Estimation of the genome size of five strains of Taylorella equigenitalis isolated in Japan.
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Electrophoresis, Gel, Pulsed-Field↗
Biomedical subjects
M Matsuda
Publications and source records attributed to M Matsuda.
A case of hepatocellular carcinoma consisting of two solitary poorly differentiated polyclonal intrahepatic tumor nodules.
Two intrahepatic solitary tumors consisting of poorly differentiated hepatocellular carcinoma (HCC) were identified as polyclonal HCC nodules by analysis of the pattern of integration of hepatitis B viral DNA into nuclear DNA. After the removal of each nodule by partial liver resection, recurrent multiple tumors appeared within 10 months postoperatively. The findings in this case suggest that the effectiveness of reduction surgery for intrahepatic multiple tumors is limited in solitary multicentric HCC that consists of poorly differentiated HCC.
Blotting, Southern↗
Adult T cell leukemia-derived factor/human thioredoxin protects endothelial F-2 cell injury caused by activated neutrophils or hydrogen peroxide.
Adult T cell leukemia-derived factor (ADF), originally defined as an interleukin 2 receptor/alpha (alpha) chain inducer produced by human T-lymphotropic virus type-I transformed cells, is identical to human thioredoxin (TRX). In this study, the protective effect of ADF/TRX on the cytotoxicity of endothelial cells caused by phorbol myristate acetate (PMA)-activated neutrophils or hydrogen peroxide (H2O2) was examined. When murine endothelial F-2 cells established from an ultraviolet light-induced tumor on a nude mouse were incubated with PMA-activated neutrophils or with 1 mM H2O2 for 6 hours, the cytotoxicity of F-2 cells was respectively 51 +/- 4% or 40 +/- 8% by the 51Cr releasing assay. Recombinant ADF/TRX (rADF/TRX) inhibited this cytotoxicity in a dose-dependent manner, although mutant ADF/TRX (cysteine 31 to serine), 2-mercaptoethanol and dithiothreitol did not. On a molar basis, rADF/TRX was more effective than glutathione but less effective than catalase. Immunoblotting analysis showed that treatment with 0.1 mM H2O2 induced murine TRX on F-2 cells. These findings indicate that ADF/TRX is an oxidative stress-inducible endogenous protein and rADF/TRX plays a protective role against activated neutrophils- or H2O2-induced endothelial cytotoxicity.
Animals↗
Expression of Fc epsilon R2/CD23 and p55 IL-2R/CD25 on peripheral blood macrophages/monocytes in multiple sclerosis.
Macrophages have been found histologically to be activated in multiple sclerosis. We analyzed the expression of CD23 and CD25 on monocytes/macrophages in peripheral blood obtained from patients with multiple sclerosis (MS) to investigate their role in the demyelinating process. Peripheral blood mononuclear cells were obtained from 30 patients with MS including four Baló's diseases (24 with acute relapsing type disease, six with chronic progressive type disease) and 12 healthy controls. The percentage of CD14+CD23+ monocytes/macrophages and CD14+CD25+ monocytes/macrophages were determined by two-color flow cytometry. The percentage of CD14+CD23+ monocytes was significantly higher in patients with MS in the active phase as compared with controls (P < 0.01). Six patients with acute relapsing MS, who had received no therapy, had higher CD14+CD23+ cells than did controls (P < 0.0001). CD14+CD25+ monocytes/macrophages were not detected in peripheral blood monocytes/macrophages of patients with MS except Baló's concentric sclerosis. The four patients with Baló's concentric sclerosis had markedly elevated levels of CD14+CD25+ monocytes/macrophages. Our findings suggest that monocytes/macrophages are activated during an exacerbation of MS, and that they may play an important role in the process of demyelination.
Adult↗
Increased levels of soluble tumor necrosis factor receptor in patients with multiple sclerosis and HTLV-1-associated myelopathy.
Tumor necrosis factor-alpha (TNF-alpha) is a potent mediator produced by activated T lymphocytes and macrophages, which may play a role in the pathogenesis and development of multiple sclerosis (MS) and HTLV-1-associated myelopathy (HAM). The first step in the induction of many biological effects elicited by TNF-alpha is its binding to specific cell surface receptors. A soluble form of TNF receptor (sTNF-R) can be detected in the body fluid. We measured sTNF-R levels in the sera and cerebrospinal fluid (CSF) of patients with either MS or HAM, and evaluated the correlation between this mediator and disease activity. The levels of sTNF-R in the sera and CSF of patients with MS were significantly increased compared with controls, particularly patients with acute relapsing MS during an exacerbation (P < 0.001). CSF levels of sTNF-R showed a strong correlation with those of TNF (r = 0.716, P < 0.001). Higher levels of sTNF-R in the sera of HAM patients were detected as compared with those of either controls (P < 0.001) or non-HAM carriers (P < 0.001). Patients with HAM exhibited significantly higher CSF levels of sTNF-R than those with other neurological diseases (P < 0.0001). These results suggest that the detection of sTNF-R in the sera and CSF may predict disease progression. Availability of such a marker would be useful in monitoring disease activity.
Adult↗
In vitro intercellular adhesion molecule-1 expression on brain endothelial cells in multiple sclerosis.
To investigate the origin of intercellular adhesion molecule-1 (ICAM-1) and its expression on brain endothelial cells, we studied the expression in vitro of ICAM-1 on human brain endothelial cells after incubation of T cells from patients with multiple sclerosis (MS) using a histochemical technique and flow cytometry. We determined soluble forms of ICAM-1 (ICAM-1) in the supernatants after mixtures of brain endothelial cells and T cells from patients with MS using an enzyme-liked immunosorbent assay. Flow cytometric analysis showed that a number of ICAM-1-positive cells were significantly increased after incubation of brain endothelial cells with T cells from patients with acute relapsing MS during an exacerbation as compared with those of controls (P < 0.01). Patients with acute relapsing MS during an exacerbation and chronic progressive MS exhibited higher levels of ICAM-1 in the supernatants of mixtures with brain endothelial cells and lymphocytes than those of controls (P < 0.001 and P < 0.01, respectively). These results suggest that lymphocytes from patients with acute relapsing MS during an exacerbation lead to an increased expression of ICAM-1 on the brain endothelial cells and add to evidence involving this adhesion molecule in the pathogenesis of MS.
Adult↗
The long-term effects of polymethylmethacrylate contact lens wear on the corneal endothelium.
PURPOSE: The purpose of this study is to determine the long-term effects of polymethylmethacrylate (PMMA) contact lens wear on the corneal endothelium. The authors had noted previously advanced polymegethism and decreased cell densities in a few long-term PMMA contact lens wearers. They evaluated a large group of such lens wearers to determine the prevalence of polymegethism and reduced endothelial cell density within this lens-wearing population. METHODS: The authors examined the morphologic characteristics of the corneal endothelium in 162 PMMA contact lens wearers or age-matched controls. Eighty-one subjects had worn contact lenses for more than 20 years. RESULTS: Patients showed advanced polymegethism and pleomorphism compared with controls. Mean cell density in the contact lens-wearing group was not different from controls, but a significantly greater percentage of contact lens wearers (11%, 9 of 81 patients) had cell densities less than 2000 cells/mm2 compared with controls (2.5%, 2 of 81 patients), and were also significantly more likely to have severe polymegethism (coefficient of variation, > 0.60) and severe pleomorphism (frequency of hexagons < 40%). CONCLUSION: This study is unique, in that it notes a subgroup of PMMA contact lens wearers who are more susceptible to significant morphometric changes and reduced endothelial cell densities with long-term contact lens use.
Adult↗
Synthesis of 12(R)- and 12(S)-hydroxyeicosatetraenoic acid by porcine ocular tissues.
Microsomal fractions from porcine ocular tissues synthesized 12(S)-5,8,10,14-hydroxyeicosatetraenoic acid [12(S)-HETE] from arachidonic acid by a membrane-bound lipoxygenase and 12(R)-HETE by the cytochrome P450-dependent monooxygenase system. Both activities were the highest in corneal microsomes. The 12(R)-HETE synthesizing activity of corneal microsomes was dependent on NADPH and inhibited by 0.1 mM SKF-525A, an inhibitor of P450 enzymes. The activity to form 12(R)-enantiomer was significantly enhanced by treatment of corneal epithelium with 3-methylcholanthrene or clofibrate. The induced activity was suppressed by cycloheximide, indicating that the induction of enzyme activities involved a translational process. The effect of these inducers on 12(R)-HETE synthesizing activity appeared to be additive. The activity to form 12(S)-enantiomer was markedly stimulated by 3 mM CaCl2. The 12-lipoxygenase of corneal microsomes was capable of oxygenating linoleic acid in addition to arachidonic acid, a characteristic of 12-lipoxygenases of the leukocyte type. 12(R)-HETE at 10(-6) M inhibited almost completely the Na,K-ATPase of corneal epithelium but had little or no effect on ciliary epithelial enzymic activity. 12(S)-HETE at 10(-6) M also inhibited corneal enzymic activity but to a lesser extent, and had no significant effect on ciliary epithelial Na,K-ATPase activity.
12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
Retrotransposon-induced ectopic expression of cut causes the Om(1A) mutant in Drosophila ananassae.
Optic morphology (Om) mutations in Drosophila ananassae map to at least 22 loci scattered throughout the genome. They are semidominant, neomorphic, nonpleiotropic, and are associated with the insertion of a retrotransposon, tom. The Om(1A) gene, which is cytogenetically linked to the cut locus, was cloned using a DNA fragment of the cut locus of Drosophila melanogaster as a probe. Three of the eight alleles of Om(1A) examined have insertion of the tom element within a putative cut region. The gamma-ray-induced revertants of Om(1A) are accompanied with cut lethal mutations and rearrangements within the cut coding region. In the eye imaginal discs of the Om(1A) mutants, differentiation of photoreceptor clusters is suppressed, abnormal cell death occurs in the center and the cut protein is expressed ectopically. D. melanogaster flies transformed with a chimeric cut gene under the control of a heat-inducible promoter show excessive cell death in the region anterior to the morphogenetic furrow, suppressed differentiation to photoreceptor clusters and defect in the imaginal eye morphology when subjected to temperature elevation. These findings suggest that the tom element inserted within the Om(1A) region induces ectopic cut expression in the eye imaginal discs, thus resulting in the Om(1A) mutant phenotype.
Animals↗
Case-control study for lung cancer and cigarette smoking in Osaka, Japan: comparison with the results from Western Europe.
In order to clarify the relation between cigarette smoking and lung cancer, a case-control study was conducted. The case series consisted of 1,376 lung cancer patients (1,082 males and 294 females) who were newly diagnosed and admitted to eight hospitals in Osaka during 1986-88. Smoking histories were compared with those of 2,230 controls (1,141 males and 1,089 females) admitted to the same hospitals during the same period without established smoking-related diseases. Odds ratios of current smoker versus nonsmoker were 18.1, 1.9, 21.4, and 3.8 for squamous, adeno, small, and large cell carcinoma, respectively, for males, and 9.7, 1.3, 12.1, 3.7, respectively, for females. Compared to the results from previous studies in Japan, the magnitude of the odds ratios for squamous and small cell carcinoma is approaching the level of Western Europe in the late 1970s. Population attributable risk of exsmokers has also been increasing to the level of Western Europe. Among male current smokers, smoking intensity, such as number of cigarettes per day or fraction smoked per cigarette, seemed to have a slightly greater influence on squamous cell carcinoma than adenocarcinoma, while factors associated with the spread of cigarette smoke, such as inhalation, seemed to have greater influence on adenocarcinoma. The difference in the distribution of these smoking characteristics between Japan and Western Europe could not fully explain the difference in lung cancer incidence and distribution of histologic types between the two areas.
Adenocarcinoma↗
Possible involvement of protein kinase C activation in down-regulation of CD3 antigen on adult T cell leukaemia cells.
The role of protein kinase C (PKC) system on CD3 expression on adult T-cell leukaemia (ATL) was examined. The down-regulation of CD3 on ATL cells is reportedly induced by CD3 down-regulating factor (CD3DF) contained in serum and culture supernatants of leukaemia cells from acute type ATL patients. After we cultured normal PBMC with a PKC inhibitor, H-7, CD3DF activity for PBMC was reduced significantly. Culture with H-7 of HTLV-1 transformed T cells, ATL-2 cells whose CD3 expression had been decreased, led to enhancement of CD3 expression in a time-dependent manner. These findings suggest that CD3DF may play an important role as a PKC system activator, resulting in CD3 down-regulation.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
A novel mutation in the erythrocyte protein 4.2 gene of Japanese patients with hereditary spherocytosis (protein 4.2 Fukuoka).
Human erythrocyte protein 4.2 (band 4.2; pallidin) is a major membrane protein that comprises 5% of the total weight of the human erythrocyte membrane. Deficiencies of this protein have been observed in hereditary spherocytosis with anaemia, suggesting a role of protein 4.2 in erythrocyte stability and integrity. The molecular basis of this disorder remains unknown. As a first step in elucidating the pathogenesis of hereditary spherocytosis associated with protein 4.2 deficiency, we cloned and sequenced the erythrocyte protein 4.2 gene from a normal Japanese person. We prepared sets of oligonucleotide primers for polymerase chain reaction (PCR) and determined nucleotide sequences of exons and exon-intron boundaries of the protein 4.2 gene from three unrelated Japanese patients with hereditary spherocytosis due to a complete defect of protein 4.2, using PCR-related techniques. Two patients were homozygous for a missense mutation in codon 142 with the Ala (GCT)-->Thr (ACT) amino acid substitution that has been reported previously (protein 4.2NIPPON), whereas one patient was compound heterozygous for the same missense mutation in codon 142 and a guanine-adenine transition in codon 119 that changes the codon for Trp (TGG) to the termination codon (TGA) (protein 4.2Fukuoka). No additional mutation was identified in other exons of the protein 4.2 genes. Dot-blot hybridization with allele-specific oligonucleotide probes showed that homozygosity for the missense mutation in codon 142 and compound heterozygosity for the codon 142 and the codon 119 mutations were related to protein 4.2 deficiency in the families. Although two alleles of missense mutation of the codon 142 were also detected in 100 alleles of healthy Japanese, results obtained in this study indicate that the two mutations described above are closely related to the pathogenesis of hereditary spherocytosis due to protein 4.2 defect.
Adult↗
Prevalence of thyroid hormone autoantibodies in healthy subjects.
OBJECTIVE: The prevalence of thyroid hormone autoantibodies in patients with thyroid disorders has been well described, although the results have been variable. However, the prevalence of thyroid hormone autoantibodies in apparently healthy subjects remains unknown and its determination was the main objective of this study. SUBJECTS AND METHODS: Sera obtained from 880 healthy subjects (365 men and 515 women) were examined for thyroid hormone autoantibodies by immune precipitation using radiolabelled thyroid hormones or thyroid hormone analogues. RESULTS: Anti-triiodothyronine (T3) and anti-thyroxine (T4) antibodies were detected in none (0%) and in 3 (0.34%), respectively, of the 880 individuals studied using radiolabelled thyroid hormones. Similar tests in 385 healthy subjects using radiolabelled thyroid hormone analogues (polyaminocarboxy T3 and T4) showed the presence of anti-T3 and anti-T4 antibodies in 3 (0.78%) and in 4 (1.04%), respectively. None of the subjects had both anti-T3 and anti-T4 antibodies. Thus, the prevalence of anti-T3 or anti-T4 antibodies among healthy population was concluded to be as high as 1.8%. Radiolabelled thyroid hormone analogue binding to purified immunoglobulin G (IgG), with or without the addition of an excess of unlabelled thyroid hormones, confirmed specific binding of thyroid hormones to the thyroid hormone autoantibody-positive IgGs. The presence and class specificity of thyroid hormone autoantibodies was confirmed by the Ouchterlony immunodiffusion/autoradiography method, which showed biphenotypic heavy chain (IgG and IgA) and kappa (kappa) light chain specificities. Serum concentrations of free thyroid hormones and TSH in thyroid hormone autoantibody-positive sera were within the normal range. CONCLUSIONS: These results indicate that the occurrence of thyroid hormone autoantibodies among the healthy Japanese population is fairly common. However, interference of thyroid hormone autoantibodies in the radioimmunoassay of free thyroid hormones is exceptional.
Adult↗
CRK protein binds to two guanine nucleotide-releasing proteins for the Ras family and modulates nerve growth factor-induced activation of Ras in PC12 cells.
It has been reported that growth factors activate Ras through a complex of an adaptor type SH2-containing molecule, Grb2, and a Ras guanine nucleotide-releasing protein (GNRP), mSos. We report on the involvement of another adaptor molecule, CRK, in the activation of Ras. Overexpression of wild-type CRK proteins CRK-I and CRK-II enhanced the nerve growth factor (NGF)-induced activation of Ras in PC12 cells, although the basal level of GTP-bound active Ras was not altered. In contrast, mutants with a single amino acid substitution in either the SH2 or SH3 domain of the CRK-I protein inhibited the NGF-induced activation of Ras. Two GNRPs for the Ras family, mSos and C3G, were coimmunoprecipitated with the endogenous Crk proteins in PC12 cells. The association between C3G and the CRK mutants was dependent upon the presence of intact SH3. The SH2 domain of CRK bound to the SHC protein phosphorylated on tyrosine residues by NGF stimulation. The results demonstrate that, in addition to Grb2, CRK participates in signaling from the NGF receptor and that two GNRPs appear to transmit signals from these adaptor molecules to Ras.
Animals↗
Potentiating effect of inhaled acetaldehyde on bronchial responsiveness to methacholine in asthmatic subjects.
BACKGROUND: It has recently been reported that acetaldehyde induces bronchoconstriction indirectly via histamine release. However, no study has been performed to assess whether acetaldehyde worsens bronchial responsiveness in asthmatic subjects so this hypothesis was tested. METHODS: Methacholine provocation was performed on three occasions: (1) after pretreatment with oral placebo and inhaled saline (P-S day), (2) after placebo and inhaled acetaldehyde (P-A day), and (3) after a potent histamine H1 receptor antagonist terfenadine and acetaldehyde (T-A day) in a double blind, randomised, crossover fashion. Nine asthmatic subjects inhaled 0.8 mg/ml acetaldehyde or saline for four minutes. After each inhalation a methacholine provocation test was performed. RESULTS: Methacholine concentrations producing a 20% fall in FEV1 (PC20-MCh) on the P-A day (0.48 mg/ml, 95% CI 0.21 to 1.08) and T-A day (0.41 mg/ml, 95% CI 0.22 to 0.77) were lower than those on the P-S day (0.85 mg/ml, 95% CI 0.47 to 1.54). There was no change in the PC20-MCh between the P-A and T-A days. A correlation was observed between the logarithmic values of PC20-MCh (log PC20-MCh) on the P-S day and the potentiating effect of acetaldehyde on the methacholine responsiveness [(log PC20-MCh on P-A day)-(log PC20-MCh on P-S day)] (rho = 0.82). CONCLUSIONS: Acetaldehyde induces bronchial hyperresponsiveness in patients with asthma by mechanisms other than histamine release.
Acetaldehyde↗
Effects of Chinese herbal medicines on DNA-synthesizing enzyme activities in mammary tumors of mice.
Sho-saiko-to (SST) and Juzen-taiho-to (JTT), Japanese modified Chinese herbal prescriptions, suppressed the activities of thymidylate synthetase and thymidine kinase involved in de novo and salvage pathways for pyrimidine nucleotide synthesis, respectively, in mammary tumors of SHN mice with the reduction of serum prolactin level. These results indicate that SST and JTT may have the antitumor effects on mammary tumors.
Animals↗
Alteration of plasma endothelin-1 by exercise at intensities lower and higher than ventilatory threshold.
The purpose of this study was to investigate whether the release of endothelin-1 (ET-1), a potent vasoconstrictor peptide produced by vascular endothelial cells, is induced by exercise. Venous plasma concentrations of ET-1 were measured by sandwich-enzyme immunoassay before and after endurance exercise with a cycle ergometer at different intensities. Male intercollegiate athletes participated in the study and performed cycle ergometer exercise of 30 min duration at intensities of 90 or 130% of their individual ventilatory threshold (VT). The plasma concentration of ET-1 was slightly but significantly increased after exercise at 90% and markedly increased after exercise at 130% of individual VT. The increase in ET-1 was greatest 30 min after exercise at both intensities. It was first demonstrated that the plasma concentration of ET-1 was significantly increased after exercise: the greater the intensity, the greater the extent of the increase in plasma ET-1 concentration. However, the precise physiological roles of ET-1 during exercise remain to be elucidated.
Adolescent↗
Effect of pulmonary blood flow on microvascular pressure profile determined by micropuncture in perfused cat lungs.
To clarify the role of the pulmonary microvasculature in adjusting to increased pulmonary blood flow, we measured arteriolar and venular pressure by the servo-null micropuncture method while changing the pulmonary blood flow in isolated perfused cat lungs. We divided the lung vasculature into three longitudinal segments: 1) arterial (pulmonary artery to 30- to 50-microns arteriole), 2) microvascular (between 30- to 50-microns arteriole and venule), and 3) venous (30- to 50-microns venule to left atrium). The vascular resistance was calculated by dividing the pressure gradient by the flow. The pressure gradient of the microvascular segment did not increase, whereas the pressure gradient of the arterial and venous segments increased simultaneously with flow rate. Total and microvascular resistance decreased with increase of flow rate. Resistances of the arterial and venous segments did not change with increase in flow. We conclude that the microvasculature plays a crucial role in preventing pulmonary hypertension with increases in flow by decreasing microvascular resistance.
Animals↗