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Biomedical subjects

M Masuda

Publications and source records attributed to M Masuda.

At least 235 records · Page 13Linked to original sources
PubMed1997

Central somatostatin prevents vagal efferent nerve excitation produced by TRH but not by 2-deoxy-D-glucose.

Thyrotropin-releasing hormone (TRH) administered intracerebroventricularly and intravenous injection of 2-deoxy-D-glucose (2-DG) stimulate pancreatic exocrine secretion via vagal efferent nerve excitation. We examined whether centrally administered somatostatin would inhibit pancreatic exocrine secretion that was stimulated by vagal efferent nerve excitation in conscious rats. The animals were prepared with cannulas draining bile and pancreatic juice separately and with a duodenal cannula, a cerebroventricular cannula, and a right jugular vein cannula. Intracerebroventricular injection of somatostatin (0.4 or 4 nmol) significantly inhibited pancreatic secretion induced by TRH (50 or 500 pmol) in a dose-dependent manner. Intravenous injection of somatostatin had no effect on pancreatic secretion stimulated by TRH. On the other hand, somatostatin injected centrally did not affect pancreatic secretion induced by 2-DG (75 mg/kg) or basal secretion. These results suggest that TRH and 2-DG stimulate vagal efferent nerves via distinct mechanisms and that central somatostatin selectively inhibits excitation of the vagus induced by peptidergic (TRH) stimulation.

Animals↗
PubMed1997

Regulation of cholecystokinin release and transcription in a rat without gene expression of cholecystokinin-A receptor.

An Otsuka Long-Evans Tokushima Fatty (OLETF) rat does not possess cholecystokinin (CKK)-A receptor gene expression because of a genetic abnormality. We examined the CCK release and its transcription in OLETF rats in comparison with control (Long-Evans-Tokushima-LETO) rats. Animals at 5-6 and 24-25 weeks of age were used. The level of CCK mRNA and CCK concentration in the small intestinal mucosa, and the level of CCK-A receptor mRNA in the pancreas were examined. To examine CCK release, rats were prepared with external bile and pancreatic fistulae. The basal plasma levels of CCK and those at 2 h after bile-pancreatic juice diversion were measured by radioimmunoassay. The levels of CCK mRNA, and tissue CCK concentration increased significantly with age in both strains, but the values in OLETF rats were significantly lower than those in LETO rats. The CCK-A receptor mRNA level also increased with age in LETO rats. The plasma CCK concentration was significantly increased by bile-pancreatic juice diversion regardless of age and strain; however, the level of plasma CCK in OLETF rats at 24-25 weeks of age was significantly lower than that of LETO rats. It is suggested that the long-term defect of CCK-A receptor may decrease CCK release and transcription.

Animals↗
PubMed1997

Increased blood plasminogen activator inhibitor-1 and intercellular adhesion molecule-1 as possible risk factors of atherosclerosis in Werner syndrome.

Werner syndrome is a rare premature aging syndrome accompanied by severe atherosclerosis. The etiology of atherosclerosis is suspected to be due to its complications, namely diabetes mellitus, hyperinsulinemia and hyperlipidemia. But from an autopsy case we found that some other risk factors may be involved in the mechanism of atherosclerosis in this syndrome. Previously we revealed that the plasminogen activator inhibitor-1 (PAI-1) gene was being overexpressed in skin fibroblasts from a patient with this syndrome. PAI-1 is a potent inhibitor of tissue plasminogen activator and a possible risk factor of atherosclerosis. This led us to assess the plasma concentration of PAI-1. Our working hypothesis was that the PAI-1 gene was upregulated or not fully suppressed in cells responsible for the production of PAI-1 in plasma as well as in fibroblasts. The results show a high concentration of plasma PAI-1. One of the well-known physiological substances that induce the PAI-1 gene is tumor necrosis factor-alpha, which also induces other possible risk factors of atherosclerosis, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1. We found the serum concentrations of ICAM-1 to be elevated in patients with this syndrome. We conclude that high concentrations of PAI-1 and ICAM-1 in blood may be one of the potent causes of severe atherosclerosis in Werner syndrome.

Adult↗
PubMed1997

The efficacy of pulmonary thromboendarterectomy on long-term gas exchange.

It has not been delineated in detail how pulmonary thromboendarterectomy (PTE) affects gas exchange through long-term follow-up. In Japan, this surgery has been undertaken in a limited number of institutions, and the results of PTE have not been well publicized. A total of 25 patients were operated on during the period from 1985 to 1996 at our institution, and the overall mortality rate was 16%. Our criteria for PTE were based on the following: 1) thrombi surgically accessible as judged by angiographic study; 2) mean pulmonary arterial pressure > or = 30 mmHg. The efficacies of PTE were analysed on haemodynamics as well as gas exchange at one month postsurgery and during follow-up (6-24 months). Significant haemodynamic improvement was obtained as early as 1 month after surgery. Improvement of gas exchange lagged, but was then observed during follow-up, and the improvement level of pulmonary haemodynamics was sustained. The early postoperative restrictive impairment and ventilation-perfusion abnormality on lung perfusion scan resolved during the follow-up period. It was concluded that the early postoperative efficacy of pulmonary throm-boendarterectomy was mainly achieved due to the reduction of pulmonary hypertension, whereas improvement in gas exchange was obtained over the longer term.

Adult↗
PubMed1997

Relationship between the release of prolactin and endothelin-1 in human decidualized endometrial cells.

The study was undertaken to investigate the interaction between the release of endothelin-1 (ET-1) and prolactin (PRL) from human decidualized endometrial cells, and the effects of transforming growth factor (TGF)-beta 1 on the release of ET-1 and PRL from human decidual cells in the early stage of pregnancy. Stromal cells derived from human endometrial tissues were cultured on a type-1 collagen membrane in serum-free medium with or without 100 nmol/l oestradiol and 1 mumol/l medroxyprogesterone acetate (MPA) for 12 days. In addition, decidual cells of early pregnancy were cultured with or without TGF-beta 1 for 48 h. PRL and ET-1 levels in the media were measured by a specific enzyme immunoassay and RIA respectively. In decidualized endometrial cells induced by ovarian steroid hormones in vitro, PRL release increased and ET-1 release decreased in a time-dependent manner. Ovarian steroid hormones significantly attenuated ET-1 release. In the decidual cells of early pregnancy, TGF-beta 1 significantly attenuated the PRL release, whereas this growth factor dose-dependently increased ET-1 release. There was a significant negative correlation between the release of PRL and that of ET-1. These results demonstrate that the regulation of PRL release is quite different from that of ET-1 release in the human decidualized endometrial cells, and suggest that TGF-beta 1 has significant effects on PRL and ET-1 release in the human decidua of early pregnancy.

Adult↗
PubMed1997

Vasodepressor effects of exercise are accompanied by reduced circulating ouabainlike immunoreactivity and normalization of nitric oxide synthesis.

Our object was to evaluate the effects of regular mild exercise on blood pressure and on circulating level of ouabainlike factors (OLF) and of nitrate anion, an endproduct of nitric oxide (NO) in humans. We measured plasma ouabainlike immunoreactivity (OLI) and nitrate ions (NO3.) before and after mild exercise for 3 months' duration in 16 patients with essential hypertension, diabetes mellitus, obesity, or hyperlipidemia. Plasma OLI was measured using an amplified ELISA system with anti-ouabain antibody and biotinyl-tyramide. Serum NO3. was measured with high-performance liquid chromatography (HPLC) with an anion-exchange column. With the reverse phase HPLC system with an octa decylsilyl silicagel column, the elution volume of plasma OLI of a healthy volunteer matched that of authentic ouabain in a gradient elution system of acetonitrile/H2O. Plasma OLI levels decreased significantly by about 34% after mild exercise, and NO3. levels tended to be within the reference interval in normal volunteers. Body weight, diastolic and systolic blood pressure, serum triglyceride and acetylcholine esterase (a marker of the fatty liver) were significantly decreased (p < 0.01) after 3 months of regular mild exercise. The plasma OLI level was significantly correlated with plasma NO3., there was a trend toward a correlation with diastolic blood pressure (p = 0.06) before and after regular exercise. Regular mild exercise led to a decrease in plasma levels of OLI, and acetylcholine esterase activity and blood pressure in adult patients. Results suggest that changes in OLF production contribute to the blood pressure regulation seen in patients who exercise regularly.

Adult↗
PubMed1997

Tyrosine phosphorylation of platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31) in mechanically stimulated vascular endothelial cells.

Fluid flow triggers signal transducing events, modulates gene expression, and remodels cytoskeletal structures in vascular endothelial cells (ECs). However, the primary steps of mechanoreception are still unknown. We have recently reported that a glycoprotein is rapidly tyrosine-phosphorylated in bovine ECs exposed to fluid flow or osmotic shock. Here were cloned a 3.4 kb cDNA encoding this protein and found that this was bovine PECAM-1. The tyrosine-phosphorylation level of PECAM-1 immunoprecipitated from mechanically stimulated bovine or human ECs increased. The PECAM-1 phosphorylation was not induced by reagents that triggered Ca2+ mobilization in ECs. An autophosphorylatable band comigrating with c-Src was co-immunoprecipitated with anti-PECAM-1, and c-Src phosphorylated and bound to a GST fusion protein containing the PECAM-1 cytoplasmic domain. A spliced mRNA form lacking amino acid residues 703-721 in the cytoplasmic domain was also expressed in bovine ECs, c-Src neither phosphorylated nor bound to the fusion protein containing the spliced PECAM-1 cytoplasmic domain which lacked one (Tyr 713) of the six tyrosine residues in the PECAM-1 cytoplasmic domain. These results suggest that the YSEI motif containing Tyr 713 is the Src phosphorylation/binding site. Our study is the first demonstration of inducible tyrosine phosphorylation of PECAM-1 and suggests involvement of PECAM-1 and Src family kinases in the sensing/signal transduction of mechanical stimuli in ECs.

Amino Acid Sequence↗
PubMed1997

[Seasonal changes of laboratory data in patients with Japanese cedar pollinosis].

Japanese cedar pollen (JCP) causes a significant seasonal allergic rhinitis in Japan during the early spring. Blood samples were collected monthly from October 1993 through October 1994 from 11 patients with Japanese cedar pollinosis. The patients were segregated into two categories based on specific IgE (RAST): single positive RAST to JCP only and multiple positive RAST to JCP, house dust (H1) and mite (D1). These two populations differed in levels of total serum IgE, numbers of eosinophils, basophils and neutrophils in peripheral blood and clinical symptoms. Seasonal increase of JCP-specific IgE was observed after pollen season in both groups. In the single positive group, but not in the multiple positive group, seasonal increase of the number of eosinophils in peripheral blood was observed with post seasonal fall and the level of total serum IgE was increased in the same manner as that of the JCP specific IgE. Although it was not significant, there was a broad seasonal increase of serum nitrate anion, a metabolite of nitric oxide.

Adult↗
PubMed1997

Molecular mechanism for retroviral neuropathogenesis: possible involvement of capillary endothelial cells.

A neuropathogenic variant of Friend MuLV, PVC-211, causes rapidly progressive spongiform neurodegeneration in susceptible rats and mice. Major targets of PVC-211 MuLV infection are brain capillary endothelial cells (BCEC), suggesting that virus-infected BCEC may play crucial roles in neurological disease induction. Consistent with this possibility, studies using chimeric viruses constructed between PVC-211 MuLV and non-neuropathogenic Friend MuLV have revealed that the BCEC tropism of the virus correlates with its neuropathogenicity. Possible involvement of cytokine expression by PVC-211 MuLV-infected BCEC in the induction of neuropathological changes will be discussed.

Animals↗
PubMed1997

Constitutive activation of Stat-related DNA-binding proteins in erythroid cells by the Friend spleen focus-forming virus.

The erythroleukemia-inducing Friend spleen focus-forming virus (SFFV) encodes a unique envelope glycoprotein which allows erythroid cells to proliferate and differentiate in the absence of the erythroid hormone erythropoietin (Epo). In an attempt to understand how the virus alters the growth of erythroid cells, studies were carried out to determine if virus infection leads to the constitutive activation of the Jak-Stat pathway, one of the signal transduction pathways activated by Epo. Our data indicates that expression of SFFV in erythroid cells leads to the constitutive activation of the same Stat proteins that are transiently activated by Epo. While constitutive activation of Stat proteins by SFFV is associated with Epo-independent proliferation of splenic erythroid progenitor cells from Fv-2-sensitive mice and Epo-dependent HCD-57 cells, it is not sufficient to induce their differentiation. Although constitutive activation of the same Stat proteins is detected in erythroid cells from SFFV-infected Fv-2-resistant mice, it does not lead to their Epo-independent growth. It is also not required for transformation of erythroid cells by SFFV. Studies are in progress to identify the mechanism by which Stat proteins are phosphorylated in SFFV-infected cells in the absence of Epo. Although it has been shown that Epo activates Stat proteins through Jak2 kinase, our results suggest that the SFFV-induced Stat protein activation is Jak2-independent.

Animals↗
PubMed1997

Prognostic value of Ki-67 for recurrence and progression of superficial bladder cancer.

PURPOSE: We retrospectively reviewed 104 cases of superficial bladder cancer to ascertain whether the Ki-67 labeling index predicts recurrence and progression. MATERIALS AND METHODS: Archival specimens from superficial bladder cancer cases were immunostained with Ki-67. RESULTS: The recurrence rate was significantly higher in cases with a Ki-67 labeling index of 5.35 or greater than in those with a value less than 5.35 (p < 0.001). The recurrence rate at 2 years was 70% in cases with a Ki-67 labeling index of 5.35 or greater and 22% in those with an index less than 5.35 (p < 0.001). Using multivariate analysis the index predicted recurrence of bladder cancer (p < 0.005). Median Ki-67 labeling index in cases with progression was significantly higher than in those without progression (p < 0.01). CONCLUSIONS: The Ki-67 labeling index is an independent predictive factor for recurrence of superficial bladder cancer.

Adult↗
PubMed1997

Effect of a new monoclonal anti-glycoprotein IX antibody, KMP-9, on high shear-induced platelet aggregation.

Human platelet glycoprotein Ib/IX complex acts as a receptor for von Willebrand factor. It is widely accepted that glycoprotein Ib is the essential receptor component, but the role of glycoprotein IX is still unclear. We produced a new monoclonal anti-glycoprotein IX antibody (KMP-9) by the hybridoma technique using platelets from a patient with Glanzmann's thrombasthenia. The epitope of KMP-9 was localized to the C-terminal 8 kD fragment of glycoprotein IX using ELISA analysis of polyethylene-pin-synthesized peptides, as well as Western blot analysis of platelets after digestion with N-glycosidase and Staphylococcus aureus V8 protease. KMP-9 partially inhibited high shear stress-induced platelet aggregation, but had no effect on aggregation induced by ristocetin or low shear stress. Its inhibitory effect on high shear stress-induced aggregation was weaker than that of anti-glycoprotein Ib or anti-glycoprotein IIb/IIIa monoclonal antibodies. A 21-mer synthetic peptide (glycoprotein IX L110-G130) inhibited the binding of KMP-9 to platelets. It also competively inhibited the suppression of high shear stress-induced platelet aggregation by KMP-9, but had no direct effect on this aggregation. KMP-9 may be useful to clarify the physiological role of GPIX.

Amino Acid Sequence↗
PubMed1997

[A case of modified Fontan operation for corrected transposition of great arteries (I.D.D.) with atrial septal defect, ventricular septal defect, pulmonary stenosis, mitral atresia and hypoplastic left ventricle].

A 14-year-old boy with corrected transposition of the great arteries (I.D.D.), atrial septal defect, ventricular septal defect, pulmonary stenosis, mitral atresia and hypoplastic left ventricle was successfully operated. He had undergone modified Blalock-Taussig shunt at the age of two. After atrial septal defect was closed with bovine pericardial patch, small ventricular septal defects were closed directly through left ventricular incision. Then the incisional line on the left ventricle was extended to pulmonary artery. The stenotic and thickened pulmonary valve was excised. The upper part of the incisional line on the right atrium and that on the left ventricle were anastomosed. Consequently the connection between the right atrium and the pulmonary artery was able to be made through hypoplastic left ventricle. This case is extremely rare type in terms of mitral atresia and is classified as Group II, type B according to Eliot's classification. This type of repair is similar to Björk's method, however, we could not make use of left ventricular contraction because it was weak. The merit of this procedure was to be able to reconstruct blood tract without using artificial conduits.

Adolescent↗
PubMed1996

Mechanism for mouse strain differences in the protective effect of Sudan III against the in vivo genotoxicity of 7,12-dimethylbenz[a]anthracene.

The effect of Sudan III-pretreatment on the in vivo genotoxicity of 7,12-dimethylbenz[a]anthracene (DMBA) was investigated using C57BL/6 (B6) and DBA/2 (D2) mice. A significant increase in the frequency of micronucleated reticulocytes was observed in both strains of mice treated with DMBA. The increase was significantly reduced in B6 but not D2 mice by Sudan III-pretreatment. However, enhancement of metabolic activation was found in the Ames assay in the hepatic post-mitochondrial supernatant fraction (S9) from Sudan III-treated animals. It was greater with S9 from B6 than S9 from the D2 group. When the assay was performed in the presence of glutathione, this enhancement was significantly reduced. Sudan III induced some drug metabolizing enzymes, mainly CYP1A and glutathione S-transferase was also induced. The induction of CYP1A was more effective in B6 than D2 mice. These results support our hypothesis that the simultaneous induction of Phase I and II drug metabolizing enzymes is the mechanism for the chemoprevention by Sudan III and suggest that strong induction of CYP1A might be essential for a protective effect.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1996

Lazaroid (U74500A) prevents vascular and myocardial dysfunction after 24-hour heart preservation. A study based on cross-circulated blood-perfused rabbit hearts.

BACKGROUND: The prevention of ventricular and vascular dysfunction has been recognized as an important factor in heart preservation. Because lipid peroxidation may cause cell membrane injury after ischemia and reperfusion, we hypothesized that the administration of a lipid peroxidation inhibitor lazaroid (U74500A) would result in an improvement of functional recovery after the 24-hour preservation period. METHODS AND RESULTS: An isolated rabbit heart preparation perfused with support rabbit blood was used. Before preservation, 4 mg/kg of either lazaroid or solvent was given to donor rabbits. The hearts were preserved with University of Wisconsin solution for 24 hours at 0 degree C. The working model preparation (n = 7 in each group) showed a better cardiac output (74.6 +/- 25.7 versus 192.7 +/- 19.6 mL/min, P < .0001) and a lower lipid peroxide level (2.1 +/- 1.3 versus 0.6 +/- 0.3 nmol/mL. P < .05) of the coronary effluent in the heart treated with lazaroid. With a Langendorff preparation (n = 7 in each group), we evaluated the vascular dilatory function. The endothelial function assessed by the percentage increase of coronary flow in response to acetylcholine in the solvent group was significantly lower than that of the lazaroid group (69 +/- 24% versus 140 +/- 67%, P < .05), whereas no significant difference was observed between the groups regarding endothelium-independent vasodilatation as assessed by the responses to nitroglycerin and nitroprusside. CONCLUSIONS: These results demonstrated an improved ventricular and endothelial function in the rabbit pretreated with lazaroid before preservation accompanied by a reduction of lipid peroxidation, indicating the potential benefits for long-term heart preservation.

Animals↗
PubMed1996

Cyclin D1 overexpression in primary hypopharyngeal carcinomas.

BACKGROUND: Hypopharyngeal squamous cell carcinomas (HPCS) are associated with an extremely poor prognosis. Generally, conventional clinicopathologic factors have only limited value as prognostic factors for this malignancy. It is therefore clinically important to identify new prognostic factors that accurately reflect the biologic aggressiveness of this malignancy. The amplification and overexpression of the cyclin D1 protooncogene have been reported in a variety of malignancies, and are thought to be related to tumor progression. Based on this phenomenon, the authors immunohistochemically evaluated overexpression of the cyclin D1 gene in 42 cases of primary HPCS. In addition, the immunohistochemical staining of the proliferation marker MIB-1 (Ki-67 antibody) was also performed. METHODS: Formalin fixed, paraffin embedded biopsy specimens obtained prior to treatment were examined. Cyclin D1 and Ki-67 were detected using monoclonal antibodies by means of the streptavidin-biotin method. The relationship between cyclin D1 overexpression and the stage, histologic grade, presence of lymph node metastases, proliferation index, and survival was then statistically analyzed. The correlation between the proliferation index, other clinicopathologic factors, and survival was also evaluated. RESULTS: Twenty-three (54.8%) HPCS specimens showed a 20% or greater immunoreactivity for cyclin D1. Cyclin D1 overexpression was related to cervical lymph node metastases (P = 0.037) but not to clinical stage, histologic grade, or the proliferation index. Cyclin D1 negative tumors were associated with a significantly better prognosis (P = 0.023), particularly in patients who underwent multimodality treatment. Finally, the MIB-1 labeling index showed no correlation with either the clinicopathologic parameters or overall survival. CONCLUSIONS: Based on these findings, cyclin D1 immunohistochemical staining is considered to be useful, not only as a prognostic factor for HPCS, but also as a means of determining the optimum treatment for each individual patient. Conversely, the MIB-1 labeling index appears to have no clinical significance in HPCS.

Adult↗