ライフサイエンスコーパス: voiding

1 d urinary retention (requiring early morning voiding).

2 the bladder dose can be reduced by frequent voiding.

3 bladder dose can be reduced by more frequent voiding.

4 ow rate suggested poor meatal opening during voiding.

5 lated using OLINDA 1.1 software, assuming no voiding.

6 MBq, depending on the assumptions on bladder voiding.

7 DFV by internalizing apical membrane during voiding.

8 es implicated in facial expression and urine voiding.

9 r to be important for coordination of proper voiding.

10 y and inhibitory effects on the frequency of voiding.

11 ynamic acquisition without disruption due to voiding.

12 , whereas withdrawals were suppressed during voiding.

13 not leak, and empties completely by natural voiding.

14 stimulation, bladder training, and prompted voiding.

15 ating detrusor pressure and flow rate during voiding.

16 aks, or does not empty completely by natural voiding.

17 ested that several transmitters may modulate voiding.

18 s in urine volume during bladder filling and voiding.

19 quency and was markedly decreased with early voiding.

20 metabolites and increasing the frequency of voiding.

21 al ureters and on radiographs obtained after voiding.

22 the uptake phase as well as before and after voiding.

23 and anorectal junction during liquid medium voiding.

24 nonsecretor phenotype, or delayed postcoital voiding.

25 CATS-1st) was developed for post-surgery mid-voiding.

26 tract or by functional impairment of urinary voiding.

27 t to the neural circuits controlling bladder voiding.

28 auses bladder contraction, typically without voiding.

29 on of these axon terminals reliably provokes voiding.

30 e of urothelium in regulating continence and voiding.

31 ack from maintaining continence to producing voiding.

32 xes to either maintain continence or promote voiding.

33 intaining continence and producing efficient voiding.

34 ollowed by place and position preference for voiding.

35 ling, which can be manually compressed after voiding.

36 te that urothelium itself directly modulates voiding.

37 hat close the ureterovesical junction during voiding.

38 /- 2.4, and 20.9 +/- 5.2 muSv/MBq for the no-voiding, 2.5-h-voiding, and 1-h-voiding models, respecti

39 2; dysuria without infection, 6; difficulty voiding, 3; and silent stones, 2.

40 ients, renography was interrupted because of voiding (30%), whereas this occurred in only 3 of the F

41 uring the first cycle of bladder filling and voiding, a second cycle was performed.

42 expert opinion, women with diabetes without voiding abnormalities presenting with acute cystitis sho

43 Voiding activity analyses revealed bladder overactivity

44 ent strategies were devised, including timed voiding alone (n=6), clean intermittent catheterization

45 ed aberrant maximum detrusor pressure during voiding and a reduction of the abnormal EMG high-frequen

46 a maximum of 10) were normal, showing normal voiding and erectile function, respectively.

47 commodate large changes in cell shape during voiding and filling cycles.

48 phrine (3000 nmol) completely blocked reflex voiding and induced overflow incontinence at a high base

49 the micturition control circuitry, to defer voiding and maintain urinary continence, even when the b

50 Urinary voiding and nocturia were worse in the radiotherapy grou

51 n, with ON cells promoting the initiation of voiding and OFF cells promoting urine storage.

52 leting Crh from Bar neurons has no effect on voiding and related bladder physiology.

53 inistration reduces the frequency of bladder voiding and restores the voided volume of CYP-treated mi

54 on, catheter size, catheter in or out during voiding and sex on flow rate, flow pattern, voiding pres

55 al cord injury disrupts voluntary control of voiding and the normal reflex pathways that coordinate b

56 ) is thought to contain neurons that trigger voiding and thereby function as the "pontine micturition

57 nabled bacteria to escape elimination during voiding and to re-emerge in the urine as the bladder dis

58 9 +/- 5.2 muSv/MBq for the no-voiding, 2.5-h-voiding, and 1-h-voiding models, respectively.

59 in controlling facial expression and urinary voiding, and also in bladder smooth muscle, consistent w

60 ctions, vesicoureteral reflux, dysfunctional voiding, and appropriate imaging studies.

61 ure had urinary tract infections, difficulty voiding, and postoperative urge incontinence.

62 eting behaviours (premature voiding, delayed voiding, and straining to void) were positively associat

63 iours (especially premature voiding, delayed voiding, and straining to void), as these unhealthy toil

64 this subset of Bar neurons is necessary for voiding, and the broader circuitry providing input to th

65 the dynamic processes of bladder filling and voiding apical membrane dynamics depend on sequential an

66 h as pelvic floor physical therapy and timed voiding, as well as pharmacologic therapy, including alp

67 Assuming bladder voiding at 2- or 4-hr intervals, the critical organ that

68 For a single bladder voiding at 6 h after (18)F-FLT injection, the (18)F-FLT

69 elvic floor physical therapy, timed voiding (voiding at specific intervals), and fluid restriction, c

70 month and 6 months posttransplant, the urine voiding behavior of recipient mice and control mice was

71 Cystometrogram study and tracing analysis of voiding behavior revealed that the ketamine-treated rats

72 bladder (megacystis) phenotype and abnormal voiding behavior similar to that found in patients.

73 Voiding behavior was monitored using specially designed

74 related to micturition and initiate specific voiding behaviors so that micturition occurs in environm

75 and lumbar spinal cord to coordinate complex voiding behaviors.

76 In vivo natural voiding behaviour, sensory nerve activity, urothelial ce

77 common among the female nurses, with delayed voiding being the unhealthiest toileting behaviour, whic

78 had a higher frequency of low-amplitude, non-voiding bladder contractions.

79 feedback programs for treating dysfunctional voiding, Botox injections for overactive bladder and an

80 ears completely with manual compression, and voiding can be maintained in this way.

81 al absorption and drug washout during normal voiding can limit sustained drug concentrations in the u

82 fort or pain during or after ejaculation and voiding complaints such as irritative and obstructive vo

83 inary retention, return of reflexive bladder voiding contractions coincident with EUS EMG activation,

84 ave a significant role in the control of non-voiding contractions in vivo.

85 acity was highest with alpha-chloralose, non-voiding contractions were greatest with alpha-chloralose

86 a therapeutic approach for management of non-voiding contractions, a condition which characterizes ma

87 capacity, residual volume, and number of non-voiding contractions, and the total elastin/collagen amo

88 e, bladder capacity, bladder compliance, non-voiding contractions, bladder pressure slopes) and anest

89 oduction and caused a marked increase in non-voiding contractions.

90 y decreased the frequency of spontaneous non-voiding contractions.

91 erfering RNA, increased the interval between voiding contractions.

92 ed clearance of infection compared to normal-voiding controls.

93 s dramatic volume changes during filling and voiding cycles.

94 e seen on Retrograde Urethrography (RGU) and Voiding Cysto-Urethrography (VCUG), i.e. linear incomple

95 Intravenous urography, voiding cysto-urethrography and MRI confirmed the ultras

96 ation was followed by intravenous urography, voiding cysto-urethrography and MRI of the abdomen.

97 Academy of Pediatrics recommend obtaining a voiding cystourethrogram and a renal ultrasonogram for y

98 coureteral reflux that is missed by standard voiding cystourethrogram but detectable during positiona

99 ammatory markers (model 2); and model 2 plus voiding cystourethrogram findings (model 3).

100 A voiding cystourethrogram for the identification of reflu

101 enatal hydronephrosis with an ultrasound and voiding cystourethrogram is reasonable and may reduce th

102 the determination of the degree of reflux by voiding cystourethrogram is to guide the institution of

103 a history of prenatal hydronephrosis with a voiding cystourethrogram may reduce this risk.

104 patients require postnatal evaluation with a voiding cystourethrogram to investigate for vesicoureter

105 ty of models requiring a blood draw and/or a voiding cystourethrogram.

106 Only 13 voiding cystourethrograms (VCUGs) (2.5%) of 517 were fou

107 diagnosis of vesicoureteral reflux involves voiding cystourethrograms, which are invasive and costly

108 Retrograde urethrography (RU) and voiding cystourethrography (VCU) are traditional diagnos

109 Retrograde Urethrography - Voiding Cystourethrography evaluation of the urethra and

110 Magnetic resonance voiding cystourethrography has been used to rule out ves

111 In many centers, voiding cystourethrography is a routine part of pretrans

112 Voiding cystourethrography should be performed routinely

113 ed within 72 hours after diagnosis, contrast voiding cystourethrography was performed one month later

114 n included US, MR imaging, autopsy, surgery, voiding cystourethrography, computed tomography, angiogr

115 ltrasonography (US), renal scintigraphy, and voiding cystourethrography.

116 air-wise comparison of changes in individual voiding data from preREL+future veh or preREL+future rap

117 Unhealthy toileting behaviours (premature voiding, delayed voiding, and straining to void) were po

118 y toileting behaviours (especially premature voiding, delayed voiding, and straining to void), as the

119 mpted to correlate common clinical measures (voiding diaries, pad testing, urodynamics) with quality-

120 A voiding diary is commonly used in clinical practice to m

121 Voiding difficulty and acute urinary retention are infre

122 balance symptom improvement and incidence of voiding difficulty.

123 l pressure, large residual urine volume, and voiding difficulty.

124 tion of the pelvic floor and contributing to voiding difficulty.

125 ncreased interest in pediatric nonneurogenic voiding disorders (NNVDs), urodynamic testing and therap

126 Idiopathic voiding disorders affect up to 10-15% of men and women.

127 athway may play an important role in urinary voiding disorders characterized by abnormal bladder moti

128 y demonstrating the inaccuracy of predicting voiding disorders on the basis of uroflow alone or the m

129 ons in both spinal cord signaling and reflex voiding during bladder filling (under anesthesia).

130 Voiding dysfunction after anti-incontinence procedures i

131 le of preoperative urodynamics in predicting voiding dysfunction after anti-incontinence surgery is r

132 of the urothelial barrier, a major cause of voiding dysfunction and bladder pain syndrome.

133 eye movement behaviour disorder and urinary voiding dysfunction appear to precede the development of

134 ase ALPL, which might mitigate the degree of voiding dysfunction by compensating for Nt5e deletion.

135 d contraction force, suggesting that bladder voiding dysfunction can be attributed to impaired BSM co

136 5-HT3A mutant mice had marked voiding dysfunction characterized by a loss of micturiti

137 of women who appear to be at higher risk of voiding dysfunction following incontinence surgery, and

138 Urinary voiding dysfunction in childhood, manifesting as inconti

139 Voiding dysfunction in children encompasses a wide spect

140 Over the last several decades voiding dysfunction in children has primarily been assoc

141 This overview of voiding dysfunction in children outlines the established

142 ill focus on the diagnosis and management of voiding dysfunction in neurologically and anatomically n

143 tive urodynamics in predicting postoperative voiding dysfunction in patients undergoing anti-incontin

144 Several aspects of voiding dysfunction in women remain under investigation,

145 hough not useful in the primary treatment of voiding dysfunction is equivalent in potency to biofeedb

146 Voiding dysfunction may play an etiological role in cong

147 Voiding dysfunction may spontaneously improve or require

148 prognostic information regarding the risk of voiding dysfunction postoperatively and the possibility

149 The rates of voiding dysfunction requiring surgery were 2.7% in those

150 afferent neurons may therefore contribute to voiding dysfunction seen in diabetes mellitus.

151 Voiding dysfunction typically presents after toilet trai

152 igher rate of lower urinary tract injury and voiding dysfunction when compared with transobturator ta

153 so assessed postoperative urge incontinence, voiding dysfunction, and adverse events.

154 lications (urinary tract infection, urgency, voiding dysfunction, and mesh erosion) were more common

155 of clinical presentations such as hematuria, voiding dysfunction, flank pain, abdominal pain, nephrol

156 se medications in the treatment of pediatric voiding dysfunction, neurogenic bladder, chronic lower u

157 rates of positive provocative stress tests, voiding dysfunction, or adverse events.

158 complications include but are not limited to voiding dysfunction, urinary retention, vaginal extrusio

159 basis of lower renal tract malformations and voiding dysfunction.

160 th overactivity syndromes and nonobstructive voiding dysfunction.

161 ck therapy for the treatment of recalcitrant voiding dysfunction.

162 ed comfort for patients with incontinence or voiding dysfunction.

163 reatment of benign prostatic hyperplasia and voiding dysfunction.

164 rned voiding patterns that contribute to the voiding dysfunction.

165 and smooth muscle contractility, leading to voiding dysfunction.

166 offers promise for managing both storage and voiding dysfunction.

167 urinary-tract infection, hydronephrosis, and voiding dysfunctions as a result of neurogenic bladders.

168 orrelation between motoneuronal survival and voiding efficiency was observed in the implanted group.

169 ong participants with fewer than 1 nocturnal voiding episode per night but 6.66 points (95% CI, 6.00

170 duction of bladder activity by more frequent voiding facilitated by increased urine volume in hydrate

171 ng urethral catheter, patients with impaired voiding following spinal cord injury, patients undergoin

172 tivity (-38%, n = 6) or completely inhibited voiding (four sites).

173 unced autonomic arousal and increased reflex voiding frequency (+237%, n = 34).

174 o reduce ongoing GABA tone, increased reflex voiding frequency (+467%, n = 16) and tonic activity in

175 er sites in the PAG, either depressed reflex voiding frequency (-60%, n = 7) and tonic EUS EMG activi

176 th factor (NGF) in contributing to increased voiding frequency and altered sensation from the urinary

177 GF-beta) signalling contributes to increased voiding frequency and decreased bladder capacity with cy

178 In aged mice, increased voiding frequency and enhanced low threshold afferent ne

179 der hyporeflexia, characterized by decreased voiding frequency and increased bladder capacity, but no

180 Bladder tau decreased with voiding frequency and was markedly decreased with early

181 for 1 h reduced the effect of acetic acid on voiding frequency as reflected by an increase in the int

182 concentrations of OxoM (5 microM) decreased voiding frequency by approximately 30%, an effect blunte

183 concentrations of OxoM (40 microM) increased voiding frequency by approximately 45%, an effect blunte

184 egardless of intervention, greater nocturnal voiding frequency was associated with worse sleep qualit

185 ed, Cav1.2 activation by Bay k8644 decreases voiding frequency while increasing void volume, indicati

186 nd across increasing categories of nocturnal voiding frequency).

187 g) did not mimic the intravesical effects on voiding frequency.

188 ion that may ultimately facilitate increased voiding frequency.

189 in the bladder perfusate, and also increased voiding frequency; these effects were suppressed by BB-F

190 technique, short-term and long-term results, voiding function after feminizing genitoplasty, and the

191 e control vector (HSV-lacZ), indicating that voiding function was improved after HSV vector-mediated

192 rent nerve interactions can influence reflex voiding function.

193 ntraspinal circuit that regulates sexual and voiding function.

194 n C-RELAP group showed a delayed recovery of voiding function.

195 in inappropriate places without a change in voiding function.

196 ladder and that luminal release can modulate voiding function.

197 r the luminal surface of the bladder affects voiding functions via mechanisms involving ATP and NO re

198 nt patient's behavior, especially his or her voiding habits, and by teaching skills for preventing ur

199 ds during bladder filling and contracts upon voiding; however, the mechanisms that drive these events

200 ssociated detrusor contractions, resulted in voiding in a significantly larger proportion of female c

201 usly hypertensive rats (SHR) and hyperactive voiding in rats with urethral obstruction are characteri

202 lood pressure, and enabled the initiation of voiding in seven individuals with motor complete SCI.

203 hyperinnervation of bladder and hyperactive voiding in SHRs.

204 brainstem neurons involved in continence and voiding in the female rat.

205 uctural integrity in order to enable urinary voiding in the standing position and second, achieving e

206 ion, and a treatment option that can restore voiding in this group of patients - sacral nerve electri

207 In contrast, the voiding-induced contraction of the AJR depended on NMMII

208 at 536 +/- 61 muGy/MBq using a 4.8-h bladder-voiding interval for the male phantom.

209 .5 +/- 0.30 mSv (at 300 MBq), with a bladder-voiding interval of 0.75 h.

210 Reducing the urinary voiding interval to 60 or 90 min lowered the urinary bla

211 Simulations in which the urinary voiding interval was decreased from 4.8 to 0.6 h produce

212 jected dose of 10 mCi (370 MBq) and a 1-hour voiding interval, a patient would be exposed to an effec

213 For a 0.75-h voiding interval, the bladder dose was reduced to 0.10 +

214 With a 2.4-h voiding interval, the calculated effective dose was 6.98

215 Assuming a 2.4-h urine voiding interval, the calculated effective doses from th

216 With a 2.4-h voiding interval, the effective dose was 5.7 microSv/MBq

217 For a 1-h voiding interval, these doses were reduced to 15 +/- 2 m

218 e dose was 0.0141 mSv/MBq when using a 3.5-h voiding interval.

219 n adult male with a 1.5 hour urinary bladder voiding interval.

220 an adult male, with a 1.5-h urinary bladder voiding interval.

221 the dynamic bladder model with a 1-h bladder-voiding interval.

222 rinary bladder wall (0.021 mGy/MBq with 2-hr voiding intervals or 0.029 mGy/MBq with 4-hr voiding int

223 , avoidance of excessive fluids, and regular voiding intervals that reduce urgency incontinence episo

224 y bladder wall (with hydration and 1- to 2-h voiding intervals).

225 voiding intervals or 0.029 mGy/MBq with 4-hr voiding intervals).

226 00868 +/- 0.00481 cGy/MBq (to bladder wall) (voiding intervals, 1-2 h), and the effective dose equiva

227 d 0.067 +/- 0.007 mGy/MBq for the 2- and 4-h voiding intervals, respectively.

228 be reduced significantly by frequent bladder-voiding intervals.

229 either restricted in this age group nor does voiding into a diaper cause disruption.

230 Normal voiding is dependent on mechanoceptive Adelta-fiber blad

231 age were excluded from consideration because voiding is neither restricted in this age group nor does

232 in the physiological control of storage and voiding is unclear.

233 a cells functions to recover membrane during voiding, is integrin regulated, occurs by a RhoA- and dy

234 By compromising urine storage and voiding, LUTDs degrade quality of life for millions of i

235 om dysfunctional voiding - unfavorable pouch voiding mechanics, insufficient pouch pressure generatio

236 re inspected for evidence of interruption or voiding midstudy.

237 rem/mCi +/- 0.436 [0.233 mSv/MBq +/- 0.118], voiding model) and uptake in the spleen (0.250 rem/mCi +

238 With the 1-h voiding model, these doses reduced to 15 +/- 1 muSv/MBq

239 376 +/- 19 muGy/MBq using the 4.8-h bladder-voiding model.

240 q for the no-voiding, 2.5-h-voiding, and 1-h-voiding models, respectively.

241 th arousal and attentional processes so that voiding occurs under appropriate conditions.

242 ange or a reduction in urethral pressure and voiding of small amounts of fluid.

243 dramatic cell deformation during filling and voiding of the bladder.

244 Storage and voiding of urine from the lower urinary tract (LUT) must

245 dder is locked in storage mode, switching to voiding only when it is judged safe and/or socially appr

246 d a significantly higher bladder pressure at voiding onset, peak pressure, and elevation in detrusor-

247 ay prior to release of obstruction (preREL), voiding parameters and residual urine volume of preREL+f

248 Voiding parameters and residual urine volume were measur

249 well as behavioral therapy to modify learned voiding patterns that contribute to the voiding dysfunct

250 discussing voiding physiology, dysfunctional voiding patterns, acute urinary retention, urine collect

251 er and more likely to receive a diagnosis of voiding-phase dysfunction, but these changes did not lea

252 earch on urinary tract infection, discussing voiding physiology, dysfunctional voiding patterns, acut

253 ptoms were not significantly associated with voiding place or position preference.

254 thermore, T13-L2 scES was shown to stimulate voiding post-transection by increasing bladder activity

255 tic target for human disease states, such as voiding postponement, urinary retention, and underactive

256 comprising the detrusor elicit transient non-voiding pressure events and associated bursts in afferen

257 t bladders, cystometry showed increased peak voiding pressure, voiding volume, bladder capacity, resi

258 revealed overactive bladder, reduced maximal voiding pressures and incontinence in IgG control, but n

259 voiding and sex on flow rate, flow pattern, voiding pressures, presence of overactivity and interpre

260 with urinary incontinence and dysfunctional voiding problems can be very difficult at times.

261 play a major role in the causation of their voiding problems, whereas delayed arousal from sleep in

262 prostate size, residual urinary volume after voiding, quality of life, laboratory values, and the rat

263 1.38), prostate size, residual volume after voiding, quality of life, or serum prostate-specific ant

264 An earlier bladder voiding reduced these doses by 25%-45%.

265 regions associated with bladder filling and voiding reflex arcs.

266 helium functions as a sensor to initiate the voiding reflex, during which it releases ATP via multipl

267 ladder of the rat increased the frequency of voiding reflexes by 8 fold and increased c-fos expressio

268 ections to Barrington's nucleus may regulate voiding reflexes during sexual behavior.

269 : (1) inhibitory control of the frequency of voiding reflexes presumably by regulating afferent proce

270 The voiding schedule includes an extended nighttime gap duri

271 .004 mSv/MBq, respectively, depending on the voiding schedule.

272 Urinary voiding should be performed during (18)F-FPEB studies to

273 erform a second cycle of bladder filling and voiding should take into account the pretest probability

274 We found that voiding-stimulated CE, which depended on beta(1) integri

275 treatment of disorders of urine storage and voiding such as overactive bladder.

276 rnal enuresis, while others manifest diurnal voiding symptoms (DVS) as well, including urinary freque

277 creased risk of a rapid change in irritative voiding symptoms and decreased urinary flow but not obst

278 ere hypothesized to contribute to irritative voiding symptoms and pain by allowing the permeation of

279 These findings support the notion that voiding symptoms and pain seen in forms of cystitis that

280 d decreased urinary flow but not obstructive voiding symptoms or prostate size.

281 ate volume, serum prostate-specific antigen, voiding symptoms, and urinary flow were minor.

282 ompared with no NSAID use) and overall LUTS, voiding symptoms, or nocturia in men or women.

283 us treatments for BPH with questionnaires on voiding symptoms, related complications, and sexual func

284 atios and 95% confidence intervals for LUTS, voiding symptoms, storage symptoms, and nocturia.

285 n of novel therapies for pain and irritative voiding symptoms.

286 ptoms, 40% had filling symptoms, and 18% had voiding symptoms.

287 omplaints such as irritative and obstructive voiding symptoms: urinary frequency, urgency, and dysuri

288 ms have a combination of both 'storage' and 'voiding' symptoms, suggesting possible coexisting bladde

289 ficantly lower rate of disruption because of voiding than the F-15 protocol, likely due to the shorte

290 of pain with bladder filling or relieved by voiding, the extent of chronic overlapping pain conditio

291 The optimal first voiding time is from 40 min to 3 hr postadministration,

292 re must be differentiated from dysfunctional voiding - unfavorable pouch voiding mechanics, insuffici

293 ewing the circumcision debate, dysfunctional voiding, vesicoureteral reflux, and the diagnosis and fo

294 cluding pelvic floor physical therapy, timed voiding (voiding at specific intervals), and fluid restr

295 etry showed increased peak voiding pressure, voiding volume, bladder capacity, residual volume, and n

296 The mean time of voiding was 18.3 min (range, 12-25 min) for F-15 patient

297 nce episodes as recorded in a 7-day diary of voiding were similar in the intervention group and the c

298 stimulation of Bar(Vglut2) neurons triggers voiding, whereas stimulating the Bar(Crh/Vglut2) subpopu

299 orders includes urge syndrome, dysfunctional voiding with an uncoordination between the detrusor and

300 includes (1) uroflowmetry, an assessment of voiding without catheters in place; (2) cystometry, whic