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Biomedical subjects

Tetsuya Hayashi

Publications and source records attributed to Tetsuya Hayashi.

At least 37 records · Page 2Linked to original sources
PubMed2005

Nifedipine enhances the cardioprotective effect of an angiotensin-II receptor blocker in an experimental animal model of heart failure.

This study was designed to examine the hypothesis that a calcium channel blocker nifedipine (CCB) could enhance the cardioprotective effect of an angiotensin-ll receptor blocker candesartan (ARB) in the treatment for heart failure. Isoproterenol (ISP) was injected into male rats at 300 mg/kg to produce progressive heart failure. Three months later, the rats were divided into 4 groups and treated for 4 weeks with 1) vehicle (n = 20), 2) ARB at 0.2 mg/kg/day (n = 6), 3) CCB at 10 mg/kg/day (n = 6), or 4) both drugs (n = 8). Rats injected with saline served as controls (n = 13). ISP caused severe myocardial degeneration and decreased the capillary density (D(cap)) of the left ventricular (LV) myocardium (mean +/- SD: 2,197 +/- 627 vs. 2,847 +/- 298 N/mm2 for normal controls), while increasing plasma thiobarbituric acid-reactive substances (TBARS; 3.6 +/- 1.1 vs. 1.9 +/- 0.5 nmol/ml). Although ARB therapy preserved cardiac morphology, it had little effect on D(cap) or oxidative stress. On the other hand, CCB decreased plasma TBARS and 4-hydroxy-2-nonenal protein expression in LV myocardium. Furthermore, the combination of CCB and ARB increased D(cap) and preserved the ultrastructure of LV myocardium, so this combination may be a useful option for the treatment of heart failure.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Chronic hypoxia accelerates the progression of atherosclerosis in apolipoprotein E-knockout mice.

The aim of this study was to investigate the effect of chronic hypoxia on the development and progression of atherosclerosis in apolipoprotein E-knockout (apoE-KO) mice. Male and female apoE-KO mice (6 weeks old) and age- and sex-matched wild-type mice were kept under hypoxic conditions (10.0 +/- 0.5% O2) in a gas chamber or in room air for 3 weeks. Aortic atherosclerotic plaque was not observed in wild-type mice under normoxic or hypoxic conditions. In the apoE-KO mice, however, hypoxia induced proliferation of smooth muscle cells and plaque formation in the aorta, which were not observed under normoxic conditions. Although sexual dimorphism of the response to hypoxia was not observed, these hypoxia-induced atherogenic changes were accompanied by a significant increase of plasma low density lipoprotein (LDL) cholesterol and NADPH-dependent vascular superoxide (O2-) production. Furthermore, matrix metalloproteinase (MMP)-9 was activated in the aorta of apoE-KO mice. In conclusion, chronic hypoxia accelerated the development of atherosclerosis in apoE-KO mice, along with increased O2- production and activated MMP-9 in the aorta.

Animals↗
PubMed2005

[A case of synchronous double primary cancers of prostate, and bladder in a hemodialysis patient: a case report].

A 60-year-old male, who had been maintained on hemodialysis for 4 years, visited our hospital to receive living renal transplantation. He complained of macrohematuria, and preoperative examination showed elevation of psostate specific antigen (PSA). Cystoscopy revealed papillary tumors on the right lateral bladder wall. Transurethral resection of bladder tumor (TUR-Bt) was performed and histopathological examination showed transitional cell carcinoma, G2, pTa. The histologic diagnosis of the transrectal needle prostate biopsy specimen was moderately differentiated adenocarcinoma. Combined androgen blockade as a neoadjuvant therapy and radical prostatectomy were performed. A case of synchronous double primary cancers, comprised of adenocarcinoma of the prostate and transitional cell carcinoma of the urinary blader in a hemodialysis patient has never been previously reported in the Japanese literature.

Adenocarcinoma↗
PubMed2004

Core protein of hepatitis C virus induces cardiomyopathy.

Hepatitis C virus (HCV) has been reported to be associated with cardiomyopathy. However, the mechanism of cardiomyopathy in chronic HCV infection is still unclear. Therefore, we investigate the development of cardiomyopathy in mice transgenic for the HCV-core gene. After the age of 12 months, mice developed cardiomyopathy that appeared as left ventricular dilatation, and systolic and diastolic dysfunction assessed by Doppler echocardiography. Histologically, hypertrophy of cardiomyocytes, cardiac fibrosis, disarray and scarcity of myofibrils, vacuolization and deformity of nuclei, myofibrillar lysis, streaming of Z-bands, and an increased number of bizarre-shaped mitochondria were found in HCV-core transgenic mice. These histological changes are just consistent with cardiomyopathy. In conclusion, the HCV-core protein directly plays an important role in the development of cardiomyopathy.

Actin Cytoskeleton↗
PubMed2004

Genomic analysis of Bacteroides fragilis reveals extensive DNA inversions regulating cell surface adaptation.

Bacteroides are predominant human colonic commensals, but the principal pathogenic species, Bacteroides fragilis (BF), lives closely associated with the mucosal surface, whereas a second major species, Bacteroides thetaiotaomicron (BT), concentrates within the colon. We find corresponding differences in their genomes, based on determination of the genome sequence of BF and comparative analysis with BT. Both species have acquired two mechanisms that contribute to their dominance among the colonic microbiota: an exceptional capability to use a wide range of dietary polysaccharides by gene amplification and the capacity to create variable surface antigenicities by multiple DNA inversion systems. However, the gene amplification for polysaccharide assimilation is more developed in BT, in keeping with its internal localization. In contrast, external antigenic structures can be changed more systematically in BF. Thereby, at the mucosal surface, where microbes encounter continuous attack by host defenses, BF evasion of the immune system is favored, and its colonization and infectious potential are increased.

Bacterial Proteins↗
PubMed2004

Hypo-osmotic potentiation of acetylcholine-stimulated ciliary beat frequency through ATP release in rat tracheal ciliary cells.

The ciliary beat frequency (CBF) of rat tracheal ciliary cells in a slice preparation was measured using video-enhanced contrast (VEC) microscopy. Acetylcholine (ACh) increased CBF mediated via intracellular Ca2+ concentration ([Ca2+]i) in a dose-dependent manner. An adequate hypo-osmotic stress (-40 mosM) potentiated ACh-stimulated CBF increase in tracheal ciliary cells and shifted the ACh dose-response curve to the left (lower concentration side). This potentiation was independent of hypo-osmotic stresses applied ranging from -20 mosM to -90 mosM. A hypo-osmotic stress induces ATP release in many cell types. The present study demonstrated that suramin (an inhibitor of purinergic receptors) and apyrase (an ATPase/ADPase) eliminate the hypo-osmotic potentiation of ACh-stimulated CBF increase and that ATP increased [Ca2+]i and CBF, as well as potentiating ACh-stimulated rises in [Ca2+]i and CBF increase. Moreover, the apical surface of tracheal ciliary cells were stained immunopositive for the P2X4 purinergic receptor. A hypo-osmotic stress (-40 mosM) transiently increased [Ca2+]i and potentiated the ACh-stimulated [Ca2+]i increase. The hypo-osmotic potentiation of ACh-stimulated CBF increase was not detected under Ca2+-free conditions. These observations suggest that a hypo-osmotic stress stimulates ATP release from the trachea. The released ATP may induce further increases in [Ca2+]i and CBF in ACh-stimulated tracheal ciliary cells, which may be mediated by purinergic receptors, such as P2X4.

Acetylcholine↗
PubMed2004

Volume overload results in exaggerated cardiac hypertrophy in the atrial natriuretic peptide knockout mouse.

OBJECTIVE: Previous studies suggest that atrial natriuretic peptide (ANP) may act as an autocrine/paracrine factor to modulate cardiac hypertrophy in response to various stimuli. The effect of ANP deficiency on the response to volume overload has not previously been studied. We hypothesised that ANP deficient mice would develop excess cardiac hypertrophy in response to volume overload stress. METHODS: Male homozygous ANP deficient (Nppa(-/-)) and wildtype (Nppa(+/+)) male mice maintained on either a normal salt (0.55% NaCl) or low salt (0.05% NaCl) diet from weaning were studied after 2 weeks of volume overload from an aorto-caval fistula (ACF). Unoperated littermates served as controls. Left ventricular (LV) structure and function was evaluated by echocardiography. Heart, LV, and lung weights were determined at sacrifice. Myocyte diameter was measured by morphometric analysis of fixed sections of the left ventricle. RESULTS: BP, heart weight, and LV weight were increased in Nppa(-/-) vs. Nppa(+/+) unoperated mice. Nppa(-/-) mice developed exaggerated heart and LV weight compared to Nppa(+/+) mice following ACF. Increased myocyte diameter paralleled increased echo LV wall thickness following ACF in Nppa(+/+) but not Nppa(-/-) mice fed with 0.55% NaCl, indicating that an alternate mechanism contributed to increased wall thickness in Nppa(-/-) mice. Mid-wall shortening was mildly depressed in the Nppa(-/-) vs. Nppa(+/+) genotype following ACF with fed 0.55% NaCl. A 0.05% NaCl diet from weaning normalized BP, but did not prevent exaggerated cardiac enlargement and LV hypertrophy following ACF in Nppa(-/-) mice. CONCLUSIONS: ANP-deficient mice exhibited an exaggerated increase in heart and LV weight in response to volume overload, which was not prevented by normalization of blood pressure. The findings suggest that ANP is an important physiologic modulator of the cardiac hypertrophy induced by volume overload.

Animals↗
PubMed2004

Effects of cellular cardiomyoplasty on ventricular remodeling assessed by Doppler echocardiography and topographic immunohistochemistry.

BACKGROUND: Myocardial infarction (MI) promotes deleterious remodeling of the myocardium, resulting in ventricular dilation and pump dysfunction. Supplementing infarcted myocardium with neonatal myocyte would attenuate deleterious remodeling and so the present study used Doppler echocardiography and histology to analyze the cardiac function and histological regeneration of the damaged myocardium after cellular cardiomyoplasty. METHODS AND RESULTS: Experimental MI was induced by 24-h coronary ligation followed by reperfusion in adult male Lewis rats and neonatal myocytes were injected directly into the infarct and peri-infarct regions. Three groups of animals were studied at 4 weeks after cellular cardiomyoplasty: noninfarcted control (control), MI plus sham injection (MI), and MI plus cell injection (MI + cell). Ventricular remodeling and cardiac performance were assessed by Doppler echocardiography or contrast echocardiography. At 4 weeks after cellular cardiomyoplasty, MI + cell hearts exhibited attenuation of global ventricular dilation and cardiac function compared with MI hearts not receiving cellular cardiomyoplasty. Immunohistochemically, connexin-43-positive small cells were observed in the vicinity of the infarction in MI + cell heart. By electron microscopy, these cells contained myofilaments with Z-bands and poorly developed intercalated disks, suggesting neonatal myocardial cells. Furthermore, the myocardial cells were often making close contact with interstitial cells. CONCLUSIONS: Implanted neonatal myocytes form viable grafts after MI, resulting in attenuated ventricular dilation and enhanced contractile function. Echocardiography, electron microscopy, and immunohistochemistry are useful methods for assessing the functional and histological regeneration of the damaged myocardium.

Actin Cytoskeleton↗
PubMed2004

Cardioprotective effect of SEA0400, a selective inhibitor of the Na(+)/Ca(2+) exchanger, on myocardial ischemia-reperfusion injury in rats.

In this study, we investigated whether the Na(+)/Ca(2+) exchanger (NCX) inhibitor SEA0400 (2-[4-[(2,5-difluorophenyl)methoxy]phenoxy-5-ethoxyaniline) might have a protective effect against myocardial ischemia-reperfusion injury in rats. In particular, we focused on cardiac function using Doppler echocardiography and cardiac gene expression. We intravenously administered either SEA0400 and delivery vehicle or only the vehicle (as a control) to Wistar rats 5 min before ischemia was induced. Reperfusion was performed after 30 min of ischemia. At 1 week after ischemia-reperfusion injury, we assessed hemodynamics by inserting a polyethylene-tubing catheter, cardiac function by Doppler echocardiography, and myocardial mRNA expression was determined by Northern blot analysis. Left ventricular (LV) end-diastolic dimensions (LVDd) and LV end-diastolic volume (LVEDV) were significantly increased in the ischemia-reperfusion rat model group compared to the control group. The SEA0400-treated group had a significantly attenuated LVDd (P<0.05) and LVEDV (P<0.01) increase, compared to the vehicle-treated group. A decrease in the LV ejection fraction (P<0.05) was significantly prevented in the SEA0400-treated group compared to the vehicle-treated group. Moreover, mRNA expression of plasminogen activator inhibitor-1 in the non-infarcted LV of the SEA0400-treated group was significantly lower than in the vehicle-treated group (P<0.05). This study demonstrates that the NCX is an important mechanism for cell death in myocardial ischemia and reperfusion in rats. SEA0400 may prove to be a promising new drug in the clinical treatment of myocardial ischemia and reperfusion.

Aniline Compounds↗
PubMed2003

Efficacy of edaravone, a free radical scavenger, on left ventricular function and structure in diabetes mellitus.

This study was designed to assess the efficacy of edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one), a free radical scavenger that possesses anti-oxidant effects, on cardiac function and fine structure of the left ventricular myocardium in diabetes mellitus. Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of spontaneous development of type II diabetes (30 weeks; n = 15) were divided into two groups and treated with edaravone 30 mg/kg/d or vehicle for 2 weeks. OLETF rats showed hyperglycemia (352 +/- 71 mg/dl vs normal control; 128 +/- 52 mg/dl), increased thiobarbituric acid-reactive substances (TBARS; 6.9 +/- 2.5 nM/ml vs 2.8 +/- 0.6 nM/ml), and decreased superoxide dismutase activity (21.5 +/- 0.9 U/ml vs 25.8 +/- 0.7 U/ml). Increased left ventricular end-diastolic pressure (12 +/- 3 mm Hg vs 6 +/- 2 mm Hg) and hypertrophied cardiocytes (23.1 +/- 1.4 vs 17.6 +/- 1.0 microm) were also observed (P < 0.05, respectively). Edaravone could not improve plasma glucose level and hemodynamic parameters but significantly decreased TBARS values (3.8 +/- 0.5) and increased superoxide dismutase activity (24.5 +/- 0.8) (vs OLETF, P < 0.05, respectively). Moreover, edaravone effectively preserved cardiocyte diameter (18.2 +/- 0.9 microm) and the fine structure of mitochondria. Thus, edaravone exhibits modest cardiac protection in diabetes mellitus independent of blood sugar level.

Animals↗
PubMed2003

Digitalis-like immunoreactive substances in maternal and umbilical cord plasma: a comparative sensitivity study of fluorescence polarization immunoassay and microparticle enzyme immunoassay.

Digitalis-like immunoreactive substances (DLIS) obtained from maternal and umbilical cord plasma at delivery were measured by fluorescence polarization immunoassay (FPIA; TDX, Abbott) and microparticle enzyme immunoassay (MEIA; IMX, Abbott). In each sample, concentrations of dehydroepiandrosterone, dehydroepiandrosterone sulfate, estradiol, estriol, hydrocortisone, progesterone, and testosterone were measured by radioimmunoassay, and cross-reaction tests of DLIS with these substances were conducted. By FPIA, the concentration of DLIS in umbilical cord plasma (0.55 +/- 0.22 ng/mL) was significantly higher than that in maternal plasma (0.23 +/- 0.11 ng/mL). In the cross-reaction tests, when the concentration of dehydroepiandrosterone sulfate was higher than 1.0 microg/mL or that of progesterone was higher than 0.5 microg/mL, DLIS were detected by FPIA. However, DLIS were not found either in the samples or in the cross-reaction tests by MEIA. By radioimmunoassay, there was no significant difference in the dehydroepiandrosterone sulfate concentration between the maternal plasma (2,917 +/- 1,001 ng/mL) and the umbilical cord plasma (1,957 +/- 376 ng/mL). The progesterone concentration in the umbilical cord plasma (310.0 +/- 85.7 ng/mL) was significantly higher than that in the maternal plasma (126.4 +/- 38.5 ng/mL). These results suggest that dehydroepiandrosterone sulfate in maternal plasma and progesterone in maternal and umbilical cord plasma may be measured as digoxin by FPIA.

Adult↗
PubMed2003

A single mediaprocessor-based programmable ultrasound system.

We have developed a programmable ultrasound imaging system using a single commercially available mediaprocessor. We have efficiently mapped all of the necessary B-mode processing algorithms on the underlying processor architecture, including envelope detection, dynamic range compression, lateral and axial filtering, persistence processing, and scan conversion. Our system can handle varying specifications ranging from 128 vectors and 512 samples per vector to more than 256 vectors and 1024 samples per vector. For an image size of 330 vectors and 512 samples per vector, it can process 30 frames per second using a 300-MHz MAP-CA mediaprocessor from Hitachi/Equator Technologies. This programmable ultrasound machine will not only offer significant advantages in terms of low cost, portability, scalability, and reduced development time, but also provide a flexible platform for developing and deploying new clinical applications to aid the clinicians and improve the quality of healthcare to patients.

Algorithms↗
PubMed2003

Two different mechanisms are involved in the extremely high-level benzalkonium chloride resistance of a Pseudomonas fluorescens strain.

A Pseudomonas fluorescens strain, PFRB, which we previously isolated as a contaminant in a batch of benzalkonium chloride (BAC) stock solution, exhibits high-level resistance, not only to BAC, but also to other cationic surfactants belonging to disinfectants classified as quaternary ammonium compounds (QACs). In this study, we analyzed the resistance mechanism of the strain to BAC and other disinfectants. We obtained results suggesting that two different mechanisms, reduced adsorption of BAC to the cell surface and an energy-dependent mechanism which is most probably an efflux system, were implicated in the high-level resistance to BAC. Reduced adsorption of BAC is likely due to the decreased negative cell surface charge of the strain. The putative efflux system seems to be unique in that it excretes only a certain range of cationic membrane-acting disinfectants belonging to QACs.

Adsorption↗
PubMed2003

[Escherichia coli].

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Bacterial Proteins↗
PubMed2002

Genomic diversity of enterohemorrhagic Escherichia coli O157 revealed by whole genome PCR scanning.

Enterohemorrhagic Escherichia coli O157 is one of the leading worldwide public health concerns, causing large outbreaks of hemorrhagic colitis as well as numerous small outbreaks and sporadic cases. The variability of restriction enzyme-digestion patterns of O157 genomes, which is widely used to distinguish strains in the molecular epidemiology of O157 infections, suggests the presence of some genomic diversity among the strains. Based on the complete genome sequence of O157 Sakai, we analyzed the whole genome structures of eight O157 strains displaying diverse XbaI-digestion patterns by a systematic PCR analysis that we have named whole genome PCR scanning. This analysis identified not only the O157-specific sequences that are highly conserved among the strains, but also revealed an unexpectedly high degree of genomic diversity. In particular, prophages, including Shiga toxin-transducing phages, exhibited extensive structural and positional diversity, implying that variation of bacteriophages is a major factor in generating genomic diversity among the O157 lineage.

Chromosomes, Bacterial↗