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Biomedical subjects

Y Sekine

Publications and source records attributed to Y Sekine.

At least 19 recordsLinked to original sources
PubMed1996

Surgical management of total anomalous pulmonary venous connection. Thirty-year trends.

BACKGROUND: Reports of surgical correction of total anomalous pulmonary venous connection (TAPVC) over the past 30 years indicate a general improvement in operative survival. However, prevention of late pulmonary venous obstruction continues to be a cornerstone of successful repair. The purpose of the study was to identify factors associated with improvement in perioperative mortality and to determine risk factors for death and reoperation due to pulmonary vein stenosis after repair of TAPVC. METHODS AND RESULTS: Using univariate and multiple regression analysis, we analyzed risk of early and late mortality and need for reoperation in 105 patients operated on between April 1966 and June 1995. Despite increased frequency of neonatal repair in the most recent time period (29% in 1966 through 1985; 55% in 1991 through 1995, P < .05), operative mortality declined (13% in 1966 through 1985; 0% in 1991 through 1995). The incidence of postoperative pulmonary hypertensive episodes and death related to pulmonary hypertension decreased significantly over the study period (P < .001). Aggressive preoperative elective medical stabilization and prophylaxis of postoperative pulmonary hypertensive episodes may have contributed to this improvement. By univariate analysis, preoperative pulmonary hypertension (P < .02) and preoperative pulmonary vein obstruction (P < .01) correlated with early mortality up to 1990 but not in the past 5 years. Multiple logistic regression analysis showed that only a small pulmonary confluence associated with diffuse pulmonary vein stenosis was an independent risk factor for early (P < .001) and late (P = .01) death as well as need for reoperation (P = .007). Type of TAPVC was not a significant risk factor throughout the three decades of our experience. At a median follow-up of 87 months, late survival was 98% (93 of 95 operative survivors), and all are NYHA class I. CONCLUSIONS: Improvements on surgical technique as well as preoperative and postoperative management account for the reduction in mortality and need for reoperation for most types of TAPVC. However, the presence of a small venous confluence and diffuse pulmonary vein stenosis remains a risk factor for adverse outcome.

Cardiac Surgical Procedures↗
PubMed1996

Identification and characterization of the linear IS3 molecules generated by staggered breaks.

Insertion sequences IS3 encodes two, out-of-phase, overlapping open reading frames, orfA and orfB. The OrfAB transframe protein that is IS3 transposase is produced by -1 translational frameshifting between orfA and orfB. Efficient production of the IS3 transposase in the cells harboring the IS3-carrying plasmid has been shown to generate miniplasmids as well as characteristic minicircles, called IS3 circles, consisting of the entire IS3 sequence and one of the 3-base pair sequences flanking IS3 in the parental plasmid. Here, we show that the IS3 transposase also generates the linear molecules of IS3 with 3-nucleotide overhangs at the 5'-ends. The nucleotide sequences of the overhangs are the same as those flanking IS3 in the parental plasmid, suggesting that the linear IS3 molecules are generated from the parental plasmid DNA by staggered double strand breaks at the end regions of IS3. The linear IS3 molecules are likely to be the early intermediates in the transposition reaction, which proceeds in a non-replicative manner.

Base Sequence↗
PubMed1996

Thymus-related liposarcoma: report of a case and review of the literature.

We report herein the case of a 77-year-old woman who was admitted to our hospital for further evaluation of an abnormal shadow in the right upper mediastinum that had been revealed by a routine chest X-ray. Computed tomography (CT) and magnetic resonance imaging (MRI) scans confirmed the presence of a thymic tumor, but did not show any evidence of invasion into the central vessels or adjacent structures. Thus, an extended thymectomy with resection of the tumor was performed. Microscopically, normal thymic tissue was found among the tumor cells, and a pathological diagnosis of well-differentiated liposarcoma was established. From the operative and microscopic findings, it is apparent that the tumor was related to the thymus. Postoperative irradiation of 60 Gy was delivered to the operative site and the patient has remained free of disease for 29 months since the operation.

Aged↗
PubMed1996

Estrogen and apoptosis in the developing sexually dimorphic preoptic area in female rats.

Effect of estrogen on apoptotic cell death was studied in the two sexually dimorphic neuronal groups in the developing rat preoptic area (POA): the anteroventral periventricular nucleus of the POA (AVPvN-POA); and the sexually dimorphic nucleus of the POA (SDN-POA). A specific labelling of nuclear fragmentation was performed by terminal deoxynucleotydyl transferase(TdT)-mediated dUTP-biotin nick end-labeling method (TUNEL method) to demonstrate apoptosis. In the AVPvN-POA whose size is larger in females than in males, the number of TUNEL-positive cells was not significantly different between day 5 control and female pups sacrificed 10 h after 25 micrograms estradiol benzoate (EB) injection. However, TUNEL-positive cells showed a significant increase in the female pups sacrificed 24 h after EB injection, compared to that shown in the control female pups. In the SDN-POA whose size is larger in males than in females, EB injection significantly decreased TUNEL-positive cells in the female pups sacrificed 24 h after EB injection, compared to that in controls. These results suggest that estrogen regulates the neuronal number by facilitating apoptotic cell death in the developing AVPvN-POA or by inhibiting it in the developing SDN-POA.

Animals↗
PubMed1996

Pulmonary hypertension after operations for congenital heart disease: analysis of risk factors and management.

BACKGROUND: Management of pulmonary hypertension, a potentially fatal complication of operations to correct congenital heart disease, has evolved through the last 15 years. Monitoring of pulmonary arterial pressure and mixed venous saturation became available, and prophylactic use of alpha-blockers and other vasodilators increased. This study examines risk factors for morbidity and mortality from pulmonary hypertension after operations to correct congenital heart disease and evaluates the impact of management changes on outcomes. METHODS: By means of multivariable logistic regression analysis, 880 high-risk patients with congenital heart disease (of 2484 patients undergoing cardiopulmonary bypass between January 1980 and December 1994) were analyzed to determine which were at risk for postoperative pulmonary hypertension and its associated morbidity and mortality. RESULTS: Patients with atrioventricular canal (n = 182), truncus arteriosus (n = 47), total anomalous pulmonary venous connection (n = 90), transposition of great arteries (n = 97), hypoplastic left heart syndrome (n = 50), and ventricular septal defect (n = 414) demonstrated a higher risk of postoperative pulmonary hypertension. By multivariable logistic regression, preoperative pulmonary hypertension (p < 0.0001), absence of mixed venous saturation monitoring (p < 0.0001), and absence of prophylactic alpha-blockade (p = 0.0004) significantly increased postoperative pulmonary hypertension. Preoperative pulmonary hypertension (p < 0.001) and absence of prophylactic alpha-blockers (p = 0.0004) were significant risk factors for in-hospital death related to pulmonary hypertension. Repair at older age (except in the case of total anomalous pulmonary venous connection) was a significant risk for postoperative pulmonary hypertension (p = 0.03). CONCLUSION: Mixed venous saturation monitoring and alpha-receptor blockade reduced the incidence of pulmonary hypertension after operations for congenital heart disease. Early definitive repair reduced morbidity and mortality from postoperative pulmonary hypertension.

Cardiac Surgical Procedures↗
PubMed1996

Structure-related inhibitory effect of antimicrobial enoxacin and derivatives on theophylline metabolism by rat liver microsomes.

Enoxacin, an antimicrobial fluoroquinolone with a 7-piperazinyl-1, 8-naphthyridine skeleton, is a potent inhibitor of cytochrome P-450-mediated theophylline metabolism. The present study was designed to clarify, using seven enoxacin derivatives, the molecular characteristics of the fluoroquinolone responsible for the inhibition. Three derivatives with methyl-substituted 7-piperazine rings inhibited rat liver microsomal theophylline metabolism to 1,3-dimethyluric acid to an extent similar to that of enoxacin (50% inhibitory concentrations [IC50s] = 0.39 to 0.48 mM). 7-Piperazinyl-quinoline derivatives, 8-hydroenoxacin (8-Hy) and 1-cyclopropyl-8-fluoroenoxacin (8-F1), which have a hydrogen and a fluorine at position 8, respectively, more weakly inhibited metabolite formation (IC50s = 0.88 and 1.29 mM, respectively). Little inhibition (IC50 > 2 mM) was observed in those with 3'-carbonyl and 4'-N-acetyl groups on the piperazine rings. The substrate-induced difference spectra demonstrated that the affinities of enoxacin, 8-Hy, and 8-F1 to cytochrome P-450 were parallel with their inhibitory activities. The substituent at position 8 was found to determine the molecular conformations of the fluoroquinolones, and the planarity in molecular shape decreased in the same order as the inhibitory activity (enoxacin > 8-Hy > 8-F1). Moreover, the 3'-carbonyl and 4'-N-acetyl groups decreased the basicity of their vicinal 4'-nitrogen atoms when judged from their electrostatic potentials, which showed a remarkably broadened negative charge around the nitrogens. As a result, the planarity of the whole molecule and the basicity of the 4'-nitrogen atom of enoxacin are likely to be dominant factors in the inhibition of theophylline metabolism by cytochrome P-450.

Animals↗
PubMed1996

Survey of risk factors for expulsive choroidal hemorrhage: case reports. Substantiation of the risk factors and their incidence.

To evaluate the interaction of risk factors for expulsive hemorrhage, we evaluated 3 cases of expulsive hemorrhage and 2 of acute intraoperative choroidal effusion that occurred at the University of Tsukuba Hospital over a 16-year-period and investigated the common findings in these 5 cases. We also selected randomly 500 cataractous cases operated at the University of Tsukuba Hospital and investigated the probabilities of risk factors for expulsive hemorrhage in these control cases. The 5 affected patients exhibited more than four risk factors of expulsive hemorrhage. The probability of more than four risk factors being involved in any cataract operation was approximately 0.33% (0.17 approximately 0.67%; 95% confidence interval). The incidence of expulsive hemorrhage at our hospital was approximately 0.2%, which is similar to the probability rate. Thus, we concluded that the development of expulsive hemorrhage was proved to be related to an accumulation of the risk factors for expulsive hemorrhage.

Aged↗
PubMed1996

[Mast cell leukemia evolved from RAEB-T (5q-syndrome) in a 12 year-old girl].

A 12-year-old, female 5q- syndrome case of refractory anemia with excess of blasts in transformation (RAEB-T) evolving to mast cell leukemia is described. This case was admitted because of general fatigue, when her peripheral blood count revealed anemia and leukocytosis with basophil-like cells. RAEB-T was diagnosed based on the laboratory findings of her peripheral blood and bone marrow aspiration, which revealed over 10% peripheral blast cells and dysmyelopoietic changes in all three lineages. Chromosomal analysis of the bone marrow cells showed 46, XX, 5q-. Six months later, the RAEB-T phase evolved to acute leukemia, despite prednisolone, vitamin D3, oxymetholone and low-dose cytosine arabinoside treatment. She had remarkable pancytopenia, hemorrhage, and hepatosplenomegaly, which were not responsive to daunomycin, enocitabine, etoposide, and 6-mercaptopurine, and eventually died. This case was unique in that her karyotype changed to normal; 46, XX, and her blast cells were mast cell lineage during the overt leukemic phase. Interestingly, some blasts were intermediate cells possessing the ultrastructural features typical of both basophils and mast cells.

Anemia, Refractory, with Excess of Blasts↗
PubMed1996

[Effect of superoxide production on nitric oxide release from the pulmonary vascular endothelium during reperfusion after warm ischemia].

It has been reported that reperfusion injury results in the diminished nitric oxide (NO) release from the pulmonary vascular endothelium. However, this mechanism is completely unknown. We examined the effect of superoxide dismutase (SOD) on NO release at reperfusion. A rabbit lung was perfused with Krebs-Henselit buffer in a recirculation system. Cyclic GMP (cGMP) content in the lung effluent from the left ventricle was assayed in a time-dependent manner. In the control group, the lung was immediately perfused without interventing ischemia. In the warm ischemia and reperfusion group, the lung was reperfused after 30 min of warm ischemia. In the SOD group, SOD (60,000 U and 120,000 U) was administered at reperfusion after warm ischemia. The cGMP release in the warm ischemia and reperfusion group significantly decreased compared with the control group. In the SOD group, cGMP release was reversed with increasing doses of SOD, and the cGMP content was significantly reversed at all time points with SOD administration of 120,000 U. The impairement of cGMP release by reperfusion injury was restored by SOD administration. This data suggests that NO release from the endothelium may be quenched by superoxide anion generated at reperfusion. In lung transplantation, efforts must be pursued to preserve the endothelial function such as NO pathway.

Animals↗
PubMed1995

Stable and general-purpose chemiluminescent detection system for horseradish peroxidase employing a thiazole compound enhancer and some additives.

A stable and highly sensitive chemiluminescent detection system for horseradish peroxidase (HRP)/luminol/hydrogen peroxide using a newly designed thiazole compound enhancer has been established. Some additives for the chemiluminescent reaction were explored to overcome some defects of the reaction such as rapid decay and high background of light emission. Recrystallization of luminol and the addition of several detergents into the reacting solution were effective to increase specific light emissions. The addition of skim milk into the reacting solution reduced the background. Consequently, skim milk combined with a detergent increased the signal to noise ratio about 20 times compared with the reactions in the absence of both additives. The optimal concentration of enhancer and the addition of egg albumin stabilized the emission. In the new method, 6x 10(-18) mol of HRP was detectable. This would be the most sensitive enhanced chemiluminescent detection system for HRP. Furthermore, we could detect picogram per milliliter (10(-17) mol) concentrations of a trace component in biological materials such as endothelin-1 by employing this reaction.

Endothelins↗
PubMed1995

IS1-encoded proteins, InsA and the InsA-B'-InsB transframe protein (transposase): functions deduced from their DNA-binding ability.

Insertion sequence IS1 encodes a transframe protein, InsA-B'-InsB, which is produced from two out-of-phase reading frames, insA and B'-insB, by translational frameshifting at a run of adenines. Unless the frameshifting event occurs, the InsA protein is produced from IS1. We found that cells harboring a plasmid carrying an IS1 mutant with a single adenine insertion in the run of adenines contained miniplasmids. Cloning and DNA sequencing analyses of the miniplasmids revealed that they had a deletion extending from an inverted repeat (IR) at the left end of IS1. This indicates that they were generated by IS1-mediated deletion due to efficient production of the InsA-B'-InsB transframe protein that is IS1 transposase. Both the InsA protein and transposase were partially purified as a fusion protein with collagen-LacZ by LacZ-specific affinity column chromatography. The InsA* and the collagenolyzed InsA* were found to bind specifically to a 24-bp region within each of the IRs at the ends of IS1. The transposase Tnp* and the collagenolyzed Tnp* were found to bind to the sequence with or without IR, but preferentially to that with IR. The nonspecific DNA-binding ability of transposase may be involved in recognition of the target DNA, an important process of transposition of IS1. Both InsA and transposase have the IR-specific DNA binding ability and a common polypeptide segment containing the alpha-helix-turn-alpha-helix motif, supporting the previous indication that InsA competes with transposase to bind to IRs and thus becomes a transposition inhibitor. Based on the observations described in this article, we speculate that transposase of IS1 consists of at least two domains, the N-terminal half, which almost entirely overlaps InsA, and the C-terminal half, which almost entirely overlaps B'-InsB. The frameshifting event adds the latter domain to the former to give the transposase activity recognizing IRs and the target sequence to initiate the transposition reaction.

Amino Acid Sequence↗
PubMed1995

Frequency of glutathione-S-transferase 1 gene deletion and its possible correlation with cataract formation.

This experiment was conducted to investigate the possible association between an increased frequency of glutathione-S-transferase (GST)1 gene deletion and the presence of cataracts in elderly patients. Genomic DNA was isolated from blood samples obtained from 138 elderly patients who had undergone cataract surgery, and from 62 random blood donors. All subjects lived in the same geographic area (Ibaraki Prefecture, Japan). The DNA sequences among three different exon ranges (exons 3-5, exons 4-5 and exons 5-6) of the GST1 gene were amplified by the polymerase chain reaction (PCR) technique to determine if GST1 gene deletion occurred. Cataract patients had a significantly higher frequency of GST1 gene deletion than random controls did (P < 0.001, odds ratio = 2.91, 1.56-5.44; 95% of confidence interval). Mean age of cataract patients lacking GST1 gene was significantly younger (n = 101, mean age = 70.4, s.d. = 10.2) than that of patients possessing the GST1 gene (n = 37, mean age = 75.0, s.d. = 8.7) (P < 0.02). These results show that the deletion of the GST1 gene may be one of determinants of genetic susceptibility to cataractgenic agents.

Aged↗
PubMed1995

Bacterial adsorption to fetuin and mucin pellicle.

The ability of Actinomyces viscosus (A. viscosus) WVU 627 to attach to hydroxyapatite (HA) beads treated with either bovine fetuin or bovine mucin was studied. All preparations used were blocked with bovine serum albumin prior to incubation with [3H] thymidine-labeled A.viscosus cells. The quantity of fetuin or mucin adsorbed on the HA beads was determined by use of [3H] fetuin or [3H] mucin. Approximately 6 micrograms protein of [3H] fetuin and 20 micrograms of protein of [3H] mucin adsorbed to 5 mg of HA beads at saturation, respectively. The presence of fetuin or mucin on HA beads promoted attachment of the organism. However, HA beads treated with human whole saliva as a positive control promoted A.viscosus attachment more effectively than HA beads treated with these glycoproteins. Attachment of two additional strains (B 236 and B 25) of A. viscosus to HA beads was also promoted by these glycoproteins. The number of A.viscosus cells which attached to fetuin-treated HA beads was dose-dependent, except for strain B 25. For all three A.viscosus strains tested, attachment to the experimental pellicle with mucin was dose-dependent. These findings suggest that the use of these newly developed bacterial adhesion assay systems may be effective for elucidating bacterial adhesion mechanisms.

Actinomyces↗
PubMed1995

[Correlation between acute rejection and the role of donor specific cytotoxic T lymphocyte in canine lung allotransplantation].

We investigated the correlation between the donor specific CTL activities and pathological findings of the grafted lungs by using mononuclear cells obtained from BAL fluids (BAL), peripheral blood (PBL), spleen (SpL) and grafted lungs (GIL) in canine lung allotransplantation. Twenty eight mongrel dogs underwent left lung allotransplantation. Fifteen dogs were not given immunosuppressive drugs. Thirteen dogs were given cyclosporine a 20 mg/kg/day per os for ten days postoperatively. Dogs were monitored by chest roentgenograms and cytotoxic activity tests of which targets were donor's fibroblasts. Pathological findings were classified by Prop's classification. The results were as follows. In latent and vascular phases no elevations of cytotoxic activities were demonstrated in PBL, BAL and GIL. But in early alveolar phase the cytotoxic activity was elevated to 19.83 +/- 14.54% in BAL. In late alveolar phase the highest cytotoxicities of 30.83 +/- 15.28% in PBL, 72.63 +/- 7.36% in BAL and 70.07 +/- 6.34% in GIL at E:T = 100:1 were demonstrated. In pneumonia cytotoxicity did not elevate at all in any effectors. As a result of them, it clearly shows that BAL is a good tool for the diagnosis of lung rejection.

Animals↗
PubMed1995

[Influence of warm ischemia and reperfusion on no-derived cyclic GMP release in the perfused rabbit lung].

To elucidate the vascular endothelial function at pulmonary ischemia and reperfusion, cyclic GMP (cGMP) release in lung perfusate at reperfusion after ischemia was examined as a marker of nitric oxide (NO) release from the endothelium in an in situ perfused rabbit lung. The lung was perfused from the pulmonary artery with Krebs-Henselite buffer and cGMP in the lung effluent from the left ventricle was assayed in a time-dependent manner. The inhibition of cGMP release by NG-nitro-L-arginine methyl ester and the reversal of the effect by L-arginine indicated that cGMP released into the perfusate was elicited by NO from the endothelium. There was a significant decrease in cGMP release during reperfusion after warm ischemia (30 min and 60 min) compared with the immediately perfusion without intervening ischemia. These data suggest that NO release is impaired by the endothelial dysfunction at reperfusion after warm ischemia in the perfused rabbit lung and the biochemical studies of the perfusate is useful in assessing the vascular endothelial function.

Animals↗
PubMed1994

Translational control in production of transposase and in transposition of insertion sequence IS3.

IS3 (1258 bp in length) contains two open reading frames, orfA and orfB, which are out of phase and overlap each other. We show here that three proteins of 10, 32 and 42 kDa in size are encoded by IS3. The 10 kDa protein is the product of orfA and is here called OrfA. The ATG codon of orfB which overlaps the termination codon of orfA is utilized to produce the 32 kDa protein (here called OrfB), in a manner depending on translation of orfA. The 42 kDa protein is a transframe protein (here called OrfB), which is synthesized from orfA and orfB by -1 translational frameshifting at the A4G motif present in the overlapping region. Both the frameshifting event to produce OrfB and the coupled translation event to produce OrfB are greatly stimulated by a pseudo knot structure located in the overlapping region between orfA and orfB. A mutant IS3 with a single base insertion in the A4G motif efficiently produces the OrfB transframe protein without frameshifting. This mutant was found not to mediate co-integration but to mediate adjacent deletion to produce various miniplasmids and minicircles in large amounts. The OrfB transframe protein is necessary and sufficient for formation of these deletion products, implying that it is the transposase. Most of the minicircles consisted solely of the entire IS3 sequence and a three base-pair sequence between the IS3 ends. The significance of minicircle formation is discussed.

Amino Acid Sequence↗
PubMed1994

A novel microtubule-based motor protein (KIF4) for organelle transports, whose expression is regulated developmentally.

To understand the mechanisms of transport for organelles in the axon, we isolated and sequenced the cDNA encoding KIF4 from murine brain, and characterized the molecule biochemically and immunocytochemically. Complete amino acid sequence analysis of KIF4 and ultrastructural studies of KIF4 molecules expressed in Sf9 cells revealed that the protein contains 1,231 amino acid residues (M(r) 139,550) and that the molecule (116-nm rod with globular heads and tail) consists of three domains: an NH2-terminal globular motor domain, a central alpha-helical stalk domain and a COOH-terminal tail domain. KIF4 protein has the property of nucleotide-dependent binding to microtubules, microtubule-activated ATPase activity, and microtubule plus-end-directed motility. Northern blot analysis and in situ hybridization demonstrated that KIF4 is strongly expressed in juvenile tissues including differentiated young neurons, while its expression is decreased considerably in adult mice except in spleen. Immunocytochemical studies revealed that KIF4 colocalized with membranous organelles both in growth cones of differentiated neurons and in the cytoplasm of cultured fibroblasts. During mitotic phase of cell cycle, KIF4 appears to colocalize with membranous organelles in the mitotic spindle. Hence we conclude that KIF4 is a novel microtubule-associated anterograde motor protein for membranous organelles, the expression of which is regulated developmentally.

Amino Acid Sequence↗