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T Nishida

Publications and source records attributed to T Nishida.

At least 55 records · Page 3Linked to original sources
PubMed2002

Impact of final coronary flow velocity reserve on late outcome following stent implantation.

Aims To assess whether coronary flow velocity reserve following stent implantation is predictive of the subsequent need of target lesion revascularization. Methods and Results The outcome was examined of 417 patients enrolled in a multicentre prospective randomized study (DESTINI), who received a successful single vessel stent implantation in native coronary arteries and in whom coronary flow velocity reserve was measured. Logistic regression analysis and the receiver operator characteristic curve were used. When compared with 358 patients not requiring target lesion revascularization, 59 patients (14%) who underwent target lesion revascularization had a lower final coronary flow velocity reserve (2.33 +/- 0.87 vs 2.48+/- 0.80, P= 0.20) and smaller final minimal lumen diameter (2.62 +/- 0.66 mm vs 2.73+/- 0.60, P= 0.19); however, those differences were not statistically significant. Patients with a coronary flow velocity reserve of < 2.0 (n=109, 26%) exhibited a significantly higher target lesion revascularization rate than patients with a coronary flow velocity reserve of > or = 2.0 (22% vs 11%, P= 0.010). This difference remained significant (odds ratio=2.01, 95% CI=1.11 to 3.66) after adjustment for other variables that were also correlated with the incidence of target lesion revascularization. Conclusion The presence of a final coronary flow velocity reserve of < 2.0 is an independent predictor of the need for target lesion revascularization after stent implantation in native coronary artery lesions.

Blood Flow Velocity↗
PubMed2001

Characterization of a novel mammalian SUMO-1/Smt3-specific isopeptidase, a homologue of rat axam, which is an axin-binding protein promoting beta-catenin degradation.

A novel SUMO-1/Smt3-specific isopeptidase, SMT3IP2/Axam2 (Smt3-specific isopeptidase 2), was cloned and characterized. The catalytic domains in the carboxyl-terminal region were very much similar to those of other SUMO-1/Smt3-specific proteases, but the amino-terminal part was quite different. The enzyme specifically bound to Smt3a and Smt3b but not to SUMO-1. The SMT3IP2 expressed by Escherichia coli could cleave SUMO-1, Smt3a, or Smt3b from a SUMO-1/RanGAP1, Smt3a/RanGAP1, or Smt3b/RanGAP1 conjugate, respectively, and had the activity of a carboxyl-terminal hydrolase to produce a glycine residue in the carboxyl terminus of these ubiquitin-like proteins. The sequence data indicated that the amino acid sequence of SMT3IP2 was mostly identical to that of rat Axam, which binds to Axin and promotes the degradation of beta-catenin, although its amino-terminal region was much shorter than that of Axam. Therefore, we designated this isopeptidase SMT3IP2/Axam2. When human SW480 cells were transfected with wild-type SMT3IP2/Axam2, the beta-catenin disappeared. When the cells were transfected with the SMT3IP2/Axam2 C500A mutant, which had neither isopeptidase nor carboxyl-terminal hydrolase activity, or with the 1-352 mutant, which lacked the catalytic domain of the enzyme, again the beta-catenin disappeared, indicating that the enzyme activities were not necessary for the instability of beta-catenin in this transfection assay system and that its competition with Dvl for binding to Axin may be important for the instability of beta-catenin as suggested previously for Axam (Kadoya, T., Kishida, S., Fukui, A., Hinoi, T., Michiue, T., Asashima, M., and Kikuchi, A. (2000) J. Biol. Chem. 275, 37030-37037). The involvement of its enzyme activities in the Wnt signaling pathway remains to be elucidated.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Purification, characterization and developmental expression of rat brain PSP protein.

We have isolated a perchloric acid-soluble protein designated as B-PSP1 from the postmitochondria supernatant fraction of rat brain. It was purified by gel filtration and anti-PSP1 affinity chromatography. Immunoblotting, peptide mapping, partial amino acid sequencing and reverse transcriptase-polymerase chain reaction showed that the amino acid sequence of B-PSP1 was identical with that of PSP isolated from rat liver. B-PSP1 was expressed in all regions including frontal cortex, posterior cortex, cerebellum, hippocampus, olfactory bulb, striatum, thalamus, midbrain, entorhinal cortex, pons, medulla and spinal cord. Immunohistochemical study showed that the expression of B-PSP1 was observed in ependymal cells of choroid plexus and glial cells of the other region. The expression of B-PSP1 in brain increased gradually from the first day to the 60th day of postnatal age, but the expression of B-PSP1 was slower than that of GFAP which is a marker protein of glial cells. The expression of PSP may be related to the cellular function rather than the developmental regulation of the glial cells. Thus, our findings are the first report on the presence of a PSP in rat brain which may be involved in the regulation of cellular function.

Animals↗
PubMed2001

A loss-of-function mutation of c-kit results in depletion of mast cells and interstitial cells of Cajal, while its gain-of-function mutation results in their oncogenesis.

Loss-of-function mutations of the c-kit receptor tyrosine kinase (KIT) result in depletion of mast cells and interstitial cells of Cajal (ICCs). In contrast, gain-of-function mutations of KIT induce neoplasms of mast cells and ICCs. In humans, the sites of mutations are different between mast cell neoplasms and those of ICCs. The former were found in the juxtamembrane domain between the transmembrane and tyrosine kinase domains, and the latter in the tyrosine kinase domain. Moreover, the mechanism of constitutive activation is different. Point mutations and/or deletions in the juxtamembrane domain induced the KIT dimerization, and the dimerized KIT was activated. A point mutation at the particular aspartic acid in the tyrosine kinase domain induced spontaneous activation without forming dimers. Mutations of the c-kit gene are a good model for understanding the relationship between mutations and diseases in both humans and mice.

Animals↗
PubMed2001

Peribronchiolar accumulation of dendritic cells and their close association with CD4(+) T cells in the murine lung hypersensitivity.

In order to understand the interaction between dendritic cells (DCs) and helper T (Th) cells in the region exposed to antigens during pulmonary delayed-type hypersensitivity (DTH), which is considered to be mediated by Th1 cells, we immunohistochemically investigated their spatial relationship in the cellular infiltrate. At 24 hours after intratracheal instillation of hapten in sensitized mice, DCs were preferentially accumulated around the bronchioles, whereas macrophages were more abundant around the accompanying arteries. DCs often formed a cluster, in which they were interconnected with each other by projections. Serial section analysis revealed that clustered DCs made a close apposition to Th cells but much less frequently to cytotoxic T cells and B cells. Immunoelectron microscopy demonstrated that lymphocytes extravasated the capillaries in the peribronchiolar interstitium and made conjugation with DCs. In the interstitial tissue, DCs often adhered to the fibroblasts, suggesting the supportive role of the latter cells in DC migration. Eosinophils were also frequent around the arteries, representing the possible involvement of Th2 cytokines. By contrast, in a chronic type of airway inflammation induced by repeated challenges of aerosolized ovalbumin, DCs were densely and diffusely accumulated around the arteries in the same way as macrophages. The present study demonstrated a close association of DCs with Th cells around the bronchioles during pulmonary DTH, suggesting that local interaction between them in the lung may play important roles in the development of this disorder.

Animals↗
PubMed2001

Carbon-carbon bond formation by electrophilic addition at the central carbon of the mu-eta(3)-allenyl/propargyl ligand on the Pd-Pd bond.

The mu-eta(3)-allenyl/propargyldipalladium complexes were synthesized by the reaction of the corresponding eta(1)-allenyl- or eta(1)-propargylpalladium complexes with Pd(2)(dba)(3). The X-ray diffraction analysis indicates that the dinuclear complex has a unique structure, in which two palladium, three carbon, two phosphorus, and one halogen atoms are in the same plane. These dinuclear complexes react with electrophiles, such as HCl or AcCl, at the central carbon of the mu-eta(3)-allenyl/propargyl ligand to give the mu-eta(3)-vinylcarbenedipalladium complexes. Intramolecular reaction proceeded smoothly to give cyclization products quantitatively. Addition of a catalytic amount of a palladium(0) complex dramatically accelerated the carbon-carbon bond formation. The MO calculations on the mu-eta(3)-allenyl/propargyl complexes indicated that the reaction proceeds via orbital control.

Journal Article↗
PubMed2001

Coordination of Lewis acid to eta(2)-enonepalladium(0) leading to continuous structure variation from eta(2)-olefin type to eta(3)-allyl type.

The reaction of alpha,beta-unsaturated carbonyl compounds, a palladium(0) complex, and Lewis acids led to the formation of a new class of complexes showing a wide variety of structures with eta(2)-type and eta(3)-type coordination of the carbonyl compounds. The reaction of Pd(PhCH=CHCOCH(3))(PPh(3))(2) with BF(3).OEt(2) or B(C(6)F(5))(3) quantitatively gave palladium complexes 1a,b having BX(3)-coordinated eta(2)-enonepalladium structure, as revealed by X-ray structure analysis of the B(C(6)F(5))(3) adduct 1b. On the other hand, the reaction of Pd(PhCH=CHCHO)(PPh(3))(2) with BF(3).OEt(2) or B(C(6)F(5))(3) gave distorted zwitterionic eta(3)-allylpalladium complexes 3a,b, where the Pd-carbonyl carbon distance in 3a (2.413(4) A) is much shorter than that (2.96(1) A) in 1b. The values of the P-P coupling constant and (13)C chemical shift for carbonyl carbon are useful criteria for predicting how the eta(3)-coordination mode contributes to the structure of the enone-palladium-Lewis acid system. Molecular orbital calculations on the series of model complexes suggest that orbital overlap in the highest occupied molecular orbital between the palladium and carbonyl carbon is enlarged by coordination of the Lewis acid to the carbonyl group. Palladium-catalyzed conjugate addition of R-M (R-M = AlMe(3), AlEt(3), ZnEt(2)) and its plausible reaction path are also reported.

Journal Article↗
PubMed2001

Combination of a brief irrigation with tissue factor pathway inhibitor (TFPI) and adenovirus-mediated local TFPI gene transfer additively reduces neointima formation in balloon-injured rabbit carotid arteries.

BACKGROUND: Tissue factor pathway inhibitor (TFPI) is a physiological antagonist of TF. We tested whether a brief irrigation with TFPI protein (rTFPI) or TFPI gene transfer into injured arteries would suppress TF activity and reduce fibroproliferative changes and investigated whether a combination of these methods would show an additive effect. METHODS AND RESULTS: We prepared adenoviruses expressing either TFPI (AdTFPI) or bacterial ss-galactosidase (AdLacZ). Rabbit carotid arteries were balloon-injured and either infected with AdTFPI (or AdLacZ) or irrigated briefly with rTFPI (or saline). After injury, TF activity in arteries increased and was sustained; however, it was suppressed during the initial 24 hours by rTFPI irrigation (but not by gene transfer) and for a substantial period of time by TFPI gene transfer (but not by rTFPI irrigation). Four weeks later, the ratio of the intimal to medial areas was 34.3+/-8.7% (mean+/-SD, n=14) in saline-treated arteries and 33.3+/-4.2% in AdLacZ-infected arteries (P:=NS versus saline). However, it was reduced to 25.5+/-8.5% in rTFPI-irrigated arteries (P:<0.01 versus saline) and to 20.7+/-5.3% in AdTFPI-infected arteries (P:<0.01 versus AdLacZ). With a combination of irrigation and gene transfer, the ratio was further reduced to 12.6+/-4.7% (P:<0.01 versus rTFPI, P:<0.05 versus AdTFPI). Systemic coagulation status was not affected in these animals. CONCLUSIONS: A combination of rTFPI irrigation and TFPI gene transfer overcomes the shortcomings shown by each method when used alone and achieves a full coverage of TF activity suppression, thereby enhancing their therapeutic effects without systemic side effects. This combination may be an effective strategy for the prevention of thrombosis and proliferative changes after angioplasty in humans.

Adenoviridae↗
PubMed2001

Characterization of binding properties of urinary trypsin inhibitor to cell-associated binding sites on human chondrosarcoma cell line HCS-2/8.

Urinary trypsin inhibitor (UTI) forms membrane complexes with UTI-binding proteins (UTI-BPs) and initiates modulation of urokinase-type plasminogen activator (uPA) expression, which results in UTI-mediated suppression of cell invasiveness. It has been established that suppression of uPA expression and invasiveness by UTI is mediated through inhibition of protein kinase C-dependent signaling pathways and that human chondrosarcoma cell line HCS-2/8 expresses two types of UTI-BPs; a 40-kDa UTI-BP (UTI-BP(40)), which is identical to link protein (LP), and a 45-kDa UTI-BP (UTI-BP(45)). Here we characterize binding properties of UTI-BPs.UTI complexes in the cells. In vitro ligand blot, cell binding and competition assays, and Scatchard analyses demonstrate that both UTI-BP(40) and UTI-BP(45) bind (125)I-UTI. A deglycosylated form of UTI (NG-UTI), from which the chondroitin-sulfate side chain has been removed, binds only to UTI-BP(40). Additional experiments, using various reagents to block binding of (125)I-UTI and NG-UTI to the UTI-BP(40) and UTI-BP(45) confirm that the chondroitin sulfate side chain of UTI is required for its binding to UTI-BP(45). Analysis of binding of (125)I-UTI and NG-UTI to the cells suggests that low affinity binding sites are the UTI-BP(40) (which can bind NG-UTI), and the high affinity sites are the UTI-BP(45). In addition, UTI-induced suppression of phorbol ester stimulated up-regulation of uPA is inhibited by reagents that were shown to prevent binding of UTI to the 40- and 45-kDa proteins. We conclude that UTI must bind to both of the UTI-BPs to suppress uPA up-regulation.

Binding Sites↗
PubMed2001

Intravascular ultrasound criteria for the assessment of the functional significance of intermediate coronary artery stenoses and comparison with fractional flow reserve.

The functional significance of coronary artery stenoses of intermediate severity is important in determining strategy in patient care. Intravascular ultrasound (IVUS) is often used to evaluate coronary stenosis severity. However, at present, few data are available about the role IVUS in the assessment of functional significance of intermediate lesions. Myocardial fractional flow reserve (FFR) <0.75 is a reliable index of a functionally severe coronary stenosis. In 53 lesions we assessed (1) by pressure wire: FFR (index of functional significance), and (2) by IVUS: minimal lumen cross-sectional area (MLA, square millimeters), minimal lumen diameter (MLD, millimeters), lesion length (millimeters), and percent area stenosis at the lesion site. By regression analysis, percent area stenosis and lesion length had a significant inverse correlation with FFR (r = -0.58, p <0.001, r = -0.41, p <0.004, respectively). MLD and MLA showed a significant positive relation with FFR (r = 0.51, p <0.001, r = 0.41, p <0.004, respectively). By using a receiver operating characteristic (ROC) curve, we identified a percent area stenosis > 70% (sensitivity 100%, specificity 68%), a MLD < or = 1.8 mm (sensitivity 100%, specificity 66%), a MLA < or =4.0 mm2 (sensitivity 92%, specificity 56%), and a lesion length of >10 mm (sensitivity 41%, specificity 80%) to be the best cut-off values to fit with a FFR <0.75. The combined evaluation of both percent area stenosis and MLD made the IVUS examination more specific (sensitivity 100%, specificity 76%). In 53 intermediate coronary lesions found by angiography, IVUS area stenosis >70%, MLD < or =1.8 mm, MLA < or =4.0 mm2, and lesion length > 10 mm reliably identified functionally critical intermediate coronary stenoses.

Cardiac Catheterization↗
PubMed2001

Gain-of-function mutation at the extracellular domain of KIT in gastrointestinal stromal tumours.

Gastrointestinal stromal tumours (GISTs) are the most common mesenchymal tumours of the human gastrointestinal tract. Previous studies of GISTs found gain-of-function mutations of the c-kit gene, which encodes a receptor tyrosine kinase (KIT). All the mutations were confined to exon 11, which encodes the juxtamembrane domain. By further examination of the whole coding region of c-kit complementary DNA in 35 GISTs, two were found to show the identical mutation at exon 9, which encodes the extracellular domain. The aims of the present study were to examine the frequency of the extracellular domain mutation and to determine whether the mutation is a gain-of-function type or not. Genomic DNA was extracted from paraffin-embedded tissues of 133 GISTs and exon 9 of the c-kit gene was amplified by polymerase chain reaction. Screening of the mutation was carried out by single-strand conformation polymorphism analysis and direct sequencing was done. Mutant c-kit cDNA was transfected into 293T human embryonic kidney cells and the magnitude of autophosphorylation of the mutant KIT was examined with or without the ligand of KIT, stem cell factor (SCF). In total, seven GIST cases (approximately 5%) were found with the identical mutation at exon 9. The mutant KIT exhibited constitutive autophosphorylation without SCF stimulation. The prognosis of the patients with the extracellular domain mutation was comparable to that of the patients with the juxtamembrane domain mutation.

Adult↗
PubMed2001

Directional atherectomy prior to stenting in bifurcation lesions: a matched comparison study with stenting alone.

The ideal catheter-based intervention for treatment of coronary lesions at bifurcation site still has to be defined. The aim of the study was to assess the acute and long-term outcome after treatment of bifurcation lesions with directional atherectomy (DCA) and stenting in comparison with stenting alone. Thirty-one consecutive patients treated for bifurcation coronary lesions (62 lesions) with DCA and stenting in at least one branch (DCA group) were compared with a matched group of 31 patients with bifurcation coronary lesions (62 lesions) treated with stenting alone in at least one branch (non-DCA group). Procedural success was 87.1% in the DCA group compared with 100% in the non-DCA group (P = 0.03). In-hospital major adverse cardiac events (MACE) occurred only in the DCA group (12.9% vs. 0%, P = 0.03), mainly non-Q-wave myocardial infarction. After the procedure, minimum lumen diameter (MLD) and acute gain were significantly greater (P = 0.004 and P = 0.05, respectively) and % diameter stenosis was significantly lower (P = 0.05) in the main branch in the DCA group. At follow-up angiogram, MLD in the main branch was still significantly greater in the DCA group compared to the non-DCA group (2.31 vs. 1.65, respectively, P = 0.04), with no significant difference in late loss and loss index between the two groups. Restenosis rate was 28.8% in the DCA group vs. 43.5% in the non-DCA group (P = 0.13). The incidence of follow-up MACE was 29% in the DCA group compared with 48.4% in the non-DCA group, mainly due to target lesion revascularization. In conclusion, treatment of bifurcation coronary lesions with DCA and stenting was associated with greater acute gain after the procedure and greater MLD at follow-up in the main branch compared with stenting alone. Procedural myocardial infarction was more frequent in the DCA group. Restenosis rates and follow-up MACE were lower following DCA and stenting, without reaching any statistical significance.

Adult↗
PubMed2001

Late acute thrombosis after coronary brachytherapy: when is the risk over?

Late total occlusion (LTO) after simultaneous coronary stenting and brachytherapy has been described in recent randomized trials. We report a case of LTO presenting with an acute clinical event 15 months after the index procedure, suggesting that the risk is not confined to the first 6-month to 1-year period.

Blood Vessel Prosthesis Implantation↗
PubMed2001

Development of a tracheal stapling device.

OBJECTIVE: Recent years have witnessed a multitude of technical advances regarding gastrointestinal and vascular anastomosis. However, difficulties still hamper tracheal and bronchial anastomosis. We have therefore developed a novel set of instruments and performed end-to-end anastomosis of the transected canine cervical trachea to establish the operative procedures. METHODS: A novel set of instruments was developed for tracheal anastomosis including two pairs of forceps for grasping the free tracheal ends, a metal connecting device, and clamping forceps for staple insertion. Briefly, the operative procedure involves fixation of forceps circumferentially to hold the cut trachea. End-to-end anastomosis is completed by joining the forceps with a clamp and stapling the tracheal ends everted outward. End-to-end anastomosis of the cervical trachea was performed on 23 dogs. Animals were monitored on a daily basis, and bronchofiberscopy was performed periodically. Deaths from all causes were evaluated by immediate necropsy. Sixteen dogs were sequentially sacrificed at 1, 2, 3 and at 6 months after surgery. RESULTS: In our dog model, stenosis at the anastomosis of the cervical trachea was found as a complication in 8 of 23 cases. Tracheal rupture occurred in a further 3 cases, slight granulation in another 4, and the remaining 8 showed no complication. Histological findings of anastomotic healing were similar to those reported for hand suture.

Anastomosis, Surgical↗
PubMed2001

Interesting RI accumulation in hepatic images with Tc-99m GSA SPECT scintigraphy in idiopathic portal hypertension.

The authors report a case of idiopathic portal hypertension (IPH), which showed interesting RI accumulation on Single Photon Emission CT (SPECT) images, with Tc-99m galactosyl human serum albumin (GSA) scintigraphy. Accumulation of Tc-99m GSA was decreased in the periphery of the liver where strong enhancement was revealed only in the arterial phase on dynamic CT. These findings imply that portal flow is decreased in the periphery of the liver where arterial flow is dominant. It was thought that secondary reduced activity of GSA due to a decrease in portal flow results in reduced radioactivity in the periphery of the liver in IPH. This interesting accumulation of Tc-99m GSA may be one of the sign of IPH.

Aged↗