| 1. |
- Abe, K., et al.
(author)
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Neutron tagging following atmospheric neutrino events in a water Cherenkov detector
- 2022
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In: Journal of Instrumentation. - : Institute of Physics (IOP). - 1748-0221. ; 17:10
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Journal article (peer-reviewed)abstract
- We present the development of neutron-tagging techniques in Super-Kamiokande IV using a neural network analysis. The detection efficiency of neutron capture on hydrogen is estimated to be 26%, with a mis-tag rate of 0.016 per neutrino event. The uncertainty of the tagging efficiency is estimated to be 9.0%. Measurement of the tagging efficiency with data from an Americium-Beryllium calibration agrees with this value within 10%. The tagging procedure was performed on 3,244.4 days of SK-IV atmospheric neutrino data, identifying 18,091 neutrons in 26,473 neutrino events. The fitted neutron capture lifetime was measured as 218 +/- 9 mu s.
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| 2. |
- Gu, BJ, et al.
(author)
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Role of supraspinal alpha 1-adrenoceptors for voiding in conscious rats with and without bladder outlet obstruction
- 2002
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In: Journal of Urology. - 1527-3792. ; 167:4, s. 1887-1891
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Journal article (peer-reviewed)abstract
- Purpose: Previous studies have shown that spinal alpha1-adrenoceptors can influence voiding in normal rats and in rats with outlet obstruction. Also, at the supraspinal level such receptors may be involved in voiding control. Therefore, we studied in rats the effects on cystometrography of intracerebroventricular administered alpha1-adrenoceptor antagonists. Materials and Methods: Continuous cystometry was performed in conscious, freely moving rats with and without bladder outlet obstruction. Cystometric parameters were evaluated before and after intracerebroventricular drug administration. Results: In normal rats intracerebroventricular administration of 8 nmol. kg.(-1) prazosin (Pfizer Central Research, Sandwich, United Kingdom) or terazosin (Abbott Laboratories, Abbott Park, Illinois) (nonsubtype selective) caused no change in cystometric parameters. At 24 or 80 nmol. kg.(-1) the 2 drugs significantly decreased voiding pressure and increased bladder capacity, voided volume and post-void residual urine volume. Administering vehicle had no effect. In rats with outlet obstruction the drug effects were significantly more pronounced than in normal animals (p <0.05), and urinary retention was produced in 50% of rats receiving prazosin. In normal rats the selective alpha1A-adrenoceptor antagonists KMD 3213 (0.8, 8 and 24 nmol. kg.(-1)) dose dependently depressed voiding pressure, and increased bladder capacity and voided volume, whereas BMY 7378 (selective for alpha1D-adrenoceptors) and A322312 (selective for alpha1B-adrenoceptors) at doses up to 80 nmol. kg.-1 had no effect. Conclusions: The results suggest that in normal rats and in rats with outflow obstruction volume induced bladder activity involves supraspinal alpha1-adrenoceptors. Bladder outlet obstruction seems to enhance the importance of these receptors. At least in normal rats the alpha1A-adrenoceptor subtype seems to mediate the effect.
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| 3. |
- Ishizuka, O, et al.
(author)
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Effect of apomorphine on intracavernous pressure and blood pressure in conscious, spinalized rats
- 2002
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In: International Journal of Impotence Research. - 1476-5489. ; 14:2, s. 128-132
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Journal article (peer-reviewed)abstract
- Apomorphine, given subcutaneously (s.c.), induces erection and bladder overactivity in rats through stimulation of dopamine (D1- and D2-like) receptors in the central nervous system. In paraplegic patients, apomorphine was reported to cause bladder overactivity. This suggests that apomorphine may have a spinal site of action also for stimulation of erection. The present study was initiated to evaluate the effect of apomorphine on erectile function in spinalized rats. Apomorphine (100 mug/kg, s.c.) was given to awake. unrestrained male Sprague-Dawley rats (300 g) with or without spinal cord injure, made at the Th 8 level 2 weeks before the experiment. Intracavernous pressure changes from baseline were evaluated as time to first response to apomorphine (TFR; see), number of phasic pressure changes in the first 30 min (PP30), duration (113; see) of the phasic pressure changes, the amount of increase in tonic peak pressure (TPP; cmH(2)O), and burst peak pressure (BPP, cmH(2)O). Blood pressure (cmH(2)O) was recorded via an intra-arterial catheter. Apomorphine, 100 mug/kg, caused no significant differences in TFR (217.8 vs 271.2), PP30 (6.4 vs 6.5), D (38.9 vs 37.6.), TPP (51.0 vs 54.0) and BPP (128.9 vs 160.4) between normal (n = 8) and spinalized rats (n = 6). However, blood pressure decreased significantly more in spinalized than in normal animals (17.7 vs 43.3: P < 0.05). The results suggest that both in normal rats, and in rats with spinal cord injury, apomorphine given s.c., can produce erection. This finding supports the use of apomorphine for treatment of erectile dysfunction in paraplegia patients. However, due consideration should be given to possible decreases in blood pressure.
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| 4. |
- Ishizuka, O, et al.
(author)
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Functional role of central muscarinic receptors for micturition in normal conscious rats
- 2002
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In: Journal of Urology. - 1527-3792. ; 168:5, s. 2258-2262
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Journal article (peer-reviewed)abstract
- Purpose: Antimuscarinic agents, which are used in to treat urgency and urge incontinence, have well-known effects on peripheral muscarinic receptors. However, some currently used drugs may have effects on muscarinic receptors in the brain and/or spinal cord involved in voiding control. We tested if muscarinic receptors within the central nervous system mediate a tonic excitatory influence on voiding in rats and if these receptors can be differently influenced by antimuscarinic drugs. Materials and Methods: The effects on cystometrography of intracerebroventricular atropine, oxybutynin, tolterodine and darifenacin were investigated in normal conscious rats. Results: Atropine (0.2 to 2 nmol.) dose dependently affected urodynamic parameters. At 2 nmol. in 6 rats the drug decreased voiding pressure (p <0.01), and increased bladder capacity (p <0.001), voided volume (p <0.05) and post-void residual volume (p <0.05). In 6 rats oxybutynin (6 to 40 nmol.) given at a dose of 6 nmol. caused no change in cystometric parameters, while at 20 nmol. the drug decreased voiding pressure (p <0.01). Tolterodine (2 to 20 nmol.) dose dependently changed urodynamic parameters, while at 20 nmol. in 6 rats the drug decreased voiding pressure (p <0.01) and increased bladder capacity (p <0.05) and voided volume (p <0.05). Darifenacin given at a dose of 20 nmol. in 6 rats caused no change in cystometric parameters. Conclusions: Muscarinic receptor mechanisms in the central nervous system mediate a tonic excitatory influence on voiding in rats, while nonsubtype selective antimuscarinic drugs may have an inhibitory effect on these mechanisms.
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| 5. |
- Ishizuka, O, et al.
(author)
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Role of supraspinal serotonin receptors for micturition in normal conscious rats
- 2002
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In: Neurourology and Urodynamics. - : Wiley. - 0733-2467 .- 1520-6777. ; 21:3, s. 225-230
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Journal article (peer-reviewed)abstract
- Serotonin (5-HT) receptors are widely distributed in the central nervous system, including several areas involved in the control of micturition reflex pathways. However, the roles of the different subtypes of 5-HT receptors are not well known. We studied in normal, conscious rats, the effects on the cystometrogram of intracerebroventricular (i.c.v.) administration of 5-HT, 8-hydroxy-2-(di-N-propylaminotetralin) (8-OH-DPAT; agonist at 5-HT1A receptors), alpha-methol-5-hydroxytryptamine maleate (agonist at 5-HT2 receptors), 2-methyl-5-hydroxytryptamine hydrochloride (agonist at 5-HT3 receptors), and 1-(4-amino-5-chloro-2methoxyphenyl)-3-(1-n-butyl-4piperidinyl)-1-propano ne hydrochloride (RS67506; agonist at 5-HT4 receptors). Female Sprague-Dawley rats, weighing approximately 230 g, were used. A polyethylene catheter was inserted into the bladder through the dome for cystometric investigations. For administration of drugs, a catheter was implanted into the right cerebral ventricle. Three days after implantation of the bladder catheter, continuous cystometry was performed. Administration of 5-HT (6 nmol/kg i.c.v.), 8-OH-DPAT (6 nmol/kg), alpha-methyl-5-hydroxytryptamine maleate (6 nmol/kg), or RS67506 hydrochloride (6 nmol/kg) significantly (P < 0.05) increased micturition pressure and decreased bladder capacity and micturition volume. The effects increased in a dose-dependent manner (18, 60 nmol/kg). Intracerebroventricular administration of 2-methyl-5-hydroxytryptamine hydrochloride (60 nmol/kg) caused no change in the cystometric parameters. The results suggest that in normal conscious rats, at the supraspinal level, 5-HT (via 5-HT1A, 5-HT2, and 5-HT4 receptors) can enhance the micturition reflex induced by bladder filling. Whether this means that 5-HT1A, 5-HT2, and 5-HT4 receptors can be targets for drugs meant for treatment of bladder hyperactivity, should be explored. (C) 2002Wiley-Liss, Inc.
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| 6. |
- Zhang, XY, et al.
(author)
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Effects of resiniferatoxin desensitization of capsaicin-sensitive afferents on detrusor over-activity induced by intravesical capsaicin, acetic acid or ATP in conscious rats
- 2003
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In: Naunyn-Schmiedeberg's Archives of Pharmacology. - : Springer Science and Business Media LLC. - 0028-1298. ; 367:5, s. 473-479
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Journal article (peer-reviewed)abstract
- Recent studies have provided evidence for a major role of urothelially released ATP acting on a subpopulation of pelvic afferent nerves in mechano-afferent transduction in the bladder. We investigated whether desensitization of capsaicin-sensitive nerve fibres by systemic resiniferatoxin (RTX)-pretreatment can counteract the detrusor over-activity induced by intravesical capsaicin, acetic acid or ATP. Cystometric investigations were performed on awake female Sprague-Dawley rats before and 24 h after injection of RTX (0.3 mg/kg s.c.) or vehicle. The effects of intravesically instilled ATP (0.1 or 1.0 mM), capsaicin (30 muM) or acetic acid (pH 4.0) were compared with those of intravesical saline. RTX, but not its vehicle, significantly increased threshold pressure, voiding interval, micturition volume and bladder capacity. In the vehicle-pretreated rats, intravesical instillation of capsaicin or acetic acid significantly decreased voiding interval, micturition volume, and bladder capacity. However, in the RTX-pretreated rats, neither capsaicin nor acetic acid affected any parameter. On the other hand, intravesical ATP (0.1 mM) significantly decreased voiding interval and micturition volume in both groups of animals. At 1.0 mM, ATP also increased basal pressure and decreased the pressure threshold for micturition in both groups. The present results support the view that increased extracellular ATP has a role in mechano-afferent transduction in the rat bladder and that ATP-induced facilitation of the micturition reflex is mediated, at least partly, by nerves other than capsaicin-sensitive afferent nerves.
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| 7. |
- Ishizuka, O, et al.
(author)
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Effects of neurokinin receptor antagonists on L-dopa induced bladder hyperactivity in normal conscious rats.
- 1995
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In: Journal of Urology. - 1527-3792. ; 154:4, s. 1548-1551
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Journal article (peer-reviewed)abstract
- PURPOSE: The urodynamic effects of intrathecal neurokinin (NK) receptor blockade on L-dopa-induced bladder hyperactivity were investigated in a rat model. MATERIALS AND METHODS: Continuous cystometry was performed in normal, conscious, female Sprague-Dawley rats. RESULTS: In rats pretreated with intraperitoneal carbidopa 50 mg./kg., intraperitoneal L-dopa 50 mg./kg. caused bladder hyperactivity that could be attenuated by intrathecal administration of the NK1 receptor selective antagonist SR 140,333 (2 nmol.), whereas the NK2 receptor selective antagonist SR 48,968 (2 nmol.) failed to do so. Combination of SR 140,333 (2 nmol.) and SR 48,968 (2 nmol.), which by itself decreased micturition pressure, practically abolished the L-dopa-induced hyperactivity. CONCLUSIONS: The present results suggest that tachykinins, via stimulation of NK1 (and/or NK2) receptors, are involved in L-dopa-induced bladder hyperactivity, most probably at the spinal level. This implies tachykinin involvement in the supraspinal pathways that control the sacral parasympathetic center innervating the urinary bladder. It also implies that spinal NK receptors are a possible target for drugs aimed for elimination of bladder hyperactivity mediated via these pathways.
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| 8. |
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| 9. |
- Ishizuka, O, et al.
(author)
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Prostaglandin E2-induced bladder hyperactivity in normal, conscious rat. Involvement of tachykinins?
- 1995
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In: Journal of Urology. - 1527-3792. ; 153:6, s. 38-2034
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Journal article (peer-reviewed)abstract
- In normal conscious rats investigated by continuous cystometry, intravesically instilled prostaglandin (PG) E2 facilitated micturition and increased basal intravesical pressure. The effect was attenuated by both the NK1 receptor selective antagonist RP 67,580 and the NK2 receptor selective antagonist SR 48,968, given intra-arterially, suggesting that it was mediated by stimulation of both NK1 and NK2 receptors. Intra-arterially given PGE2 produced a distinct increase in bladder pressure before initiating a micturition reflex, indicating that the PG had a direct contractant effect on the detrusor smooth muscle. The effect of intra-arterial PGE2 could not be blocked by intra-arterial RP 67,580 or SR 48,968, which opens the possibility that the micturition reflex elicited by intra-arterial PGE2 was mediated by pathways other than the reflex initiated when the PG was given intravesically. The present results thus suggest that intra-arterial PGE2, given near the bladder, may initiate micturition in the normal rat chiefly by directly contracting the smooth muscle of the detrusor. However, when given intravesically, PGE2 may stimulate micturition by releasing tachykinins from nerves in and/or immediately below the urothelium. These tachykinins, in turn, initiate a micturition reflex by stimulating NK1 and NK2 receptors. Prostanoids may, via release of tachykinins, contribute to both urge and bladder hyperactivity seen in inflammatory conditions of the lower urinary tract.
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