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Biomedical subjects

H Matsui

Publications and source records attributed to H Matsui.

At least 37 records · Page 2Linked to original sources

[Congenital supravalvular aortic stenosis; report of a case].

We experienced a successful surgical case of extended aortoplasty by means of Doty's method (two sinus reconstruction) for congenital supravalvular aortic stenosis (SAS). Case was 12-year-old boy, who had no complaint except heart murmur. The retrograde aortography demonstrated localized stenosis just above the aortic valve, and it was an hour-glass type. The preoperative peak systolic pressure gradient between the left ventricle and ascending aorta was 56 mmHg, which was improved postoperatively. This case showed excellent results. Doty's aortoplasty was favorable method for SAS without deformity of aortic valve and coronary obstruction.

Aorta↗

Observation of band renormalization effects in hole-doped high-Tc Superconductors.

We report a systematic high-resolution angle-resolved photoemission spectroscopy on high-T(c) superconductors Bi(2)Sr(2)Ca(n-1)Cu(n)O(2n+4) (n=1-3) to study the origin of many-body interactions responsible for superconductivity. For n=2 and 3, a sudden change in the energy dispersion, so called "kink", becomes pronounced on approaching (pi,0) in the superconducting state, while a kink appears only around the nodal direction in the normal state. For n=1, the kink shows no significant temperature dependence even across T(c). This could suggest that the coupling of electrons with Q=(pi,pi) magnetic mode is dominant in the superconducting state for multilayered cuprates, while the interactions at the normal state and that of single-layered cuprates have a different origin.

Journal Article↗

Role of genetic polymorphisms of the RNASEL gene on familial prostate cancer risk in a Japanese population.

The RNASEL gene on chromosome 1q25 has been identified as a prostate cancer susceptibility gene. We screened for RNASEL germline mutations in familial prostate cancer patients, and performed a case-control study to examine the association of specific variants with prostate cancer risk in the Japanese. Three variants within the RNASEL gene, G282A, G1385A and T1623G were identified. G1385 and T1623G variants result in previously reported Arg462Gln and Asp541Glu variants, respectively. The novel G282A variant does not cause amino-acid substitution. A case-control study consisting of 101 familial prostate cancer cases and 105 noncancer controls showed that the Gln/Gln genotype of codon462 was observed in 7.6% of controls. However, the Gln/Gln genotype was not observed in cases, and reduced prostate cancer risk (odds ratio (OR)=0.061, P=0.014). The Asp/Asp genotype of codon541 increased the familial prostate cancer risk (OR=7.37, P=0.0004). In subset analysis, a significant association was observed in patients with more than two affected members (OR=3.15, P=0.028), and weak associations were found in patients with metastatic disease (OR=2.40, P=0.11) and high-grade disease (Gleason score >or=7) (OR=3.07, P=0.14). These findings suggested that the polymorphic changes within the RNASEL gene may be associated with familial prostate cancer risk in a Japanese population.

Adult↗

BCS-like Bogoliubov quasiparticles in high-T(c) superconductors observed by angle-resolved photoemission spectroscopy.

We performed high-resolution angle-resolved photoemission spectroscopy on triple-layered high-T(c) cuprate Bi(2)Sr(2)Ca(2)Cu(3)O(10+delta). We have observed the full energy dispersion (electron and hole branches) of Bogoliubov quasiparticles and determined the coherence factors above and below E(F) as a function of momentum from the spectral intensity as well as from the energy dispersion based on BCS theory. The good quantitative agreement between the experiment and the theoretical prediction suggests the basic validity of BCS formalism in describing the superconducting state of cuprates.

Journal Article↗

The origin of multiple superconducting gaps in MgB2.

Magnesium diboride, MgB2, has the highest transition temperature (T(c) = 39 K) of the known metallic superconductors. Whether the anomalously high T(c) can be described within the conventional BCS (Bardeen-Cooper-Schrieffer) framework has been debated. The key to understanding superconductivity lies with the 'superconducting energy gap' associated with the formation of the superconducting pairs. Recently, the existence of two kinds of superconducting gaps in MgB2 has been suggested by several experiments; this is in contrast to both conventional and high-T(c) superconductors. A clear demonstration of two gaps has not yet been made because the previous experiments lacked the ability to resolve the momentum of the superconducting electrons. Here we report direct experimental evidence for the two-band superconductivity in MgB2, by separately observing the superconducting gaps of the sigma and pi bands (as well as a surface band). The gaps have distinctly different sizes, which unambiguously establishes MgB2 as a two-gap superconductor.

Journal Article↗

Gene cloning, expression, and crystallization of a thermostable exo-inulinase from Geobacillus stearothermophilus KP1289.

The gene ( inuA) encoding exo-inulinase (EC 3.2.1.80) was cloned from the thermophilic Geobacillus stearothermophilus ( Bacillus stearothermophilus) KP 1289 growing at between 41 degrees C and 69 degrees C. The inuA gene consisted of 1,482 bp encoding a protein of 493 amino acids. The deduced polypeptide of molecular mass ( M) 56,744 Da showed strong sequence similarity to Pseudomonas mucidolens exo-inulinase, Bacillus subtilis levanase, Paenibacillus polymyxa ( Bacillus polymyxa) fructosyltransferase, and so on, indicating that the enzyme belonged to glycosyl hydrolase family 32. The M of the purified exo-inulinase, expressed in Escherichia coli HB101, was estimated as approximately 54,000 Da by both SDS-PAGE and gel filtration. These results suggested that the active form of the enzyme is a monomer. The enzyme was active between 30 and 75 degrees C with an optimum at 60 degrees C. The properties were identical to those of the native enzyme. Additionally, for the first time for a prokaryotic GH32 protein, crystals of the recombinant enzyme were obtained.

Amino Acid Sequence↗

Interaction of leptin with gastric myofibroblast transdifferentiation in Helicobacter pylori-infected Mongolian gerbils: the effect of rebamipide.

BACKGROUND: Our recent histochemical studies have revealed the marked increase of myofibroblasts in the Helicobacter pylori-infected Mongolian gerbil fundic mucosa, while the mediators, which facilitate the conversion of fibroblasts to the myofibroblasts have remained unknown. AIM: The present study was undertaken to clarify the alteration of leptin in the control and H. pylori-infected Mongolian gerbil stomach. The effector sites of rebamipide were also investigated in relation to leptin. METHODS: The localization of leptin was investigated by the indirect immunofluorescence. Plasma leptin levels were determined by ELISA method. The localization of 3H-rebamipide binding sites was investigated by autoradiography. RESULTS: Serum leptin content in H. pylori-infected Mongolian gerbils was significantly increased. The presence of leptin immunoreactivity was recognized in the endothelial cells of the microcirculatory network and very weakly in the glandular cells in the control group, while in the H. pylori-infected group leptin was markedly recognized in the mesenchymal cells. Rebamipide bound to the fibroblasts and surface mucous cells and decreased the leptin immunoreactivity in the gastric mucosa. CONCLUSIONS: Leptin was mostly found in the mesenchymal cells. Rebamipide administration brought about the decrease of leptin in the gastric mucosaof the H. pylori-infected gerbils.

Alanine↗

Rebamipide binds to iNOS-positive cells in acetic acid-treated but not in ethanol-treated rat gastric mucosa.

BACKGROUND: Rebamipide is a gastroprotective agent to stimulate prostaglandin generation in gastric mucosa and attenuate the activity of neutrophils, but direct evidence for the effector sites of this agent has remained to be clarified. AIM: The present study was undertaken to show the effector sites of rebamipide in control and ulcer-provoked rats. METHODS: The rats were divided into control, acetic acid- and ethanol-treated rats. In the acetic acid-treated group, 100% acetic acid was attached to the serosal surface of the stomach for 30 s, 7 days before the experiments. In the ethanol-treated group, a dose of 0.5 mL/100 g body weight of 50% ethanol was administered through orogastric intubation 2 h before the experiments. Using the unfixed cryostat sections, aqueous solution of 3H-rebamipide was applied and the localization of the binding sites of rebamipide was investigated by autoradiography. RESULTS: In the control rats, rebamipide was found to bind to the surface epithelial cells. In the ethanol-treated group, few binding sites were observed in the damaged gastric mucosa. In the acetic acid-treated group, the marked accumulation of the binding sites of 3H-rebamipide was observed in the mesenchymal cells in the lamina propria mucosae between the regenerated gastric epithelial cells. Combination of autoradiography and immunohistochemistry has revealed that iNOS-immunoreactive cells had the strong binding of rebamipide in the acetic acid-treated group. Some of these cells were CD68-positive macrophages, while others were CD68-negative, corresponding to polymorphonuclear leucocytes. In the ethanol-treated acute gastric mucosal injury group, few binding sites were observed in the damaged gastric mucosa. CONCLUSIONS: Autoradiography has made it clear that rebamipide binds to iNOS-positive cells in the gastric mucosa 7 days after acetic acid-treatment.

Acetic Acid↗

Low energy excitation and scaling in Bi(2)Sr(2)Ca(n-1)Cu(n)O(2n+4) (n=1-3): angle-resolved photoemission spectroscopy.

Angle-resolved photoemission spectroscopy (ARPES) has been performed on the single- to triple-layered Bi-family high-T (c) superconductors (Bi(2)Sr(2)Ca(n-1)Cu(n)O(2n+4), n=1-3). We found a sharp coherent peak as well as a pseudogap at the Fermi level in the triple-layered compound. Comparison among three compounds has revealed a universal rule that the characteristic energies of superconducting and pseudogap behaviors are scaled with the maximum T (c).

Journal Article↗

Iron lactate induction of pancreatic and endometrial proliferative lesions and a lack of increased tumors in a 104-week carcinogenicity study in F344 rats.

Iron lactate has been used as a food additive for iron supplementation. The present study was conducted to determine whether it might have carcinogenic potential. A total of 150 male and 150 female Fischer 344 rats were divided into three groups and fed basal diet containing 0, 1 or 2% of iron lactate for 104 weeks. No iron lactate-induced tumors were observed in any groups, although the incidences of pancreatic acinar cell and endometrial gland hyperplasias were increased in males and females, respectively, in the 2% group. Thus our in vivo animal data indicate that iron lactate lacks carcinogenicity in male and female F344 rats. However, estrogenic effects might be concluded based on the data for endometrial lesions. In a second experiment, an estrogen responsive rat pituitary tumor cell line, MtT/Se, and a human breast cancer cell line, MCF-7, were therefore employed to examine the estrogenic potential of iron lactate with regard to receptor binding affinity and ERE-reporter gene activation. Results in both cases were negative. Further investigations are needed to elucidate the mechanisms of induction of pancreatic and endometrial proliferative lesions by iron lactate.

Animals↗

Arsenic trioxide therapy for relapsed or refractory Japanese patients with acute promyelocytic leukemia: need for careful electrocardiogram monitoring.

Recent studies have shown that arsenic trioxide (As(2)O(3)) can induce complete remission in patients with acute promyelocytic leukemia (APL). We tested the efficacy and safety of As(2)O(3) for the treatment of patients with APL who had relapsed from or become refractory to all-trans retinoic acid (ATRA) and conventional chemotherapy in a prospective study. As(2)O(3) at a dose of 0.15 mg/kg was administered until the date of bone marrow remission to a maximum of 60 days. In patients who achieved complete remission (CR), one additional course of As(2)O(3) was administered using the same dose for 25 days. Of 14 patients, 11 (78%) achieved CR. Six of 10 patients who achieved CR showed disappearance of PML-RARalpha transcript by RT-PCR assay. The duration of As(2)O(3)-induced CR ranged from 4 to 22 months (median, 8 months) at a median follow-up of 17 months. Adverse events included 13 electrocardiogram abnormalities (13 QTc prolongation, eight ventricular premature contraction, four nonsustained ventricular tachycardia and two paroxysmal supraventricular tachycardia), seven nausea and vomiting, four pruritus, three peripheral neuropathy, three fluid retention and one APL differentiation syndrome. Four patients received antiarrhythmic agents. Hyperleukocytosis developed in five patients and in three cytotoxic drugs were necessary. Other adverse events were relatively mild. As(2)O(3) treatment is effective and relatively safe in relapsed or refectory patients with APL. Cardiac toxicities in patients with QTc prolongation should be carefully monitored.

Adult↗

Reduced effect of gemtuzumab ozogamicin (CMA-676) on P-glycoprotein and/or CD34-positive leukemia cells and its restoration by multidrug resistance modifiers.

Gemtuzumab ozogamicin (CMA-676), a calicheamicin-conjugated humanized anti-CD33 mouse monoclonal antibody, has recently been introduced clinically as a promising drug for the treatment of patients with acute myeloid leukemia (AML), more than 90% of which express CD33 antigen. However, our recent study suggested that CMA-676 was excreted by a multi- drug-resistance (MDR) mechanism in P-glycoprotein (P-gp)-expressing leukemia cell lines. We analyzed the in vitro effects of CMA-676 on leukemia cells from 27 AML patients in relation to the amount of P-gp, MDR-associated protein 1 (MRP1), CD33 and CD34, using a multi-laser-equipped flow cytometer. The cytocidal effect of CMA-676, estimated by the amount of hypodiploid portion on cell cycle, was inversely related to the amount of P-gp estimated by MRK16 monoclonal antibody (P = 0.004), and to the P-gp function assessed by intracellular rhodamine-123 accumulation in the presence of PSC833 or MS209 as a MDR modifier (P = 0.0004 and P = 0.002, respectively). In addition, these MDR modifiers reversed CMA-676 resistance in P-gp-expressing CD33(+) leukemia cells (P = 0.001 with PSC833 and P = 0.0007 with MS209). In CD33(+) AML cells from 13 patients, CMA-676 was less effective on CD33(+)CD34(+) than CD33(+)CD34(-) cells (P = 0.002). PSC833 partially restored the effect of CMA-676 in CD33(+)CD34(+) cells. These results suggest that the combined use of CMA-676 and a MDR modifier will be more effective on CD33(+) AML with P-gp-related MDR.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Persistent increase in myofibroblasts in Helicobacter heilmannii-infected mice but not in Helicobacter pylori-infected Mongolian gerbils: colocalization of COX-2 and bFGF immunoreactivity.

BACKGROUND: The clinical significance of Helicobacter heilmannii infection remains uncertain, owing to the lack of a specific detection method. Recently, we reported a marked increase in myofibroblasts in the early stage of Helicobacter pylori infection in Monglian gerbils. AIM: The present study was designed to clarify changes in myofibroblasts, and in the immunoeactivities of basic fibroblast growth factor, cyclooxygenase-2 and inducible nitric oxide synthase after H. pylori infection in Monglian gerbils and H. heilmannii infection in mice. METHODS: After oral inoculation, changes in the location of bacteria and the immunoreactivity of myofibroblasts, basic fibroblast growth factor, cyclooxygenase-2 and inducible nitric oxide synthase were stained with the indirect immunofluorescent method and observed by confocal laser microscopy. RESULTS: In H. heilmannii-infected mice, the increases in myofibroblasts and in immunoreactivities of these three markers were sustained 12 months after infection. In H. pylori-infected Monglian gerbils, however, these increases were significant at 3 months but had returned to control levels at 12 months. CONCLUSIONS: Two types of Helicobacter infection showed different patterns of myofibroblast proliferation, coinciding with the extent of inflammation. These findings suggest that this difference may be related to the consequences of the infection.

Animals↗

Ubiquitin-proteasome inhibitor enhances tumour necrosis factor-alpha-induced apoptosis in rat gastric epithelial cells.

BACKGROUND: Tumour necrosis factor (TNF-alpha) is a candidate factor for involvement in inflammation-mediated gastric mucosal injury. However, the effect of this cytokine on gastric epithelial cells has been poorly investigated. In the present study, we examined whether gastric epithelial cells are resistant to TNF-alpha-induced apoptosis, and whether this resistance is related to ubiquitin-proteasome-associated nuclear factor-kappaB (NF-kappaB) activation. METHODS: The rat gastric mucosal cell line RGM-1 was grown in DMEM/F12 medium supplemented with 10% FCS. Confluent monolayers of cells were pretreated or not for 60 min with PSI, a peptide aldehyde known to specifically inhibit the chymotrypsin-like activity of 26S proteasome. Cells were subsequently stimulated with recombinant rat TNF-alpha and their viability was determined by WST-1 assay. Apoptosis was confirmed by fluorescence microscopy after staining with Hoechst 33342 and propidium iodide, and DNA fragmentation was determined by flow cytometry using an APO-BRDU kit. IkappaB-alpha and the p65 binding subunit of NF-kappaB were detected by Western blots. RESULTS: Twenty-four-hour incubation with TNF-alpha alone or PSI alone did not affect the cell viability of RGM-1 cells. Pretreatment with PSI significantly enhanced the level of apoptosis induced by TNF-alpha. In RGM-1 cells treated with TNF-alpha, cytoplasmic IkappaB-alpha decreased and p65 in nuclear extracts increased markedly 30 min after cytokine stimulation. Pretreatment with PSI at 12.5 micromol/L blocked these TNF-alpha-induced changes. CONCLUSION: PSI enhances TNF-alpha-induced apoptosis through inhibition of NF-kappaB activation in RGM-1 cells.

Animals↗

Macrophage migration inhibitory factor activates antigen-presenting dendritic cells and induces inflammatory cytokines in ulcerative colitis.

The level of macrophage migration inhibitory factor (MIF) and the functions of dendritic cells (DC) are up-regulated in the peripheral blood, and the numbers of MIF-expressing cells and mature DC are increased at the colonic mucosa from patients with ulcerative colitis (UC). However, a functional relationship between MIF and DC, and the role of MIF in the pathogenesis of UC, are not clear. In this study, we showed that a pure population of peripheral blood DC is a new and still unknown source of MIF. DC from UC patients produced significantly higher levels of MIF (17 x 5 +/- 9 x 8 ng/ml, n = 10) compared with patients with Crohns disease (CD) (4 x 6 +/- 2 x 5 ng/ml, n = 5, P< 0 x 01) and control subjects (5 x 0 +/- 2 x 6 ng/ml, n = 10, P< 0 x 01). A double immunofluorescence study revealed the expression of MIF by CD83-positive mature DC at the colonic mucosa from UC patients. Blood DC treated with high amounts of MIF (500 ng/ml) showed a significantly higher stimulatory capacity (43287 +/- 5998 CPM, n = 5) in an allogenic mixed leucocyte reaction compared with untreated DC (27528 +/- 8823 CPM, n = 5, P< 0 x 05). Study of intracellular cytokine expression showed that MIF induced significant levels of interleukin (IL)-1 and IL-8 in monocytes and DC from UC and CD patients. These results showing the capacity of MIF to induce increased functional capacity of DC, and to produce IL-1 and IL-8 from monocytes and DC, indicate a role of MIF in the induction and/or perpetuation of the inflammatory environment in UC.

Cells, Cultured↗

Endoscopic fluorescence observation of gastric mucosa after indomethacin treatment in rats.

BACKGROUND AND STUDY AIMS: The present authors have already reported that mucosal autofluorescence intensity was increased in gastric lesions induced by nonsteroidal anti-inflammatory drugs. The aim of this study was to clarify whether the observation of mucosal autofluorescence with a newly established endoscopic fluorescence analyzing system could help us to recognize indomethacin-induced gastric lesion formation in vivo. MATERIALS AND METHODS: Gastric mucosal fluorescence intensity was measured time-sequentially after indomethacin treatment in rats, using a fluorescence endoscope system. The concentration of thiobarbituric acid-reactive substances in gastric mucosa was measured as an indicator of tissue lipid peroxidation. Fluorescent substances from rat stomachs were analyzed using high performance liquid chromatography. RESULTS: Treatment with indomethacin induced a time-dependent increase of fluorescence intensity. The concentration of thiobarbituric acid-reactive substances was also increased after the treatment. Pretreatment with radical scavenging reagent constrained the increase of both the fluorescence intensity and the concentration of thiobarbituric acid-reactive substances. The fluorescence products were coproporphyrin, protoporphyrin and mesoporphyrin. CONCLUSIONS: These findings indicate that the intensity of porphyrin fluorescence increased in gastric mucosal lesions induced by oxygen radicals. Endoscopic observation of mucosal fluorescence was shown to aid the sensitive and objective diagnosis of gastric injuries.

Animals↗