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Biomedical subjects

H Oda

Publications and source records attributed to H Oda.

At least 271 records · Page 15Linked to original sources
PubMed1995

Aortic arch malformations and ventricular septal defect in mice deficient in endothelin-1.

Endothelin-1 (ET-1) is a 21-amino acid peptide with various biological activities including vasoconstriction and cell proliferation. To clarify the physiological and pathophysiological role of ET-1, we disrupted the mouse Edn1 locus encoding ET-1 by gene targeting and demonstrated that ET-1 is essential to the normal development of pharyngeal arch-derived tissues and organs. In this study, we focused on the phenotypic manifestations of Edn1-/- homozygous mice in the cardiovascular system. Edn1-/- homozygotes display cardiovascular malformations including interrupted aortic arch (2.3%), tubular hypoplasia of the aortic arch (4.6%), aberrant right subclavian artery (12.9%), and ventricular septal defect with abnormalities of the outflow tract (48.4%). The frequency and extent of these abnormalities are increased by treatment with neutralizing monoclonal antibodies or a selective ETA receptor antagonist BQ123. At an earlier embryonic stage, formation of pharyngeal arch arteries and endocardial cushion is disturbed in Edn1-/- homozygotes. In situ hybridization confirmed ET-1 expression in the endothelium of the arch arteries and cardiac outflow tract and the endocardial cushion as well as in the epithelium of the pharyngeal arches. Thus, ET-1 is involved in the normal development of the heart and great vessels, and circulating ET-1 and/or other ET isoforms may cause a functional redundancy, at least partly, through the ETA receptor.

Animals↗
PubMed1995

A case of unprotected left main coronary stenosis rescued by directional coronary atherectomy as a last resort.

The prognosis of left main coronary stenosis complicating cardiogenic shock is very poor. Unprotected left main coronary stenosis usually preclude percutaneous transluminal coronary angioplasty because of the appearance of elastic recoil and the risk of hemodynamic collapse after acute closure of the artery. An 85-year-old woman with no history of heart disease developed cardiogenic shock. Coronary arteriography showed an unprotected left main coronary stenosis. Due to her advanced age, her family opposed coronary artery bypass surgery. We report here the successful treatment of this case of unprotected left main coronary stenosis by directional coronary atherectomy as a last resort.

Aged↗
PubMed1995

ATP receptor-mediated increase of Ca ionophore-stimulated arachidonic acid release from PC12 pheochromocytoma cells.

Phospholipase A2 has recently been proposed as the effector enzyme involved in the receptor-mediated release of arachidonic acid (AA). Released AA and its metabolites have been demonstrated to play an important role in the regulation of cell functions. [3H]AA release from prelabeled PC12 cells was stimulated by a Ca ionophore such as ionomycin or A23187. Although ATP and its effective analog, adenosine 5'-O-(3-thiotrisphosphate) (ATP gamma S), 2-methylthio ATP and 3'-O-(4-benzoyl)benzoyl ATP, did not stimulate [3H]AA release on their own, they did enhance Ca ionophore-stimulated [3H]AA release. The effect of ATP analogs was dose-dependent. ADP, UTP, GTP, ITP, alpha beta-methylene ATP, beta gamma-methylene ATP and 8-bromo ATP showed no effect or very limited effect. The effect of ATP gamma S was antagonized by suramin, a putative P2Y receptor antagonist. The effective ATP analogs also increased [Ca2+]i (cytosolic free Ca2+ concentration) via Ca2+ influx. However, the addition of 50 mM KCl or 10 microM bradykinin, which are well-known to increase [Ca2+]i by different pathways, did not stimulate [3H]AA release, either with or without the Ca ionophore. The addition of phorbol 12-myristate 13-acetate, an activator of protein kinase C, showed no effect on [3H]AA release, either with or without the Ca ionophore. These data suggest that 1) ATP increased Ca ionophore-stimulated AA release via a P2Y-like ATP receptor, and that 2) the elevation of [Ca2+]i by ATP does not quantitatively explain the ATP-stimulated AA release in PC12 cells.

Adenosine Triphosphate↗
PubMed1995

High cell density cultivation and high recombinant protein production of Escherichia coli strain expressing uricase.

Uricase from Cellulomonas flavigena SK-4 is an industrially useful enzyme for commercial formulations of hair coloring. The uricase production by recombinant Escherichia coli strain with a high cell density cultivation technique was described. Of three kinds of media, synthetic media with the feeding of a high concentration of glucose solution were suitable for high cell density cultivation. As for feeding, both biomass concentration and uricase productivity were increased by about two (61.2 g dry cell weight (DCW)/liter) and three times (1037 U/ml broth), respectively, in 24 h by continuous supply. In the case of feeding by a DO-stat method, however, cell concentration was comparable to continuous glucose supply but uricase activity was reduced. By supplying pure oxygen to compensate for oxygen limitation during cultivation, the highest values of 77.4g DCW/liter and 1113 U/ml broth of the uricase activity were achieved with the total cultivation time of 15 h.

Actinomycetales↗
PubMed1995

Leukotriene B4 in bronchoalveolar lavage fluid of patients with diffuse panbronchiolitis.

Leukotriene B4 (LTB4) is a potent proinflammatory mediator that may be of particular relevance to the pathology of several respiratory diseases. We have previously reported that neutrophil chemotactic mediators in the lavage fluid of patients with diffuse panbronchiolitis (DPB) consist of many components. In this study, we evaluated the effect of erythromycin (EM) on the pathogenesis of DPB, by examining the level of LTB4 in the bronchoalveolar lavage (BAL) fluid, and determining the relationship between the level and neutrophil accumulation into the respiratory tract. Pre-EM treatment neutrophil chemotactic activity (NCA) in the patients with DPB was significantly increased compared with that in five healthy nonsmoking volunteers (HVs) (p < 0.001), and the level was markedly reduced after EM treatment (p < 0.001). The amounts of LTB4, detected in the BAL fluid from the patients, was also significantly higher than those in control subjects (3.5 +/- 1.1 ng/mL vs 0.1 +/- 0.0 ng/mL, p < 0.001), and the level was significantly reduced after EM treatment (0.6 +/- 0.3 ng/mL, p < 0.01). In addition, the percent reduction of the level of LTB4 was significantly correlated with NCA (r = 0.832, p < 0.01); the reduction was also significantly correlated with neutrophil percentage before and after EM treatment (r = 0.778, p < 0.05). These findings provide evidence for the potent role of LTB4 in the respiratory tracts of patients with DPB and suggest that this lipoxygenase metabolite is involved in the recruitment of neutrophils into the airways of the patients. Our findings suggest that LTB4 is one of the most important chemotactic mediators that has a pathogenetic role in the airway damage of DPB. Erythromycin might inhibit the production of this mediator, restrict the neutrophil accumulation, modulate the excessive inflammation in the respiratory tract, and ultimately improve the pathogenesis of DPB.

Adult↗
PubMed1995

The effect of various bacteria and sera on functional activity of mouse macrophages.

The study has been performed to compare the ability of mouse peritoneal macrophages to ingest various types (catalase positive and negative) of bacteria and compared the influence of various sera on intracellular killing of Escherichia coli C (E. coli C). Among the tested microbes only E. coli C was ingested very luxuriantly and other organisms were taken up luxuriantly and moderately by mouse peritoneal resident macrophages (RMQs). Broad difference of ingestion was found even within the same genus (i.e., E. coli B and E. coli C). Intracellular killing of E. coli C by RMQs also varied depending on the type of serum. The maximum intracellular killing was found in the presence of normal mouse serum, although the difference was not much. The study has revealed that bacterial ingestion and intracellular killing ability of RMQs varies depending on bacterial strains and sera respectively.

Animals↗
PubMed1995

Glomerular localization of interleukin-6 suppressed by steroid mini-pulse therapy in an IgA nephropathy patient.

A 16-year-old female with IgA nephropathy harboring histologically active lesions was treated with steroid mini-pulse therapy. Immunohistochemical examination revealed a diffuse distribution of interleukin-6 (IL-6) in the renal biopsy tissue. After treatment, her clinical factors and renal function improved, and renal biopsy showed reduced histological lesions and disappearance of the IL-6 distribution. Immunohistological studies of cytokines, such as IL-6, may be useful for evaluating the therapeutic effects in IgA nephropathy.

Adolescent↗
PubMed1995

Role of the tissue renin-angiotensin system in the action of angiotensin-converting enzyme inhibitors.

The mechanism of the blood pressure-lowering action of chronic administration of angiotensin-converting enzyme (ACE) inhibitors is still controversial. We investigated the effects of the ACE inhibitors, captopril and perindopril, on the renin-angiotensin system (RAS) in plasma and tissues (adrenal gland and kidney) in the rat. Captopril or perindopril was infused intraperitoneally into rats via a mini-osmotic pump for 6 days at a rate of 0.5 or 0.25 mg/kg/hr, respectively. Perindopril markedly increased plasma renin concentration (PRC) from 12.7 +/- 1.1 to 867 +/- 59 ng Ang I/ml/hr and significantly inhibited plasma angiotensin II (Ang II) from 17.5 +/- 3.5 to 7.8 +/- 0.6 pg/ml and plasma ACE activity from 31.6 +/- 1.7 to 1.7 +/- 0.3 U/liter. Captopril also increased PRC from 12.1 +/- 2.1 to 147 +/- 17 ng Ang I/ml/hr. However, it did not inhibit plasma Ang II (20.6 +/- 1.9 vs 22.0 +/- 2.1 pg/ml, N.S.) and increased plasma ACE activity from 35.9 +/- 1.8 to 65.0 +/- 4.8 U/liter. Perindopril increased kidney renin from 625.3 +/- 84.6 to 2152.3 +/- 233.4 micrograms/g/hr, while captopril produced a modest but insignificant rise in kidney renin (708.0 +/- 107.1 vs 1083.3 +/- 155.5 micrograms Ang I/g/hr, N.S.). On the other hand, both captopril and perindopril decreased adrenal Ang II significantly (from 21.1 +/- 2.7 to 9.2 +/- 0.5 pg/capsule and from 15.5 +/- 2.9 to 2.0 +/- 0.6 pg/capsule, respectively). Adrenal renin was not altered by either treatment. In spite of no inhibition of plasma Ang II, the pressor response to intravenous Ang I was still suppressed after captopril treatment. Both captopril and perindopril lowered the blood pressure of the rats significantly. Our results support the hypothesis that inhibition of tissue RAS is important for the hypotensive action of ACE inhibition.

Adrenal Glands↗
PubMed1995

[Long-term results of surgical treatment for renal pelvic and ureteral tumors].

Fifty eight cases of primary tumors in the renal pelvis and ureter were treated at Toranomon Hospital between 1983 and 1992. They consisted of 32 renal pelvic tumors, 21 ureteral tumors and 5 tumors at both sites. The age of the patients ranged from 30 to 84 years (mean 63.1). Surgery was performed in 56 cases. Radical nephroureterectomy with concomitant ipsilateral retroperitoneal lymph node dissection was performed in 38 cases. The other surgeries were radical nephroureterectomy without lymph node dissection in 9, nephrectomy in 4, resection of ureter and reanastomosis in 3, radical nephroureterectomy and cystectomy in 1 and partial nephrectomy in 1. Pathologically, 53 were transitional cell carcinoma (TCC), 2 were TCC plus squamous cell carcinoma and 1 was TCC plus adenocarcinoma. Over-all survival rates (Kaplan-Meier) of 56 surgical cases at 1, 3, 5 years were 92.2, 83.7 and 72.8%, respectively. Combination chemotherapy (M-VAC or CAP) was performed in 9 cases of metastatic disease and 1 case of bilateral disease. Of these 10 cases, one achieved complete remission, 2 no change and 7 had progressive disease. Adjuvant chemotherapy was performed in 21 cases after surgery. These 21 patients were of high risk in recurrence either Grade 3 or pT3. However, the 5-year survival rate was 77.3% in these patients. Thus we conclude that the adjuvant chemotherapy in high risk patients was effective in our cases.

Adult↗
PubMed1995

Renal osteodystrophy in hemodialysis patients.

Patterns of bone loss in the axial and appendicular skeleton were studied in 88 chronic hemodialysis patients (59 males and 29 females) and 60 normal volunteers (30 males and 30 females). The hemodialysis patients were properly medicated with phosphate binders and 1 alpha-OH D3 where necessary. The metacarpal index (MCI), sigma gray scale/diameter (sigma GS/D) and bone mineral content (BMC) were measured as bone mass indices, and the relationship investigated between clinical factors [age, duration of hemodialysis, serum phosphate (P), calcium (Ca), carboxy-terminal fragments of parathyroid hormone (C-PTH), osteocalcin (OC), alkaline phosphate (ALP) and Ca x P]. The bone loss in the hemodialysis patients was greater than that in the normal controls and was accelerated after menopause in women. However, the bone mass indices in a few of the hemodialysis patients of advanced age (over 60) showed higher values than those of the controls. The bone mass indices in male hemodialysis patients showed a negative correlation with the hemodialysis duration, C-PTH and OC, as did those in female patients with hemodialysis duration. On the other hand, BMC in female hemodialysis patients showed a negative correlation with P, C-PTH and Ca x P. In conclusion, age and the duration of hemodialysis are the most essential factors in skeletal and trabecular bone loss in male and female hemodialysis patients. Subsequent factors responsible for skeletal bone loss in male patients are C-PTH and OC, and those for trabecular bone loss in female patients are P, C-PTH and Ca x P. Control of the levels of C-PTH, OC, P and Ca x P is recommended for prevention of bone loss in hemodialysis patients.

Adult↗
PubMed1995

Usefulness of immunoadsorption therapy for systemic lupus erythematosus associated with transverse myelitis. A case report.

Transverse myelitis (TM) is a very rare complication of systemic lupus erythematosus (SLE) and its prognosis is poor. It therefore needs to be treated aggressively. We describe a patient suffering from SLE associated with TM, who responded well to a combination of immunoadsorption therapy and steroid mini-pulse therapy. His serum interleukin 6 levels as well as clinical indicators fell to normal after this treatment.

Adult↗
PubMed1994

Michael addition-type 4-hydroxy-2-nonenal adducts in modified low-density lipoproteins: markers for atherosclerosis.

It has been proposed that plasma low-density lipoprotein (LDL) undergoes oxidative modification before it can give rise to foam cells in atherosclerosis. Oxidation of LDL generates a variety of reactive aldehyde products including 4-hydroxy-2-nonenal (HNE), which may covalently attach to the LDL apolipoproteins. We here present direct evidence that HNE derivatization of LDL forms Michael addition-type adducts of HNE with histidine and lysine residues of apolipoprotein B-100 (apoB) and also demonstrate the utility of an antibody specific to the HNE adducts generated in the LDL treated with HNE or oxidatively modified by Cu2+ or cultured endothelial cells. HNE adducts present in the LDL that had been treated with HNE were attested to be Michael addition-type adducts on the basis of the fact that incubation of LDL with 1 mM HNE (2 h, 37 degrees C) resulted primarily in the formation of Michael addition-type HNE-histidine (39.9 mol/mol of LDL) and HNE-lysine (19.3 mol/mol of LDL) adducts. An enzyme-linked immunosorbent assay (ELISA) and an SDS-polyacrylamide gel electrophoresis (SDS-PAGE)/immunoblot analysis of HNE-modified LDL demonstrated that these HNE adducts were detectable with the HNE-specific antibody affinity-purified with the Michael adduct (HNE-histidine) as a ligand. The following lines of evidence indicated the presence of Michael addition-type HNE adducts in the oxidatively modified LDL in vitro: (i) Amino acid analysis of LDL that had been treated with Cu2+ (24 h, 37 degrees C) demonstrated the presence of a Michael addition-type HNE-histidine adduct (7-9 mol/mol of LDL).(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehydes↗
PubMed1994

Detection of active UV-photoproduct repair in monkey skin in vivo by quantitative immunohistochemistry.

Ultraviolet-induced cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4)photoproducts in DNA were quantitatively measured in monkey skin using an immunohistochemical method with two specific monoclonal antibodies. The skins of Cynomolgus monkeys (Macaca fascicularis) were irradiated with UV light and processed for preparation of conventional formalin-fixed, paraffin-embedded histological sections. Both of the photoproducts were detectable in the nuclei of epidermal cells at doses of 500 J/m2 for UVB and 50 J/m2 for UVC, respectively, nuclear staining being clearly dose-dependent. Time course studies also showed a statistically significant decrease in nuclear staining with time after exposure to either UVB or UVC irradiation. Although only 30% of CPDs were removed from DNA in the first 24 h, about half of the (6-4) photoproducts were repaired within 3 h post-UV irradiation. Staining completely disappeared by 48 h in the (6-4) photoproduct case and by 72 h in the case of CPDs. The results suggest that epidermal cells of monkey skin can efficiently repair UV-photoproducts in DNA, but that the capacity is slightly less than in man.

Animals↗
PubMed1994

Additional ST-segment elevation immediately after reperfusion and its effect on myocardial salvage in anterior wall acute myocardial infarction.

Rapid resolution of ST-segment elevation is a reperfusion-associated electrocardiographic change in acute myocardial infarction. However, some patients have additional ST-segment elevation immediately after reperfusion before such resolution. The clinical significance and the effect on myocardial salvage of this electrocardiographic change are unknown. To examine this electrocardiographic feature and determine its clinical basis for occurrence and influence on left ventricular function, 58 consecutive patients with a first anterior wall acute myocardial infarction who had intracoronary thrombolysis or coronary angioplasty, or both, were assessed. With the use of frequent electrocardiographic procedures during reperfusion therapy, patients were divided in 2 groups: those with additional ST-segment elevation (n = 35; group A, > or = 0.5 mV increase in summed ST-segment elevation in lead V1-V6 within 15 minutes after reperfusion), and those without this phenomenon (n = 23; group B). Baseline characteristics, creatine kinase kinetics and left ventricular function were compared between both groups. Before reperfusion, group A had a greater summed ST-segment elevation (2.44 +/- 1.07 vs 1.57 +/- 0.98 mV; p = 0.003) and poorer collaterals (p = 0.001) than did group B. Peak creatine kinase was significantly higher in group A than in B (6,550 +/- 3,477 vs 4,310 +/- 1,880 IU/liter; p = 0.003). Group A had less improvement in ejection fraction (-4.2 +/- 9.9% vs 1.7 +/- 9.6%; p = 0.04) and regional wall motion (0.28 +/- 0.74 vs 0.76 +/- 0.79 SD/chord; p = 0.03) than did group B. It is thought that additional ST-segment elevation immediately after reperfusion occurred in myocardium with severe ischemic damage before reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Elevated blood pressure and craniofacial abnormalities in mice deficient in endothelin-1.

The endothelin-1 (ET-1) gene was disrupted in mouse embryonic stem cells by homologous recombination to generate mice deficient in ET-1. These ET-1-/- homozygous mice die of respiratory failure at birth and have morphological abnormalities of the pharyngeal-arch-derived craniofacial tissues and organs. ET-1+/- heterozygous mice, which produce lower levels of ET-1 than wild-type mice, develop elevated blood pressure. These results suggest that ET-1 is essential for normal mouse development and may also play a physiological role in cardiovascular homeostasis.

Animals↗
PubMed1994

A Drosophila homolog of cadherin associated with armadillo and essential for embryonic cell-cell adhesion.

We have identified a Drosophila homolog of vertebrate classic cadherins. A monoclonal antibody to Drosophila alpha-catenin (D alpha-catenin) copurifies a 150-kDa glycoprotein (gp150) along with the alpha-catenin. To further characterize this protein, we generated monoclonal antibodies to gp150 and isolated its cDNAs using the antibodies. Predicted sequences of the encoded product revealed that it is a transmembrane protein with similarity to vertebrate classic cadherins, and so we designated this molecule DE-cadherin. The extracellular domain has six cadherin-specific repeats, although the first repeat seems to be cleaved off upon maturation, and the cytoplasmic domain shows significant identity to that of vertebrate classic cadherins. DE-cadherin is distinguishable from its vertebrate counterparts by a large insertion with local sequence similarity to Fat, laminin A chain, Slit, and neurexin I at the proximal region of the extracellular domain. Despite such differences, DE-cadherin is functionally similar to vertebrate classic cadherins. For example, it is associated with alpha-catenin and beta-catenin (Armadillo), and protected from trypsin digestion only in the presence of Ca2+, as is the case for many of classic cadherins. Transfection of S2 cells with the DE-cadherin cDNA enhances their Ca(2+)-dependent cell aggregation. Antibodies to this molecule inhibited aggregation of not only the transfectants but also early embryonic cells. DE-cadherin is concentrated at the apical poles of epithelial cell-cell junctions. All these results suggest that DE-cadherin is a homolog of vertebrate classic cadherins and that the vertebrate and invertebrate share common mechanisms for regulation of cell-cell adhesion.

Amino Acid Sequence↗