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Biomedical subjects

M Minami

Publications and source records attributed to M Minami.

At least 37 records · Page 2Linked to original sources
PubMed1998

Elevated frequency of sister chromatid exchanges in lymphocytes of victims of the Tokyo sarin disaster and in experiments exposing lymphocytes to by-products of sarin synthesis.

More than 5000 passengers of Tokyo subway trains were injured with toxic chemicals including the nerve gas sarin. Most of the victims examined had marked miosis and decreased serum cholinesterase activity. To monitor the genetic aftereffects of sarin exposure, we measured sister chromatid exchanges (SCEs) of the victims using peripheral blood lymphocytes. The frequency of SCEs was significantly higher in the victims than in the control group. Analyzing results using samples of urine from the victims suggested that the victims were exposed to not only sarin per se, but by-products of sarin synthesis, i.e. diisopropyl methylphosphonate (DIMP), diethyl methylphosphonate (DEMP) and ethyl isopropyl methylphosphonate (EIMP). Thus, the in vitro SCE-inducing effect of DIMP, DEMP and EIMP was examined using human lymphocytes and we obtained positive results.

Adult↗
PubMed1998

IL-12 promotes the adhesion of NK cells to endothelial selectins under flow conditions.

This study examined the adhesive interactions of peripheral blood NK cells with P- and E-selectin and analyzed the effect of IL-12 on the binding of NK cells to these selectins. P-selectin glycoprotein ligand-1 (PSGL-1) is expressed on most resting and IL-12-activated NK cells. However, the percentage of resting NK cells bound to P-selectin-IgG was 15%, and that of activated NK cells bound to P-selectin-IgG was 65%. Furthermore, the number of IL-12-activated NK cells bound to P-selectin-transfected Chinese hamster ovary cells was significantly higher than that of resting NK cells under flow conditions. These interactions were abolished by the incubation of these NK cells with anti-PSGL-1 (PL-1) mAb. Thus, PSGL-1/P-selectin interaction is important in the binding of resting and activated NK cells to P-selectin. NK cells express sialyl-Lewis(x) (sLe(x)) structure recognized by anti-sLe(x) mAb (KM-93), and IL-12 activation of NK cells increased the mean fluorescence intensity of KM-93-reactive NK cells. Adhesion of IL-12-activated NK cells to E-selectin-transfected Chinese hamster ovary cells was stronger than that of resting NK cells under flow conditions. These interactions were reduced markedly by incubation with anti-sLe(x) mAb. Thus, sLe(x) is the major ligand of resting and activated NK cells for E-selectin. These findings indicate that IL-12 stimulation of NK cells promotes their adhesion activity to endothelial selectins.

Animals↗
PubMed1998

Induction by lysophosphatidylcholine, a major phospholipid component of atherogenic lipoproteins, of human coronary artery smooth muscle cell migration.

BACKGROUND: The objectives of the present study were (1) to determine whether lysophosphatidylcholine (lyso-PC), a prominent component of oxidatively modified LDL, induces migration of human coronary artery smooth muscle cells (SMCs) and, if so, to clarify the mechanism, and (2) to investigate the possible interactions of lyso-PC and platelet-derived growth factor (PDGF)-BB, endothelin- (ET-1), adrenomedullin (AM), or vitamin E on SMC migration by the Boyden's chamber method. METHODS AND RESULTS: Lyso-PC induced SMC migration in a concentration-dependent manner between 10(-6) and 5 x 10(-5) mol/L. By contrast, phosphatidylcholine was without significant activity, and lysophosphatidylinositol and lysophosphatidylserine were much less effective than lyso-PC. Lyso-PC increased basic fibroblast growth factor (bFGF) production in a concentration-dependent manner between 10(-6) and 5 x 10(-5) mol/L in these cells. Furthermore, lyso-PC-induced SMC migration was inhibited by neutralizing antibody to bFGF but not by neutralizing antibody to transforming growth factor-beta1. Lyso-PC-induced migration was significantly enhanced by PDGF-BB or ET-1 but was clearly inhibited by human AM and vitamin E. CONCLUSIONS: These results indicate that (1) lyso-PC induces human coronary artery SMC migration at least in part through release of endogenous bFGF and (2) this lyso-PC-induced migration can be further induced by PDGF-BB and ET-1 and can be inhibited by human AM and vitamin E. Lyso-PC may recruit medial SMCs during the process of coronary atherosclerosis in part by releasing bFGF in concert with PDGF-BB or ET-1 in vascular tissues. This lyso-PC-induced SMC migration may be suppressed by AM and vitamin E under certain pathological conditions.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

IFN-gamma induces coordinate expression of MHC class I-mediated antigen presentation machinery molecules in adult mouse Schwann cells.

The expression of major histocompatibility complex (MHC) class I molecules on adult mouse Schwann cells (SCs) was examined using immunofluorescence analysis. MHC class I molecules were not expressed on the surface of untreated SCs. Interferon (IFN)-gamma treatment induced expression of the molecules on the SCs. Expression of genes coding for the molecules involved in MHC class I-mediated antigen presentation was also analysed in SCs by reverse transcription-polymerase chain reaction (RT-PCR). Expression of MHC class I heavy chain genes was faintly detected in untreated SCs. IFN-gamma treatment augmented the expression. In addition, IFN-gamma induced expression of the genes for beta2-microglobulin, the peptide transporter TAP-1 and the proteasomal subunit LMP-2, whose expression was not detected in untreated SCs. The expressions of MHC class II molecules and their genes were not detected even after IFN-gamma treatment. These data suggest that MHC class I-mediated antigen presentation machinery functions in adult mouse SCs and that the SCs themselves work as antigen presenting cells and as targets for cytotoxic T cells in some physiological conditions.

Animals↗
PubMed1998

Expression of stromal cell-derived factor-1 and CXCR4 chemokine receptor mRNAs in cultured rat glial and neuronal cells.

The expression of the mRNAs for stromal cell-derived factor-1alpha and -1beta (SDF-1alpha and -1beta) and their receptor CXCR4 in cultured rat glial and neuronal cells was examined. SDF-1alpha mRNA was expressed intensely in astrocytes and weakly in neurons, but not in microglia. SDF-1beta mRNA was expressed weakly in these three types of cells. The expressions of SDF-1alpha and -1beta mRNAs in astrocytes were decreased by treatment with LPS (100 ng/ml) for 1-6 h but markedly increased by that for 24-72 h, whereas the expression of SDF-1beta mRNA in microglia was hardly changed by the treatment for 0.5-6 h, and was decreased by that for 24-48 h. The expression of CXCR4 mRNA was observed in astrocytes, microglia and neurons, and was not altered by LPS treatment.

Animals↗
PubMed1998

Localization of fractalkine and CX3CR1 mRNAs in rat brain: does fractalkine play a role in signaling from neuron to microglia?

Localization of the mRNAs for fractalkine, a CX3C chemokine, and for its receptor CX3CR1 was investigated in the rat brain. In situ hybridization study revealed that fractalkine mRNA was dominantly expressed in neuronal cells particularly in the olfactory bulb, cerebral cortex, hippocampus, caudate putamen and nucleus accumbens. In vitro study using enriched neuronal or glial culture supported the dominant expression of fractalkine mRNA in neurons. On the other hand, CX3CR1 mRNA was dominantly expressed in glial cells throughout the whole brain. The in vitro study suggested the cells expressing CX3CR1 mRNA are microglia, not astrocytes or neurons. Fractalkine appears to function as a signal molecule from neuron to microglia.

Amino Acid Sequence↗
PubMed1998

DAMGO recognizes four residues in the third extracellular loop to discriminate between mu- and kappa-opioid receptors.

Previously, we reported that replacement of the region from the fifth transmembrane domain to the C-terminus of kappa-opioid receptor with the corresponding region of mu-opioid receptor gives high affinity for [D-Ala2, N-MePhe4, Gly-ol5]enkephalin (DAMGO), a mu-opioid receptor-selective ligand, to the resultant chimeric receptor, suggesting that the difference in the amino acid sequence within this region is critical for the discrimination between mu- and kappa-opioid receptors by DAMGO. In the present study, we constructed further six mu/kappa-chimeric receptors and revealed that at least two separate regions around the third extracellular loop are critical for the discrimination between mu- and kappa-opioid receptors by DAMGO. Furthermore, we constructed several mutant receptors by a site-directed mutagenesis technique and found that the difference between Glu297 of kappa-opioid receptor and Lys303 of mu-opioid receptor in one region, and the difference between Ser310, Tyr312 and Tyr313 of kappa-opioid receptor and Val316, Trp318 and His319 of mu-opioid receptor in the other region, are critical for the discrimination between these receptors by DAMGO. The mutant receptor, kappa (E297K + Y313H + Y312W + S310V), in which the Glu297, Ser310, Tyr312 and Tyr313 of kappa-opioid receptor were changed to Lys, Val, Trp and His, respectively, bound to DAMGO with high affinity (Kd = 8.7 +/- 1.2 nM) and efficiently mediated the inhibitory effect of DAMGO on intracellular cAMP accumulation. The present results showed that these four amino acid residues act as determinants for the discrimination between mu- and kappa-opioid receptors by DAMGO.

Adenylyl Cyclases↗
PubMed1998

Acute and subchronic immunotoxicity of p-chloronitrobenzene in mice. I. Effect on natural killer, cytotoxic T-lymphocyte activities and mitogen-stimulated lymphocyte proliferation.

We evaluated the immunotoxicity of p-chloronitrobenzene (p-CNB) after intraperitoneal (i.p.) injection of p-CNB in BDF1 mice; single i.p. injection of 300 mg/kg (acute experiments), or 30 mg/kg three times a week for 4 weeks (subchronic experiments). The following items were investigated: number of splenocytes, natural killer (NK) activity, cytotoxic T-lymphocyte (CTL) activity and LPS-stimulated lymphocyte proliferation using splenocytes, hemoglobin (Hb) concentration in peripheral blood and body weight. NK activity in exposed mice significantly decreased compared to control in both acute and subchronic experiments. CTL activity in acute exposed mice showed a significant decrease on the 3rd day only after injection, and significant decrease at 3 and 4 weeks in subchronic exposed mice compared to controls. Comparing the effect of p-CNB on NK activity with that of CTL for both the acute and subchronic exposures, NK activity was more inhibited by p-CNB than CTL activity in the acute stage, whereas both the NK and CTL activities were inhibited by p-CNB in the subchronic stage. There was an indication that p-CNB also inhibited LPS- stimulated B-lymphocyte proliferation. On the other hand, Hb concentration did not show significant difference between the exposed and control mice in both acute and subchronic experiments. Body weight in subchronically exposed mice was significantly lower than the control from day 19. The above evidence indicated that p-CNB has an inherent immunotoxic effect on mice.

Animals↗
PubMed1998

Complete genomic structure DNA polymorphisms, and alternative splicing of the human AF-6 gene.

In our previous work, detailed deletion mapping of ovarian cancers indicated that a 300-kb region of chromosome 6q27 was likely to contain one or more putative tumor suppressor genes associated with development of this type of cancer. DNA sequencing in the region disclosed the presence of AF-6, a gene that had been identified as the ALL-1 fusion partner involved in acute myeloid leukemias with t(6;11)(q27;q23) translocations. In the work reported here, we determined the complete genomic sequence of the AF-6 gene, including exon-intron boundaries, and found six DNA polymorphisms. One of them, an insertion/deletion polymorphism, determined the presence or absence of seven amino acids in the AF-6 product. We also identified two alternatively spliced forms of the gene; the two novel transcripts would encode additional C-terminal peptides in comparison to the reported protein. Sequencing of seven cosmid clones that covered the entire gene revealed 32 exons (not including one exon involved in the insertion/deletion polymorphism), spanning approximately 140 kb of genomic DNA. These results may contribute to an understanding of the mechanism causing chromosomal translocations in leukemic cells.

Alternative Splicing↗
PubMed1998

Separate determination of human urinary conjugated and unconjugated 3-methoxy-4-hydroxyphenylethyleneglycol.

A new determination procedure for human urinary 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) was established. In addition to the previously established solid-phase extraction method for unconjugated MHPG, another solid-phase extraction method for conjugated MHPG was developed. Unconjugated MHPG was adsorbed on a Sep-Pak Diol cartridge and selectively recovered by elution with ethyl acetate. The eluate was evaporated and the residue was redissolved and analyzed by reversed-phase high-performance liquid chromatography with fluorimetric detection. Conjugated (sulfate plus glucuronide) MHPG was adsorbed on a Sep-Pak Accell QMA cartridge and quantitatively eluted with 0.2 M NaCl. After enzymatic hydrolysis, deconjugated MHPG was extracted using a Sep-Pak Diol cartridge and analyzed in the same manner as unconjugated MHPG. The new method is simple and rapid and can quantitate conjugated and unconjugated MHPG discriminatively.

Adult↗
PubMed1998

[Prognosis and management in patients with left main shock syndrome--emergency PTCA following CABG].

To clarify the optimal management and delineate the characteristics of patients with severe left main disease and cardiogenic shock as a result of an acute anterolateral myocardial infarction (left main shock syndrome), we analyzed the course of 13 such patients from September 1989 to June 1997. Of the 13 patients, 7 (53.8%) were managed with emergency coronary angioplasty (group A), 3 (23.1%) were treated with emergency coronary angioplsty following coronary bypass graft surgery (group B) and 3 (23.1%) underwent emergency coronary bypass graft surgery alone (group C). The interval from the beginning of myocardial ischemia to revascularization was 266 +/- 303 min. The degree of diameter stenosis found in the left main coronary artery was 98.1 +/- 1.8%. Overall in-hospital mortality for the 13 patient with left main shock syndrome was 76.9% (group A: 7/7; group B: 1/3; group C: 2/3, NS) and operative mortality was 61.5% (group A: 6/7; group B: 0/3; group C: 2/3, p = 0.03). When all 13 patients were examined together, the presence of ventricular tachycardia (VT) x ventricular fibrillation (Vf) was found to be the most powerful univariate predictor of operative death (p = 0.03). This is, 7 (87.5%) of the 8 patients with VT x Vf at presentation died within 30 postoperative days, and only 1 (20%) of the 5 patients without VT x Vf died (p = 0.03). Age, percent stenosis of the left main or right coronary arteries, the interval from the beginning of myocardial ischemia to revascularization, intubation, systolic pressure, fractional shortning, pulmonary artery pressure, pulmonary capillary wedge pressure, coronary risk factors, pulmonary edema, mitral regurgitation and percutaneous cardiopulmonary support failed to attain univariate significance at the P = .1 level. The postoperative peak CPK level was 15665 +/- 6710 IU/1 in operative death compared to 4733 +/- 2749 IU/1 in operative survival (p = 0.01). In conclusion, emergency coronary angioplasty following coronary bypass graft surgery for left main shock syndrome has been a very successful therapeutic option. Finally, for the entire group of 13 patients with left main shock syndrome, VT x Vf significantly decreased short-term survival.

Adult↗
PubMed1998

Clinical study on lung cancer as a second primary cancer.

This study evaluates the effect of a previous cancer on the clinical characteristics and the outcome of lung cancer patients. The 313 primary lung cancer patients operated on in the Osaka University Hospital during the period 1984-1993 were reviewed. Of those, 37 had a history of previous cancer. In the lung cancer patients with a history of previous cancer, 20 had adenocarcinomas, 14 had squamous cell carcinomas, while 3 had other cancers. The previous malignancies included 13 gastric cancers, 10 head and neck cancers, 6 colorectal cancers, and 8 others. The pathological stage was 17 stage I, 1 stage II, 15 stage IIIA, 1 stage IIIB, and 3 stage IV. The 5-year survival rate was 37.9%. In patients without a history of previous cancer, there were 139 adenocarcinomas, 100 squamous cell carcinomas, and 37 others. The pathological stage was 126 stage I, 33 stage II, 74 stage IIIA, 23 stage IIIB, and 20 stage IV. The 5-year survival rate was 43.3%. There were no significant differences in the cell type, stage, or survival between the lung cancers found as the first and second cancers. Lung cancer patients with a history of previous cancer are expected to respond to a resection as well as those with lung cancer appearing as their first cancer.

Adenocarcinoma↗
PubMed1998

Hodgkin's disease of the chest wall: report of a case.

Hodgkin's disease primarily originating from the chest wall is very rare. A 48-year-old man was admitted to our hospital because of an abnormal shadow on a chest X-ray. Radiographic examinations suggested a neurogenic tumor located in the right second-intercostal space, and it was thus extirpated thoracoscopically. The tumor was thought to have arisen from the subpleural space, probably from a lymph node of the chest wall. The resected specimen measured 5.5 x 2.0 cm in size, and the pathological diagnosis was Hodgkin's disease of the diffuse lymphocyte predominant type. A clinical examination showed no other lesions in any other part of the body, including the bone marrow. Following surgery, adjuvant chemotherapy (COPP-ABVD) was given because of the possible scattering of malignant cells during surgery. To the best of our knowledge, this is the first report of Hodgkin's disease originating in the chest wall.

Chemotherapy, Adjuvant↗
PubMed1998

Microvascular permeability of the non-heart-beating rabbit lung after warm ischemia and reperfusion: role of neutrophil elastase.

BACKGROUND: The duration of warm ischemia and reperfusion injury is a major limiting factor in the setting of lung transplantation with non-heart-beating donors (NHBD). We hypothesized that reperfusion with neutrophil elastase inhibitor or leukocyte-depleted blood has an inhibitory effect on the ischemia-reperfusion injury of NHBD rabbit lungs. METHODS: To assess the lung injury, we used a perfused rabbit lung model and measured the hemodynamic parameters and filtration coefficient. The rabbit lungs after hypoxic cardiac arrest for 30, 50, and 60 minutes were harvested at room temperature, and ventilated lungs were reperfused for 1 hour at a constant flow (120 mL/min). The group with 60 minutes of warm ischemia and hypoxia was further divided into three groups to determine the effects of leukocyte-depleted reperfusion or neutrophil elastase inhibitor, (1) no other special treatment, (2) reperfusion with leukocyte-depleted blood, and (3) administration of 10 mg of specific neutrophil elastase inhibitor. The lungs reperfused immediately after harvest from the heart-beating donor were regarded as the control. RESULTS: Sixty minutes of warm ischemia and hypoxia resulted in an increase in filtration coefficient (0.68+/-0.20 g x min(-1) x cm H2O(-1) per 100 g) compared with the control values of 0.13+/-0.03 g x min(-1) x cm H2O(-1) per 100 g. The increase in filtration coefficient after 60 minutes of warm ischemia and hypoxia in NHBD was remarkably suppressed by leukocyte depletion (0.23+/-0.07) and by neutrophil elastase inhibitor (0.21+/-0.08). The shunt fraction and histology results were also near normal. CONCLUSIONS: These results suggested that leukocyte depletion or treatment with neutrophil elastase inhibitor during reperfusion reduces alveolar-capillary damage caused by lung ischemia-reperfusion injury in the NHBD lung transplantation setting. This effect might be mediated by inhibition of neutrophil elastase activity or sequestration, and thus may lead to the increased availability of NHBD lungs.

Animals↗
PubMed1998

Effect of docosahexaenoic acid on smooth muscle cell functions.

There is increasing evidence that fish oil-enriched diets attenuate the progression of several types of human and experimental renal, intestinal and cardiovascular disorders, including hypertension. Docosahexaenoic acid (DHA), may be one of the active biological component. We previously reported that dietary DHA suppressed the progression of hypertension in stroke-prone spontaneously hypertensive rats (SHRSP). The purpose of this study is to clarify the in vitro effect of DHA on cultured smooth muscle cell functions such as cell growth, hypertrophy, NO release, and intracellular Ca2+ metabolism, which are involved in the regulatory mechanisms of vascular tone. Addition of DHA to the culture medium of aortic smooth muscle cells isolated from SHRSP and normotensive Wistar Kyoto rats (WKY) had no significant effects on cell growth or on cell hypertrophy induced by angiotensin II as measured by flow cytometry. DHA had no stimulatory effect on interleukin-1beta (10 ng/ml)-induced nitric oxide release from smooth muscle cells of SHRSP, but rather slightly inhibited it. However, the treatment of smooth muscle cells with DHA (30 microM) for 2 days significantly suppressed the increase in intracellular Ca2+ concentration induced by angiotensin II, but not by thapsigargin. This was due to the suppression of Ca2+ influx, as determined by Mn2+ influx experiment. These results indicate that DHA specifically suppresses Ca2+ mobilization into smooth muscle cells. This may be one of the mechanisms by which dietary DHA prevents the development of hypertension in SHRSP.

Animals↗