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H Masaki

Publications and source records attributed to H Masaki.

At least 19 recordsLinked to original sources
PubMed2001

Effect of angiotensin II type 2 receptor on tyrosine kinase Pyk2 and c-Jun NH2-terminal kinase via SHP-1 tyrosine phosphatase activity: evidence from vascular-targeted transgenic mice of AT2 receptor.

Angiotensin II (Ang II) has two major receptor isoforms, AT1 and AT2. AT1 transphosphorylates Ca(2+)-sensitive tyrosine kinase Pyk2 to activate c-Jun NH2-terminal kinase (JNK). Although AT2 inactivates extracellular signal-regulated kinase (ERK) via tyrosine phosphatases (PTP), the action of AT2 on Pyk2 and JNK remains undefined. Using AT2-overexpressing vascular smooth muscle cells (AT2-VSMC) from AT2-transgenic mice, we studied these undefined actions of AT2. AT1-mediated JNK activity was increased 2.2-fold by AT2 inhibition, which was abolished by orthovanadate. AT2 did not affect AT1-mediated Pyk2 phosphorylation, but attenuated c-Jun mRNA accumulation by 32%. The activity of src-homology 2 domain-containing PTP (SHP-1) was significantly upregulated 1 min after AT2 stimulation. Stable overexpression of SHP-1 dominant negative mutant in AT2-VSMC completely abolished AT2-mediated inhibition of JNK activation and c-Jun expression. These findings suggest that AT2 inhibits JNK activity by affecting the downstream signal of Pyk2 in a SHP-1-dependent manner, leading to a decrease in c-Jun expression.

Angiotensin Receptor Antagonists↗
PubMed2001

Detection of Salmonella enteritidis in shell and liquid eggs using enrichment and plating.

Detection methods using various enrichment and plating media and immunoconcentration for Salmonella enteritidis in shell and liquid eggs were evaluated. For liquid egg samples naturally contaminated with S. enteritidis, pre-enrichment in 225 ml of buffered peptone water with cysteine followed by selective enrichment in 10 ml of tetrathionate broth was the superior, resulting in the detection of S. enteritidis in all samples on six of the seven types of selective agar substrate investigated. This enrichment procedure also enabled detection of S. enteritidis in most of artificially inoculated shell egg and pasteurized liquid egg samples.

Animals↗
PubMed2001

Angiotensin AT(1) and AT(2) receptors differentially regulate angiopoietin-2 and vascular endothelial growth factor expression and angiogenesis by modulating heparin binding-epidermal growth factor (EGF)-mediated EGF receptor transactivation.

Angiotensin II (Ang II)-mediated signals are transmitted via heparin binding epidermal growth factor (EGF)-like growth factor (HB-EGF) release followed by transactivation of EGF receptor (EGFR). Although Ang II and HB-EGF induce angiogenesis, their link to the angiopoietin (Ang)-Tie2 system remains undefined. We tested the effects of Ang II on Ang1, Ang2, or Tie2 expression in cardiac microvascular endothelial cells expressing the Ang II receptors AT(1) and AT(2). Ang II significantly induced Ang2 mRNA accumulations without affecting Ang1 or Tie2 expression, which was inhibited by protein kinase C inhibitors and by intracellular Ca(2+) chelating agents. Ang II transactivated EGFR via AT(1), and inhibition of EGFR abolished the induction of Ang2. Ang II caused processing of pro-HB-EGF in a metalloproteinase-dependent manner to stimulate maturation and release of HB-EGF. Neutralizing anti-HB-EGF antibody blocked EGFR phosphorylation by Ang II. Ang II also upregulated vascular endothelial growth factor (VEGF) expression in an HB-EGF/EGFR-dependent manner. AT(2) inhibited AT(1)-mediated Ang2 expression and phosphorylation of EGFR. In an in vivo corneal assay, AT(1) induced angiogenesis in an HB-EGF-dependent manner and enhanced the angiogenic activity of VEGF. Although neither Ang2 nor Ang1 alone induced angiogenesis, soluble Tie2-Fc that binds to angiopoietins attenuated AT(1)-mediated angiogenesis. These findings suggested that (1) Ang II induces Ang2 and VEGF expression without affecting Ang1 or Tie2 and (2) AT(1) stimulates processing of pro-HB-EGF by metalloproteinases, and the released HB-EGF transactivates EGFR to induce angiogenesis via the combined effect of Ang2 and VEGF, whereas AT(2) attenuates them by blocking EGFR phosphorylation. Thus, Ang II is involved in the VEGF-Ang-Tie2 system via HB-EGF-mediated EGFR transactivation, and this link should be considerable in pathological conditions in which collateral blood flow is required.

Angiopoietin-1↗
PubMed2001

Emergence and spread of low-level mupirocin resistance in methicillin-resistant Staphylococcus aureus isolated from a community hospital in Japan.

The objective of this study was to investigate the state of mupirocin resistance in methicillin-resistant Staphylococcus aureus (MRSA) in a community hospital in Japan. Ninety strains of MRSA were isolated from the respiratory tract of 56 patients (group I, Jun 1990-Aug 1996) before introduction of mupirocin in Japan, which were compared with 168 strains from 48 patients (group II, Sept 1996-Jan 1998) and 146 strains from 85 patients (group III, Feb 1999-Dec 1999) isolated after introduction of mupirocin. Comparisons were made by determining the minimum inhibitory concentrations (MIC) against nine antibiotics. Fifty-five MRSA isolates from 27 patients [13 (27.1%) of 48 in group II and 14 (16.5%) of 85 in group III] after introduction of mupirocin showed low-level resistance to mupirocin (MIC, 6.25 to 50 microg/ml) but the remaining isolates were sensitive to mupirocin (MIC < or =3.13 microg/ml). Most patients colonized with low-level mupirocin-resistant MRSA were elderly (> or =65 years of age), on total parenteral nutrition or nasal feeding and had other underlying diseases. The proportion of patients colonized with low-level mupirocin-resistant MRSA following repeated use of mupirocin was higher in patients of group II than those of group III. Molecular typing by pulsed-field gel electrophoresis (PFGE) demonstrated that the pattern of 13 MRSA isolates from 13 patients of group II consisted of three patterns (A, B, C) with predominance of pattern A, while the pattern of 13 MRSA isolates from 13 patients of group III consisted of three patterns (A, C, D) with predominance of patterns A and D. Our results indicated that resistance of MRSA to mupirocin remains at a low level at present in Japan. However, we should be aware of the possible emergence of MRSA highly resistant to mupirocin in the future.

Anti-Bacterial Agents↗
PubMed2001

Ethanol and protein metabolism.

This article represents the proceedings of a workshop at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Carol C. Cunningham and Victor R. Preedy. The presentations were (1) Ribosomal content, ribosomal localization and the levels of ribosomal protein mRNA and rRNA in rat skeletal muscle exposed to ethanol, by Alistair G. Paice, John E. Hesketh, Timothy J. Peters, and Victor R. Preedy; (2) Altered hepatic mitochondrial ribosome structure after chronic ethanol administration, by Vinood B. Patel and Carol C. Cunningham; (3) Clinical aspects of hepatic protein metabolism and alcohol, by Elena Volpi; and (4) Effects of oral intake of alanine plus glutamine on ethanol metabolism and ethanol-related depression in motor activity, by Kazunori Mawatari, H. Masaki, M. Mori, and Kunio Torii.

Alanine↗
PubMed2001

[Detection of gram-negative bacteria in patients and hospital environment at a room in geriatric wards under the infection control against MRSA].

We prospectively surveyed gram-negative bacteria in patients and hospital environment in a room in the geriatric ward which was specifically under the infection control against MRSA once every two weeks between September and December 1996. We investigated the inpatients in an 8-bed room in the geriatric wards (190 beds) of AINO Memorial Hospital, affiliated with Nagasaki University. During the study period, we performed a total of 431 cultures. The number of specimens cultured was 116 from airways (nose, 42; pharynx, 42; sputum, 32), 24 from decubitus ulcer, 40 from urine, 42 from feces, a total of 125 from skin (head, 42; forearm, 42; inguinal region, 41), and 84 from the hospital environment (floor swab, 42; settled agar plate, 42), respectively. A total of 15 species were isolated from the hospital environment. Some species were the same as those which were recovered from the hospital environment were those observed on each body site. In the hospital environment, the isolation rates of Acinetobacter baumanii and Klebsiella pneumoniae were significantly high in the settled agar plate (A. baumanii, p < 0.01; K. pneumoniae, p < 0.05, respectively). Isolation rates of Pseudomonas aeruginosa, Citrobacter spp., and Enterobacter sakazakii were also high in the settled agar plate (p = 0.078, 0.078, 0.078, respectively). In conclusion, gram-negative bacteria in patients may be associated with the environmental bacteria in the room in the geriatric wards.

Aged↗
PubMed2001

[Importance of a cleaning in upper airways by using povidone iodine for the prevention of nosocomial pneumonia].

We investigated the efficacy of infection control measures against nosocomial pneumonia in geriatric wards. Cases with nosocomial pneumonia were retrospectively analyzed between January 1991 and March 1995. The study period was divided into four annual periods (periods 1, 2, 3 and 4). Period 1, January to December 1991, was applied as the cotrol. We investigated patients with nosocomial pneumonias in geriatric wards (190 beds) of AINO Memorial Hospital, affiliated with Nagasaki University. During the study period, nosocomial pneumonia significantly diminished. (period 1 vs periods 2, 3 and 4, p < 0.05, p < 0.05, p < 0.05, respectively). Major causative organisms of nosocomial pneumonia were MRSA and Pseudomonas aeruginosa. During the four periods, a significant reduction in cases with MRSA- and P. aeruginosa-induced nosocomial pneumonia was observed (MRSA: period 1 vs periods 2, 3 and 4, p < 0.05, p < 0.05, p < 0.01, respectively; P. aeruginosa: period 1 vs period 3, p < 0.01, period 2 vs periods 3 and 4, p < 0.01, p < 0.05, respectively). On the other hand, the improvement of decubitus ulcers was associated with a significant reduction in nosocomial pneumonia (period 1 vs. periods 2 and 3, p < 0.05 and p < 0.05, respectively). In conclusion, stringent infection control programs, including a cleaning in the upper airways by povidone iodine, are necessary in geriatric wards to reduce and prevent nosocomial pneumonia.

Aged↗
PubMed2001

Significant reduction of methicillin-resistant Staphylococcus aureus bacteremia in geriatric wards after introduction of infection control measures against nosocomial infections.

OBJECTIVES: (1) To investigate the efficacy of infection control measures against methicillin-resistant Staphylococcus aureus (MRSA) bacteremias in geriatric wards. (2) To identify predisposing risk factors for MRSA bacteremia. METHODS: Cases with nosocomial bacteremias were retrospectively analyzed between January 1991 and March 1995. The study period was divided into four annual periods and the period 1, January to December 1991, was applied as the control. MATERIALS: We investigated patients with nosocomial bacteremias in geriatric wards (190 beds) of AINO Memorial Hospital, affiliated with Nagasaki University. RESULTS: A significant reduction in cases with MRSA-induced nosocomial bacteremia was observed after the introduction of a stringent infection control and prevention program (period 1 vs. periods 2, 3, and 4: p<0.00833, p<0.00167, and p<0.00167, respectively). The major source of bacteremia included urinary tract infections, intravenous catheter-related infections, and infected decubitus ulcers. Improvement of decubitus ulcer was associated with a significant reduction in MRSA bacteremia (period 1 vs. periods 2 and 3: p<0.00017 and p<0.00833). CONCLUSION: Stringent infection control programs, including prevention and treatment of decubitus ulcers, are necessary in geriatric wards to reduce and prevent MRSA bacteremia.

Aged↗
PubMed2001

[Gene-therapy for peripheral vascular diseases].

The prognosis for patients with chronic critical leg ischemic is often poor. The treatment of peripheral vascular disease, although greatly improved over recent decades by drug medication, surgical and minimally-invasive techniques, remains limited by vascular proliferative lesions and by our inability to modulate the progression of native disease. The therapeutic angiogenesis is now the most expected therapy for peripheral vascular diseases. This review explores some of concepts and methods of therapeutic angiogenesis including gene therapy using angiogenic growth factor such as VEGF and basic FGF and an implantation of bone marrow derived endothelial progenitor cells.

Animals↗
PubMed2001

[Pathophysiology of blood pressure variability in patients with chronic renal failure under maintenance hemodialysis].

The rise of blood pressure is negatively related with the glomerullar filtration rate(GFR) in patients with terminal renal failure. Hypertension may be a mechanism to maintain renal blood flow and GFR constant by the increased driving force of blood to the kidney. Elevated levels of a so-called third factor, now designated as endogenous digitalis, are found in those patients. The most likely candidate of the endogenous digitalis is ouabain, which causes hypertension with chronic administration. On the other hand, extreme hypotension often occurs during maintenance hemodialysis, and since hemodynamic alterations closely resemble endotoxin shock, the involvement of nitric oxide(NO) over-production has been suggested. When we measured nitrate anion as the final metabolite of NO, the concentration was significantly higher in patients with marked hypotension during hemodialysis than those without hypotension. Since reflex tachycardia was not observed during hypotension, we speculated that those patients had autonomic disturbances, and assessed autonomic function by heart rate spectral analysis. Although the high frequency spectral power, regarded as the vagal tone, was not significantly different between the groups, low/high frequency spectral power ratio, which was thought to be a sympathetic component, was significantly lower in patients with hypotension during hemodialysis than that in patients without hypotension. We speculated that NO synthase may be induced by the stimuli to monocytes by tubes and dialyser membrane made of synthetic materials leading to the over production of NO during and after regular hemodialysis. Thus, cytokines may be the mediator of the induction of NO synthase. Dilated capacitance vessels decrease the venous return to the heart, which may be the direct cause of dialysis-induced hypotension.

Autonomic Nervous System↗
PubMed2001

[A case of primary racemose hemangioma of bronchial artery with recurrent hemoptysis].

A 42-year old man was admitted to our hospital because of hemoptysis. Bronchial arteriography revealed a tortuous and dilated left bronchial artery with a shunt formation between the bronchial and pulmonary arteries. Bronchial artery embolization using a sponge was performed three times to treat the hemoptysis, but all attempts failed. The patient therefore underwent left lower lobectomy, after which no hemoptysis was observed. Histopathologically, the resected tissue showed no inflammatory change. Interestingly, abnormal vessels resembling arteriovenous malformations were also found. Although the embolization therapy was effective in several reported cases, we concluded that surgery was required for this patient with persistent hemoptysis because of the development of collaterals and a bronchial-pulmonary artery shunt.

Adult↗
PubMed2000

Angiotensin II initiates tyrosine kinase Pyk2-dependent signalings leading to activation of Rac1-mediated c-Jun NH2-terminal kinase.

Ca(2+)-sensitive tyrosine kinase Pyk2 was shown to be involved in angiotensin (Ang) II-mediated activation of extracellular signal-regulated kinase (ERK) via transactivation of epidermal growth factor receptor (EGF-R). In this study, we tested the involvement of Pyk2 and EGF-R in Ang II-induced activation of JNK and c-Jun in cardiac fibroblasts. Ang II markedly stimulated JNK activities, which were abolished by genistein and intracellular Ca(2+) chelators but partially by protein kinase C depletion. Inhibition of EGF-R did not affect Pyk2 and JNK activation by Ang II. Stable transfection with a dominant negative (DN) mutant for Pyk2 (PKM) completely blocked JNK activation by Ang II. DN mutants of Rac1 (DN-Rac1) and MEK kinase (DN-MEKK1) also abolished it, whereas those of Cdc42, RhoA, and Ha-Ras had no effect. Induction of c-Jun gene transcription by Ang II was abolished in PKM, DN-Rac1, and DN-MEKK1, in which Ang II-induced binding of ATF2/c-Jun heterodimer to the activator protein-1 sequence at -190 played a key role. These results suggest that 1) in cardiac fibroblasts activation of JNK and c-Jun by Ang II is initiated by Pyk2-dependent signalings but not by downstream signals of EGF-R or Ras, 2) Rac1 but not Cdc42 is required for JNK activation by Ang II upstream of MEKK1, and 3) ATF-2/c-Jun binding to the activator protein-1 sequence at -190 plays a key role for induction of c-Jun gene by Ang II.

Angiotensin II↗
PubMed2000

A cytotoxic ribonuclease which specifically cleaves four isoaccepting arginine tRNAs at their anticodon loops.

Colicin D has long been thought to stop protein synthesis in infected Escherichia coli cells by inactivating ribosomes, just like colicin E3. Here, we show that colicin D specifically cleaves tRNAs(Arg) including four isoaccepting molecules both in vivo and in vitro. The cleavage occurs in vitro between positions 38 and 39 in an anticodon loop with a 2',3'-cyclic phosphate end, and is inhibited by a specific immunity protein. Consistent with the cleavage of tRNAs(Arg), the RNA fraction of colicin-treated cells significantly reduced the amino acid-accepting activity only for arginine. Furthermore, we generated a single mutation of histidine in the C-terminal possible catalytic domain, which caused the loss of the killing activity in vivo together with the tRNA(Arg)-cleaving activity both in vivo and in vitro. These findings show that colicin D directly cleaves cytoplasmic tRNAs(Arg), which leads to impairment of protein synthesis and cell death. Recently, we found that colicin E5 stops protein synthesis by cleaving the anticodons of specific tRNAs for Tyr, His, Asn, and Asp. Despite these apparently similar actions on tRNAs and cells, colicins D and E5 not only exhibit no sequence homology but also have different molecular mechanisms as to both substrate recognition and catalytic reaction.

Anticodon↗
PubMed2000

Definition of an epitope on Japanese encephalitis virus (JEV) envelope protein recognized by JEV-specific murine CD8+ cytotoxic T lymphocytes.

We defined an epitope on the Japanese encephalitis virus (JEV) envelope (E) protein recognized by CD8+ cytotoxic T lymphocytes (CTLs). CTLs induced in JEV-infected BALB/c (H-2d) mice recognized E and/or premembrane (PrM) proteins, while CTLs in C57BL/6J (H-2b) and C3H/HeJ (H-2k) mice did not. JEV-specific CTLs had a phenotype of CD3+ CD4- CD8+. Twenty-four 9-amino acid (a.a.) peptides, which had binding motifs for H-2Kd, H-2Ld or H-2Dd, were synthesized according to the amino acid sequences of PrM and E proteins. CTLs induced by JEV infection recognized only the peptide K-3. Immunization of BALB/c mice with only a group of peptides including K-3 induced CTLs which recognized the homologous K-3 peptide, while immunization with other peptides did not. The peptide K-3 had a binding motif for H-2Kd. This is consistent with the finding that JEV-specific CTLs in BALB/c mice was H-2Kd-restricted. These results indicate that the epitope recognized by CTLs in BALB/c mice is located between a.a. 60 and 68 on the E protein, corresponding to an a.a. sequence of CYHASVTDI.

Amino Acid Sequence↗
PubMed2000

Transactivation of EGF receptor induced by angiotensin II regulates fibronectin and TGF-beta gene expression via transcriptional and post-transcriptional mechanisms.

The signaling cascade elicited by angiotensin II (Ang II) resembles that characteristic of growth factor, and recent evidence indicates transactivation of epidermal growth factor receptor (EGF-R) by G protein-coupled receptors. Here, we report the involvement of EGF-R in Ang II-induced synthesis of fibronectin and TGF-beta in cardiac fibroblasts. Ang II stimulated fibronectin mRNA levels dose-dependently with a maximal increase (approximately 5-fold) observed after 12 h of incubation. Ang II-, or calcium ionophore-induced fibronectin synthesis was completely abolished by tyrosine kinase inhibitors and intracellular Ca2+ chelating agents. Ang II-induced fibronectin mRNA was not affected by PKC inhibitors or PKC depletion, whereas specific inhibition of EGF-R function by a dominant negative EGF-R mutant and tyrphostin AG1478 abolished induction of fibronectin mRNA. We isolated the rat fibronectin gene including the 5'-flanking region and found that the AP-1 binding site present in the promoter region was responsible for the Ang II responsiveness of this gene. Gel retardation assay revealed the binding of nuclear protein to the AP-1 site, which was supershifted with anti-c-fos and anti-c-jun but not anti-ATF-2 antibodies. Conditioned medium from Ang II-treated cells contained TGF-beta bioactivity and addition of neutralizing TGF-beta antibody modestly (46%) inhibited induction of fibronectin. Ang II-induced synthesis of TGF-beta was also abolished by inhibition of EGF-R function. The effect of TGF-beta was exerted by stabilizing fibronectin mRNA without affecting the promoter activity and required de novo protein synthesis. We concluded that Ang II-induced expression of fibronectin and TGF-beta is mediated by downstream signaling of EGF-R transactivated by Ca2+-dependent tyrosine kinase, and that Ang II-induced fibronectin mRNA expression is regulated by two different mechanisms; transcriptional control by binding of c-fos/c-jun complex to the AP-1 site, and post-transcriptional control by mRNA stabilization due to autocrine and/or paracrine effects of TGF-beta. Thus, this study suggested that the action of Ang II on extracellular matrix formation should be interpreted in association with the EGF-R signaling cascade.

Angiotensin II↗
PubMed2000

Changes in patterns of left ventricular hypertrophy after aortic valve replacement for aortic stenosis and regurgitation with St. Jude Medical cardiac valves.

In this study, we analyzed the extent and pattern of regression of left ventricular (LV) hypertrophy after aortic valve replacement in patients with aortic stenosis (AS) and compared the results with those of another group of patients with aortic regurgitation (AR). Seventy patients who underwent isolated aortic valve replacement were divided into 2 groups. Group 1 was comprised of 29 patients who underwent aortic valve replacement for aortic stenosis, and Group 2 of 41 patients who underwent aortic valve replacement for aortic regurgitation. A third group of 10 healthy subjects served as a healthy control group. Echocardiographic studies were done before the operation and 5 years postoperatively. At follow-up, a significant reduction in the left ventricular mass was found in both groups, but it remained significantly greater than in the healthy control group. The ratio of LV wall thickness to radius (th/r) in Group 1 decreased significantly, and at follow-up it was within the normal value. In Group 2, the th/r ratio increased, and at follow-up it was within the normal value. After aortic valve replacement, the wall thickness remained significantly greater than normal for patients with AS, and the chamber radius remained significantly greater than normal for patients with AR. For these reasons, LV hypertrophy still existed in both groups at postoperative follow-up. The actuarial survival rate was 85.3% at 16 years for Group 1 and 83.4% at 18 years for Group 2. There was no significant difference in the long-term survival rates between the 2 groups. Actuarial freedom from valve-related events was 91.9% at 16 years for Group 1 and 82% at 18 years for Group 2. There was no significant difference in the valve-related event free curves between groups. After 5 years of follow-up, th/r reached normal for both groups, indicating remodeling of the LV geometry after aortic valve replacement.

Adult↗