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Biomedical subjects

K Fujii

Publications and source records attributed to K Fujii.

At least 865 records · Page 48Linked to original sources
PubMed1982

Accumulation of 5-methyltetrahydrofolate in cobalamin-deficient L1210 mouse leukemia cells.

Cobalamin-deficient L1210 mouse leukemia cells were propagated on [3H]folate under conditions designed to completely label the intracellular folate compounds. The latter, present almost entirely as polyglutamate forms, were converted to the corresponding monoglutamates by treatment with gamma-glutamylcarboxypeptidase; the monoglutamates were subsequently separated and identified by chromatography on Sephadex G-25. 5-Methyltetrahydrofolate accounted for approximately 70% of the total folate pool (17.8 nmol/10(9) cells), while the remainder was comprised largely of 5-formyltetrahydrofolate (13.0%), and tetrahydrofolate (9.5%). The identity of 5-methyltetrahydrofolate were further confirmed by chromatography on DEAE-cellulose and by its quantitative conversion to tetrahydrofolate after treatment with a highly purified preparation of methionine synthetase (5-methyltetrahydrofolate:homocysteine methyltransferase, EC 2.1.1.13). In contrast, cobalamin-replete cells contained only 5.3% 5-methyltetrahydrofolate, along with 30% each of the other three reduced folate compounds. These results provide direct experimental proof of the "methyl trap" hypothesis, which predicted that 5-methyltetrahydrofolate should accumulate in cobalamin-deficient cells.

Animals↗
PubMed1982

Genetic analysis of human lymphocyte proteins by two-dimensional gel electrophoresis: 2. Genetic polymorphism of lymphocyte cytosol 64K polypeptide.

We describe a genetic polymorphism of human lymphocyte cytosol major polypeptide with mol. wt. 64,000, detected in peripheral blood lymphocytes by high resolution two-dimensional electrophoresis. Three different electrophoretic types (1-1, 2-1, 2-2) of the polypeptide have been identified. Family and population studies indicate that the three phenotypes of the polypeptide are determined by two common alleles at a single autosomal locus. The polypeptide occurs in the cytosol and is predominant in peripheral blood lymphocytes, B-lymphoblastoid cells, T-lymphoblastoid cells, lymph node, and spleen. The polypeptide has not been detected HeLa cells, fibroblasts, erythrocytes, serum, and cerebrum. Traces of the polypeptide exist in liver, kidney, and skeletal muscle. It is proposed that the polypeptide and its locus be temporarily designated lymphocyte cytosol 64K polypeptide (LC64K polypeptide) and LC64P, respectively. In a Japanese population, the gene frequencies of LC64P1 and LC64P2 were 0.936 and 0.064, respectively. The data suggest that LC64P is a new locus, product of which shows genetic polymorphism and is associated with the function and/or the structure of lymphocytes.

Alleles↗
PubMed1982

Neural and humoral factors influence gastric receptive relaxation in dogs.

To clarify the neural and humoral factors which control gastric receptive relaxation, the effects of various types of vagotomy or splanchnicotomy on receptive relaxation of the canine innervated corpus pouch were investigated. The influence of gastrin, histamine H1-receptor antagonist, and anti-histamine releasing agents on receptive relaxation were also examined. Selective proximal vagotomy or splanchnicotomy resulted in a slight disturbance in receptive relaxation. Truncal vagotomy produced a marked disturbance in receptive relaxation. Administration of tetragastrin potently inhibited receptive relaxation, however, recovery occurred by injecting a histamine H1-receptor antagonist. Increased serum gastrin induced by perfusion of the antrum with liver extract solution disturbed receptive relaxation and this response was inhibited by pretreatment with transamine, an inhibitor of histamine release from histamine secreting cells. These results indicate that receptive relaxation in the canine stomach is controlled not only by vagal and splanchnic nerves, but also by gastrin and histamine.

Animals↗
PubMed1982

Effect of L-leucine-supplemented diet on the nicotinamide adenine dinucleotide content of rat liver.

The hepatic nicotinamide adenine dinucleotide (NAD) content was significantly lower in rats fed a diet supplemented with 0.45-10% L-leucine for 1-3 weeks than in control rats fed laboratory chow (24.6% protein). High dietary levels of leucine did not affect the activity of hepatic tryptophan pyrrolase or quinolinate phosphoribosyltransferase, which are key enzymes in the tryptophan leads to NAD pathway. The increased hepatic NAD contents 4 hours after intraperitoneal injections of the NAD precursors L-tryptophan, niacin and nicotinamide were not influenced by excess dietary leucine. These observations suggest that decrease in the hepatic NAD content by excess dietary leucine is not due to alteration of NAD metabolism resulting from accumulation of leucine or its metabolite. The uptake of 1 mM L-[side chain-2,3-3H]tryptophan into isolated jejunal segments was inhibited markedly by 10 mM-leucine. Similar inhibitory effects were observed with 10 mM L-valine, L-isoleucine, L-phenylalanine and L-methionine, but not-L-lysine, L-aspartate, L-alanine or glycine. The radioactivity in portal blood after administration of a solution of 10 mumol of L-[side chain-3-14C]tryptophan in 1 ml of physiological saline by stomach tube was inhibited markedly by addition to the solution of 100 mumol of L-leucine or the other amino acids that inhibited L-tryptophan uptake by isolated jejunal segments. These findings strongly suggest that decrease in the liver NAD content by excess dietary leucine is mainly due to competitive inhibition by L-leucine of intestinal absorption of L-tryptophan.

Animals↗
PubMed1982

A spin trap study on anaerobic dehalogenation of halothane by a reconstituted liver microsomal cytochrome P-450 enzyme system.

In the presence of a spin trapping reagent, N-tert-butyl-alpha-phenylnitrone, anaerobic incubation of halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) with a reconstituted cytochrome P-450 enzyme system of rabbit liver microsomes exhibited an electron spin resonance spectrum containing signals of a nitroxide radical, and all components of the reconstituted system were necessary to produce the nitroxide radical. Formation of 2-chloro-1,1,1-trifluoroethane, the product of anaerobic dehalogenation of halothane by the reconstituted system, was inhibited by N-tert-butyl-alpha-phenylnitrone. These results indicate that a radical intermediate of halothane is produced during the anaerobic dehalogenation reaction, and that the radical is trapped by N-tert-butyl-alpha-phenylnitrone to form a N-tert-butyl-alpha-phenylnitrone radical adduct.

Anaerobiosis↗
PubMed1982

A partially degraded form of human plasminogen in circulating blood.

A method for separate measurement of the amounts of the native form and partially degraded form of plasminogen and plasmin in human circulating blood was devised based on their different mobilities on disc polyacrylamide gel electrophoresis. The relative amounts in the circulating blood as estimated by the method were as follows: 78.5% native form, 6.1% partially degraded form and 15.5% plasmin, in the resting state of healthy adults. The partially degraded form increased to about 50% after strenuous exercise load. The present study showed that relatively large amounts of the partially degraded form can be produced in the circulating blood, even though abundant plasmin inhibitors exist there. These data suggest that the partially degraded form may play an important role in thrombolysis in vivo.

Electrophoresis, Polyacrylamide Gel↗