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Biomedical subjects

H Masaki

Publications and source records attributed to H Masaki.

At least 73 records · Page 4Linked to original sources
PubMed1999

Angiotensin II type 2 receptor overexpression activates the vascular kinin system and causes vasodilation.

Angiotensin II (Ang II) is a potent vasopressor peptide that interacts with 2 major receptor isoforms - AT1 and AT2. Although blood pressure is increased in AT2 knockout mice, the underlying mechanisms remain undefined because of the low levels of expression of AT2 in the vasculature. Here we overexpressed AT2 in vascular smooth muscle (VSM) cells in transgenic (TG) mice. Aortic AT1 was not affected by overexpression of AT2. Chronic infusion of Ang II into AT2-TG mice completely abolished the AT1-mediated pressor effect, which was blocked by inhibitors of bradykinin type 2 receptor (icatibant) and nitric oxide (NO) synthase (L-NAME). Aortic explants from TG mice showed greatly increased cGMP production and diminished Ang II-induced vascular constriction. Removal of endothelium or treatment with icatibant and L-NAME abolished these AT2-mediated effects. AT2 blocked the amiloride-sensitive Na(+)/H(+) exchanger, promoting intracellular acidosis in VSM cells and activating kininogenases. The resulting enhancement of aortic kinin formation in TG mice was not affected by removal of endothelium. Our results suggest that AT2 in aortic VSM cells stimulates the production of bradykinin, which stimulates the NO/cGMP system in a paracrine manner to promote vasodilation. Selective stimulation of AT2 in the presence of AT1 antagonists is predicted to have a beneficial clinical effect in controlling blood pressure.

Actins↗
PubMed1999

Isolation and characterization of the actin gene from the cellulolytic fungus Humicola grisea and analysis of transcription levels of actin and cellulase genes.

An actin gene was isolated from the cellulolytic fungus Humicola grisea. The gene structure, which has 5 introns in the coding region, is similar to those of the so far cloned fungal actin genes. But there are some differences in intron sizes and codon usage. Transcription levels of actin and cellulase genes were also investigated.

5' Untranslated Regions↗
PubMed1999

Transcriptional regulation of the Bacillus ohbensis cyclodextrin glucanotransferase gene in B. subtilis.

The expression of the cyclodextrin glucanotransferase (CGTase) gene (cgt) of Bacillus ohbensis, when introduced into an alpha-amylase-defective strain of B. subtilis on a multicopy plasmid, pHY300PLK, was induced in the presence of starch and was subject to catabolite repression by glucose as well as in the original strain, B. ohbensis. We constructed a cgt'::'lacZ translational fusion to study the expression in B. subtilis, and this construct was confirmed to be subject to both starch induction and catabolite repression. In order to define the region involved in the regulation of the cgt gene, a series of cgt'::'lacZ gene with various lengths of deletion in the promoter region was constructed on pHY300PLK. DNA regions responsible for starch induction and catabolite repression by glucose could be separated in the deletion experiment. Primer extension analysis showed that the catabolite repression was controlled at the initiation of transcription, while the starch induction is likely to be controlled by a transcriptional termination-antitermination mechanism.

5' Untranslated Regions↗
PubMed1999

Primary aldosteronism with aldosterone-producing adrenal adenoma in a pregnant woman.

A 30-year-old pregnant woman complained of muscle weakness at 29 weeks' gestation. She was hypertensive with severe hypokalemia. Lower plasma renin activity and higher aldosterone level than the normal values in pregnancy suggested primary aldosteronism. A cesarean delivery was performed at 31 weeks' gestation because of pulmonary congestion. The neonatal course was uncomplicated. The laparoscopic adrenalectomy for a 2.0-cm right adrenal adenoma resulted in normalizing of her blood pressure and serum potassium level. Although primary aldosteronism is rare, especially during pregnancy, it should be always considered as one of etiologies of hypertension in pregnancy.

Adrenal Cortex Neoplasms↗
PubMed1999

Multiple spontaneous small bowel perforations due to systemic cholesterol atheromatous embolism.

A-65-year-old man was admitted for coronary and peripheral angiography to evaluate angina pectoris and peripheral vascular disease. Following angiography, he suffered from blue toes, livedo reticularis and progressive renal failure. The patient's condition continued to deteriorate, including the development of malnutrition. Four months later he suddenly developed panperitonitis, went into shock and died. The autopsy verified multiple perforations of the small bowel with disseminated cholesterol atheromatous embolism. The other organs including kidney were also invaded by atheroembolism. This was a rare case of multiple spontaneous perforations of small bowel due to systemic cholesterol atheromatous embolism.

Acute Kidney Injury↗
PubMed1999

Attachment of Burkholderia pseudomallei to pharyngeal epithelial cells: a highly pathogenic bacteria with low attachment ability.

Respiratory infections are initiated by the attachment of bacteria to pharyngeal epithelial cells. We studied the attachment of Burkholderia pseudomallei to pharyngeal epithelial cells. After one, two, three, and four washes, there were 22.6+/-8.9, 15.7+/-7.0, 6.8+/-3.1, and 4.6+/-1.1 (mean+/-SD) attached bacteria/cell, respectively. If the bacterial concentration was maintained at 1 X 10(8) colony-forming units (cfu)/ml and three washes were done, at concentrations of 2.5 x 10(4), 5 X 10(4), and 1 x 10(5) cells/ml there were 9.9+/-3.6, 3.3+/-0.8, and 2.5+/-1.1 attached bacteria/cell, respectively. If the cell concentration was kept at 2.5 x 10(4) cells/ml and three washes were done, at bacterial concentrations of 1 x 10(5), 1 X 10(6), 1 X 10(7), 1 x 10(8), and 1 x 10(9) cfu/ml, there were 0.3+/-0.3, 0.6+/-0.6, 1.0+/-0.2, 5.1+/-2.3, and 9.6+/-1.9 attached bacteria/cell, respectively. There were 4.8+/-1.9, 5.5+/-2.5, 5.6+/-1.9, and 6.4+/-2.6 attached bacteria/cell at 0, 30, 120, and 240 min of incubation, respectively. Pharyngeal cells from 10 persons (seven men and three women, mean+/-SD age = 30.7+/-8.1 years, 12 experiments with a single isolate) showed that there were 7.8+/-4.3 attached bacteria/cell. It was found that the efficiency of attachment of this bacteria was very low (7.0+/-3.3 bacteria/cell). Electron microscopy revealed that there were no fimbriae but a thin capsular polysaccharide layer on the surface of B. pseudomallei. Attachment to pharyngeal epithelial cells appeared to be mediated by this structure.

Adult↗
PubMed1999

Mediation of attachment of Burkholderia pseudomallei to human pharyngeal epithelial cells by the asialoganglioside GM1-GM2 receptor complex.

Melioidosis is the term given to any infection caused by Burkholderia pseudomallei. This bacteria is one of the important causative agents of life-threatening pulmonary infections in the tropical and subtropical areas. The initiation of respiratory infections is attachment of this bacteria to pharyngeal cells. The precise mechanism of attachment of B. pseudomallei is not known. In this study, we found that asialoganglioside GM1 at concentrations of 25, 12.5, and 5 microg/ml significantly decreased the attachment of B. pseudomallei strain Sp-186 in a dose-dependent manner. On the other hand, asialoganglioside GM2 decreased the attachment of B. pseudomallei, but only at a concentration of 25 microg/ml. At a concentration of 1 mg/ml, glucose, N-acetyl-galactosamine, and galactose caused a significant decrease in attachment. However, at concentrations of 250 microg/ml, no decrease in attachment was observed in B. pseudomallei treated with these carbohydrates. Mannose and fucose at concentrations of 1 mg/ml had no effects on the inhibition of attachment of B. pseudomallei. Four other isolates of B. pseudomallei showed a significant decrease in attachment after treatment with asialoganglioside GM1. We conclude that asialogangliosides GM1 and GM2 are part of the receptor complex for B. pseudomallei on human pharyngeal epithelial cells.

Bacterial Adhesion↗
PubMed1999

Differential kinetics of circulating angiotensin IV and II after treatment with angiotensin II type 1 receptor antagonist and their plasma levels in patients with chronic renal failure.

BACKGROUND: Angiotensin II (Ang II) C-terminal hexapeptide (referred to as Ang IV) possesses the characteristics of a real hormone with specific receptors and biological effects. Clinical application of Ang II type 1 receptor (AT1-R) antagonists cause an increase in plasma Ang II level, which may result in enhanced production of Ang IV. PATIENTS AND METHODS: In this study, we measured plasma Ang IV and Ang II levels in patients with chronic renal failure (CRF), and also examined the changes in Ang IV and Ang II levels after administration of an ATI-R antagonist. RESULTS: Ang II and Ang IV levels in CRF patients untreated with hemodialysis (n = 16) were 15.8+/-3.6 and 6.0+/-1.1 pg/ml, respectively, which did not differ significantly from Ang II (20.6+/-2.4) and Ang IV levels (8.6+/-1.1) in normal controls (n = 23). The ratio of Ang IV to Ang II was 38%, similar to that in the controls (41%). Ang II or Ang IV levels in CRF patients treated with hemodialysis (n = 12) were also similar to the control values. Ang IV levels had a significant correlation with Ang II levels (r = 0.59). When hypertensive patients were treated with an AT1-R antagonist candesartan for 7 days, Ang II and Ang IV levels were increased 5.5- and 4.1-fold relative to the control levels, respectively. Ang II levels 28 and 56 days after treatment were significantly lower than those 7 days after treatment, whereas Ang IV levels did not differ significantly from those 7 days after treatment. Similar differential kinetics in Ang II and Ang IV levels after long-term (90 days) treatment with an AT1-R antagonist was also confirmed in experiments using rats. Significant decrease in blood pressure continued during long-term treatment with an AT1-R antagonist. CONCLUSION: These findings demonstrated that plasma Ang IV levels in patients with CRF did not differ significantly from those in normal subjects, and that treatment with an AT1-R antagonist caused marked increases in both Ang II and Ang IV levels. In contrast, during long-term treatment plasma Ang II levels were more rapidly decreased than Ang IV levels, suggesting longer-lasting enhancement of the action of Ang IV rather than that of Ang II after treatment with an AT1-R antagonist.

Aged↗
PubMed1999

[Recent trends in radiation therapy for pediatric cancer].

A recent strategy in the treatment of pediatric cancer is the "total cell kill", in which the main part of therapy depends on intensive, aggressive chemotherapy with or without bone marrow transplantation. Radiotherapy, like surgery, plays a role in local treatment. Recent progress in therapy has permitted cures even of patients with advanced cancer. Disease-free patients should have the same quality of life as that of healthy children of the same sex and age. Therefore, both saving the patient's life and providing him or her with a good quality of life are important in treatment policy. To obtain these goals, radiation therapy has been included in combined multi-modality therapy for the management of pediatric cancer. Other important concerns are to reduce the radiation dose and determine the timing of radiation therapy.

Child↗
PubMed1998

Angiotensin II type 2 receptor is upregulated in human heart with interstitial fibrosis, and cardiac fibroblasts are the major cell type for its expression.

The expression pattern of angiotensin (Ang) II type 2 receptor (AT2-R) in the remodeling process of human left ventricles (LVs) remains poorly defined. We analyzed its expression at protein, mRNA, and cellular levels using autopsy, biopsy, or operation LV samples from patients with failing hearts caused by acute (AMI) or old (OMI) myocardial infarction and idiopathic dilated cardiomyopathy (DCM) and also examined functional biochemical responses of failing hearts to Ang II. In autopsy samples from the nonfailing heart group, the ratio of AT1-R and AT2-R was 59% and 41%, respectively. The expression of AT2-R was markedly increased in DCM hearts at protein (3.5-fold) and mRNA (3.1-fold) levels compared with AMI or OMI. AT1-R protein and mRNA levels in AMI hearts showed 1.5- and 2.1-fold increases, respectively, whereas in OMI and DCM hearts, AT1-R expression was significantly downregulated. AT1-R-mediated response in inositol phosphate production was significantly attenuated in LV homogenate from failing hearts compared with nonfailing hearts. AT2-R sites were highly localized in the interstitial region in either nonfailing or failing heart, whereas AT1-R was evenly distributed over myocardium at lower densities. Mitogen-activated protein kinase (MAPK) activation by Ang II was significantly decreased in fibroblast compartment from the failing hearts, and pretreatment with AT2-R antagonist caused an additional significant increase in Ang II-induced MAPK activity (36%). Cardiac hypertrophy suggested by atrial and brain natriuretic peptide levels was comparably increased in OMI and DCM, whereas accumulation of matrix proteins such as collagen type 1 and fibronectin was much more prominent in DCM than in OMI. These findings demonstrate that (1) AT2-R expression is upregulated in failing hearts, and fibroblasts present in the interstitial regions are the major cell type responsible for its expression, (2) AT2-R present in the fibroblasts exerts an inhibitory effect on Ang II-induced mitogen signals, and (3) AT1-R in atrial and LV tissues was downregulated during chronic heart failure, and AT1-R-mediated functional biochemical responsiveness was decreased in the failing hearts. Thus, the expression level of AT2-R is likely determined by the extent of interstitial fibrosis associated with heart failure, and the expression and function of AT1-R and AT2-R are differentially regulated in failing human hearts.

Adult↗
PubMed1998

Overproduction of recombinant Trichoderma reesei cellulases by Aspergillus oryzae and their enzymatic properties.

We have established an expression system of Trichoderma reesei cellulase genes using Aspergillus oryzae as a host. In this system, the expression of T. reesei cellulase genes were regulated under the control of A. oryzae Taka-amylase promoter and the cellulase genes were highly expressed when maltose was used as a main carbon source for inducer. The production of recombinant cellulases by A. oryzae transformants reached a maximum after 3-4 days of cultivation. In some cases, proteolysis of recombinant cellulases was observed in the late stage of cultivation. The recombinant cellulases were purified and characterized. The apparent molecular weights of recombinant cellulases were more or less larger than those of native enzymes. The optimal temperatures and pHs of recombinant cellulases were 50-70 degrees C and 4-5, respectively. Among the recombinant cellulases, endoglucanase I showed broad substrate specificities and high activity when compared with the other cellulases investigated here.

Aspergillus oryzae↗
PubMed1998

Angiotensin II type 1 receptor-induced extracellular signal-regulated protein kinase activation is mediated by Ca2+/calmodulin-dependent transactivation of epidermal growth factor receptor.

The signaling cascade elicited by angiotensin II (Ang II) resembles that characteristic of growth factor stimulation, and recent evidence suggests that G protein-coupled receptors transactivate growth factor receptors to transmit mitogenic effects. In the present study, we report the involvement of epidermal growth factor receptor (EGF-R) in Ang II-induced extracellular signal-regulated kinase (ERK) activation, c-fos gene expression, and DNA synthesis in cardiac fibroblasts. Ang II induced a rapid tyrosine phosphorylation of EGF-R in association with phosphorylation of Shc protein and ERK activation. Specific inhibition of EGF-R function by either a dominant-negative EGF-R mutant or selective tyrphostin AG1478 completely abolished Ang II-induced ERK activation. Induction of c-fos gene expression and DNA synthesis were also abolished by the inhibition of EGF-R function. Calmodulin or tyrosine kinase inhibitors, but not protein kinase C (PKC) inhibitors or downregulation of PKC, completely abolished transactivation of EGF-R by Ang II or the Ca2+ ionophore A23187. Epidermal growth factor (EGF) activity in concentrated supernatant from Ang II-treated cells was not detected, and saturation of culture media with anti-EGF antibody did not affect the Ang II-induced transactivation of EGF-R. Conditioned media in which cells were incubated with Ang II could not induce phosphorylation of EGF-R on recipient cells. Platelet-derived growth factor-beta receptor was not phosphorylated on Ang II stimulation, and Ang II-induced c-jun gene expression was not affected by tyrphostin AG1478. Our results demonstrated that in cardiac fibroblasts Ang II-induced ERK activation and its mitogenic signals are dominantly mediated by EGF-R transactivated in a Ca2+/calmodulin-dependent manner and suggested that the effects of Ang II on cardiac fibroblasts should be interpreted in association with the signaling pathways regulating cellular proliferation and/or differentiation by growth factors.

Animals↗
PubMed1998

Cardiac-specific overexpression of angiotensin II AT2 receptor causes attenuated response to AT1 receptor-mediated pressor and chronotropic effects.

Angiotensin (Ang) II has two major receptor isoforms, AT1 and AT2. Currently, AT1 antagonists are undergoing clinical trials in patients with cardiovascular diseases. Treatment with AT1 antagonists causes elevation of plasma Ang II which selectively binds to AT2 and exerts as yet undefined effects. Cardiac AT2 level is low in adult hearts, whereas its distribution ratio is increased during cardiac remodeling and its action is enhanced by application of AT1 antagonists. Although in AT2 knock-out mice sensitivity to the pressor action of Ang II was increased, underlying mechanisms remain undefined. Here, we report the unexpected finding that cardiac-specific overexpression of the AT2 gene using alpha-myosin heavy chain promoter resulted in decreased sensitivity to AT1-mediated pressor and chronotropic actions. AT2 protein undetectable in the hearts of wild-type mice was overexpressed in atria and ventricles of the AT2 transgenic (TG) mice and the proportions of AT2 relative to AT1 were 41% in atria and 45% in ventricles. No obvious morphological change was observed in the myocardium and there was no significant difference in cardiac development or heart to body weight ratio between wild-type and TG mice. Infusion of Ang II to AT2 TG mice caused a significantly attenuated increase in blood pressure response and the change was completely blocked by pretreatment with AT2 antagonist. This decreased sensitivity to Ang II-induced pressor action was mainly due to the AT2-mediated strong negative chronotropic effect and exerted by circulating Ang II in a physiological range that did not stimulate catecholamine release. Isolated hearts of AT2 transgenic mice perfused using a Langendorff apparatus also showed decreased chronotropic responses to Ang II with no effects on left ventricular dp/dt max values, and Ang II-induced activity of mitogen-activated protein kinase was inhibited in left ventricles in the transgenic mice. Although transient outward K+ current recorded in cardiomyocytes from AT2 TG mice was not influenced by AT2 activation, this study suggested that overexpression of AT2 decreases the sensitivity of pacemaker cells to Ang II. Our results demonstrate that stimulation of cardia AT2 exerts a novel antipressor action by inhibiting AT1-mediated chronotropic effects, and that application of AT1 antagonists to patients with cardiovascular diseases has beneficial pharmacotherapeutic effects of stimulating cardiac AT2.

Angiotensin II↗
PubMed1998

Overexpression of phospholamban alters inactivation kinetics of L-type Ca2+ channel currents in mouse atrial myocytes.

In mammalian ventricular myocytes, inactivation of L-type Ca2+ channels (CaCh) is controlled by voltage- and Ca2+-dependent mechanisms. The Ca2+-dependent component is regulated by the Ca2+ released from the sarcoplasmic reticulum (SR). However, little is known about the inactivation properties of CaCh in atrial myocytes, which lack spatial coupling between CaCh and SR Ca2+ release channels. The cardiac SR Ca2+ load is determined by the activity of SR Ca2+-ATPase, which is inversely regulated by the levels of phospholamban (PLB). To investigate the role of SR Ca2+ in atrial myocytes, Ca2+ currents (I Ca) were recorded in mouse atrial myocytes recorded from wild-type (WT) mice and the characteristics were compared to those obtained from atrial myocytes from the transgenic mice overexpressing PLB (PLB-OEX). ICa from WT exhibited fast and slow components of inactivation and the rate of inactivation was slowed when SR Ca2+ was depleted by caffeine, suggesting that the inactivation of atrial ICa is modulated by SR Ca2+ load. The current density and voltage-dependence of ICa were similar between the two groups. However, the fast component of inactivation was significantly reduced in PLB-OEX. When Ca2+ was replaced by Ba2+ or in the presence of caffeine, inactivation was slowed and the decay of the current was not significantly different between WT and PLB-OEX. These results suggest that the inactivation of ICa in mouse atrial myocytes involves Ca2+-dependent and voltage-dependent components. The decrease in the faster component of inactivation in PLB-OEX is consistent with the idea that CaCh and SR Ca2+ release channels are functionally coupled and Ca2+ released from the SR contributes the Ca2+-dependent inactivation component.

Animals↗
PubMed1998

[A case of ruptured descending thoracic aortic aneurysm due to Salmonella infection].

A 66-year-old male was admitted to our hospital because of pyrexia, chest pain and hemosptum. Inflammatory findings were made and salmonella enteritidis was detected by bacterial examination of sputum and stool. Enhanced chest CT examination disclosed a descending thoracic aortic aneurysm which had ruptured into the left lower lobe of the lung. Under a diagnosis of ruptured mycotic descending thoracic aortic aneurysm, an emergency operation was performed. A left posterolateral thoracotomy carried out after axillo-bilateral femoral bypass grafting. A pseudoaneurysm of the descending thoracic aorta had ruptured into the left lower lobe of the lung. After resection of the aneurysm, closure of both ends of the intact descending thoracic aorta and a left lower lobectomy were carried out. An ascending aorta-infrarenal abdominal aorta bypass was performed because of insufficient visceral arterial blood flow through the axillo-bilateral femoral bypass. The patient's immediate postoperative recovery was complicated by paraplegia. Chloramphenicol and levofloxacin were administered for three months, after which his recovery followed a good course.

Aged↗
PubMed1998

Differential role of catalase and glutathione peroxidase in cultured human fibroblasts under exposure of H2O2 or ultraviolet B light.

The purpose of this study was to elucidate the differential contribution of catalase and glutathione peroxidase (GSH-Px) to H2O2 scavenging in cultured human dermal fibroblasts. Responses of the cells in terms of both enzyme activities were examined by using two sorts of inhibitors, 3-amino-1H-1,2,4-triazole (AT) for catalase and DL-buthionine-[S,R]-sulfoximine (BSO) for GSH-Px, under exposure to H2O2 or ultraviolet (UV) B radiation. AT treatment resulted in a decrease in H2O2 scavenging activity, while BSO treatment did not affect H2O2 scavenging. When fibroblasts were exposed to a low concentration of H2O2 (100 microM). AT treatment resulted in a significant decrease in cell survival, but BSO treatment did not affect survival. At higher concentrations of H2O2 ranging from 500 microM to 1 mM, BSO-treated fibroblasts showed reduced survival. In addition, AT treatment was much more cytotoxic in the presence of UVB than BSO treatment. The intracellular levels of H2O2 in fibroblasts treated with AT or BSO were also determined. BSO-treated cells showed similar H2O2 levels to control cells, but the intracellular H2O2 levels of AT-treated fibroblasts were 1.4-fold higher than found in control cells. These results with human dermal fibroblasts indicate that catalase acts as a primary defence against oxidative stress from exogenous or endogenous H2O2 at low concentrations. In contrast, GSH-Px helps protect the cell from damage during exposure to high concentrations of H2O2.

Amitrole↗
PubMed1998

Enhanced negative slope of the readiness potential preceding a target force production task.

Readiness potentials (RPs) preceding a trigger pulling movement were recorded in 9 right-handed male subjects. We investigated two tasks, non-purposive and purposive movement tasks. In this study we defined simple trigger pull as non-purposive, and target force production by pulling the trigger as purposive. In the non-purposive task, the subjects were instructed to pull the trigger at their own pace and at an easily-exerted force level. After two sessions in the non-purposive movement task, the subjects were submitted to the purposive movement task, and were requested to pull the trigger in an attempt to produce target force, the range of which was decided individually on the basis of mean force level in the second session of the non-purposive movement task. The RP preceding the purposive movement was larger than that preceding the non-purposive movement. In addition, enhancement of the RP was specific to the negative slope (NS'). Since neither peak force nor time to peak force of the movement differed in the two tasks, it was concluded that the increased NS' was due to a psychological change associated with execution of the purposive movement.

Adult↗