reduction in the hepatic content of purine nucleotides that are inhibitory for amidophosphoribosyltransferase, the enzyme that catalyzes the first reaction unique to the pathway of purine biosynthesis. PP-ribose-P, an important metabolite in the control of purine biosynthesis, was increased 2,3-fold in liver following fructose, but not glucose administration. In conjunction with the decrease in inhibitory nucleotides and increase in PP-ribose-P 29% of amidophosphoribosyltransferase was shifted from the large inactive to the small active form of the enzyme. Results of these studies demonstrate that the end-products of the pathway, purine nucleotides, control the activity of the enzyme that catalyzes the first reaction leading to purine nucleotide synthesis either through a direct effect of purine nucleotides on the enzyme, through an indirect effect of the change in nucleotides on PP-ribose-P synthesis, or a combination of these effects. The resultant changes in amidophosphoribosyltransferase conformation and activity provide a basis for understanding the increase in purine biosynthesis that results from hepatic depletion of purine nucleotides.

Amidophosphoribosyltransferase↗
PubMed1980

Abnormalities of serum cholinesterase isozyme in liver cirrhosis and hepatoma (Part II).

The pattern of serum cholinesterase (ChE) isozyme appeared to be characteristically abnormal in liver cirrhosis and hepatoma. In liver cirrhosis an abnormal fast moving peak was observed in 92.5% of fifty three patients studied. Further, diminishing activities of ChE 3 and 4, accompanied by an emergence of weak bands with unusual rates of flow, were noted in 58.5%. The latter abnormality was always associated with the former one. The pattern in hepatoma was essentially the same with liver cirrhosis, though diversity of bands was also present in some cases. It was ascertained that these abnormalities was due to sialic acid content bound to the enzyme, but was not due to production of abnormal enzyme protein moiety. It was suggested by clinical analysis that the degree of the abnormality of the isozyme may be useful for the diagnosis and prognostic evaluation of liver cirrhosis.

Carcinoma, Hepatocellular↗
PubMed1980

Cruveilhier-Baumgarten disease in Japan--on the basis of our own case.

The article reports on a patient with Cruveilhier-Baumgarten disease. The anamnesis of the 59-year-old housewife revealed previous anemia, splenomegaly and abnormal liver function 21 years ago. Three years ago, esophageal varices were found. A tortuously distended vein was seen in the falciform ligament at the time of laparoscopy, and this finding was confirmed by angiography and ultrasonography. Esophageal varices and hypersplenism were also noted. Despite these findings, liver biopsy specimens of both lobes showed only slight fibrosis with minimal lymphocyte infiltration in some portal areas, and no evidence of cirrhosis. Patency of the umbilical vein and portal hypertension without significant histologic change of the liver, are both in keeping with the features of this disease. Dilatation of the umbilical vein seemed to be congenital and did not contribute to active blood flow of portal hypertension in this patient. In Japan, development of "caput medusae" in portal hypertension is rather rare, whereas esophageal varices and splenomegaly are more frequent. Venous hum is also seldom found. 14 cases of Cruveilhier-Baumgarten disease and 28 cases of Cruveilhier-Baumgarten syndrome have been reported from Japan in the literature since 1911.

Celiac Artery↗
PubMed1980

Evaluation of blood cultures following laparoscopy.

To determine the incidence of transient bacteremia associated with laparoscopy, a prospective study was carried out in 113 patients with diverse liver diseases. Blood samples for aerobic and anaerobic cultures were obtained for each patient immediately before laparoscopy, within three minutes after creation of pneumoperitoneum and within three minutes after needle biopsy of the liver. Five subjects were culture positive, and all isolates were of the propionibacterium species. Positive cultures did not correlate with the nature of underlying liver disease, and none of these patients developed clinical evidence of bacterial infection. Positive isolates might be assumed to be contaminants, but the fact propionibacterium has been known to cause endocarditis cannot be ignored. Until further evidence accumulates, antibiotic coverage in "high risk" patients with cardiac lesions who are predisposed to endocarditis undergoing laparoscopy may be warranted.

Adult↗
PubMed1979

Human amidophosphoribosyltransferase. An oxygen-sensitive iron-sulfur protein.

Glutamine 5-phosphoribosyl-1-pyrophosphate amidotransferase (EC 2.4.2.14), amidophosphoribosyltransferase, was partially purified from human placenta. Upon exposure to oxygen, both the glutamine and ammonia activities were lost in parallel. Inactivation by oxygen increased as the temperature of incubation rose and the partial pressure of oxygen increased. Molecular oxygen rather than a radical derivative was responsible for inactivation since scavengers of oxygen radicals did not protect against inactivation. AMP,GMP,PP-ribose-P, and inorganic phosphate partially protected both the glutamine and ammonia activities from inactivation by oxygen. Incubation with 1,10-orthophenanthroline, but not 1,7-metaphenanthroline or tiron, led to inactivation of amidophosphoribosyltransferase. Both the 1,10-orthophenanthroline- and oxygen-inactivated enzymes could be reconstituted by incubation with ferrous iron and inorganic sulfide in the presence of dithiothreitol under anaerobic conditions. The iron requirement could not be replaced by zinc, copper, cobalt, nickel, magnesium, or calcium. The sulfide requirement could not be replaced by higher concentrations of dithiothreitol. It is concluded from these studies that human amidophosphoribosyltransferase is an iron-sulfur protein and oxidation of this structure may be responsible for the marked lability of this enzyme in vitro.

Amidophosphoribosyltransferase↗
PubMed1978

Renal handling of lysozyme in experimental Fanconi syndrome.

The relationship between lysozyme and sodium reabsorption by the kidney tubule was studied in the experimental Fanconi syndrome. Female, anesthetized Sprague-Dawley rats were injected intravenously with maleic acid (an inhibitor of sodium transport) neutralized with sodium hydroxide in doses of either 2 or 8 mmol/kg. Clearance studies were performed immediately afterward, and plasma and urine were analyzed for inulin, pH, sodium, glucose, and lysozyme. Two hours after the maleic acid injection, renal cortical tissue was removed and homogenized. Specific activity of Na-K-ATPase was assayed in the light microsomal fraction. The results showed that both concentrations of maleic acid caused significant increases in urinary volume, glucose excretion, and pH. There were significantly correlated decreases in TNafract and TLyfract. The slope of the regression line (TLyfract = 1.03 TNafract - 5.82; r = 0.92) approximated unity. Renal cortical Na-K-ATPase activity was significantly decreased by 25% in the animals receiving 2 mmol maleic acid and 43% in the animals receiving 8 mmol. The evidence suggests that lysozyme reabsorption in the proximal tubule might be mediated directly or indirectly by active tubular transport of sodium, a process that is related to the Na-K-ATPase transport system.

Adenosine Triphosphatases↗