ライフサイエンスコーパス: overactivity

1 ion of autophagosomes as well as cathepsin B overactivity).

2 compared to urodynamically-observed detrusor overactivity.

3 r hyperactivity as a feature of KATP channel overactivity.

4 oms/overactive bladder syndrome/and detrusor overactivity.

5 ing novel pathways thought to play a role in overactivity.

6 tially a function of VEGF receptor signaling overactivity.

7 s associated with robust hepatic sympathetic overactivity.

8 ractivity and those with idiopathic detrusor overactivity.

9 mportance in the pathophysiology of detrusor overactivity.

10 ht play a role in the development of bladder overactivity.

11 sting bladder outlet obstruction and bladder overactivity.

12 ic and probably also non-neurogenic detrusor overactivity.

13 oliferation and an OPC-like identity via Ets overactivity.

14 ting alternative pathways affecting detrusor overactivity.

15 ysregulation, predominantly with sympathetic overactivity.

16 r motor neurone syndrome, rather than muscle overactivity.

17 tem cells, to screen for suppressors of dCBP overactivity.

18 ing, with a compensatory cardiac sympathetic overactivity.

19 s recommend urodynamics to identify detrusor overactivity.

20 ubiquitination partially suppressed channel overactivity.

21 nomously functioning thyroid nodules [AFTN]) overactivity.

22 ed by mechanistic target of rapamycin (mTOR) overactivity.

23 hibiting pathways displaying IKAROS-mediated overactivity.

24 cated in mice with fibroblast-specific TGF-B overactivity.

25 ith neurologically driven urethral sphincter overactivity.

26 o reverse AF-related pathologies due to GIRK overactivity.

27 art of the mechanism involved in sympathetic overactivity.

28 vel of DPCs, as well as signs of ALT pathway overactivity.

29 ent and not copy number that is the cause of overactivity.

30 eated mice, a commonly used model of bladder overactivity.

31 formed the management of neurogenic detrusor overactivity.

32 that Pirt deficiency in mice causes bladder overactivity.

33 signal leads to an equatorial band of myosin overactivity.

34 Neo-A damage resulted in central CRF systems overactivity.

35 s associated with sympathetic nervous system overactivity.

36 are essential restrictors of stress-response overactivity.

37 was characterized by disinhibition, restless overactivity, a fatuous affect, puerile behaviour and ve

38 gia following spinal cord injury and bladder overactivity after cerebral infarction.

39 This chronic mPFC overactivity also stably suppresses natural reward-motiv

40 Approximately half have detrusor overactivity and a smaller number have impaired detrusor

41 important mechanism contributing to bladder overactivity and afferent hyperexcitability induced by p

42 e mechanisms responsible for the sympathetic overactivity and blunted baroreflex control in chronic h

43 morphisms may contribute to Ca(v)3.2 channel overactivity and consequently to absence epilepsy and es

44 pressing this construct demonstrated TGFbeta overactivity and developed dermal and pulmonary fibrosis

45 (CIHH) during sleep that elicit sympathetic overactivity and diminished parasympathetic activity to

46 Since sympathetic overactivity and dysregulation of the renal-adrenal syst

47 failure (HF) is characterized by sympathetic overactivity and enhanced circulating catecholamines (CA

48 that a significant component of sympathetic overactivity and enhanced transmission may arise from im

49 on localized in the prostate induces bladder overactivity and enhances bladder afferent function.

50 al muscle mass is associated with ergoreflex overactivity and exercise limitation in CHF, particularl

51 e (Fcgr3-rs), as a determinant of macrophage overactivity and glomerulonephritis in Wistar Kyoto rats

52 blunted glycogen synthase kinase (GSK)3beta overactivity and hyperactivation of its downstream mitog

53 is important in devising methods to regulate overactivity and hyperplasia of the parathyroid gland af

54 was observed, suggesting that ageing induces overactivity and hypersensitivity of the bladder.

55 s suggest that constipation induced detrusor overactivity and increased excitatory serotonin receptor

56 flow pattern, voiding pressures, presence of overactivity and interpretation of findings on both urod

57 then leptin could contribute to sympathetic overactivity and its adverse consequences in human obesi

58 Moreover, in two mouse models of cholinergic overactivity and NMJ Ca(2+) overload, anti-cholinesteras

59 lly expressed GD is characterized by thyroid overactivity and orbital tissue inflammation and remodel

60 hed in the management of refractory detrusor overactivity and overactive bladder.

61 Autonomic imbalance (sympathetic overactivity and parasympathetic withdrawal) has emerged

62 L225P underlies K(ATP) channel overactivity and PNDM by specifically increasing Mg-nucl

63 erapeutic alternatives for managing detrusor overactivity and possible future developments are discus

64 sostriatal regions to contribute to dopamine overactivity and psychosis.

65 sulin resistance associated with sympathetic overactivity and regulation of brown fat metabolism.

66 rease cystometric capacity, inhibit detrusor overactivity and resolve overactive bladder symptoms acu

67 AA irritated the bladder, induced bladder overactivity and significantly (P < 0.001) reduced bladd

68 nsity of 3-4T, suppressed AA-induced bladder overactivity and significantly increased bladder capacit

69 t, both in patients with neurogenic detrusor overactivity and those with idiopathic detrusor overacti

70 The clinical significance of mild thyroid overactivity and underactivity is uncertain, which has l

71 that prostatic inflammation induces bladder overactivity and urothelial NGF overexpression in the bl

72 deleterious effects of mutant L-type channel overactivity, and addressed potential effects of altered

73 ducing incontinence associated with detrusor overactivity, and repeated treatments appear safe and ef

74 ranscription, and therefore tandem duplicate overactivity appears to be a previously unidentified for

75 molecular mechanisms underlying such kinase overactivity are not fully understood in the context of

76 t lessening chemoreceptor-driven sympathetic overactivity are now under investigation; thus, the abil

77 ntinence, overflow incontinence and detrusor overactivity are the major categories of urinary inconti

78 could contribute to the emergence of bladder overactivity as well as somal hypertrophy and hyperexcit

79 ductive cycle in contributing to sympathetic overactivity associated with cardiovascular disease.

80 Bladders of DKO animals exhibited detrusor overactivity at an early stage: increased frequency of n

81 ree remissions had less evidence of HPA axis overactivity at entry than those who were not in remissi

82 ical status at 2-year follow-up and HPA axis overactivity at entry were examined.

83 , i.v.) suppressed PNS inhibition of bladder overactivity at low intensity (1T) but not at high inten

84 lure (CHF) and may contribute to sympathetic overactivity, attenuated baroreflex sensitivity (BRS), a

85 nnexin 43 plays an important role in bladder overactivity, but its localization has not been clearly

86 ponent which is characterized by sympathetic overactivity, but the impact of sex and age remains larg

87 ampal perineuronal net (PNN) replicates this overactivity, but uncertainty over rodent/human prefront

88 SGLT2 inhibitors also attenuate sympathetic overactivity by modulating neurohumoral activation and r

89 that prostatic inflammation causes detrusor overactivity by using a rat model of chemically induced

90 pses and decreased in axonal synapses during overactivity by veratridine.

91 Chronic sympathetic nervous system overactivity can also contribute to a further decline of

92 Further, this reflex overactivity can be partially normalized by antagonizing

93 The effects of C3G overactivity can be suppressed by reducing the gene dose

94 tical for maintenance of euglycemia and that overactivity can cause diabetes by inhibiting insulin se

95 a model for sleep apnoea) causes sympathetic overactivity, cardiovascular remodelling and hypertensio

96 n anesthetized pig model of myogenic bladder overactivity, compound 14 and (-)-cromakalim 1 were foun

97 n the genome that we tested, suggesting that overactivity could be a general property of tandem gene

98 harmacoresistance, overcoming P-glycoprotein overactivity could be investigated as a potential treatm

99 HPSE overactivity degrades HSPGs within the ECM, facilitating

100 of bladder fullness reported by patients and overactivity detected early in DBD.

101 Whether sympathetic overactivity develops early during pregnancy, remaining

102 of autism spectrum disorder, inattention and overactivity, disinhibited social engagement, conduct or

103 SCI)-induced bladder dysfunction is detrusor overactivity (DO).

104 is occurring in patients, including detrusor overactivity (DO).

105 es tissue-resident Treg differentiation, and overactivity drives dose-dependent skin and systemic inf

106 tent with the conclusion that extreme B cell overactivity drives the initial stages of SLE leading to

107 ase NPM1-ALK, but the mechanism by which ALK overactivity drives toxicity upon TKI withdrawal remaine

108 s in PDGFRalpha(+) cells and prevent bladder overactivity during filling.

109 These results support PL BLA circuit overactivity during stress as a biomarker of trait vulne

110 These results support PL->BLA circuit overactivity during stress as a biomarker of trait vulne

111 adder dysfunction, characterized by detrusor overactivity during the early stage of the disease and d

112 UTS including urinary frequency and detrusor overactivity evaluated by awake cystometry.

113 We demonstrated that bladder overactivity, evident as decreased voided volume and sho

114 ole of CD154-CD40 interactions in the B cell overactivity exhibited by patients with active systemic

115 infections and tumours of immunodeficiency, overactivity in allergic and autoimmune disease.

116 Here we report that UNC-115 overactivity in C. elegans neurons promotes the formatio

117 potential early role for mesolimbic dopamine overactivity in CHR.

118 disorder (MDD) raise the possibility that LC overactivity in depression may be secondary to reduced G

119 f thoracic aortic disease, and that TGF-beta overactivity in diseased aortas is a secondary, unproduc

120 Cholinergic overactivity in diseases of neuromuscular transmission e

121 mechanism for the development of sympathetic overactivity in experimental hypertension.

122 l molecular mechanism underlying sympathetic overactivity in genetic hypertension and suggest potenti

123 ng hypothalamic pituitary adrenal (HPA) axis overactivity in healthy controls (HCs) and patients with

124 r, these findings suggest that mechanoreflex overactivity in heart failure may be a compensatory resp

125 ular pathways that contribute to sympathetic overactivity in hypertension and discuss their potential

126 f inhibition in the motor cortex, leading to overactivity in M1 and a disruption in spatial-temporal

127 endocrine studies have demonstrated HPA axis overactivity in major depression, a relationship of HPA

128 Voiding activity analyses revealed bladder overactivity in Mcoln1 (-/-) mice.

129 Induced fluency decreased or eliminated the overactivity in most motor areas, and largely reversed t

130 e that simultaneous underactivity in OFC and overactivity in NAC can negatively impact behavioral con

131 eurone channelopathy induced by carotid body overactivity in neurogenic hypertension that may contrib

132 bladder DRG neurons and to alleviate bladder overactivity in Pirt(-/-) mice.

133 nce that supports the hypothesis of dopamine overactivity in schizophrenia is the psychomimetic poten

134 n relevant animal models have indicated that overactivity in selective hippocampal circuits contribut

135 ere is an association between P-glycoprotein overactivity in some regions of the brain and pharmacore

136 cineurin signaling in the PVN in sympathetic overactivity in spontaneously hypertensive rats (SHR), a

137 tion of a tankyrase inhibitor attenuated Wnt overactivity in the AXIN1-mutant model systems.

138 Overactivity in the detrusor is a common clinical proble

139 findings support the hypothesis of glutamate overactivity in the development of dyskinesias.

140 A novel finding was the presence of relative overactivity in the lateral premotor and inferolateral p

141 exities, evidence of significant sympathetic overactivity in the manifestation and progression of HF

142 First, we found overactivity in the midbrain, which was at the level of

143 d touch' synesthetic experience is caused by overactivity in the neural system that responds to the o

144 Parkinson's disease patients showed relative overactivity in the precuneus, premotor and parietal cor

145 Overactivity in the subthalamic nucleus (STN) is believe

146 Indeed, Hh-deficient embryos showed Notch overactivity in their defective gut mesenchyme and expos

147 sure-flow urodynamics demonstrating detrusor overactivity, in the setting of a clinically relevant ne

148 children have substantial difficulties with overactivity, inattention, and impulsivity that are just

149 features with other PPKs caused by protease overactivity, including erythema, peeling, and exacerbat

150 Sympathetic overactivity is a compensatory mechanism at first, but m

151 Detrusor overactivity is a relatively common yet embarrassing sym

152 Cardiac sympathetic overactivity is a well-established contributor to the pr

153 Chronic sympathetic overactivity is also known to be present in central obes

154 schizophrenia, anterior hippocampus (aHipp) overactivity is associated with orbitofrontal cortex (OF

155 This overactivity is consistent with suggestions in previous

156 However, given that exercise pressor reflex overactivity is known to elicit enhanced circulatory res

157 The cause of this overactivity is not clear, but may be driven by certain

158 hat the phenomenon of extrasynaptic receptor overactivity is observed in a broader range of patients

159 Sympathetic nerve overactivity is pro-arrhythmic and a key contributor to

160 We have demonstrated that this overactivity is responsible for the exaggeration in the

161 nderstanding of the pathogenesis of detrusor overactivity is slow but steady.

162 Detrusor overactivity is the occurrence of abnormal increases in

163 Bladder overactivity is traditionally treated with anticholinerg

164 rapolating from other forms of AKI where RAS overactivity is well documented.

165 its endogenous ligand, angiotensin II, with overactivity leading to vascular remodeling and hyperten

166 ell impedance platform, we showed that TRPV4 overactivity leads to cell barrier disruption, while pha

167 Since the pathology of TGF-beta overactivity manifests primarily within the arterial med

168 This overactivity may be associated with the addictive scratc

169 This overactivity may be one of the underlying mechanisms of

170 re, we show that chronic hepatic sympathetic overactivity mediates hepatic steatosis.

171 nia" factor, in particular the subdimension "overactivity." Ncan(-/-) mice were hyperactive and showe

172 Neurogenic detrusor overactivity (NDO) is a well known consequence of spinal

173 Neurogenic detrusor overactivity (NDO) is among the most challenging complic

174 sclerosis often develop neurogenic detrusor overactivity (NDO), which currently lacks a universally

175 Overactivity occurs at the level of RNA transcription, a

176 iety-like behavior, our results suggest that overactivity of 5-HT(1B) autoreceptors in DRN neurons ma

177 se mutations of the Gs alpha gene leading to overactivity of adenylyl cyclase have been identified in

178 diabetic complications is well-studied, with overactivity of ALR2 in the hyperglycemic state leading

179 receptor binding, then causes inappropriate overactivity of basal ganglia-frontal projections, resul

180 al ganglia opioid transmission, resulting in overactivity of basal ganglia-frontal projections.

181 within the brain to another, as a result of overactivity of certain nerve cells.

182 enetic disease cystic fibrosis (CF), whereas overactivity of CFTR may lead to secretory diarrhea and

183 Overactivity of ClC-7 induces pathologically enlarged va

184 latory lesions, suggesting that sprouting or overactivity of contralateral corticostriatal input cont

185 Overactivity of EGFR signaling, as achieved by heat-shoc

186 The overactivity of ergoreceptors (intramuscular afferents s

187 ersistent free heme overload in malaria, the overactivity of HO-1 resulted in continuous transient ge

188 Overactivity of immune responses at a systemic level is

189 We demonstrate overactivity of insulin-like growth factor (IGF) signali

190 p1 and Gasp2 have phenotypes consistent with overactivity of MSTN and GDF-11.

191 the brain may be caused by overexpression or overactivity of multidrug transporters, such as P-glycop

192 ssion and might be more appropriately termed overactivity of normal PRS.

193 roblasts and lymphoblasts from patients with overactivity of normal PRS.

194 e-feedback mechanism to protect neurons from overactivity of Pum.

195 other cardiometabolic diseases are linked to overactivity of renal sympathetic and sensory nerves, bu

196 ess of movement in PD has been attributed to overactivity of striatal projection neurons forming eith

197 Overactivity of subthalamic nucleus (STN) neurons is a c

198 lation and cell cycle arrest derive from the overactivity of TGF-beta receptor signaling, which is no

199 al actions of alcohol that may contribute to overactivity of the ACC during withdrawal and excessive

200 f sleep-wake regulation consisting of either overactivity of the arousal systems, hypoactivity of the

201 Overactivity of the brain renin-angiotensin system is a

202 enetic and epigenetic events cause universal overactivity of the cell cycle cdks in human cancer, and

203 ns and pathologies share the common theme of overactivity of the complement system's alternative path

204 in some electrophysiological studies showing overactivity of the corticostriatal glutamatergic system

205 ion in Alzheimer patients has been linked to overactivity of the cyclin-dependent kinase 5 (CDK5) and

206 Obesity is associated with overactivity of the endocannabinoid system, which is inv

207 major cause of end-stage kidney disease, and overactivity of the endocannabinoid/cannabinoid 1 recept

208 affected relatives, findings consistent with overactivity of the enzyme.

209 Overactivity of the hexosamine pathway mediates glucose-

210 activation of protein kinase C isoforms, and overactivity of the hexosamine pathway.

211 The E23K variant leads to overactivity of the K(ATP) channel, resulting in reduced

212 ic pathobiology in depression is a result of overactivity of the LC.

213 of functional neurological disorder includes overactivity of the limbic system, the development of an

214 ate changes and overproliferation, mimicking overactivity of the RAS-MAPK pathway.

215 rtension, a genetic disease characterized by overactivity of the renal sodium chloride cotransporter

216 To establish that overactivity of the renal TGF-beta system mediates the f

217 Overactivity of the subcallosal cingulate has been assoc

218 from the eccrine sweat glands, is caused by overactivity of the sympathetic nerves.

219 Overactivity of the sympathetic nervous system is a hall

220 m of this increased inflammation is unknown, overactivity of the sympathetic nervous system is a hall

221 buting to changes in insulin sensitivity and overactivity of the sympathetic nervous system.

222 e strongly in support of the hypothesis that overactivity of the TGF-beta system in the kidney is a c

223 Overactivity of these serotonergic sympatho-somatomotor

224 exogenous endothelin-1, possibly reflecting overactivity of this system and ET(A) receptor downregul

225 following chronic challenges may result from overactivity of this system.

226 se effects of chronic stress may result from overactivity of this system.

227 contractions during filling, and rescued the overactivity of Trpv4 (-/-) bladders.

228 s circulating atrial natriuretic peptide and overactivity of various intrarenal paracrine systems, in

229 ty mucocutaneous pigmentation, and endocrine overactivity (Ophthalmic Surg Lasers Imaging 39(6):514-6

230 a cyclophosphamide cystitis model of bladder overactivity, optogenetic activation of CRH-PMC neurons

231 al treatments like drug therapy for detrusor overactivity or sling procedures for female stress incon

232 ecation for patients with neurogenic bladder overactivity or spinal cord lesions.

233 modulin-dependent protein kinase II (CaMKII) overactivity plays a crucial role in the pathophysiology

234 Detrusor overactivity poses a major challenge to physicians from

235 These findings indicate that dopamine overactivity predates the onset of schizophrenia in indi

236 Because a state of adrenergic overactivity prevails when triiodothyronine (T3) concent

237 COMT genetic overactivity produced a selective overdrive of the endoc

238 function, especially for those with detrusor overactivity refractory to anticholinergics, is, however

239 ry feedback, the people who stuttered showed overactivity relative to controls in the anterior insula

240 The cellular mechanisms behind this overactivity remain poorly understood, with most attenti

241 We propose that detrusor overactivity results from exaggerated symptomatic expres

242 king a full set of microtubule triplets, its overactivity results in over-elongated and structurally

243 rams under an awake condition showed bladder overactivity revealed by time-dependent reductions in in

244 nerve stimulation in the management of both overactivity syndromes and nonobstructive voiding dysfun

245 s of medications aimed at targeting cytokine overactivity that act directly on brain function and/or

246 chanisms that are responsible for the B cell overactivity that is observed in patients with SLE, we h

247 nd pseudoephedrine might reduce the synaptic overactivity that occurs in the slow-channel myasthenic

248 n in the female LC could contribute to LC-NE overactivity that underlies the hyperarousal symptoms of

249 a consequence of aberrant or prolonged TNK2 overactivity, the latter being a failure in TNK2 degrada

250 nsitivity as well as non-neurogenic detrusor overactivity, there is up-regulation of unmyelinated ner

251 bited social engagement, and inattention and overactivity through to young adulthood (pooled p<0.0001

252 NLRP3 overactivity triggered inflammatory cytokines (IL-1beta

253 ed as an important mediator inducing bladder overactivity under pathological conditions such as spina

254 el, and emerging evidence indicates that its overactivity underpins the progression of several human

255 Ergoreceptor overactivity was associated with a worse symptomatic sta

256 Hippocampal overactivity was due to a failure to deactivate during l

257 Foxo3a inhibits NF-kappaB activation, whose overactivity was responsible for T cell hyperactivity in

258 nsitization and associated basal sympathetic overactivity were abolished by GLP1R activation in the C

259 Focusing on hippocampal overactivity, which has emerged as a central feature of

260 cular the role of the various forms of motor overactivity, which might be amenable to botulinum toxin

261 nical trials that attempted to treat bladder overactivity with calcium channel blockers (CCBs) have b

262 Mice exhibited incontinence and overactivity with diminished voiding pressure.

263 on alternative pathways underlying detrusor overactivity with the intention of improving storage sym