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Biomedical subjects

S Furuta

Publications and source records attributed to S Furuta.

At least 397 records · Page 22Linked to original sources
PubMed1983

[Two-dimensional echocardiographic observation of a rapidly growing floating left atrial ball thrombus: report of a case with mitral stenosis].

This report dealt with a rapidly growing ball thrombus floating in the left atrium in a case with mitral stenosis detected by serial two-dimensional echocardiography and confirmed at operation. A 45-year-old female was admitted to our hospital on January 7, 1982 because of dyspnea, orthopnea and fever. On admission she had typical auscultatory signs of mitral stenosis, and her chest roentgenogram revealed slight pulmonary venous congestion and marked left atrial enlargement. Laboratory findings including complete blood counts, coagulation studies and blood chemistry were normal except a positive CRP test. Two-dimensional echocardiography performed on January 8 revealed a tight mitral stenosis with the mitral orifice area of about 0.9 cm2, and a floating ball thrombus in the left atrium, which was 2.5 X 3 cm in size. Fuzzy echoes flowing slowly around the thrombus were also observed. Intravenous administration of heparin was started immediately. In the next morning (January 9), the two-dimensional echocardiography was reexamined, which revealed a markedly growing thrombus which became 4 X 4 cm in size. Several hours after the reexamination mitral valve replacement was performed. The removed thrombus was 5.5 X 7 cm in size and consisted of three laminated structures. This finding was consistent with the echocardiographic observations. Coagulation studies made just before operation showed increased coagulability. Increased stagnation of blood in the left atrium due to heart failure and a transient increase of blood cell aggregation and coagulability induced by preceding infection might be responsible for the genesis of such a thrombus.

Echocardiography↗
PubMed1982

Reduction of beta-oxidation capacity of rat liver mitochondria by feeding orotic acid.

Rats were maintained on fat-free high carbohydrate diets either with or without orotic acid (1%, w/w), pantethine (1%, w/w), adenine (0.25%, w/w), and/or p-chlorophenoxyisobutyrate (0.25%, w/w). Oxidation of fatty acid by liver mitochondria was inhibited to less than half that of the control after administration of orotic acid. Activities of acyl-CoA dehydrogenases were markedly decreased by orotic acid administration, but the following enzyme activities were not, or only slightly decreased: acyl-CoA synthetase, carnitine acyltransferases, enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase and 3-ketoacyl-CoA thiolase. Simultaneous addition of pantethine in the orotic acid-containing diet prevented induction of fatty liver. It also prevented decreases in fatty acid oxidation capacity and acyl-CoA dehydrogenase activity. Introduction of adenine or p-chlorophenoxyisobutyrate, which reverse orotic acid-induced fatty liver, reversed oxidation and acyl-CoA dehydrogenase activities to control levels. The oxidation capacity of the peroxisomal system remained unchanged after administration of orotic acid.

Acyl-CoA Dehydrogenases↗
PubMed1982

Studies on DNA content of hepatocytes in cirrhosis and hepatoma by means of microspectrophotometry and radioautography.

In order to clarify the underlying mechanism of malignant transformation from cirrhosis to hepatoma the cell kinetics of hepatocytes were studied in these two conditions. The content and synthesis of DNA in hepatocyte nuclei were investigated, by means of Feulgen-microspectrophotometry and tritiated thymidine radioautography, in cirrhotic and noncancerous parts of hepatoma with concomitant cirrhosis. The distribution of ploidy patterns was widely spread, from hypodiploid to hyperpolyploid, in the noncancerous parts of a cirrhotic liver containing hepatoma. In normal liver, each paired nuclear DNA content of a binucleate cell recorded almost the same amount, whereas in the noncancerous as well as in hepatoma cells much difference of DNA content was observed between the paired nuclei of the binucleate cells. The ploidy pattern of hepatocytes in patients with liver cirrhosis, who had developed hepatoma during follow-up periods of several months to several years, appeared to resemble that in noncancerous parts of hepatoma cases. On the other hand, the incorporation of tritiated thymidine into hepatocytes was found to be markedly increased in noncancerous parts as well as in cirrhotic liver developing hepatoma during follow-up periods. These results suggest the possibility that the hepatocytes in noncancerous parts of hepatoma have deranged cell-kinetics which might be a driving factor for the development of malignancy.

Acute Disease↗
PubMed1982

Riboflavin deficiency and beta-oxidation systems in rat liver.

Weanling rats were fed a riboflavin-deficient diet. The mitochondrial fatty acid oxidation in liver was depressed in riboflavin deficiency but restored after supplementation of riboflavin. Among the enzymes involved in this system, only the acyl-CoA dehydrogenase (EC 1.3.99.2 and 1.3.99.3) activities varied with the change in fatty acid oxidation. An accumulation of the apoforms of acyl-CoA dehydrogenases was found in riboflavin deficiency. The levels of electron transfer flavoprotein and other enzymes involved in the beta-oxidation system remained unchanged. The peroxisomal fatty acid oxidation and levels of individual enzymes of this system remained constant. No accumulation of the apoform of acyl-CoA oxidase was observed under simple, riboflavin-deficient conditions. However, accumulation of a large amount of apo-acyl-CoA oxidase was observed when the peroxisomal system was induced by administration of a peroxisome proliferator, di(2-ethylhexyl)phthalate, under riboflavin-deficient conditions.

Acyl-CoA Oxidase↗
PubMed1982

Sixteen years follow-up of a patient with alcoholic pancreatitis: serial findings of morphology and function on the pancreas and the liver.

Sixteen years follow-up was performed in a male of long-standing alcohol indulgence who had an alcoholic liver disease at the outset, followed by alcoholic pancreatitis which progressed finally to pancreatic calcification. During this course, the abnormalities of endoscopic pancreatogram were unremittingly progressive, whereas exocrine and endocrine pancreatic dysfunction remained fluctuating, but ultimately deteriorated. In contrast functional and histological abnormalities of the liver were not progressive but returned toward normal. The follow-up observations in this case suggest that some cases of typical alcoholic pancreatitis may have unremittingly progressive morphologic changes with fairly well reserved capacity of exocrine and endocrine pancreatic functions and their hepatic lesions may not be in parallel with pancreatic lesions.

Adult↗
PubMed1982

A case of acute non-A, non-B sporadic hepatitis with evolution of liver cirrhosis on serial histologic follow-up.

Progression of acute non-A, non-B (NANB) posttransfusion hepatitis to liver cirrhosis has been well recognized as in hepatitis B infection, whereas no progression of acute NANB sporadic hepatitis to liver cirrhosis has yet been documented. We reported a 29-year-old male with prolonged transaminase elevations in whom acute NANB sporadic hepatitis progressed to histologically confirmed cirrhosis during follow-up of about 3 years. It is suggested that some of the cryptogenic cirrhosis of non-B type may develop from acute NANB sporadic hepatitis and long-term observation is also needed in patients with acute hepatitis of this category.

Adult↗
PubMed1982

Biosynthesis of enzymes of peroxisomal beta-oxidation.

Male Wistar rats were fed a diet with or without di(2-ethylhexyl)phthalate (DEHP), a peroxisome proliferator, for 2 weeks. The increases in the individual enzymes of the hepatic peroxisomal beta-oxidation system after administration of DEHP were 31- to 33-fold. It was found by in vivo experiments using L-[4,5-3H]leucine and the immunoprecipitation technique that the rates of synthesis of the enzymes were 16- to 20-fold higher and those of degradation were 1.7- to 1.9-fold lower in the DEHP group. The translation rates of these enzymes in vitro with liver RNA in the reticulocyte-lysate system were 12- to 14-fold higher in the DEHP group. Short-term kinetic labeling experiments on acyl-CoA oxidase consisting of three subunits were conducted in vivo to explore the biogenesis of peroxisomes. The label was found in the biggest subunit of the enzyme in the supernatant fraction shortly after the label injection, but was distributed to the smaller subunits later. The labeling in the smaller subunits in the peroxisomal fraction was greater than that of the supernatant. The distribution of the label among the subunits in these subcellular fractions was the same as that of the protein amounts 1 day after the label injection. This paper reports that the increase in the quantities of peroxisomal enzymes upon administration of DEHP is mainly due to the increase in their synthesis rates caused by the increase in amounts of mRNA coding for these enzymes.

Acyl-CoA Oxidase↗
PubMed1982

The significance of blood transfusion in non-A, non-B chronic liver disease in Japan.

We performed a follow-up study on 70 patients with acute non-A, non-B (NANB) posttransfusion hepatitis and a retrospective study on 283 chronic hepatitis, 70 cirrhosis and 53 hepatocellular carcinoma patients of type NANB. In acute NANB post-transfusion hepatitis, as judged by the transaminase levels, th duration of the disease exceeded 6 months in 46/70 = 65.7% and 1 year in 32/70 = 45.7%. The histological diagnosis of the 32 cases persisting for more than 1 year was chronic active hepatitis in 5, chronic persistent hepatitis in 2 and unresolved hepatitis in 6. The frequency of previous transfusion in chronic hepatitis, cirrhosis and hepatocellular carcinoma of type NANB was 42.8, 37.1 and 15.1%, respectively, whereas the incidence of early posttransfusion hepatitis was 8.5, 8.6 and 7.5%, respectively. in chronic liver diseases with a history of jaundice and/or hepatitis, previous transfusions are more frequently associated with type NANB than with type B disease. The present study demonstrates that NANB posttransfusion hepatitis tends to develop to chronic liver disease when analyzed prospectively as well as retrospectively.

Adult↗
PubMed1982

Etiology of mitral regurgitation in secundum atrial septal defect.

Non-rheumatic mitral regurgitation was found in 9.1% (27 patients) of all patients with secundum atrial septal defect (298 patients) who were operated on during a 13-year period at the Mitsui Memorial Hospital. This combined lesion was more frequent in female (12.3%, 19 patients) than male (5.6%, 8 patients), and the incidence tended to increase with age. Inspection at operation revealed a marked fibrous thickening of the anterior and posterior mitral valve leaflets with a localized bulging into the left atrium in the posteromedial commissural area. Similar, but less prominent change was found in nearly all patients above 20 years of age with mitral regurgitation, although the small area where the commissural chordae were attached was not involved. A friction between anterior and posterior mitral leaflets due to abnormal left ventricular motion secondary to the right ventricular volume overload might be responsible to the genesis of this lesion. Mitral annuloplasty was performed on 21 of 27 patients with a satisfactory result without operative mortality. Except one case of early death from cerebral thromboembolism they were all restored to a functional status of class I by NYHA standard within one year after operation, and there were no late death during a follow-up period of as long as 12 years. We propose a new entity "ASD, MR complex" for this combined lesion, as it demonstrates a specific pathophysiology, and necessitates a different procedure for surgical correction from that of a secundum atrial septal defect without other anomalies.

Adolescent↗