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Biomedical subjects

H Ohashi

Publications and source records attributed to H Ohashi.

At least 163 records · Page 9Linked to original sources
PubMed1999

Classic Blalock-Taussig shunt in neonates.

BACKGROUND: The choice of palliative procedure for neonates with congenital cyanotic heart defects remains controversial. Several reports have questioned whether the classic Blalock-Taussig shunt is adequate in neonates, because it shows a high rate of mortality and early shunt failure. The purpose of this study is to evaluate the early and late results of classic Blalock-Taussig shunt in neonates. METHODS: From December 1981 to December 1996, 31 neonates underwent a classic Blalock-Taussig shunt. Mean age at operation was 15.9 days (range, 2 to 28 days), and mean body weight was 3214 g (range, 2229 to 4468 g). The major diagnoses were pulmonary atresia with intact ventricular septum (6 patients) and with ventricular septal defect (4), univentricular heart (6), tricuspid atresia (5), tetralogy of Fallot (4), transposition of the great arteries (3), and double outlet right ventricle (3). RESULTS: There were no early deaths. There was one early shunt failure. The patient underwent a replacement of Blalock-Taussig shunt by vascular graft on the 1st postoperative day. Two patients with non-confluent central pulmonary artery underwent a contralateral modified Blalock-Taussig shunt on the 22nd and 42nd postoperative day, respectively. There were two late deaths before the definitive repair was performed. Twelve patients required an additional shunt operation. The mean interval between the initial and the second shunt procedure was 27.7 months (range, 6 to 67 months). Ten patients underwent definitive operation and the mean interval to that procedure was 55.5 months (range, 14 to 121 months). Shunt patency was 94.7+/-5.1% at 3 years. The freedom from cardiac event (cardiac deaths or repeat shunting procedure) was 80.5+/-7.1% at 1 year and 54.9+/-9.4% at 3 years. CONCLUSIONS: The classic Blalock-Taussig shunt has a low operative mortality and has provided excellent long-term palliation in the neonate. We conclude that a classic Blalock-Taussig shunt should be considered a reasonable choice in neonates requiring a palliative procedure for congenital cyanotic heart defects.

Heart Defects, Congenital↗
PubMed1999

[Early postoperative results of coronary revascularization with the radial artery: an analytical study of vascular diameter ratio of the graft and the coronary artery].

Between October 1996 and June 1988, radial artery grafts were used in 49 patients undergoing myocardial revascularization. There were three hospital deaths, none of them due to the use of radial artery. In 32 patients studied early, 33 of 34 radial artery grafts were patent (patency 97%), and 30 of 32 internal thoracic artery grafts (94%), 32 of 35 saphenous vein grafts (90%), 3 of 3 gastroepiploic artery grafts (100%) were patent respectively. The mean diameter ratio of graft and recipient coronary artery was 1.03 +/- 0.17 in radial artery, 0.92 +/- 0.16 in internal thoracic artery and 1.67 +/- 0.55 in saphenous vein graft. Our result suggest that the radial artery is an excellent conduit for myocardial revascularization, although a longer follow-up is mandatory.

Adult↗
PubMed1999

Possible involvement of bcl-2 in regulation of cell-cycle progression of haemopoietic cells by transforming growth factor-beta1.

Transforming growth factor-beta1 (TGF-beta1) acts directly on haemopoietic progenitor cells to regulate their growth. To investigate a possible link between the action of TGF-beta1 and cell death regulators such as bcl-2, we utilized Ba/F3 cells, the interleukin-3 (IL-3)-dependent growth of which could be modulated by TGF-beta1, as well as haemopoietic progenitor cells. We demonstrate here that up-regulation of bcl-2 protein (Bcl-2) as well as that of an inhibitor of cyclin/cyclin-dependent kinase complex, p27, was associated with TGF-beta1-induced deceleration of the cell-cycling of haemopoietic progenitor cells and Ba/F3 cells. The data from cell-cycle analysis of Ba/F3 cells showed that TGF-beta1 retarded the G1 to S phase transition. Analysis of cells with the potential to express Bcl-2 in an inducible manner indicated that up-regulation of Bcl-2 was sufficient for not only an increase in the level of p27 but also to inhibit the cell growth. Using c-kit-overexpressing cells, we observed that the potential of TGF-beta1 to up-regulate the expression of Bcl-2 and p27 could be counteracted by the c-kit ligand, stem cell factor. These results demonstrate that Bcl-2 exerts an essential function in the regulation of G1 to S phase transition of haemopoietic cells by TGF-beta1.

Animals↗
PubMed1999

Clonality analysis of granulocytes and T lymphocytes in healthy females by the PCR-based HUMARA method.

Clonality analysis utilizing X-chromosome inactivation has been used in the study of various diseases, including hematological malignancies. The human androgen receptor gene (HUMARA) assay is the newest of such methods, and the majority of the female population can be assessed by this relatively simple procedure. One problem in using these clonality analysis methods, however, is that there may be significant variation in Lyonization in blood cells in normal individuals. To determine the diversity in X-chromosome methylation patterns, which reflect Lyonization, assessed by the HUMARA assay in the supposedly normal population, we analyzed granulocytes and T cells from 97 relatively young (18- to 35-year-old) healthy female volunteers. We found that the methylation patterns in the two HUMARA alleles were distributed even more widely, both in granulocytes and in T cells, than previously reported with other methods. We also found that the deviation of methylation in granulocytes and T cells was well correlated. Thus, we conclude that appropriate controls from the same individuals, such as T cells in the case of stem cell disorders, should always be employed to conclusively determine whether certain cells of hematopoietic origin are clonal.

Adolescent↗
PubMed1999

[Emergency coronary artery bypass grafting for acute coronary syndrome].

Emergency CABG for acute coronary syndrome (ACS) was studied. Sixty patients had CABG for medically refractory UAP, 78 patients for AMI and 8 patients for post-infarction angina (PIA). In UAP group 7 patients (12%) died postoperatively, mainly due to perioperative myocardial infarction (PMI) and operative complications. In AMI group, 26 patients (33%) died, 14 of them due to myocardial failure. The operative mortality was extremely high in shock-state patients group (48%) and cardiac pulmonary arrest state patients group (85%). Operative result was poor in those patients whose infarct-related artery was not recanalized preoperatively. Operative mortality was 13% in PIA group. It was concluded that the reduction of mortality of those patients required much refined myocardial preservation technique and powerful mechanical assist system to support the postoperative myocardial failure.

Aged↗
PubMed1999

Characterization of native human thrombopoietin in the blood of normal individuals and of patients with haematologic disorders.

Thrombopoietin (TPO) isolated from thrombocytopenic plasma of various animal species has previously been shown to comprise only truncated forms of the molecule, presumably generated by proteolysis. Native TPO has now been partially purified from normal human plasma by immunoaffinity chromatography and was confirmed to be biologically active. Gel filtration in the presence of SDS revealed that TPO eluted in two peaks: a major peak corresponding to the elution position of fully glycosylated recombinant human TPO (rhTPO) consisting of 332 amino acid residues, and a minor peak corresponding to a smaller molecular size. Immunoblot analysis also revealed that most plasma-derived TPO migrated at the same position as fully glycosylated rhTPO, corresponding to a molecular size of approximately 80 to 100 kDa. Furthermore, the size distribution of circulating TPO in patients with various haematologic disorders did not differ markedly from that of plasma-derived TPO from healthy individuals. These results indicate that the truncation of circulating TPO is not related to disease pathophysiology, and that the predominant form of TPO in blood is a biologically active approximately 80- to 100-kDa species. The size distribution of TPO extracted from normal platelets was similar to that of TPO in plasma; the proportion of truncated TPO was decreased by prior incubation of platelets with hirudin. indicating that the endogenous truncated TPO, at least in platelet extract, was generated by thrombin-mediated cleavage.

Hematologic Diseases↗
PubMed1999

[Treatment of cancer ascites by combined intraperitoneal administration of low-dose CDDP and reinfusion of ultra-filtrated and concentrated ascitic fluid in patients].

Ascites due to carcinomatous dissemination is a severe problem for end-stage cancer patients. We attempted treating patients on an outpatient basis with the administration of low-dose CDDP-i.p. and reinfusion of ultrafiltrated and concentrated ascites. From 1995, we performed this therapy on 16 patients with concentrated ascites 6-8 fold and reinfusion, combined with low-dose CDDP-i.p. and drip infusion of 5-FU intravenously. The ascitic fluid was significantly decreased after treatment in 8 patients, and 2 patients had lasting low concentrations of CA 125. CA 125 decreased in 83.3% of patients, who tended to have extended survival times after remarkable ascites pooling and treatment with low-dose CDDP-i.p. and reinfusion therapy. This treatment is a useful cant method for decreasing ascites and improving QOL.

Adult↗
PubMed1999

Predictors of survival in continuous ambulatory peritoneal dialysis patients: the importance of left ventricular hypertrophy and diabetic nephropathy.

We retrospectively evaluated the factors that are prognostic in long-term continuous ambulatory peritoneal dialysis (CAPD). From 1986 to 1997, 91 CAPD patients (59 male, 32 female, mean age 48 years) entered the study. Their primary renal diseases were chronic glomerulonephritis (CGN, n = 80), diabetic nephropathy (DN, n = 10), and polycystic kidney disease (PKD, n = 1). The roles of primary renal disease, hypertension, left ventricular hypertrophy (LVH), left ventricular ejection fraction (LVEF), cardiac sympathetic activity, anemia, hypoalbuminemia, and plasma concentration of parathyroid hormone (PTH) on patient prognosis were analyzed. Among the 91 CAPD patients, 26 died during the observation period. Of these deaths, 17 resulted from cardiovascular diseases including cerebrovascular events (n = 7), myocardial infarction (n = 2), sudden death (n = 7), and aortic aneurysmal rupture (n = 1). Nine patients died of non cardiovascular events. Sclerosing encapsulating peritonitis and others, mainly cachexia, accounted for 2 and 7 of these deaths, respectively. The 5-year survival rate was 74%; the 10-year rate was 49%. The cumulative 5- and 10-year success rates of CAPD were 69% and 39%, respectively. DN, hypertension, severe LVH (more than 200 g/m2), and hypoalbuminemia were contributors to poor prognosis. Among these, DN and severe LVH were the two main predictors by Cox proportional hazards model. We conclude that CAPD patients with DN or severe LVH, or both, have a greater chance of drop-out from cardiovascular events.

Aortic Aneurysm↗
PubMed1999

An autopsy report of graft-versus-host disease (GVHD) following blood transfusion.

A case of graft-versus-host disease (GVHD) associated with blood transfusion in a 71-year-old man is reported. The patient received transfusions (irradiation red cells M.A.P 14 units, fresh frozen plasma 11 units) and developed features of GVHD including fever, a skin rash, diarrhea, liver dysfunction, hypoplastic bone marrow, and pancytopenia. He died on day 32 posttransfusion. Pathologically, lymphocyte infiltration of skin and liver lesions, degeneration of small bile ducts, crypt cell necrosis in the gastrointestinal tract, and bone marrow hypoplasia were observed. Immunohistochemically, infiltrating lymphocytes were CD8+ T type, the result suggesting that they role a part in posttransfusion GVHD.

Aged↗
PubMed1998

Thrombopoietin induces association of Crkl with STAT5 but not STAT3 in human platelets.

Crkl, a 39-kD SH2, SH3 domain-containing adapter protein, is constitutively tyrosine phosphorylated in hematopoietic cells from chronic myelogenous leukemia (CML) patients. We recently reported that thrombopoietin induces tyrosine phosphorylation of Crkl in normal platelets. In this study, we demonstrate that thrombopoietin induces association of Crkl with a tyrosine phosphorylated 95- to 100-kD protein in platelets and in UT7/TPO cells, a thrombopoietin-dependent megakaryocytic cell line. With specific antibodies against STAT5, we demonstrate that the 95- to 100-kD protein in Crkl immunoprecipitates is STAT5. This coimmunoprecipitation was specific in that Crkl immunoprecipitates do not contain STAT3, although STAT3 becomes tyrosine phosphorylated in thrombopoietin-stimulated platelets. The coimmunoprecipitaion of Crkl with STAT5 was inhibited by the immunizing peptide for Crkl antisera or phenyl phosphate (20 mmol/L). After denaturing of Crkl immunoprecipitates, Crkl was still immunoprecipitated by Crkl antisera. However, coimmunoprecipitation of STAT5 was not observed. Coincident with STAT5 tyrosine phosphorylation, thrombopoietin induces activation of STAT5 DNA-binding activity as demonstrated by electrophoretic mobility shift assays (EMSA). Using a beta-casein promoter STAT5 binding site as a probe, we have also demonstrated that Crkl antisera supershift the STAT5-DNA complex, suggesting that Crkl is a component of the complex in the nucleus. Furthermore, interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), and erythropoietin also induce Crkl-STAT5 complex formation in responding cells in a stimulation-dependent manner. In vitro, glutathione S-transferase (GST)-Crkl bound to STAT5 inducibly through its SH2 domain. These results indicate that thrombopoietin, IL-3, GM-CSF, and erythropoietin commonly induce association of STAT5 and Crkl and that the complex translocates to the nucleus and binds to DNA. Interestingly, such association between STAT5 and Crkl was not observed in cytokine-stimulated murine cells, suggesting an intriguing possibility that components of the human STAT5-DNA complex may be different from those of the murine counterpart.

Acute-Phase Proteins↗
PubMed1998

Measurements of zeta potentials of particulate biomaterials in protein-rich hyaluronan solution with changes in pH and protein constituents.

This study was undertaken to determine the zeta potentials of particulate biomaterials in three types of protein-rich hyaluronan solution with changes in pH; a microelectrophoretic method was used. For the purpose of determining the pH value of synovial fluid in various inflammatory conditions, we collected synovial fluid samples from joints with osteoarthritis (OA), rheumatoid arthritis (RA), and those undergoing revisions arthroplasties. The mean values of the pH in the synovial fluid from joints with OA, RA, and revision arthroplasty were shown to be 7.9, 7.5, and 8.1, respectively. The pH-zeta potential curves obtained differed, depending on the biomaterial and the medium. Addition of gamma-globulin to the medium reduced the absolute value of the zeta potentials of some of the biomaterials. The findings of this study suggest that the electrophoretic behaviors of the particulate biomaterials tested in this study are affected by the protein constituents of and pH changes in protein-rich synovial fluid. The values we obtained will be useful as reference standards and will also aid in the study of the surface phenomena of biomaterials.

Biocompatible Materials↗
PubMed1998

Molecular cloning and characterization of human PDE8B, a novel thyroid-specific isozyme of 3',5'-cyclic nucleotide phosphodiesterase.

We have identified a novel human isozyme of 3',5'-cyclic nucleotide phosphodiesterase (PDE), which we designated PDE8B. cDNA of 2844 bp encoding the C-terminal 659 amino acids of PDE8B was cloned following the identification of an expressed sequence tag (EST) obtained through a search of the EST database. The predicted protein sequences of PDE8B showed highest homology (65% identity, 83% similarity) to that of PDE8A. Northern blot analysis indicated that the mRNA encoding PDE8B is expressed specifically and abundantly in thyroid gland as a approximately 4.2 kb mRNA, in contrast to the wide expression of PDE8A mRNA in various tissues. The carboxyl-terminal 584 amino acids of PDE8B were expressed in E.coli as a fusion protein. The recombinant PDE8B exhibited cAMP PDE activity which was not inhibited by various PDE inhibitors including vinpocetine, milrinone, rolipram, and IBMX with the exception of dipyridamole which caused 50% inhibition at a concentration of 40 microM. cAMP hydrolytic activity was unaffected by cGMP and no cGMP PDE hydrolysis were detectable at concentrations up to 100 microM. These findings suggest that PDE8B is a new member of the PDE8 family.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1998

Carbachol-induced oscillations in membrane potential and [Ca2+]i in guinea-pig ileal smooth muscle cells.

1. Cytosolic free Ca2+ concentration ([Ca2+]i) and membrane potential were simultaneously recorded from single smooth muscle cells of guinea-pig ileum, using a combination of nystatin-perforated patch clamp and fura-2 fluorimetry techniques. 2. Carbachol (CCh, 2 microM) produced oscillatory changes in [Ca2+]i and membrane potential which coincided well in time with each other, and peaks of membrane potential oscillations reached a saturated level of around -7 mV. Thapsigargin (1 microM) abolished these effects of 2 microM CCh. La3+ (3 microM) immediately prevented the discharge of spike potentials, but allowed both on-going oscillatory responses to persist for a while. 3. CCh (0.25-0.75 microM) caused membrane potential and [Ca2+]i to oscillate in some 20 % of cells studied. Every membrane potential oscillation was preceded by the discharge of single or multiple spike potentials. The effects of CCh were readily abolished by La3+ (3 microM). 4. In cells exhibiting no oscillatory response to 0.25-0.75 microM CCh, an electrically evoked action potential usually generated changes in [Ca2+]i and membrane potential similar to those following spontaneously evoked action potentials, and sometimes it did so only after [Ca2+]i or InsP3 had been slightly elevated by repeatedly evoking action potentials or by increasing CCh concentration in the bath medium. 5. The results suggest that in ileal smooth muscle cells, the oscillations of [Ca2+]i and membrane potential arising from muscarinic stimulation result from release of Ca2+ from internal stores and that there is a Ca2+-induced potentiation of coincidently elicited cation channel openings. Under weak muscarinic stimulation, Ca2+ entry upon action potential discharge can trigger such a release of stored Ca2+, resulting in synchronous generation of a large rise in [Ca2+]i and a slow, large membrane depolarization.

Action Potentials↗
PubMed1998

Standard transport channels of X-ray beamlines at SPring-8.

SPring-8 is constructing most of its beamlines using a combination of standardized components. The structures of the beamlines are also standardized according to the light-source characteristics. Specifications of components as well as the unified method of assembly and alignment are described.

Journal Article↗
PubMed1998

Pseudoachondroplasia with de novo deletion [del(11)(q21q22.2)].

Pseudoachondroplasia (PSACH) is a relatively common osteochondrodysplasia characterized clinically by short-limbed short stature with normal face, and radiographically by platyspondyly and dysplasias of epiphyses and metaphyses of the tubular bones. Recently, mutation of cartilage oligomeric matrix protein has been identified in PSACH. However, clinical variability and genetic heterogeneity have been reported in PSACH, indicating a possible existence of a second PSACH gene. Here, we report on a patient with a typical severe form of PSACH who had a de novo interstitial deletion in the long arm of chromosome 11 [del(11)(q21q22.2)]. The size of the deletion was estimated at 0.8-7.3 Mb using fluorescent in situ hybridization (FISH). This deletion may contain or disrupt a second PSACH locus.

Achondroplasia↗