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Biomedical subjects

H Oda

Publications and source records attributed to H Oda.

At least 217 records · Page 12Linked to original sources
PubMed1997

An autopsied case of acute myocarditis with myocardial calcification.

A 47-year-old woman was admitted with fever, hypotension, an elevated serum creatinine kinase level, and electrocardiographic abnormalities, which led to the diagnosis of acute myocarditis. She was placed on percutaneous cardiopulmonary support because of hemodynamic collapse on the third hospital day. Serial echocardiography showed gradual recovery of profound hypokinesis and edematous thickening of the left ventricle, but she died of sepsis on the 17th day without overt renal insufficiency or electrolytic abnormalities. Autopsy revealed myocardial necrosis with lymphocytic infiltrates and extensive myocardial calcification. Calcification was dense in the area of severe myocardial necrosis, and the distribution of calcium deposits suggested that the calcification was a consequence of significant inflammation of the myocardium. Recovery of regional wall motion was prominent in the area of severe inflammatory change. Dissociation between the pathologic and echocardiographic findings suggested the possibility of functional reversibility of severely damaged myocardium and possible mechanisms of abnormal contractile function other than inflammatory change.

Acute Disease↗
PubMed1997

High responsiveness to thyroid hormone of adult rat primary hepatocytes cultured on EHS-gel.

The induction of malic enzyme gene expression by triiodothyronine and insulin was severely blunted in rat monolayer hepatocytes cultured on type I collagen compared with that in spherical hepatocytes cultured on a reconstituted basement membrane gel (EHS-gel). Although the mRNA level of thyroid hormone receptor beta (TR beta) gradually decreased in the monolayer hepatocytes during culture, the mRNA level in the hepatocytes on EHS-gel was maintained at around the in vivo level. Our results suggest that the maintenance of TR beta mRNA on EHS-gel is responsible for the high responsiveness to thyroid hormone in a hepatocyte culture.

Animals↗
PubMed1997

A case of nonpenetrating traumatic aortic regurgitation detected by transesophageal echocardiography.

A 67-year-old man, who had fell 5 meters, landing on his back, one month before, was referred because of heart failure due to aortic regurgitation (AR). Transesophageal echocardiogram (TEE) confirmed injuries in the aortic valve and the Valsalva sinus of the aorta before the surgery: the intimal flap in the Valsalva sinus of right coronary cusp (RCC), the prolapse of the RCC, and the dissection by longitudinal length of 3 cm in the Valsalva sinus of noncoronary cusp (NCC), ending as a blind pouch. Postoperative TEE confirmed the dissection was not repaired in the Valsalva sinus of the NCC. In this instance, TEE was extremely useful, compared with transthoracic echocardiography, computed tomography and magnetic resonance imaging, to assess the mechanism of AR following a nonpenetrating trauma, and to know to what degree the aortic valve and the Valsalva sinus of the aorta were destroyed.

Aged↗
PubMed1997

Thoracic myelopathy due to intraspinal rheumatoid nodules.

A fifty-six-year-old woman with classical rheumatoid arthritis had subacute onset of paraparesis due to thoracic epidural rheumatoid nodules. Although plain radiograms and computed tomograms of the thoracic spine were negative except for old compression fractures, magnetic resonance imaging revealed thoracic spinal cord compression due to masses at multiple levels. There was a steady recovery after excision surgery.

Female↗
PubMed1997

High concentration of recombinant murine interferon-beta enhances the growth of Orientia (formerly Rickettsia) tsutsugamushi Gilliam in mouse L929 cells.

We studied the effect of recombinant murine interferons (rMuIFNs) on the growth of Orientia (formerly Rickettsia) tsutsugamushi Gilliam in mouse L929 cells. Rickettsial growth was measured by flow cytometry. rMUIFN-gamma inhibited the growth of O. tsutsugamushi at the concentrations of 100 i.u./ml and 1,000 i.u./ml in accord with previous reports. Relatively low concentrations (10 i.u./ml and 100 i.u./ml) of rMUIFN-beta also inhibited the growth of O. tsutsugamushi. On the other hand, high concentrations (1,000 i.u./ml and 10,000 i.u./ml) of rMuIFN-beta enhanced the growth of the rickettsia. This enhancement of rickettsial growth was blocked by anti-murine IFN-beta monoclonal antibody (MoAb). rMuIFN-beta also enhanced the growth of Rickettsia sibirica 246 in L929 cells to some extent.

Animals↗
PubMed1997

Role of intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and macrophages in ddY mouse nephropathy.

ddY mouse nephropathy is an animal model of human IgA nephropathy that is characterized by spontaneous IgA deposition in the glomerular mesangium, mesangial cell proliferation, and matrix expansion. We investigated the involvement of intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and macrophages in the pathogenesis of ddY mouse nephropathy. Five mice each underwent urinalysis, light microscopic examination of the kidneys, immunofluorescent detection of immunoglobulins and complement, and immunohistochemical examination for intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and infiltrating macrophages at 5, 10, 20, 30, 40, 50, 60, and 70 weeks of age. Albuminuria was observed from the age of 20 weeks and all mice showed albuminuria by 70 weeks. Histological glomerular damage was significantly related to the appearance of albuminuria (p < 0.01). In the glomeruli, positivity for intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1, as well as the number of infiltrating macrophages, were significantly increased in mice with nephropathy compared to pre-nephropathy mice (p < 0.01). These results suggest that intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and infiltrating macrophages are involved in the progression of histological damage in ddy mouse nephropathy.

Animals↗
PubMed1997

[Non-Hodgkin's lymphoma associated with polymyositis].

A 67-year-old man was admitted to with severe nasal congestion. One year previously, he had been suffered from polymyositis (PM) and had been treated with prednisolone. Physical examination and computed tomography revealed a mass in the upper pharynx. Biopsy revealed non-Hodgkin's lymphoma (diffuse medium, B-cell type). Bone marrow aspiration also revealed the infiltration by lymphoma cells. The patient achieved a complete remission after combination chemotherapy (cyclophosphamide, adriamycin, vincristine, prednisolone). However, one month later, he suffered from central nervous system involvement of lymphoma cells, and he died of an aspiration pneumonia. Polymyositis/dermatomyositis associated with non-Hodgkin's lymphoma is extremely rare.

Aged↗
PubMed1997

Lipids in progression of renal disease.

There is increasing evidence for the role of hyperlipidemia as a contributing factor to the progression of chronic renal disease. Experimental studies in animal models suggest that lipids might be important modulators in progressive renal disease. On one hand maneuvers designed to elevate cholesterol worsen renal disease while reduction of lipid-lowering agents have demonstrated beneficial effects. In humans, correcting abnormalities in lipid metabolism with antilipemic therapy may help slow the rate of functional decline in patients with progressive renal disease as well as reduce the frequency of acute rejection after renal transplantation. However, large controlled clinical trials examining the effect of lipid-lowering strategies on progression of renal disease have not been carried out. Further clinical trials delineating the precise role of antilipemic agents in treating patients with renal disease appears warranted.

Animals↗
PubMed1997

Irbesartan lowers blood pressure and ameliorates renal injury in experimental non-insulin-dependent diabetes mellitus.

In the present study, we investigated the effects of the angiotensin (Ang) II receptor antagonist, irbesartan, on blood pressure and renal structural injury in obese Zucker rats (OZR), an experimental model of non-insulin-dependent diabetes mellitus (NIDDM). Twenty-six-week-old OZR with established renal disease were administered either low-dose (15 mg/kg) or high-dose (50 mg/kg) irbesartan in the drinking water for a period of 18 weeks. Irbesartan caused dose-related reductions in blood pressure, and reduced by 47 to 60% the percent of glomeruli with sclerosis at 44 weeks of age (P < 0.05). In addition, irbesartan at the higher dose reduced the tubulointerstitial injury score at 44 weeks by approximately 75% (P < 0.05). By contrast, irbesartan did not significantly reduce albuminuria in OZR. The results of the present study demonstrate that the Ang II receptor antagonist irbesartan can reduce blood pressure and ameliorate glomerular and tubulointerstitial injury in an experimental model of NIDDM.

Albuminuria↗
PubMed1997

[A case of allergic bronchopulmonary aspergillosis caused by Aspergillus terreus].

A 66-year-old woman was admitted to our hospital with a cough, wheezing, and expectoration. Chest X-ray and CT scanning revealed atelectasis and infiltration of the middle lobe, but no central bronchiectatic change. The patient had eosinophilic infiltration elevated serum IgE, RAST against Aspergillus )(A.) fumigatus, a positive immediate skin reaction, and a positive test for antibodies against A. funmigatus. Bronchoscopy demonstrated mucoid impaction that plugged the middle lobe bronchus. The mucoid plug contained A. terreus and numerous eosinophils. Because the level of the precipitating antibody for counter immunoelectrophoresis against A. terreus was higher than that at A. fumigatus, allergic bronchopulmonary aspergillus caused be A. terreus was diagnosed. Oral and inhalation therapy of corticosteroids ameliorated the symptoms and abnormal laboratory findings.

Aged↗
PubMed1996

Drosophila alpha-catenin and E-cadherin bind to distinct regions of Drosophila Armadillo.

Adherens junctions are multiprotein complexes mediating cell-cell adhesion and communication. They are organized around a transmembrane cadherin, which binds a set of cytoplasmic proteins required for adhesion and to link the complex to the actin cytoskeleton. Three components of Drosophila adherens junctions, analogous to those in vertebrates, have been identified: Armadillo (homolog of beta-catenin), Drosophila E-cadherin (DE-cadherin), and alpha-catenin. We carried out the first analysis of the interactions between these proteins using in vitro binding assays, the yeast two-hybrid system, and in vivo assays. We identified a 76-amino acid region of Armadillo that is necessary and sufficient for binding alpha-catenin and found that the N-terminal 258 amino acids of alpha-catenin interact with Armadillo. A large region of Armadillo, spanning six central Armadillo repeats, is required for DE-cadherin binding, whereas only 41 amino acids of the DE-cadherin cytoplasmic tail are sufficient for Armadillo binding. Our data complement and extend results obtained in studies of vertebrate adherens junctions, providing a foundation for understanding how junctional proteins assemble and a basis for interpreting existing mutations and creating new ones.

Amino Acid Sequence↗
PubMed1996

Insulin suppresses the induction of CYP2B1 and CYP2B2 gene expression by phenobarbital in adult rat cultured hepatocytes.

The effect of insulin on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated. Insulin, which has been regarded as an essential hormone for primary hepatocytes, was found to strongly suppress the induction of CYP2B1/2B2 gene expression in hepatocytes cultured on EHS-gel. Although the induction by PB was not seen in monolayer hepatocytes cultured on type I collagen under standard culture conditions, the induced expression of the CYP2B1/2B2 gene was observed in monolayer hepatocytes by removing insulin from the medium. Further, we succeeded in maintaining the prolonged induction of CYP2B1/2B2 by PB in monolayer hepatocytes by using a medium containing dexamethasone but not insulin. Since the PB-induced UDP-glucuronosyltransferase gene expression was not reduced by insulin, the suppressive effect of insulin was considered to be specific to the CYP2B1/2B2 gene. These results demonstrate that insulin in media masks the PB-induced expression of the CYP2B1/2B2 gene in conventional monolayer hepatocytes and that the use of insulin-free media with primary hepatocytes provides a useful tool for investigating the molecular mechanism of CYP2B1/2B2 gene expression.

Animals↗
PubMed1996

Marked expression of plasma brain natriuretic peptide is a special feature of hypertrophic obstructive cardiomyopathy.

OBJECTIVES: We examined whether plasma brain natriuretic peptide levels are abnormally elevated in hypertrophic obstructive cardiomyopathy compared with other cardiac diseases. BACKGROUND: We previously reported that plasma brain and atrial natriuretic peptide levels were elevated in hypertrophic cardiomyopathy. METHODS: We compared plasma concentrations of brain and atrial natriuretic peptide and hemodynamic and echocardiographic data in 50 patients with hypertrophic obstructive cardiomyopathy (n = 15, mean [+/-SD] intraventricular pressure gradient 37 +/- 16 mm Hg), hypertrophic nonobstructive cardiomyopathy (n = 15), aortic stenosis (n = 10, mean pressure gradient 41 +/- 18 mm Hg) and hypertensive heart disease (n = 10, mean systolic/diastolic blood pressure 203 +/- 16/108 +/- 11 mm Hg, respectively) and 10 normal subjects. RESULTS: Plasma brain natriuretic peptide levels were higher in the hypertrophic obstructive cardiomyopathy group (397.1 +/- 167.8 pg/ml*) than in the hypertrophic nonobstructive cardiomyopathy (60.0 +/- 48.1 pg/ml*), hypertensive heart disease (53.9 +/- 31.4 pg/ml*), aortic stenosis (75.4 +/- 54.3 pg/ml*) and normal groups (9.8 +/- 6.4 pg/ml [*p < 0.05 vs. normal group, p < 0.05 vs. hypertrophic obstructive cardiomyopathy group]). Although plasma atrial natriuretic peptide levels were higher in the hypertrophic obstructive cardiomyopathy group than the other patient groups, the brain/atrial natriuretic peptide ratio in the hypertrophic obstructive cardiomyopathy group was higher (4.5 +/- 2.3) than those in the other three patient groups (1.1 to 1.4) and the normal group (0.7 +/- 0.5). Left ventricular end-diastolic pressure and left ventricular end-diastolic volume index were similar among the four patient groups. The interventricular septal thickness and the ratio of interventricular septal thickness to left ventricular posterior wall thickness were similar between the hypertrophic obstructive and nonobstructive cardiomyopathy groups. CONCLUSIONS: Abnormal elevations of plasma brain natriuretic peptide levels are difficult to explain on the basis of hemodynamic and echocardiographic data and are a special feature of hypertrophic obstructive cardiomyopathy.

Adult↗
PubMed1996

G(o) protein does not regulate ATP-stimulated [Ca2+]i elevation or noradrenaline release in PC12 cells.

The roles of G(o), a heterotrimeric GTP binding (G) protein with a 40-kDa alpha subunit and which is localized predominantly in neuronal cells, in exocytosis have been discussed recently. PC12 pheochromocytoma cell line is a convenient model in which to study the Ca(2+)-dependent mechanisms of the neurosecretory process. The stimulation of ATP receptors or addition of KCl stimulated an elevation of cytosolic free Ca2+ concentration ([Ca2+]i) and [3H]noradrenaline (NA) release in PC12 cells. In this study, we investigated the roles of G(o) in ATP- and KCl-stimulated reactions. Nerve growth factor treatment for 2 days and transfection of PC12 cells with cDNA of subunit of (G(o alpha) had no effect on ATP-stimulated [3H]NA release, although both treatments increased levels of the G(o alpha) and its trimeric form by about twofold over those in unstimulated cells. The [Ca2+]i rise induced by ATP in NGF-treated cells was similar to that in control cells, although the maximal response was slightly smaller. Cholera toxin treatment for 2 days inhibited ATP- and KCl-stimulated NA release, although this treatment caused an approximately twofold increase in the level of G(o). Pertussis toxin treatment, which ADP ribosylated over 90% of endogenous G proteins such as G(o), had no effect on ATP-stimulated reactions. These findings show that G(o) does not directly regulate ATP-stimulated Ca2+ channels or the NA release process in PC12 cells. Cholera toxin-sensitive protein(s) may regulate exocytosis.

Adenosine Triphosphate↗
PubMed1996

Somatic mutations of the APC gene in sporadic hepatoblastomas.

Hepatoblastoma is a rare hepatic malignancy that occurs in children with an average age of 2 or 3 years and is known to be one of the extracolonic manifestations of familial adenomatous polyposis. Only a single hepatoblastoma with a germ-line mutation of the adenomatous polyposis coli (APC) gene has been reported thus far. To elucidate the possible roles of APC gene alterations in sporadic hepatoblastomas, we examined loss of heterozygosity (LOH) at the APC and MCC loci and performed a sequencing analysis of a part of the APC gene, including the mutation cluster region, in 13 hepatoblastomas of non-familial adenomatous polyposis patients. LOH at the APC and/or MCC loci was observed in four of seven (57%) informative cases. Of the 13 cases, somatic mutations were detected in 8 (61.5%), with 9 (69%) cases showing genetic alterations in the APC gene as LOH or somatic mutations. Two cases demonstrated double mutations. Furthermore, the nature of the somatic mutations observed in the present study was unusual because 9 of the 10 mutations were missense, with only 1 case featuring a frame-shift mutation due to an insertion. Previous reports have described almost all (>90%) mutations of the APC gene in colorectal tumors to result in a truncated APC protein due to either frame-shift or nonsense mutations. These findings suggest that a mutation of the APC gene may play an important role in the genesis of sporadic hepatoblastomas, and the mechanisms of APC gene alteration may be different from those reported previously for colorectal tumors.

Base Sequence↗
PubMed1996

Oxidative stress response in iron-induced renal carcinogenesis: acute nephrotoxicity mediates the enhanced expression of glutathione S-transferase Yp isozyme.

An iron chelate, ferric nitrilotriacetate (Fe-NTA), induces acute renal proximal tubular necrosis, a consequence of free radical-mediated oxidative tissue damage, that eventually leads to a high incidence of renal adenocarcinoma in rodents. In the present study, we investigated the free radical-induced oxidative stress response in this carcinogenesis model, focusing on the expression of glutathione S-transferases (GSTs) which catalyze the conjugation of reactive chemicals with glutathione and play an important role in protecting cells. A single intraperitoneal Fe-NTA treatment (15 mg Fe/kg body weight) induced a rapid oxidative stress, which was monitored by the accumulation of lipid peroxidation products and the loss of sulfhydryl contents in the kidneys, resulting in a 30% reduction of GST activity 1 h after an Fe-NTA treatment. The enzyme activity returned to the control level after 16 h. The immunoblot analysis of GST isozymes demonstrated that the level of alpha-class GSTs (GST-Ya and GST-Yc) and pi-class GST (GST-Yp), major GST isozymes constitutively produced in the kidney, decreased immediately within 1 h of the Fe-NTA treatment. The onset of the recovery of GST-Yp protein levels was detected 3 h after the Fe-NTA treatment. The enhanced production of GST-Yp in gene expression was evident in the drastic elevation of mRNA levels and these increases coincided with a substantial rise in the GST activity and protein levels. The alpha-class GSTs were not inducible by treatment with Fe-NTA. The immunohistochemical analysis demonstrated that the expression of GST-Yp was strongly induced in the regenerating proximal tubular cells. A steady accumulation of GST-Yp protein was observed in the subacute toxicity experiments with multiple injections of Fe-NTA. These results suggest that the enhanced expression of GST-Yp is important in mediating cell repairs or increasing the resistance to subsequent injury.

Adenocarcinoma↗
PubMed1996

Zygotic Drosophila E-cadherin expression is required for processes of dynamic epithelial cell rearrangement in the Drosophila embryo.

Dynamic epithelial reorganization is essential for morphogenesis of various organs. In Drosophila embryos, for example the Malpighian tubule is generated by cellular rearrangement of a preexisting epithelium and the tracheal network is formed by outgrowth, branching, and fusion of epithelial vesicles. Here we report that the previously identified locus shotgun (shg) encodes DE-cadherin, an epithelial cell-cell adhesion molecule of the classic cadherin type and that zygotic shg mutations rather specifically impair processes of the dynamic epithelial morphogenesis. In the mutants, the Malpighian tubule disintegrated into small spherical structures, and the tracheal network formation was blocked in selected steps. The malformation of these organs could be rescued by overexpression of DE-cadherin cDNA under a heat shock promoter. Unexpectedly, the zygotic null condition did not severely affect general epithelial organization; most epithelial tissues maintained not only their cell-cell associations but also their apicobasal polarity in the mutants. The zygotic null mutant retained a certain level of maternally derived DE-cadherin molecules until the end of embryogenesis. These results suggest that zygotic DE-cadherin expression is critical for the rearrangement processes of epithelial cells, whereas the maternally derived DE-cadherin may serve only for the maintenance of the static architecture of the epithelia.

Animals↗