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Biomedical subjects

I Matsuda

Publications and source records attributed to I Matsuda.

At least 127 records · Page 7Linked to original sources
PubMed1995

PCR detection of Ti and Ri plasmids from phytopathogenic Agrobacterium strains.

A universal primer set (VCF/VCR) for PCR analysis based on the sequences of the virC operon located on Ti and Ri plasmids was designed to detect these plasmids from phytopathogenic Agrobacterium strains. With the VCF (sequence, 5'-ATCATTTGTAGCGACT-3') and VCR (sequence, 5'-AGCTCAAACCTGCTTC-3') primer set, DNA fragments of 730 bp in length were amplified from cell lysates of 10 rhizogenic and 65 tumorigenic agrobacteria. DNA sequencing and Southern hybridization analysis confirmed that the amplified fragments corresponded to the target region. The PCR method is considered convenient for routine determination of the potential pathogenicity of Agrobacterium strains.

Base Sequence↗
PubMed1995

Intra-arterial liposomal adriamycin for metastatic adenocarcinoma of the liver.

A liposome-entrapped liposome form of Adriamycin (Lip-ADM) has been demonstrated to cause less myocardial and gastrointestinal toxicity than free ADM. In the present study, Lip-ADM prepared by the remote loading method was administered to 3 patients with metastatic adenocarcinoma of the liver via a reservoir with the catheter located in the proper hepatic artery. The primary tumor was gastric cancer in 2 patients and sigmoid colon cancer in 1. Lip-ADM was administered at doses of 10, 20 or 50 mg per time. The total ADM dose was 170, 490, and 760 mg, respectively. No severe adverse effects, such as nausea, vomiting, stomatitis, alopecia or cardiotoxicity, were observed in any of the patients. Although mild leukocytopenia (2,800/microliters) was observed in 1 patient, anemia or thrombocytopenia did not occur. The survival time was respectively 6, 15, and 17 months from the start of Lip-ADM administration. A partial response was obtained in 1 patient and stable disease in 1 patient. Administration of Lip-ADM via a reservoir appears to be a useful treatment for patients with metastatic adenocarcinoma of the liver, since the low toxicity of this preparation allows an increase of the total dose of ADM.

Adenocarcinoma↗
PubMed1995

Characterization of antineutrophil antibodies in patients with neutropenia associated with nutritional copper deficiency.

Six antineutrophil antibody (ANA)-positive patients with copper deficiency were classified into two groups; those with (group A, n = 3) and those without (group B, n = 3) neutropenia. The percent binding of ANA for normal peripheral neutrophils was similar in both groups (83.5 +/- 7.2 vs. 79.1 +/- 10.5%). The percent binding of sera to cultured promyelocytic leukemia cells (HL-60) was increased in group A (from 3.7 +/- 3.2 to 12.2 +/- 2.3%) but not in group B (from 65.3 +/- 21.7 to 40.7 +/- 6.3%) after stimulation of HL-60 with DMSO. The stimulated HL-60 cells expressed CD 16 and CD 11b antigens. In the presence of monoclonal antibody for CD 16, the titer of ANA was nil in group A and unchanged in group B. Thus, ANA of patients with neutropenia may recognize mainly the CD 16 antigen, the Fc gamma receptor III of neutrophils.

Adolescent↗
PubMed1995

Different effects of subclasses of HDL containing apoA-I but not apoA-II (LpA-I) on cholesterol esterification in plasma and net cholesterol efflux from foam cells.

We investigated the effects of subclasses of plasma LpA-I (HDL containing apoA-I but not apoA-II) on cholesterol esterification in plasma and net cholesterol efflux from foam cells. LpA-I was composed of particles of three diameters: large (11.1 nm; Lg-LpA-I), medium (8.8 nm; Md-LpA-I), and small (7.7 nm; Sm-LpA-I). Plasma concentrations of LpA-I were positively correlated only with the level of Lg-LpA-I. Plasma concentrations of Lg-LpA-I were inversely correlated with the rate of cholesterol esterification in plasma and VLDL- and LDL-depleted plasma. Plasma concentrations of Md-LpA-I and Sm-LpA-I did not correlate with the rate of cholesterol esterification in plasma or VLDL- and LDL-depleted plasma. When macrophage foam cells were incubated with Md- and Sm-LpA-I, cellular cholesterol mass was reduced by approximately 70%. In contrast, the cellular cholesterol-reducing capacity of Lg-LpA-I was negligible. Lg-LpA-I inhibited net cholesterol removal from foam cells that was mediated by Md- and Sm-LpA-I and cholesteryl ester production with these particles. These results suggest that Md- and Sm-LpA-I may actively participate in cellular cholesterol removal and cholesterol esterification in plasma and HDL, while Lg-LpA-I may regulate these functions of Md- and Sm-LpA-I.

Adolescent↗
PubMed1995

Signaling through CD40 rescues IgE but not IgG or IgA secretion in X-linked immunodeficiency with hyper-IgM.

The ligand for CD40 (CD40L) is a membrane protein on activated T cells that induces B cell proliferation and differentiation. Several mutations of the CD40L gene were reported responsible for defective class switching of B cells in an X-linked immunodeficiency with hyper IgM (X-HIM). We studied four affected males from three families and found three independent mutations including new mutations of CD40L gene. In every X-HIM patient tested, however, anti-CD40 plus IL-10 did not induce class switching from IgM to IgG or IgA, even in the presence of Staphylococcus aureus Cowan I strain (SAC). CD4+ T cell clones, expressing CD40L on their surface, also did not rescue IgG or IgA induction by X-HIM peripheral blood B cells in vitro. But signaling through CD40 induced both B cell proliferation and IgE secretion when IL-4 was added to the culture. Taken together, these results show that in vitro signaling through CD40 rescues IgE but not IgG or IgA secretion by peripheral blood X-HIM B cells and suggest that in vivo CD40 and CD40L interaction might be necessary for IgG and IgA differentiation in X-HIM.

Amino Acid Sequence↗
PubMed1995

A late-appearing Philadelphia chromosome in acute lymphoblastic leukemia confirmed by expression of BCR-ABL mRNA.

We report two cases of acute lymphoblastic leukemia (ALL) with a late-appearing Philadelphia chromosome (Ph1), confirmed by the expression of BCR-ABL mRNA, using the reverse transcriptase/polymerase chain reaction (RT/PCR) technique. The first patient was a 10-year-old boy with precursor B cell type ALL-L1 (FAB classification). At diagnosis, no metaphase cells were found by chromosome analysis and BCR-ABL mRNA was not observed. At the beginning of relapse, which occurred after 7 months of complete remission, a normal karyotype was observed. At the terminal stage, leukemic cells with Ph1 and BCR-ABL mRNA for the P190 variety were observed. The second patient was a 12-year-old boy with immature T cell type ALL-L1. The metaphase cells showed a 9p- chromosome at diagnosis and Ph1 appeared in addition to 9p- at relapse. Hybrid mRNA for the P210 variety was detected only when Ph1 had developed. The blast cells with Ph1 were derived from the original leukemic clone through clonal evolution, since the same clonal rearrangements of IGH or TCRB were detected in leukemic cells obtained both at diagnosis and relapse in both patients. Thus, in both cases, Ph1 was detected only in the course of ALL along with expression of BCR-ABL mRNA. This observation also confirmed that, as in de novo Ph1-positive ALL, both the P190 and P210 varieties of BCR-ABL mRNA are observed in ALL with late-appearing Ph1.

Base Sequence↗
PubMed1995

Structural and functional differences of subspecies of apoA-I-containing lipoprotein in patients with plasma cholesteryl ester transfer protein deficiency.

ApoA-I-containing lipoproteins exist in plasma in two main forms: one contains only apoA-I (LpA-I) while the other contains both apoA-I and apoA-II (LpA-I/A-II). We characterized structural and functional changes of these lipoproteins in six patients with cholesteryl ester transfer protein (CETP) deficiency. In these patients, the amount of LpA-I and LpA-I/A-II had increased significantly. Sixty-five percent of plasma apoA-I was associated with LpA-I/A-II, which indicated that LpA-I/A-II was predominant. The chemical composition of both LpA-I and LpA-I/A-II was characterized by increased ratios of neutral to polar lipid, compared with findings in normal subjects. Particle sizes of these lipoproteins shifted to larger diameter ranges, as compared to the size seen in normal subjects. Incubation of patients' LpA-I and LpA-I/A-II with CETP markedly corrected the chemical and physical abnormalities in these lipoproteins. Cholesterol-reducing capacities of these lipoproteins from macrophage foam cells were significantly lower than in normal controls. Cholesterol esterification rates in LpA-I, LpA-I/A-II, and plasma were significantly lower in patients than in normal controls. We propose that the structure and function of LpA-I and LpA-I/A-II are severely affected in the presence of CETP deficiency.

Apolipoprotein A-I↗
PubMed1995

Extraordinarily high eosinophilia and elevated serum interleukin-5 level observed in a patient infected with Paragonimus westermani.

OBJECTIVE: Although eosinophilia is one of the typical clinical features of some helminth infections, the degree of eosinophilia in helminthiasis is usually 10% to 30% with a total white blood cell count of 10,000 to 20,000/mm3. Here we report a case of extraordinarily high eosinophilia (91%; absolute eosinophil count, 84,000/mm3) caused by Paragonimus westermani infection. To determine the mechanisms of eosinophilia, the levels of several eosinophilopoietic cytokines in the patient's sera were measured during the course of treatment. METHODS: Serum levels of three cytokines, granulocyte-macrophage colony-stimulating factor, interleukin-3 (IL-3), and IL-5 were measured by enzyme-linked immunosorbent assay using commercial kits or our own assay system for IL-5. RESULTS: Although the kinetic changes of IL-5 correlated well with eosinophilia, the serum IL-3 level remained below the detection level throughout the period examined. Although the granulocyte-macrophage colony-stimulating factor level was twofold to threefold higher than the normal level, its kinetics did not parallel the degree of eosinophilia. CONCLUSIONS: These results show that Paragonimus westermani infection can induce an extraordinarily high level of eosinophilia with an associated increase in IL-5 production. Immunoserologic diagnosis for parasitic diseases should be included in the differential diagnosis of eosinophilia.

Animals↗
PubMed1995

Ultrastructural, immunocytochemical and stereological investigation of hepatocytes in a patient with the mutation of the ornithine transcarbamylase gene.

We studied a male newborn suffering from deficiency of ornithine transcarbamylase (OTC) that is due to a G-to-A substitution in codon 269 of the OTC gene. This study intends to define the cell biological mechanisms in this naturally occurring OTC mutation which may explain the mild clinical course in spite of the very low residual enzyme activity. Using immunogold labeling of thawed thin frozen sections of liver from this patient and a control liver, we analyzed the quantitative distribution of several mitochondrial proteins in the cytosol and the mitochondria of hepatocytes. In addition, the absolute volumes and surface densities of mitochondria and peroxisomes were determined. Our results show that the absolute volume of mitochondria in the patient's hepatocytes was increased to 141% (P < 0.001) without any change in the surface density indicating an increased number of mitochondria. In the patient's hepatocytes the peroxisomes were increased in size but not in number. The concentration of OTC was elevated in the cytosol (P < 0.001) and to a lesser extent in mitochondria (P < 0.01) of the patient's hepatocytes thus indicating a doubling of OTC relative to control liver cells. The quantity of OTC in mitochondria was 63% higher in diseased liver cells. By conventional thin section electron microscopy, mitochondria-like structures with poorly defined cristae and an electron-dense matrix were observed in the cytoplasm of the diseased hepatocytes. By immunoelectron microscopy, they contained the cytochrome c oxidase II subunit as well as DNA but lacked OTC, carbamylphosphate synthetase, F1-ATPase beta subunit and catalase. Thus it appears that these structures represent defective and probably degenerating mitochondria. Our data indicate that the reduced enzyme activity of the mutant OTC is partly compensated by an increased amount of enzyme molecules in the cytosol as well as mitochondria combined with an increase in the biogenesis of mitochondria.

Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzin↗
PubMed1995

[Postoperative abdominal lymph node recurrence of intrathoracic esophageal cancer with a long-term complete response to radiation and split CF therapy (CDDP and 5-FU)--a case report].

We experienced complete remission in a patient with postoperative abdominal lymph node recurrence of intrathoracic esophageal cancer after treatment with radiation (60Co: 30 Gy) and split CF therapy (CDDP: 20 mg/day + 5-FU: 1 g/day for 5 days). Since then, this patient has remained in complete remission for 43 months with intermittent split CF therapy one or two times a year.

Abdomen↗
PubMed1995

A case of triple early gastric cancer in the remnant stomach.

A 63-yr-old man, who had undergone distal gastrectomy and gastrojejunostomy (Billroth II method) 32 yr previously for duodenal ulcer, was admitted with suspected gastric remnant cancer. An upper gastrointestinal series and endoscopy revealed a protruding lesion at the stoma of the remnant stomach. Total gastrectomy with resection of the adjacent jejunum was performed. Histological examination demonstrated two well-differentiated adenocarcinomas (a mixed type I and IIc lesion with submucosal invasion and a type IIa lesion with intramucosal invasion) and a type IIc mucocellular carcinoma located in the mucosa. Gastritis cystica polyposa also was observed in the remnant stomach. The combination of three early gastric cancers and gastritis cystica polyposa suggests that the mucosa of the remnant stomach had a high malignant potential. The patient has survived without recurrence for 5 yr since the operation.

Adenocarcinoma↗
PubMed1995

[Neutropenia in patient with X-linked hyper-IgM syndrome].

The X-linked form of hyper-IgM syndrome (HIGM1) is a rare disorder characterized by the inability of B cells to undergo isotype switch by a deficiency of CD40 ligand (CD40L) on activated T lymphocytes. The patients suffer from recurrent infections not only due to a lack of B lymphocyte activation but also due to defect of T lymphocyte functions. In addition, neutropenia is frequently accompanied by these symptoms. A patient with HIGM1, we experienced, suffered from recurrent infections and neutropenia. But he had a normal number of hematopoietic stem cell by the in vitro colony forming assay. CD34+ myeloid stem cell has been known to express CD40. We speculated by these facts that myeloid cell numbers are regulated by CD40-CD40L interaction.

Adolescent↗
PubMed1994

Interaction between apo A-I-containing lipoproteins and lecithin:cholesterol acyltransferase.

HDL2 and HDL3 subfractions of two species of apo A-I-containing lipoprotein, one containing only apo A-I (LpA-I) and the other containing both apo A-I and apo A-II (LpA-I/A-II), were tested for reactivity to lecithin:cholesterol acyltransferase (LCAT). These subfractions and their mixtures were incubated with lipoprotein-deficient plasma (LCAT source), and the rate of cholesterol esterification and kinetic parameters were determined. Apparent Vmax (appVmax) and apparent Km (appKm) for HDL2 subfractions of LpA-I and LpA-I/A-II were significantly lower than those of their HDL3 counterparts. Differences between subfractions were much more prominent in LpA-I than in LpA-I/A-II. appVmax of the HDL2 subfraction of LpA-I (LpA-IHDL2) was one-fifth, and appKm was one-third of those for the HDL3 subfraction (LpA-IHDL3). appVmax and appKm of LpA-IHDL2 were both lowest among the apo A-I-containing lipoprotein subfractions. When LpA-IHDL2 was added to other subfractions, the molar rate of cholesterol esterification was suppressed. Since LpA-IHDL2 consists of a particle 11.1 nm in diameter, our observations suggest that LpA-IHDL2 suppresses cholesterol esterification in apo A-I-containing lipoprotein, possibly by displacing LCAT from other subfractions with higher appKm and higher appVmax to 11.1 nm LpA-I particles with lower appKm and lower appVmax. All of these data suggest that the relative amount of 11.1 nm LpA-I particles in plasma regulates the reactivity of apo A-I-containing lipoprotein to LCAT and may play a key role on the production of cholesteryl esters in plasma.

Apolipoprotein A-I↗
PubMed1994

Evidence for impaired cellular cholesterol removal mediated by apo A-I containing lipoproteins in patients with familial lecithin: cholesterol acyltransferase deficiency.

We investigated the cholesterol reducing capacity of two species of lipoproteins containing apo A-I, one containing only apo A-I (LpA-I) and the other containing apo A-I and apo A-II (LpA-I/A-II), in 7 patients (4 homozygotes and 3 heterozygotes) with familial lecithin: cholesterol acyltransferase (LCAT) deficiency. Interaction of normal LpA-I or LpA-I/A-II with macrophage foam cells induced a mass reduction in cholesterol from these cells and the cholesterol reducing capacity of LpA-I was greater than that of LpA-I/A-II. When foam cells were incubated with these lipoproteins from homozygotes or heterozygotes, the capacity of LpA-I and LpA-I/A-II particles to reduce cellular cholesterol was decreased by approx. 50% in the homozygotes but was increased by 25-50% in the heterozygotes. These results suggest that LpA-I and LpA-I/A-II isolated from homozygotes and from heterozygotes differ in their ability to accept cellular cholesterol. The former are poor and the latter good acceptors of intracellular cholesterol. We conclude that factors other than reverse cholesterol transport via apo A-I containing lipoproteins have to be considered to explain why homozygotes for LCAT deficiency are not at high risk for premature atherosclerosis.

Adult↗
PubMed1994

Lactoferrin inhibits cholesterol accumulation in macrophages mediated by acetylated or oxidized low-density lipoproteins.

When macrophages are incubated with acetylated or oxidized low-density lipoproteins (Ac- or OxLDL), cellular cholesteryl esters (CE) increase significantly. In the present study, we investigated the effect of whey protein on Ac- or OxLDL mediated accumulation of CE in macrophages and found that lactoferrin (Lf), a minor protein component of whey, inhibits the accumulation of CE dose-dependently. In the presence of bovine Lf (1 mg/ml), CE accumulation in macrophages incubated with AcLDL (100 micrograms of protein/ml) decreased by more than 80%. Human Lf was less potent than bovine Lf, and bovine transferrin had no effect. Binding of 125I-AcLDL to macrophages was also inhibited by Lf. Agarose gel electrophoresis revealed that Lf binds to Ac- or OxLDLs and neutralizes their negative charges. These results indicate that Lf inhibits the binding of modified LDLs to macrophages by direct interaction with modified LDLs, resulting in their loss of function as ligands of the scavenger receptor. Modification of the arginine residues of Lf with 1,2-cyclohexanedione abolished its ability to bind to AcLDL, suggesting that a region rich in basic amino acid residues near the N-terminus of Lf, which resembles the ligand-binding site of the scavenger receptor, may be responsible for this binding ability. As a result, the inhibitory effect of Lf on CE accumulation in macrophages was significantly weakened by this modification. Our results suggest the possibility that Lf in the blood stream may act as an anti-atherogenic agent in vivo.

Amino Acid Sequence↗
PubMed1994

Structural organization and analysis of the human fumarylacetoacetate hydrolase gene in tyrosinemia type I.

Fumarylacetoacetate hydrolase (FAH) is a metabolic enzyme functioning at the last step of tyrosine catabolism. Deficiency in this enzyme activity is associated with tyrosinemia type I, characterized by hypertyrosinemia, liver dysfunction, renal tubular dysfunction, liver cirrhosis, and hepatic tumors. We isolated from a human gene library a chromosomal gene related to FAH. The human FAH gene is 30 kilobases long and is split into 14 exons. All of the splice donor and acceptor sites conform to the GT/AG rule. We also analyzed findings in a patient with tyrosinemia type I with respect to the mutation responsible for defects in the enzyme. A nucleotide change from T to G was found in the exon 2 of the gene and this change was accompanied by an amino acid substitution (Phe62Cys). Transfection and expression analysis of the cDNA in cultured BMT-10 cells with the nucleotide substitution demonstrated that the substitution was indeed responsible for the decreased activity of the enzyme in the patient. These results confirmed that the T to G mutation was one of the causes of tyrosinemia type I. Structure of the FAH gene and tests for expression of the mutant FAH will facilitate further understanding of various aspects of FAH.

Base Sequence↗
PubMed1994

Plasma HDL levels are regulated by the catabolic rate of large particles of lipoprotein containing apo-A-I.

Lp-A-I was isolated by immunoaffinity chromatography and then separated into two fractions of large and small Lp-A-I particles by conventional ultracentrifugation with a cut-off density of 1.125 g/ml. The large and small particle-rich fractions were then radiolabeled with [125I]-Na and [131I]-Na, respectively. Both of the labeled lipoproteins were injected (20 microCi, i.v.) simultaneously into normolipidemic rabbits. The FCR of the large Lp-A-I particles was much less than that of the small Lp-A-I particles (0.801 +/- 0.026/day vs. 2.227 +/- 0.067/day, P < 0.0001). These data indicate that the two particles have distinctly different metabolic pathways and that the lower FCR of larger Lp-A-I particles can effectively raise plasma HDL levels.

Animals↗