ライフサイエンスコーパス: overactive

1 hereas the mechanically sensitive fibres are overactive.

2 , regulatory components upstream of WspR are overactive.

3 cal malignancies in which the AKT pathway is overactive.

4 orders in which CRF neurotransmission may be overactive.

5 other disorders in which CaRs are under- or overactive.

6 other pathologies in which FAAH and Cox are overactive.

7 n of an unrelated synthetic reporter gene is overactive (2.3- to 5.1-fold) at all sites in the genome

8 t that, in C, the mirror system for touch is overactive, above the threshold for conscious tactile pe

9 domain-binding motif of Crumbs die due to an overactive actomyosin network associated with disrupted

10 miR-146a-deficient mice, leading to both an overactive acute inflammatory response and chronic infla

11 variety of clinical outcome measures (e.g. 'Overactive, aggressive behaviour'), symptoms proved supe

12 In the context of cancer, overactive Akt promotes cell survival and proliferation.

13 This loss leads to overactive Akt signaling, which is correlated with incre

14 Overactive Akt/mTOR signaling induced by ASXL1-MT result

15 thy with severe renal injury secondary to an overactive alternative complement pathway (AP).

16 Central to this overactive and destructive host response are macrophages

17 In sprouty mutants, the FGF pathway is overactive and ectopic branches are induced on the stalk

18 Female subjects exposed to ethanol were overactive and exhibited spatial learning deficits, effe

19 However, overactive and prolonged inflammation compromises healin

20 eoclasts that are large, multinucleated, and overactive and that contain paramyxovirus-like nuclear i

21 -associated neurodegeneration accompanied an overactive anterior cingulate cortex, which in turn resu

22 In aHUS patients with an underlying overactive AP, additional stimulation of the AP and inhi

23 estrogen production within the breast due to overactive aromatase.

24 We hypothesized that in the presence of overactive ATP-insensitive KATP channels, a reduction in

25 wild-type, patient cells were found to have overactive auto-phosphorylation with downstream activati

26 emic lupus erythematosus is characterized by overactive B cells that differentiate into autoantibody-

27 Opn5-null mice show overactive BAT, increased body temperature, and exaggera

28 e, in late-gestation upper-layer precursors, overactive beta-catenin signaling was able to partially

29 OCD in the form of poor frontal control over overactive BG, and a frontostriatoinsular maldevelopment

30 Anticholinergic medications to treat overactive bladder (OAB) have been associated with incre

31 Overactive bladder (OAB) is a highly prevalent symptom c

32 As overactive bladder (OAB) is a prevalent and chronic medi

33 Overactive bladder (OAB) is often treated with medicatio

34 Overactive bladder (OAB) symptoms in Parkinson disease (

35 human beta3-AR agonist for the treatment of overactive bladder (OAB), is described.

36 tor agonists (beta3-AR) for the treatment of overactive bladder (OAB).

37 ld be an effective therapy for patients with overactive bladder (OAB); however, this approach is cont

38 Overactive bladder affects 10-12% of men, of which 13% a

39 Overactive bladder affects 10-27% of men, a significant

40 -five urine specimens (from 41 patients with overactive bladder and 24 controls) were examined using

41 drugs remain the first-line treatment of the overactive bladder and a favorable efficacy/tolerability

42 dysfunctional voiding, Botox injections for overactive bladder and an adult anticholinergic for over

43 Overactive bladder and benign prostatic hyperplasia comm

44 Control patients did not have overactive bladder and did not have a clinically relevan

45 ents for common urological disorders such as overactive bladder and interstitial cystitis/bladder pai

46 cantly less likely to receive a diagnosis of overactive bladder and more likely to receive a diagnosi

47 Men with overactive bladder and other lower urinary tract symptom

48 nation with an alpha-blocker, in men with an overactive bladder and summarize the efficacy and safety

49 d clinical trials, to establish the cause of overactive bladder and to determine the best method of m

50 ndicate that BK channel dysfunction leads to overactive bladder and urinary incontinence.

51 ure drug targets for effective management of overactive bladder are discussed.

52 ry to benign prostatic hyperplasia (BPH), an overactive bladder detrusor (a syndrome of urinary urgen

53 mon among men and are usually caused by BPH, overactive bladder detrusor, or both.

54 may be a viable target for the treatment of overactive bladder disorders.

55 from urothelium results in incontinence and overactive bladder due to abnormal mechanotransduction;

56 New theories and modified definitions of overactive bladder have been proposed, structured eviden

57 r existing anticholinergics, in treating the overactive bladder in children need closer scrutiny.

58 l nerve neuromodulation for the treatment of overactive bladder in patients who do not respond to opt

59 The overactive bladder is a common and distressing condition

60 Overactive bladder is a common problem affecting women w

61 Overactive bladder is an important lower urinary tract s

62 Overactive bladder is now recognized as a chronic debili

63 ur understanding of the basic science of the overactive bladder it is becoming clear that the control

64 However, coexisting overactive bladder may be responsible for storage sympto

65 al treatment of men with incontinence due to overactive bladder or to stress urinary incontinence pub

66 In women with refractory overactive bladder or urgency predominant mixed urinary

67 on the Urogenital Distress Inventory and the Overactive Bladder Questionnaire (both P <0.001) at both

68 both before and after RTx as measured by the Overactive Bladder Questionnaire and International Prost

69 nd 2010 were asked to complete the validated Overactive Bladder Questionnaire based on patient sympto

70 oCA score (1.3 points vs. 0.3 points) or the Overactive Bladder Questionnaire score (-3.3 points vs.

71 inumtoxinA showed greater improvement in the Overactive Bladder Questionnaire SF for symptom bother (

72 om baseline in urinary symptom scores in the Overactive Bladder Questionnaire Short Form (SF); range,

73 00, higher scores indicating worse symptoms; Overactive Bladder Satisfaction questionnaire; range, 0-

74 rusor instability with subsequent obstructed/overactive bladder symptom complexes not dissimilar to t

75 y, inhibit detrusor overactivity and resolve overactive bladder symptoms acutely.

76 g that prostatic inflammation contributes to overactive bladder symptoms in male patients; however, l

77 Men with enlarged prostates experience overactive bladder symptoms of urgency and frequency.

78 hat in men with persistent storage symptoms (overactive bladder symptoms), clinically meaningful impr

79 ht be useful clinically for the treatment of overactive bladder symptoms.

80 ection and a control group the prevalence of overactive bladder syndrome (OAB), and how it was associ

81 lay a significant role in the development of overactive bladder syndrome (OAB).

82 Lower urinary tract disorders such as overactive bladder syndrome (OABS) and interstitial cyst

83 Overactive bladder syndrome (OBS) results from disturban

84 gastroesophageal reflux disease (GERD), and overactive bladder syndrome (OBS), as well as other gast

85 apy of lower urinary tract disorders such as overactive bladder syndrome and cystitis.

86 ower urinary tract storage disorders such as overactive bladder syndrome and urinary incontinence sig

87 lower urinary tract symptoms, including the overactive bladder syndrome, and that combination of the

88 tment of nonobstructed urinary retention and overactive bladder syndrome, especially when accompanied

89 treatment of obstructive airway disease and overactive bladder syndrome.

90 ifenacin, as a treatment alternative of male overactive bladder syndrome.

91 he treatment of lower urinary tract symptoms/overactive bladder syndrome/and detrusor overactivity.

92 ive bladder and an adult anticholinergic for overactive bladder that underwent testing in children; e

93 tion and therefore are candidate targets for overactive bladder therapy.

94 oms and nonobstructive pattern recognized as overactive bladder type has also been successfully evalu

95 Treatment options for the overactive bladder were recently discussed at the 4th In

96 This mix of obstructed, overactive bladder with hidden stress incontinence incre

97 ere are persistent urinary storage symptoms (overactive bladder) following therapy with an alpha-bloc

98 on is required to identify the true cause of overactive bladder, allowing new targeted treatments to

99 veral potential targets for treatment of the overactive bladder, particularly within the mechanosenso

100 ynamic cystometry in conscious mice revealed overactive bladder, reduced maximal voiding pressures an

101 actions is pivotal to the disease process in overactive bladder, urge incontinence, and spinal cord i

102 example is sacral nerve stimulation to treat overactive bladder, urinary incontinence and interstitia

103 ment of refractory detrusor overactivity and overactive bladder.

104 ) agonist approved only for the treatment of overactive bladder.

105 involved in the management of patients with overactive bladder.

106 ecent developments in pharmacotherapy of the overactive bladder.

107 ted pig bladder strips, an in vitro model of overactive bladder.

108 evere lower urinary tract symptoms including overactive bladder.

109 and are obvious targets for treatment of the overactive bladder.

110 openers may have utility in the treatment of overactive bladder.

111 sorders of urine storage and voiding such as overactive bladder.

112 bladder compliance, ultimately resulting in overactive bladder.

113 ement, urinary retention, and underactive or overactive bladder.SIGNIFICANCE STATEMENT The pontine mi

114 Overactive bladders exhibited greater TRPV4-induced ATP

115 Present treatments for overactive bladders have significant non-compliance rate

116 dies using anticholinergics in patients with overactive bladders supports these findings.

117 nd identify TRPV4 up-regulation in aging and overactive bladders.

118 his suggests a role for BMPR-IA in mediating overactive BMP signaling in the absence of Noggin.

119 Loss of Noggin function leads to overactive BMP signaling, particularly in the palatal ep

120 This may be due to an overactive bowel, as suggested by previous studies.

121 in corticolimbic interneurons results in an overactive but desynchronized PFC before adolescence.

122 ations in the human TRPM3 render the channel overactive, but likely via different mechanisms.

123 c C3 complexes, and promoted formation of an overactive C3/C5 convertase.

124 Overactive Cdc42 has been implicated in the pathology of

125 Most human cancers contain overactive CDK4/6-cyclin D, and CDK4/6-specific inhibito

126 The inhibition of overactive CDKs during cancer remains an important strat

127 tween circuits, probably by calming down the overactive cells.

128 These overactive channels remained sensitive to sulfonylurea,

129 An overactive complement system is associated with AMD path

130 ical strategies that selectively correct the overactive components of the PI3K pathway while leaving

131 ase-relevant mutations that formed either an overactive convertase (M433I) or a convertase resistant

132 Biological monoclonal antibody drugs inhibit overactive cytokine signalling that drives chronic infla

133 Overactive defense signaling can result in dwarfism as w

134 tic cell uptake is essential for suppressing overactive dendritic cell-mediated inflammatory response

135 ults from low cAMP due to a misregulated and overactive DhkC phosphorelay in the amtC null strain.

136 ess, nausea, sweating, and being restless or overactive) did not differ between the groups.

137 or depressive disorder is associated with an overactive dorsal raphe nucleus with overactive projecti

138 resting periods and single units in KO were overactive during SWR events.

139 provide a checkpoint function to inactivate overactive E2F-1, but the association may also inactivat

140 Therefore, overactive EC signaling elicits an increase in plasma tr

141 rovements in dyslipidemia, direct effects of overactive EC signaling on plasma lipoprotein metabolism

142 Obesity is associated with an overactive endocannabinoid (EC) system.

143 of diseases whose pathogenesis is linked to overactive ER stress response.

144 01) and baroreflex sensitivity (P=0.03), and overactive ergoreceptors (P=0.003) compared with patient

145 We conclude that a population of overactive, excessively synchronized iSPNs could orchest

146 diovascular responsiveness is mediated by an overactive exercise pressor reflex (EPR).

147 o exercise in hypertension is mediated by an overactive exercise pressor reflex.

148 o exercise in hypertension is mediated by an overactive exercise pressor reflex.

149 ontainment of the inflammatory response, and overactive fibrosis may cause adverse remodeling in pati

150 s of function, suggesting that it encodes an overactive form of Cdc20p.

151 and hyperactive behaviors of mutants with an overactive Galpha(q) pathway.

152 ignificant role in normal renal function and overactive GH signaling has been implicated in proteinur

153 iatal AA release in HD is consistent with an overactive glutamate system and diminished glutamate tra

154 r phosphorylation and excessive signaling by overactive GPCR mutants result in a wide variety of dise

155 he stressed and failing heart, inhibition of overactive GRKs has been proposed as a novel therapeutic

156 Overactive growth during nutrient limitation ("nutrient-

157 Ptc(+/-) mice, which have an overactive Hh pathway, exhibited sustained overinduction

158 interaction in mutated GATA1s converges with overactive IGF signaling to promote cellular transformat

159 tissues from excessive collateral damage by overactive immune cells and their proinflammatory cytoki

160 triggers of the emergency downregulation of overactive immune cells.

161 e-protecting negative feedback inhibition of overactive immune cells.

162 the chronic stages of disease attenuates the overactive immune inflammatory response, especially infl

163 However, an overactive immune response can cause tissue damage and s

164 reventing uncontrolled tissue destruction by overactive immune responses, but also for protecting tum

165 igher with worse mood, implicating a broadly overactive immune system in chronic post-stroke depressi

166 We propose that an overactive immune system, including the "metabolic syndr

167 ability and defective immunoregulation drive overactive immunity to a subset of resident intestinal b

168 be cancer cell selective if this pathway is overactive in a cancer cell relative to a nontransformed

169 It is abnormally overactive in almost all human cancers.

170 lished that ryanodine receptors (RyanRs) are overactive in Alzheimer's disease (AD), and it has been

171 CK2 is overexpressed and overactive in B cell acute lymphoblastic leukemia and di

172 The ergoreflex was particularly overactive in cachectics (P<0.05), accompanied by marked

173 e first evidence that neddylation pathway is overactive in ccRCC and that MLN4924 induces dose-depend

174 These processes are often overactive in diseased cells, leading to unregulated cel

175 e results suggest the muscle metaboreflex is overactive in hypertension.

176 y prefrontal-striatal circuits, which may be overactive in individuals suffering from trauma-related

177 he midbrain and hippocampus were found to be overactive in major depressive disorder during unsuccess

178 by distal cues predictive of threats and is overactive in major depressive disorder.

179 We find that STAT3, a transcription factor overactive in many cancers, regulates PCBP2, a protein i

180 proteinase 9 (MMP9), which degrades NGF, was overactive in MCI and AD.

181 factor receptor (EGFR) signaling pathway is overactive in more than half of human cancers and mediat

182 s barely active in normal primary MCs and is overactive in neoplastic MCs.

183 Several proteases are overactive in NS, including kallikrein-related peptidase

184 dy weight, and systemic metabolism, which is overactive in obesity and type 2 diabetes.

185 pathways were significantly upregulated and overactive in patients who developed SIRS (P < 0.0001).

186 inhibitors targeted against driver kinases, overactive in selected subsets of solid tumors, elicit i

187 STEP is overactive in several neuropsychiatric and neurodegenera

188 The orexin system is overactive in SHRs and contributes to the augmented CO2

189 mGluR5-ERK1/2 pathway is not constitutively overactive in the Fmr1 KO, however, suggesting that mRNA

190 Similarly, ethanol-exposed subjects were overactive in the open field, an effect attenuated with

191 e formation of signaling complexes that stay overactive in the presence of the attractant.

192 xpression and function in CD8(+) T cells, is overactive in these cells in patients with lymphoma, and

193 disease, the type 2 immune response that is overactive in these diseases can also mediate beneficial

194 The same frontomesial network was overactive in TS patients compared with healthy subjects

195 a gain-of-functionNlrp3allele and subsequent overactive inflammasome activity displayed abnormal sacc

196 or managing genetic diseases associated with overactive inflammasomes, but also for treating common m

197 Following myocardial infarction (MI), overactive inflammation remodels the left ventricle (LV)

198 cance due to the attractiveness of targeting overactive inflammation without significant adverse effe

199 a key negative regulator to tightly control overactive inflammation.

200 actions, how glucocorticoids tightly control overactive inflammatory response is not fully understood

201 rt by delayed vascularization accompanied by overactive inflammatory responses following surgery.

202 OM characterized by the presence of overactive inflammatory responses is due to the aberrant

203 understanding of the role factors such as an overactive innate immune response play in the pathogenes

204 These mutant HPs contain increased ROS, overactive intracellular signalling through the AKT/mamm

205 arises from suppressed insulin secretion by overactive KATP channels in pancreatic beta-cells, but t

206 tion circuits bilaterally, together with an "overactive" left-sided ventral striatal-ventrolateral an

207 One such alteration could be an overactive locus coeruleus (LC)-norepinephrine system, w

208 ochemical studies have provided evidence for overactive mAChR signaling in the fragile X knock-out (F

209 erein, we report that in disease models with overactive mammalian target of rapamycin complex 1 (mTOR

210 Here, we show that overactive matriptase, reflected in an increased ratio o

211 itro, a condition that is secondary to their overactive metabolic state.

212 leotide drugs are being developed to inhibit overactive miRNAs linked to disease.

213 Moreover, ASD fibroblasts showed overactive mitochondrial bioenergetics associated with a

214 ciated increase in glucose metabolism and an overactive mitochondrial electron transport chain and is

215 Pals1 deficiency as a potential inhibitor of overactive mitogenic signaling.

216 on (inactive form), lower AMPK activity, and overactive mTOR pathway in AMD RPE as compared to normal

217 The paradoxical excitation was caused by overactive muscarinic receptors (mAChRs), leading to a s

218 icating that each defect is a consequence of overactive myosin.

219 a great level of enthusiasm to downregulate overactive N-methyl-D-aspartate (NMDA) receptors to prot

220 agonists, are appealing methods to constrain overactive neuronal activity.

221 differentiation and function as a result of overactive NF-kappaB and reduced Wnt/beta-catenin signal

222 Our findings suggest that an overactive NHEJ system and, specifically, aberrant Ku70/

223 However, overactive NMDARs can trigger cell death signalling path

224 mor suppressor is excessively degraded by an overactive oncogenic E3 ligase.

225 e inhibition and may be a strategy to target overactive oncogenic kinase cascades in cancer.

226 Overactive or dysregulated TGFbeta responses have also b

227 These include agents that either block overactive or enhance underresponsive cellular pathways.

228 iological evidence indicating this system is overactive or hyperresponsive in depression and with gen

229 a(2+) release, rather than the expression of overactive or leaky SR Ca(2+) release channels.

230 rest in defining cellular factors that limit overactive or misdirected Th17-type inflammation.

231 iety disorder (SAD), are characterized by an overactive or underactive serotonin system has not been

232 TRPpathies, disease states that result from overactive or underactive TRP channels?

233 sured samples, in which these regulators are overactive or underactive, respectively.

234 Overactive or unresolved inflammation is the primary det

235 esized that an augmented CO2 chemoreflex and overactive orexin system are linked with high ABP in bot

236 We suggest that an overactive orexin system may play an important role in t

237 FAK KO keratinocytes exhibited overactive p38 and MMP9 signaling in vitro, findings rec

238 Cell Stem Cell, Ceccaldi et al. identify an overactive p53/p21 stress response and cell cycle arrest

239 oregulation, and survival, and targeting the overactive parasympathetic system may be a useful therap

240 diac arrhythmias in mutant mice, implicating overactive parasympathetic tone.

241 rative glomerulonephritis is associated with overactive PDGF receptor signal transduction.

242 It supports the hypothesis that overactive performance monitoring is an endophenotype th

243 Overactive performance monitoring, as measured by the er

244 nitrogen stress, resulting in precocious and overactive PHG.

245 ion in Atg5(-)/(-) cells does not occur from overactive phosphatases.

246 Overactive phosphoinositide 3-kinase (PI3K) in cancer an

247 These results suggest that overactive phosphorylation of cytoplasmic residues of be

248 Our studies reveal that CD4(+) T cells with overactive PI3K have aberrant activation and differentia

249 s and a novel murine disease model caused by overactive PI3K signaling.

250 Overactive PIEZO2 causes anatomical defects through incr

251 els are increased in HD cells as a result of overactive positive feedback loop.

252 reduces BR only when the blink generator is overactive, possibly influencing tear film retention.

253 rotransmission in SAD is characterized by an overactive presynaptic serotonin system, with increased

254 The overactive proinflammatory immune signatures offers targ

255 with an overactive dorsal raphe nucleus with overactive projections to the amygdala, periaqueductal g

256 The presumed role of an overactive protein arginine deiminase 4 (PAD4) in the pa

257 arget actin-myosin interactions to alleviate overactive protein interactions.

258 Overactive pyramidal cells, notably those in the hippoca

259 nsgenic expression suppressed the effects of overactive Rac, including ectopic lamellipodia and filop

260 Overactive RAS signaling is prevalent in juvenile myelom

261 A core abnormality in both tumor groups is overactive RAS/ERK signaling, a pro-proliferative signal

262 These overactive reflexes may also contribute to the chronic s

263 However, overactive, relapsing fear behavior in the absence of da

264 on is critical for host defense; however, an overactive response is detrimental to the host.

265 er, loss of function of these cells or their overactive response to tissue injury often causes seriou

266 Overactive responses by interleukin 17 (IL-17)-producing

267 ganglionosis (Hirschsprung disease), whereas overactive RET can lead to multiple endocrine neoplasia

268 aking, which is postulated to result from an overactive reward system in the brain.

269 dampened reward anticipation while reducing overactive reward updating in patients with bipolar diso

270 ar-IR laser irradiation to thermally disrupt overactive sebaceous glands in the skin which define the

271 nd indicate that ODA is likely the result of overactive SHH signaling in humans harboring mutations i

272 Previous work has suggested that overactive signaling by group I metabotropic glutamate r

273 Overactive signaling is therefore capable of producing u

274 , despite the potential benefits of blocking overactive signaling, no P2X7 receptor antagonists have

275 Selective modulation of overactive SMA-STN projection pathways may underlie the

276 Overactive SMO signaling is oncogenic and is therefore a

277 ion may counteract the inhibitory effects of overactive sphincter afferents on the detrusor, and dete

278 This condition involves an overactive spinal reflex loop that resists the passive l

279 cent hypotheses suggest an involvement of an overactive stress axis.

280 idiopathic torsion dystonia (ITD) have shown overactive striatum and frontal accessory areas and unde

281 es have suggested that PTSD patients have an overactive sympathetic nervous system (SNS) that could c

282 However, an overactive T(H)17 response results in tissue inflammatio

283 erable evidence supports the hypothesis that overactive T-channels may contribute to thalamocortical

284 The PD-L1-PD-1 axis protects the host from overactive T-effector cells not only in cancer but also

285 oint is achieved through competition between overactive telomerase and TRD.

286 e ECM of Bgn(-/0) Fmod(-/-) MCCs, leading to overactive TGF-beta1 signal transduction.

287 ing an explant culture system, we found that overactive TGF-beta1 signals induced chondrogenesis and

288 However, prolonged and overactive TGFbeta signalling in pressure-overloaded car

289 ound that cells that underwent EMT exhibited overactive transforming growth factor beta (TGFbeta) sig

290 n cancer because of increased expression and overactive transport.

291 enuating invasiveness and metastasis of Her2 overactive tumors.

292 Overactive type 2 CD4+ helper T (Th2) cells are known to

293 ecently been introduced for the treatment of overactive urinary bladder syndrome.

294 the normal function of T(reg) cells, because overactive variants of some target genes are known to be

295 dolescence results in part from a relatively overactive ventral striatal (VS) motivational circuit th

296 c2 +/- ASD mice where mTOR is constitutively overactive, we observed postnatal spine pruning defects,

297 ventral epidermis, and double mutants mimic overactive Wg signaling in this tissue.

298 In both experimental models, Fam20C becomes overactive when associated with a 500-kDa multiprotein c

299 lays a role in disease such as cancer, where overactive Wnt signaling drives LEF/TCFs to transform ce

300 xpression at the cell surface contributes to overactive Wnt signaling in subsets of pancreatic, ovari