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Sökning: WFRF:(Igawa K)

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1.
  • 2017
  • swepub:Mat__t
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2.
  • Harmankaya, Necati, 1983, et al. (författare)
  • Healing of complement activating Ti implants compared with non-activating Ti in rat tibia.
  • 2012
  • Ingår i: Acta biomaterialia. - : Elsevier BV. - 1878-7568 .- 1742-7061. ; 8:9, s. 3532-40
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent studies have revealed that ozone ultraviolet (UVO) illumination of titanium (Ti) implants improves bone-implant anchorage by altering the physico-chemical and immune activating properties of the titanium dioxide (TiO(2)) layer. In the present rat tibia model, the authors compared the early events of inflammation and bone formation around UVO-treated Ti and complement activating immunoglobin g (IgG)-coated Ti. Machined Ti and machined Ti coated with a physical vapour-deposited Ti layer were used as references. Screw-shaped test and reference implants were implanted into rat tibia and harvested after 1, 7 and 28 days. Messenger RNA expression of implant adhered cells and peri-implant tissue ~250 μm from the surface were subsequently analysed with regard to IL-1β, TNF-α, osteocalcin, cathepsin K, BMP-2 and PDGF. Separate implants were retrieved after 7 and 28 days for removal torque measurements, and histological staining and histomorphometric analysis of bone area and bone-to-implant contact. While enhanced expression of inflammatory markers, TNF-α and IL-1β, was observed on IgG-coated surfaces throughout the observation time, UVO-treated surfaces indicated a significantly lower early inflammatory response. In the early phases (1 and 7 days), the UVO-treated surfaces displayed a significantly higher expression of osteoblast markers BMP-2 and osteocalcin. In summary, complement activating Ti implants elicited a stronger inflammatory response than UVO-treated Ti, with low complement activation during the first week of healing. In spite of this, the UVO-treated Ti induced only marginally more bone growth outside the implants.
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3.
  • Harmankaya, Necati, 1983, et al. (författare)
  • Raloxifene and alendronate containing thin mesoporous titanium oxide films improve implant fixation to bone.
  • 2013
  • Ingår i: Acta biomaterialia. - : Elsevier BV. - 1878-7568 .- 1742-7061. ; 9:6, s. 7064-73
  • Tidskriftsartikel (refereegranskat)abstract
    • This study tested the hypothesis that osteoporosis drug-loaded mesoporous TiO2 implant coatings can be used to improve bone-implant integration. Two osteoporosis drugs, Alendronate (ALN) and Raloxifene (RLX), were immobilized in nanoporous oxide films prepared on Ti screws and evaluated in vivo in rat tibia. The drug release kinetics were monitored in vitro by quartz crystal microbalance with dissipation and showed sustained release of both drugs. The osteogenic response after 28days of implantation was evaluated by quantitative polymerase chain reaction (qPCR), removal torque, histomorphometry and ultrastructural interface analysis. The drug-loaded implants showed significantly improved bone fixation. In the case of RLX, stronger bone-remodelling activity was observed compared with controls and ALN-loaded implants. The ultrastructural interface analysis revealed enhanced apatite formation inside the RLX coating and increased bone density outside the ALN coating. Thus, this novel combination of a thin mesoporous TiO2 carrier matrix and appropriate drugs can be used to accelerate implant fixation in trabecular bone.
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4.
  • Igawa, T, et al. (författare)
  • Evolutionary history of the extant amphioxus lineage with shallow-branching diversification
  • 2017
  • Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 7:1, s. 1157-
  • Tidskriftsartikel (refereegranskat)abstract
    • Amphioxus or lancelets have been regarded as a key animal in understanding the origin of vertebrates. However, the evolutionary history within this lineage remains unexplored. As the amphioxus lineage has likely been separated from other chordates for a very long time and displays a marked left-right asymmetry, its evolutionary history is potentially helpful in better understanding chordate and vertebrate origins. We studied the phylogenetic relationships within the extant amphioxus lineage based on mitochondrial genomes incorporating new Asymmetron and Epigonichthys populations, and based on previously reported nuclear transcriptomes. The resulting tree patterns are consistent, showing the Asymmetron clade diverging first, followed by the Epigonichthys and Branchiostoma clades splitting. Divergence time estimates based on nuclear transcriptomes with vertebrate calibrations support a shallow diversification of the extant amphioxus lineage in the Tertiary. These estimates fit well with the closure of seaways between oceans by continental drift, ocean currents, and present geographical distributions, and suggest a long cryptic history from the origin of amphioxus to its most recent diversification. Deduced character polarities based on phylogenetic analyses suggest that the common ancestor of the extant amphioxus existed in a tiny epibenthic state with larva-like appearance of extant amphioxus, likely with ciliate epidermis.
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6.
  • Kaidoh, K, et al. (författare)
  • Effects of selective beta 2 and beta 3-adrenoceptor agonists on detrusor hyperreflexia in conscious cerebral infarcted rats
  • 2002
  • Ingår i: Journal of Urology. - 1527-3792. ; 168:3, s. 1247-1252
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: We evaluated the effects of beta-adrenoceptor agonists on detrusor hyperreflexia in cerebral infarcted rats. Materials and Methods: To produce cerebral infarction in Sprague-Dawley rats the left middle cerebral artery was occluded by introducing a monofilament nylon thread into the artery. In sham operated rats the same artery was exposed but not occluded. After these operations cystometric and cardiovascular experiments were performed with no anesthesia or restraint. Results: After the operation bladder capacity was significantly decreased and voiding pressure was significantly increased in cerebral infarcted but not in sham operated animals. The difference in cerebral infarcted and sham operated rats was significant for each parameter (p < 0.01). Post-void residual urine volume was not affected in either group. In the cerebral infarction group intravenous administration of CL316243 ([R,R]-5-2-[[2-(3-chlorophenyl-2-hydroxyethyl]-amino] propyl]-1,3-benzodioxole-2,2-dicarboxylate) (Kissei Central Laboratories, Hotaka, Japan) a selective beta3-adrenoceptor agonist, significantly increased bladder capacity at 10 and 100 mug./kg. without affecting voiding pressure or post-void residual urine volume. Procaterol, a selective beta2-adrenoceptor agonist, significantly increased bladder capacity and post-void residual urine volume at 10 mug./kg. intravenously without affecting voiding pressure. In separate experiments procaterol (1 to 100 mug./kg. intravenously) decreased mean blood pressure and increased heart rate in a dose dependent manner. In contrast, the effects of CL316243 (0.1 to 100 mug./kg. intravenously) on mean blood pressure and heart rate were minimal. Conclusions: These results indicate that in cerebral infarcted rats detrusor hyperreflexia can be suppressed by the selective beta3-adrenoceptor agonist CL316243 without increasing post-void residual volume and without significant cardiovascular side effects. If the current results hold true in humans, selective beta3-adrenoceptor agonists may prove useful for treating detrusor hyperreflexia associated with cerebral infarction.
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7.
  • Persson, Katarina, et al. (författare)
  • Effects of inhibition of the L-arginine/nitric oxide pathway in the rat lower urinary tract in vivo and in vitro
  • 1992
  • Ingår i: British Journal of Pharmacology. - 0007-1188 .- 1476-5381. ; 107, s. 178-184
  • Tidskriftsartikel (refereegranskat)abstract
    • 1 The present study was performed to investigate how blockade of the L-arginine/nitric oxide (NO)pathway influences the function of the lower urinary tract in vivo, as studied by cystometry in consciousrats and in vitro, in isolated muscle preparations from the rat detrusor and urethra.2 L-N0-nitro arginine methyl ester (L-NAME), 10 and 20 mg kg-, administered intra-arterially,decreased micturition volume and bladder capacity, and increased spontaneous bladder contractions.D-NAME (20mgkg-') had no effect. No changes in the urodynamic parameters were recorded ifL-NAME (20mgkg-') was administered in combination with L-arginine (200mgkg-').3 Cystometries performed after intra-arterial administration of sodium nitroprusside (SNP) (3mgkg-') and 3-morpholino-sydnonimin hydrochloride (SIN-1, 2mgkg-') showed a decrease in bladdercapacity, micturition volume and threshold pressure. SIN-1, but not SNP, induced spontaneous bladdercontractions.4 Isolated precontracted urethral preparations responded to electrical stimulation with a frequencydependenttetrodotoxin-sensitive relaxation. L-NAME (10-4 M), but not D-NAME, reduced the maximalrelaxation to 31 ± 8% (n = 8) of the response prior to drug administration. The inhibition induced byL-NAME was completely reversed by L-arginine (10-3 M). SNP (10-1 10-4 M), SIN-1 (10-6-3 x l0-4M) and NO (10-5-10-3M; present in acidified solution of NaNO2), caused relaxation (93-100%) ofurethral preparations. L-NAME did not affect these relaxations.5 Detrusor strips contracted by carbachol or K' showed contractions in response to electricalstimulation, even when pretreated with a,p-methylene ATP and/or atropine. Small relaxations (14-41%)of detrusor strips were evoked by SNP (10-6-10-4M), SIN-1 (10-5-3 x 10-4M) and NO (10-5-10-3M). Electrically (20 Hz) induced contractions of the detrusor muscle were unaffected by addition ofL-NAME (10-6_10-4 M) or L-arginine (10-3 M).6 The present results suggest that the L-arginine/NO pathway is of functional importance for thebladder outlet region, but that its role in the detrusor is questionable. They also suggest that the site ofaction of L-NAME for inducing bladder hyperactivity in the rat is the outlet region rather than thedetrusor muscle. 
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8.
  • Takeda, H, et al. (författare)
  • Effects of beta(3)-adrenoceptor stimulation on prostaglandin E-2-induced bladder hyperactivity and on the cardiovascular system in conscious rats
  • 2002
  • Ingår i: Neurourology and Urodynamics. - : Wiley. - 0733-2467 .- 1520-6777. ; 21:6, s. 558-565
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims. To investigate the effects of selective beta(2)- and selective beta(3)-adrenoceptor (AR) agonists on prostaglandin (PG) E-2-induced bladder hyperactivity in conscious free-moving rats. Methods. Female Sprague-Dawley rats were anesthetized for implantation of bladder, intravenous, and intra-arterial catheters. The effects of a beta(3)-AR agonist (CL316,243) on cystometric and cardiovascular parameters were assessed in conscious rats. Intravesical instillation of PGE(2) (20-60 muM, 6 mL/hr) in conscious rats produced a concentration-dependent increase in voiding frequency. Results. In this model i.v. CL316,243 (beta(3)-AR agonist) reduced basal bladder pressure, increased micturition volume, and prolonged micturition interval in a dose-dependent manner, without affecting threshold pressure or micturition pressure. On the other hand, i.v. procaterol (beta(2)-AR agonist) did not counteract the bladder hyperactivity. Atropine (muscarinic antagonist) reduced micturition pressure and micturition volume, and shortened micturition interval. CL316,243 slightly decreased mean blood pressure and increased heart rate only when given at high doses (10 and 100 mug/kg, iv.). In contrast, procaterol caused a significant decrease in mean blood pressure and a significant increase in heart rate. Atropine significantly increased heart rate. Conclusions. The present results clearly demonstrated that the beta(3)-AR agonist prolonged the micturition interval without producing significant cardiovascular side effects. The human detrusor, like the rat detrusor, relaxes on beta(3)-AR stimulation. Provided that these results are valid in humans, selective beta(3)-AR agonists might be clinically useful for controlling a certain type of bladder overactivity.
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