Biomedical subjects
Publications and source records attributed to T Nishimaki.
A competitive inhibition test for anti-nRNP antibody was developed, using horseradish-peroxidase-labelled anti-nRNP IgG derived from the serum of a patient with mixed connective tissue disease. In this test, the anti-nRNP antibody was clearly distinguished from the anti-Sm antibody in the patients' sera, and the sensitivity of the assay for anti-nRNP antibody was close to 50 ng/ml.
The peroxidase-labelled IgG fraction of anti-nRNP antibody obtained from a MCTD patient stained the nuclei of almost any kind of cells of man and rat. In addition, the cytoplasma of anterior horn cells of the rat spinal cord was exclusively reacted with this antibody. Both cytoplasmic and nuclear staining of the anterior horn cells were reduced after treatment of tissue sections with RNase.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We report a rare case of duplication of the stomach concomitant with idiopathic portal hypertension. The woman underwent a gastrectomy, under a tentative diagnosis of gastric carcinoma. The resected specimen revealed a submucosal type duplication of the stomach located on the greater curvature. The lesion had three communications with the true stomach and had the gross appearance of a "triple antrum".
Crude extract of Escherichia coli was found to elongate medium chain acyl-CoA primers. The reaction products were fatty acids one or two C2 units longer than the primer. Acetyl-CoA acted as the condensing unit in this reaction, while malonyl-CoA did not. The optimal pH for the reaction was 5.0 in 0.1 M citrate-phosphate buffer. NADH was the predominant electron donor for the incorporation of acetyl-CoA into fatty acids, and NADPH was one-third as effective as NADH at pH 5.0. Acyl carrier protein and cerulenin had no effect on the acetyl-CoA incorporation into the chain elongation products. Acyl-CoA compounds with medium carbon chain lengths proved to be the best as primers, and the maximum incorporation was observed with octanoyl-CoA. N-Ethylmaleimide and p-hydroxymercuribenzoate blocked the chain elongation reaction by inhibiting either condensation or 3-ketoacyl reduction.
Sera of patients with various liver diseases were examined for the presence of Hanganutziu-Deicher (H-D) antibodies by enzyme immunoassay with high-molecular weight glycoprotein (HMWGP) isolated from bovine red blood cell stromata. IgG class H-D antibodies were demonstrated in sera of 5.9% of acute hepatitis, 28.1% of chronic hepatitis and 21.9% of liver cirrhosis patients. H-D specificity of the antibodies under investigation was determined by absorption experiments. Evidence was also presented that the H-D antibodies in the liver disease sera are directed to N-glycolyl neuraminic acid (NGNA) and/or NGNA-dependent determinants of HMWGP.
Explore the source record for details and available documents.
Antiglycolipid antibodies were measured in normal and pathologic sera and synovial fluids by means of a modified microplate method of complement-mediated immune lysis of fluorescent dye-trapped liposomes. All sera of normal subjects had antibodies against globopentaosylceramide (IV3 GalNAcGbOse4Cer), ganglioside GM1, gangliotriaosylceramide, gangliotetraosylceramide, and galactosylneolactotetraosylceramide antigens. Most sera of normal subjects had antibodies against lactotriaosylceramide, N-glycolylneuraminosyl-neolactotetraosylceramide (NeuGcnLcOse4Cer), GM3 ganglioside with N-glycolylneuraminic acid (NeuGcGM3) and GD1a antigens. Differences of titers against IV3GalNAcGbOse4Cer, neolactotetraosylceramide, NeuGcGM3 and NeuGcnLcOse4Cer antigens were observed between sera of normal subjects and pathologic sera from cases of leukemias, lymphomas, several autoimmune diseases and liver diseases.
Dextran and antidextran antibodies were examined by enzyme immunoassay (EIA) and immunodiffusion in sera of 108 patients with various liver diseases. In EIA, IgG class antidextran antibody was detected in 16 patients (14.8%), mostly with chronic liver diseases such as liver cirrhosis (26.9%) and chronic hepatitis (22.2%). IgM class antibody was detected in 10 patients (9.2%). Results obtained by EIA inhibition revealed that dextran antigen was present mostly in sera of patients with acute liver diseases such as fulminant hepatitis (75.0%) and acute hepatitis (17.2%). Identity of the dextran antigen in the liver diseases serum and the dextran preparation recognized by an antibody-containing serum was demonstrated. These results suggest that the damaged hepatocytes in the process of the liver disease may release the dextran antigen into the patient's circulation which is responsible for the formation of antidextran antibodies by the patients with liver diseases.
Explore the source record for details and available documents.
NADPH-dependent trans-2-enoyl-CoA reductase was purified to homogeneity from Escherichia coli. The molecular weight of the native enzyme was estimated to be 80,000 by gel filtration and that of the subunit was estimated to be 40,000 by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The enzyme was most active toward trans-2-hexenoyl-CoA and trans-2-octenoyl-CoA but was less active toward longer chain substrates, whereas the Km values decreased progressively with increasing carbon chain length of substrates. The reductase appears to have a functional thiol group. The enzyme activity was rapidly decreased by p-hydroxymercuribenzoate and 5,5'-dithiobis(2-nitrobenzoic acid), and slowly by N-ethylmaleimide. The enzyme was protected from inhibition by these SH-reagents by the addition of NADPH. The enzyme was also inhibited by saturated acyl-CoA esters.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The immunoglobulin class of rheumatoid factor (RF) in sera and synovial fluids of patients with rheumatic diseases was measured by a solid-phase enzyme immunoassay. IgG-RF was frequently found in seronegative sera as well as in seropositive sera of rheumatic patients. Titers of IgG-RF were higher in the active phase than in the inactive phase of SLE and showed a correlation to the levels of hypocomplementemia and circulating immune complexes in SLE sera. Titers of IgA-RF were likewise higher in the active-phase of SLE with a correlation to titers of circulating immune complexes. IgA-RF was also found frequently in sera of patients with Sjögren's syndrome.
Incorporation of deuterium atoms from deuterium-labeled NADPH and 2H2O during the reaction catalyzed by 2,4-dienoyl-CoA reductase of Escherichia coli (E. coli) was investigated. When trans-2,cis-4-decadienoyl-CoA was incubated with 4R- or 4S-[4-2H1]NADPH in the presence of purified 2,4-dienoyl-CoA reductase, no deuterium was detected in the reaction product by gas chromatography-mass spectrometry after derivatization to its pyrrolidine amide. On the other hand, when the dienoyl-CoA was incubated in the presence of NADPH and the reductase in 2H2O, two deuterium atoms were incorporated: One deuterium atom was located at the C-4 position of trans-2-decenoate, and the other at the C-5 position. The UV and shorter wavelengths of the visible spectrum of the reductase solution revealed that the reductase contained flavin as a prosthetic group. Therefore it is considered that a hydrogen atom of NADPH was first transferred to the flavin moiety of the reductase, and then the hydrogen atom was rapidly exchanged for one in the medium before its direct transfer to the substrate.
The highest mean value of the serum C1q concentrations among chronic liver diseases was obtained in patients with liver cirrhosis (LC). C1q serum levels seemed to increase along the progression of liver damage. Serum levels of C1q and CH50 in patients with LC and systemic lupus erythematosus (SLE) were simultaneously estimated. No correlation between C1q and CH50 levels was observed in LC sera, while a significant correlation was demonstrated in SLE sera. It could be suggested that the mechanism for the low CH50 in LC sera seemed different from that in SLE sera, and that the activation of classical complement pathway was not the predominant cause in LC sera. Correlations of serum levels between immune complexes and C1q were examined in patients with LC and SLE. It could be deduced from the results of a positive correlation in LC sera and the reverse tendency in SLE sera that the significances of C1q and immune complexes in LC sera differed from those in SLE sera.