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Biomedical subjects

F Matsuda

Publications and source records attributed to F Matsuda.

At least 91 records · Page 5Linked to original sources
PubMed1987

A novel family of variable region genes of the human immunoglobulin heavy chain.

We isolated and sequenced six variable-region (V) gene segments of the human immunoglobulin heavy-chain (H) using the V71-2 segment as probe. These VH segments were more than 90% homologous to each other and less than 65% homologous to members of the three known VH families. The VH fragments hybridized to an identical set of restriction fragments on Southern blots of human placenta DNA. The new family was designated as the VH-IV family. The complexity of the VH-IV family was estimated to be at least nine genes, of which the sequenced seven were functional genes. The VH-IV family is homologous (76%) to the mouse Vh36-60 family.

Amino Acid Sequence↗
PubMed1986

Sensitive determination of deuterated and non-deuterated tryptophan, tryptamine and serotonin by combined capillary gas chromatography and negative ion chemical ionization mass spectrometry.

Sensitive methods for the determination of deuterated and non-deuterated tryptophan, tryptamine and serotonin by combined capillary gas chromatography and negative ion chemical ionization mass spectrometry were developed. [3,3-2H2]-L-Tryptophan, which was used as a tracer, was synthesized for studies of their in vivo metabolism. Tryptophan was converted into its trifluoroacetylmethyl derivative after prepurification with an AG 50W-X2 cation-exchange column. Tryptamine and serotonin were extracted with 20% butanol in diethyl ether and derivatized with trifluoroacetic anhydride. These derivatives were separated and determined by selected ion monitoring. In these determinations, [2',3,3,4',5',6',7'-2H7]-D,L-tryptophan, [alpha,alpha,beta,beta-2H4]tryptamine and [alpha,alpha,beta,beta-2H4]serotonin were used as internal standards.

Chemical Phenomena↗
PubMed1986

Cloning of cDNA for human T-cell replacing factor (interleukin-5) and comparison with the murine homologue.

We have cloned cDNA for T-cell replacing factor (interleukin-5), which replaces T-cell helper function for normal B cells which secrete immunoglobulin, from human T cell leukemia line, ATL-2, using mouse interleukin-5 cDNA as probe. Total nucleotide sequence of the cDNA (816 base pairs) was determined and compared with that of mouse interleukin-5 cDNA. The cloned cDNA encoded the interleukin-5 precursor of 134 amino acids containing an N-terminal signal sequence. Although the human interleukin-5 precursor is one amino acid longer than the murine homologue, the sizes of the mature proteins appear similar. The nucleotide and amino acid sequence homologies of the coding regions of human and murine interleukin-5 are 77% and 70%, respectively. Human interleukin-5 synthesized by the direction of the cloned cDNA induced immunoglobulin synthesis in human B cells stimulated by Staphylococcus aureus mitogen.

Amino Acid Sequence↗
PubMed1986

Organization and evolution of variable region genes of the human immunoglobulin heavy chain.

We have isolated 23 different cosmid clones of the heavy-chain variable region genes (VH) of human immunoglobulin. These clones encompass about 1000 X 10(3) base-pairs of DNA containing 61 VH genes. Characterization of the 23 clones by Southern blot hybridization showed that VH genes belonging to different families were physically linked in many regions. Cluster 71, which was analyzed in detail, comprised seven VH segments arranged in the same orientation with different intervals. This clone contained internal homology regions, each carrying two VH segments of different families. Comparison of the nucleotide sequences of VH segments within each family showed that profiles of accumulation of mutations in framework (FR) and complementarity-determining (CDR) regions were different. CDR had more mutations at amino-acid-substituting positions than at silent positions, whereas FR had the reverse distribution of mutations. Five out of seven VH segments of this cluster were pseudogenes containing various mutations. VH pseudogenes were classified into two distinct groups; one with a few replacement mutations (conserved pseudogenes), and the other with rather extensive mutations (diverged pseudogenes). The possibility that conserved pseudogenes serve as a reservoir of VH segments is discussed.

Base Sequence↗
PubMed1985

Non-Hodgkin's lymphoma of Waldeyer's ring and nasal cavity. Clinical and immunologic aspects.

Twenty-nine cases of non-Hodgkin's lymphoma of Waldeyer's ring (W-NHL) and nasal cavity or paranasal sinus (N-NHL) were studied for tumor-surface marker phenotype and histopathologic correlation with clinical features. Immunostaining procedures on tissue sections by using xenoantisera and monoclonal antibodies to human B- and T-cells enabled the authors to demonstrate precise surface marker phenotypes of tumor cells and, moreover, the histologic localization of normal or neoplastic B- and T-cells in preserving the original structure of lymphoid organs or tumor tissues. In 22 cases of W-NHL, 19 (86%) had B-cell markers and 3 (14%) had T-cell markers, whereas 6 of 7 cases (86%) of N-NHL had T-cell markers. Tumor cells in T-cell lymphomas in W-NHL and N-NHL reacted with antibodies to peripheral T-cells except one case of W-NHL. Rappaport "histiocytic" subtype was heterogeneous with respect to both surface marker characteristics and morphologic features, i.e., seven had B-cell markers and four had T-cell markers, and they were all subdivided into "large cell" or "large cell, immunoblastic" in Working Formulation and "large cell" or "pleomorphic" in Lymphoma Study Group classification. The actuarial survival curve for all T-cell lymphoma patients was characterized by a rapid initial decline and a subsequent plateau, which contained two of the long survivors. In contrast, the B-cell lymphoma group had a more graded decline. The median and actuarial survivals of the T-cell lymphoma group were far inferior to those for the lymphoma group that expressed B-cell markers.

Adolescent↗
PubMed1985

An early effect of the S component of staphylococcal leukocidin on methylation of phospholipid in various leukocytes.

On incubation of rabbit polymorphonuclear leukocytes with the S component of staphylococcal leukocidin at 37 degrees C, the 3H-labeled methyl group of S-adenosyl[methyl-3H]methionine was rapidly incorporated into phospholipid. Subsequently, the methylated phosphatidylcholine was degraded by activated phospholipase A2. Complete blockage of the methylation of phospholipid by a mixture of erythro-9-[2-hydroxy-3-nonyl]adenine, adenosine, and L-homocysteine thiolactone markedly inhibited the activation of phospholipase A2 by the S component. It also inhibited the binding of 125I-labeled F component to the cells, but not that of the labeled S component. These results suggest that methylation of phospholipid in the cell membranes by the S component results in activation of phospholipase A2, which induces the binding of the F component to the cells.

Adenine↗
PubMed1984

Binding of pseudomonal leukocidin to rabbit polymorphonuclear leukocytes.

The leukocytotoxic toxin pseudomonal leukocidin, produced by Pseudomonas aeruginosa, was radioiodinated with chloramine-T reagent. Binding of [125I]leukocidin to rabbit polymorphonuclear leukocytes was found to be concentration dependent at 37 degrees C. A Scatchard plot of binding data was linear, indicating that leukocidin binds to a single population of sites. The dissociation constant, KD, was calculated from the Scatchard plot to be 2.5 X 10(-7) M, and the number of binding sites per leukocyte was approximately 4.4 X 10(5). Unlabeled leukocidin or antileukocidin antibody reduced the binding of [125I]leukocidin to the leukocytes. A leukocidin-binding protein was extracted from rabbit polymorphonuclear leukocytes with Triton X-100 and purified by leukocidin-Sepharose 4B affinity column chromatography. Approximately 60 micrograms of binding protein was obtained from 8.1 mg of material extracted from the leukocytes. The binding protein had a molecular weight of about 50,000 as shown by sodium dodecyl sulfate-polyacrylamide slab gel electrophoresis and staining with silver nitrate. Under nondenaturing conditions, its molecular weight was also about 50,000, as shown by gel filtration-Sephadex G-200 chromatography. The 50,000-dalton protein purified in this way from rabbit polymorphonuclear leukocytes competitively inhibited the binding of leukocidin to leukocytes and inactivated leukocidin activity. With equimolar amounts of the 50,000-dalton protein and leukocidin, up to 90% inactivation of leukocidin was observed.

Animals↗
PubMed1983

Crystallization and some properties of leukocidin from Pseudomonas aeruginosa.

A leukocidin was isolated and purified from autolysates of Pseudomonas aeruginosa strain 158 by a combination of procedures such as column chromatography on DEAE-Sephadex A-50, gel filtration on Sephadex G-100, and zone electrophoresis on pevikon. The purified preparation showed a single band in each experiment using electrophoreses in the presence or absence of sodium dodecyl sulfate (SDS), and the agar-gel Ouchterlony immunodiffusion test. The purified pseudomonal leukocidin was crystallized by salting out with saturated ammonium sulfate at pH 7.0 in a needle-leaf like form. The molecular weight of the leukocidin was estimated to be 42,500 by SDS-polyacrylamide gel electrophoresis, 40,000 by gel filtration, and 44,700 (3.3 S20,W) by sucrose density gradient centrifugation. The isoelectric point of the leukocidin was estimated to be at pH 6.3 by isoelectrofocusing. Morphological studies of a leukocidin-treated leukocyte showed that the formation of vacuoles of cytosolic granules and the swelling of the lobulated nuclei occurred prior to leukocyte enlargement. In a slide adhesion test with rabbit polymorphonuclear leukocytes (1 X 10(6], the minimum cytotoxic dose for the destruction of all leukocytes was 13-20 ng of the crystallized toxin. Rabbit lymphocytes were one-thirtieth as sensitive as rabbit leukocytes. Leukocidin did not act on rabbit erythrocytes or on platelets.

Amino Acids↗
PubMed1983

Alcoholic cardiomyopathy--acetaldehyde poisoning rat: myocardial and serum enzyme changes in acute exposure.

In order to clarify the pathogenesis of alcoholic cardiomyopathy, acetaldehyde (Ach) was administered to rats using the inhalation method. Serum enzyme changes and structural alterations of the heart were observed at various time intervals after 2 ml of Ach exposure for 2 hours. Possible myocardium-related enzymes, such as glutamic oxaloacetic transaminase, lactic dehydrogenase and creatine phosphokinase, were elevated within 24 hours and then returned almost to the previous levels. The most significant change seen using light microscopy was a prominent contraction band scattered throughout the specimen in the groups exposed for 12 and 24 hours, respectively. Ultrastructually, mitochondrial swelling and crystal disarray concomitant with myofibrillar change (swelling of Z-band) were observed. The former was seen most prominently immediately after exposure, while the latter was observed 24 hours after exposure. The significance of these findings and the difference between alcoholic cardiomyopathy and ischemic lesions were discussed.

Acetaldehyde↗