ライフサイエンスコーパス: deficit

1 2) and, as hypothesized here, vapor-pressure deficit.

2 (fl/+) mice) results in a motor coordination deficit.

3 tion of normoglycemia in response to glucose deficit.

4 SPS exposure induced an extinction-retention deficit.

5 T(H)1(*) cells unable to compensate for this deficit.

6 ot ABA content in poplars subjected to water deficit.

7 s 28% showed moderate, and 17% severe growth deficit.

8 and this correlates with locomotor behavior deficit.

9 rice (Oryza sativa) root growth under water deficit.

10 ains maintain cell wall flexibility in water deficit.

11 15 years of experimentally imposed moisture deficit.

12 hypomyelination, and permanent sensorimotor deficit.

13 treated with a G4 stabilizer develop memory deficits.

14 hereas nTg mice with MPTP exposure showed no deficits.

15 loss of dopamine neurons, resulting in motor deficits.

16 mitigates juvenile isolation-induced social deficits.

17 s may lead to tissue damage and neurological deficits.

18 d abnormal gamma oscillations and behavioral deficits.

19 nitively intact and without focal neurologic deficits.

20 ation of dopamine levels and rescue of motor deficits.

21 re not very effective in reversing cognitive deficits.

22 (DS) results in various degrees of cognitive deficits.

23 , as well as a range of chronic neurological deficits.

24 early identification and remediation of gait deficits.

25 g a circuit mechanism underlying sociability deficits.

26 oss of dopamine neurons and motor behavioral deficits.

27 rs, including major depression and cognitive deficits.

28 aired social interactions, and communication deficits.

29 est was sensitive enough to detect locomotor deficits.

30 strategies that minimize risk of production deficits.

31 term effects, including cognitive and memory deficits.

32 , as observed in patients with cardiodynamic deficits.

33 al networks could account for spatial memory deficits.

34 resulting in both cognitive and noncognitive deficits.

35 were associated with permanent visual field deficits.

36 ry brain injuries and permanent neurological deficits.

37 ent neurodegeneration and accompanying motor deficits.

38 inflammatory response and cellular function deficits.

39 1 mimicked the cilia-beating and ventricular deficits.

40 nts for psychiatric disorders with attention deficits.

41 is abortive, causing devastating neurologic deficits.

42 ally powerful tool to treat microcirculation deficits, a common pathology in numerous diseases.

43 Physical and psychologic deficits after an ICU admission are associated with lowe

44 l strains displaying similar functional gait-deficits after injury.

45 bility in the type and severity of cognitive deficits after traumatic brain injury.

46 licting evidence on whether sensory learning deficits align on the nonclinical end of the psychosis c

47 l patients with papilledema and visual field deficits also exhibited improvement (p<0.0005).

48 Right hippocampal volume deficit and inferior temporal cortex thinning demonstrat

49 models to estimate the prevalence of growth deficit and linear mixed models to calculate adjusted me

50 was significantly down-regulated under water deficit and posttranscriptionally regulated by microRNA3

51 settings to monitor the progression of motor deficit and response to treatment.

52 creasing CP and VO2max , increasing the O(2) deficit and sowing the seeds of exercise intolerance.

53 g viral Ags exhibit both discrete functional deficits and a notable surplus.

54 ore, ISRIB treatment reverses spatial memory deficits and ameliorates working memory in old mice.

55 re hyperproliferative, yet have regenerative deficits and are shifted towards a de-differentiated sta

56 liable identification of specific underlying deficits and biases in neurocognitive functions.

57 owed activation-related metabolic remodeling deficits and decreased mitochondrial membrane potential;

58 yramidal cells successfully corrected memory deficits and did so in a regionally specific manner: ven

59 patients (Foxp2(+/R552H) mice) display motor deficits and impaired synaptic plasticity in the striatu

60 have been successful in understanding memory deficits and in linking to neural data.

61 xon regeneration failure causes neurological deficits and long-term disability after spinal cord inju

62 sorder characterized by social communication deficits and other behavioral abnormalities.

63 Modulation of this circuit induced social deficits and repetitive behaviors, whereas activation of

64 id improved metabolic and neurodevelopmental deficits and reversed leptin resistance in the offspring

65 Mitochondrial deficits and specifically reduced mitophagy are evident

66 epression of AMPKalpha1 alleviated cognitive deficits and synaptic failure displayed in 2 separate li

67 ationship with the development of behavioral deficits and tau neuropathology.

68 (low-luminance visual acuity, low-luminance deficit, and microperimetric sensitivity) from the poore

69 to light and acoustic stimuli, prey-capture deficits, and a failure to habituate to acoustic stimuli

70 euroinflammation, attenuated neurobehavioral deficits, and limited tissue loss long after TBI.

71 ng, associated with persistent soil moisture deficit, appears to intensify surface warming and anticy

72 through a resilience approach rather than a deficit approach and offers a blueprint for approaching

73 Age-related memory deficits are correlated with neural hyperactivity in the

74 Visual deficits are dominated by cone loss, which progresses sl

75 ociated neuroinflammation and the neurologic deficits are dramatically exacerbated.

76 ues, that these putative temporal processing deficits are not apparent in responses of single-unit au

77 The mechanisms underpinning attentional deficits are only partially understood.

78 pathological states, in which mitochondrial deficits are prominent and difficult to fix.

79 blems even before memory and other cognitive deficits are reported.

80 To treat the deficit arising from Chrna5 disruption without triggerin

81 xide dismutase (SOD) family exemplifies this deficit, as the specific metal used by any family member

82 show that specific areas of localised volume deficit, as visible on routine imaging data, are associa

83 Thalamo-striatal progressive volumetric deficit associated with symptomatic improvement after cl

84 ibuted to the brain and can rescue cognitive deficits associated with aging in mice.

85 ential therapeutic target to treat cognitive deficits associated with MS.SIGNIFICANCE STATEMENT To id

86 anxiety-like behavior and substantial memory deficits associated with the presence of extrauterine en

87 The iMSN-Drd2KO mice showed performance deficits at all phases of rotarod skill learning.

88 cells, results in not only muscle aging-like deficit but also trabecular bone loss, a feature of oste

89 nd enriched environment may rescue cognitive deficits by improving network activation accuracy.

90 ns in adulthood could rescue the sociability deficits caused by juvenile isolation.

91 an be distinguished from unrelated nutrition deficit characteristics.

92 displayed repetitive behaviors, sociability deficits, cognitive dysfunction, and abnormal dendritic

93 urodevelopmental abnormalities and cognitive deficits commonly observed in psychiatric disorders.

94 d risk for language and other neurocognitive deficits compared to term controls (TC).

95 regulation of stomatal movements under water-deficit conditions.

96 7b (miR397b) in roots under normal and water-deficit conditions.

97 periods of development is proposed to drive deficits consistent with schizophrenia in adults.

98 of these CRRs and failure to correct glucose deficit, constituting a potentially lethal condition kno

99 ASD-associated cellular and behavioral deficits could be rescued by pharmacological inhibition

100 Perceptual deficits could emerge for different perceptual tasks or

101 tress impairs extinction learning, and these deficits depend, in part, on stress-induced norepinephri

102 is acutely knocked down in adult MB, memory deficits displayed by amn hypomorphic mutants are rescue

103 unaffected, suggesting a primary attentional deficit during acute abstinence.

104 Maternal micronutrient deficits during preconception and pregnancy may persist

105 ty of acute impairments, of which limb motor deficit, dysphagia, and incontinence have declined betwe

106 dinately respond to distinct levels of water deficits (e.g., mild, moderate or severe drought) remain

107 tion is associated with permanent functional deficit even after advanced microsurgical repair.

108 were correlation between percentages of flow deficits (FD(3mm) and FD(6mm)) and sMS in the central 10

109 ed to measure the choriocapillaris (CC) flow deficits (FDs) under drusen was tested in eyes with larg

110 erence between treatment training within the deficit field and control training within the sighted fi

111 on code and produced commensurate behavioral deficits for late-solved images.

112 These results show that perceptual deficits from AN damage are smaller than generally expec

113 ing the 18-year period, including limb motor deficit (from 77% [95% CI 74%-81%] to 62% [56%-68%], p <

114 he transport sites and to balance the charge deficit generated by the exchange of Ca(2+).

115 ) using model-based predictions of cognitive deficits generated from the Iowa cohort lesion-behavior

116 in the percentage of time points with an MPP deficit > 20%, multivariable-adjusted odds of developing

117 By contrast, at 19 weeks, when motor deficits had become dramatically evident, both measures

118 as a mediator between symptoms of attention deficit hyperactivity disorder (ADHD) and associated cog

119 rder (BIP), major depression (MD), attention-deficit hyperactivity disorder (ADHD) and autism (AUT).

120 cetaminophen exposure and risks of attention deficit hyperactivity disorder (ADHD) and autism spectru

121 Attention deficit hyperactivity disorder (ADHD) is a common, highl

122 Attention deficit hyperactivity disorder (ADHD) is a highly herita

123 Childhood attention deficit hyperactivity disorder (ADHD) shows a highly var

124 ide association studies (TWASs) of attention deficit hyperactivity disorder (ADHD), autism spectrum d

125 Attention deficit hyperactivity disorder (ADHD), autism spectrum d

126 ition, educational attainment, and attention deficit hyperactivity disorder (ADHD).

127 and overall cognition in boys with attention deficit hyperactivity disorder (ADHD).

128 al disability, facial dysmorphism, attention-deficit hyperactivity disorder) and revealed further dis

129 der (ASD), schizophrenia (SZ), and Attention-Deficit-Hyperactivity-Disorder (ADHD), but their impact

130 sive-compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD) are clinically and

131 Although the prevalence of attention-deficit/hyperactivity disorder (ADHD) has been stable ov

132 Attention deficit/hyperactivity disorder (ADHD) is a common and he

133 Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopm

134 age-related change in symptoms of attention-deficit/hyperactivity disorder (ADHD) is heritable.

135 structural changes associated with attention-deficit/hyperactivity disorder (ADHD).

136 anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder in children were assessed

137 quotient (IQ) and higher levels of attention deficit/hyperactivity disorder symptoms.

138 precision when cases with comorbid attention-deficit/hyperactivity disorder were removed from the ana

139 cts of PDD005 for the treatment of cognitive deficit in aging mice.

140 acerbated negative emotional behavior, and a deficit in BNST synaptic potentiation.

141 dendrite morphogenesis defects result from a deficit in Cbln1/GluD2-dependent competitive interaction

142 The OxPhos deficit in cINs could be reversed by Alpha Lipoic Acid/A

143 IL-6 receptor only in osteoblasts exhibit a deficit in exercise capacity of similar severity to the

144 s and there is post-mortem evidence of their deficit in FTLD.

145 wth restriction is associated with a nephron deficit in humans, and is commonly caused by placental i

146 The deficit in long-term object recognition memory was resto

147 A male-specific 35% nephron deficit in microRNA-210 knockout mice was observed.

148 uals and HD patients, supporting the lack of deficit in mitochondrial protein import.

149 However, the source of this outgroup deficit in observational learning remained unknown, whic

150 eavy" roots as an adaptive response to water deficit in rice.

151 rontal GABAergic function could arise from a deficit in the recruitment of fast-spiking interneurons

152 a nigra, which is the root cause of dopamine deficit in the striatum in Parkinson's disease.

153 motor cortex correlated with motor learning deficits in a mouse model of FASD.

154 we quantified the prediction of behavioural deficits in a prospective cohort of 132 first-time strok

155 side the damaged area contributes to spatial deficits in a way that depends on the different cognitiv

156 se results suggest that allocentric strategy deficits in ageing can result from difficulties related

157 ation, are considered hallmarks of cognitive deficits in Alzheimer's disease.

158 of Hh-deficient mesoderm revealed selective deficits in anterior mesoderm populations, culminating i

159 plantation from MIA mice produced behavioral deficits in antibiotic-treated mock mice.

160 Deficits in associative and Pavlovian learning are thoug

161 , these results indicate that age-associated deficits in auditory and visual processing emerge in par

162 described the effects of oxytocin on social deficits in autism spectrum disorder (ASD), no large-sca

163 efficiently recovers aralar-KO neurons from deficits in basal-stimulated and glutamate-stimulated re

164 Thus, deficits in behavioral flexibility observed in disorders

165 oural abnormalities but do have sex-specific deficits in body mass and motor function.

166 e DSS colitis enhanced neurogenesis but with deficits in cell cycle kinetics of proliferating progeni

167 ry in order to make predictions about memory deficits in clinical populations.

168 f CypD also prevented KET-induced behavioral deficits in cognitive flexibility, social interaction, a

169 These findings show GEE induces long-lasting deficits in cognitive function that may contribute to hu

170 et groups that included less severe adaptive deficits in communication skills, similar functional lan

171 etrant cleft palate, mandible hypoplasia and deficits in cranial base ossification.

172 ocalization to dendritic spines and synaptic deficits in cultured rat hippocampal neurons.

173 d parietal-prefrontal information processing deficits in delusional psychopathology and in genetic ri

174 etiology and treatment of reward processing deficits in depression.

175 ed 5-HT levels contribute to social learning deficits in depression.

176 impairment (MCI), which are characterized by deficits in executive functions, memory and attention.

177 iate engram reactivation underlies cognitive deficits in FXS, and enriched environment may rescue cog

178 static factors contributed to the functional deficits in gene regulatory activity of the mutant ERalp

179 Marked deficits in glucose availability, or glucoprivation, eli

180 accounting for action selection performance deficits in healthy older adults.

181 yl starch (HES) to correct for intravascular deficits in high-risk surgical patients is either effect

182 g picture of the cardiac and musculoskeletal deficits in human AD.

183 Feeding and suckling deficits in infants with PWS are replaced with excessive

184 Neonatal tissue damage induces long-term deficits in inhibitory synaptic transmission within the

185 We uncovered deficits in insulin secretion, partly due to reduced mit

186 We uncovered deficits in insulin secretion, partly due to reduced mit

187 strain of C. difficile; however, significant deficits in intestinal neutrophils and eosinophils were

188 an abnormal neuronal morphology resulting in deficits in learning and memory.

189 s are associated with long term neurological deficits in life and have also been associated with dysb

190 Visceral adipose NLRP3 was required for deficits in long-term potentiation (LTP) in transplant r

191 null neurons rescues synaptic and behavioral deficits in Mecp2 conditional knockout mice, whereas abo

192 rocytes relevant to the development of motor deficits in mice.

193 eference test is often used to assess social deficits in mouse models of ASD.

194 c factor (BDNF) correlate with neuromuscular deficits in mouse models of Kennedy's disease (KD), sugg

195 Deficits in muscle brain-derived neurotrophic factor (BD

196 27L, were associated with pulmonary function deficits in obese children with asthma.Conclusions: We f

197 knockdown in mouse OFC resulted in specific deficits in OFC-mediated cognitive flexibility.

198 We establish that the social behaviour deficits in offspring exposed to MIA can be temporarily

199 ty, lower baseline anxiety, and motivational deficits in operant conditioning for palatable food rewa

200 prediction errors), which formally captured deficits in outgroup learning.

201 k, which reliably measures cognitive control deficits in patients (Henderson et al., 2012) and used l

202 ficulties in aged people are associated with deficits in processing and encoding spatial cues.

203 This results in deficits in promoter methylation of activity-dependent g

204 plicated in the pathophysiology of cognitive deficits in psychiatric disorders.

205 Deficits in recognition memory were evident at the late

206 t that interventions that target insomnia or deficits in reward processing may mitigate the risk of d

207 erefore, the aim of this study was to assess deficits in reward system functioning and mesolimbic DA

208 acid (DomA) produces long-lasting behavioral deficits in rodent and primate models; however, the mech

209 eatment with alpha7 nAChR agonists for these deficits in SCZ may be promising.

210 delays and uncoordinated movement to subtle deficits in sensory and learning behaviors.

211 brain.SIGNIFICANCE STATEMENT Age-associated deficits in sensory processing arise from structural and

212 n corticolimbic interneurons ameliorates the deficits in spatial working memory and PPI, presumably b

213 Behavioural deficits in stroke reflect both structural damage at the

214 The deficits in submucosal neurons are reflected functionall

215 d behavioral outcomes and indicated that the deficits in task performance were plausibly explained by

216 -related hearing loss typically present with deficits in temporal processing tasks.

217 ion regulation strategies amongst those with deficits in the ability to deploy such strategies.

218 dies have reported improvement of behavioral deficits in the Ts65Dn mouse model of Down syndrome (DS)

219 s locomotor impairment and social behavioral deficits in these animals.

220 Genetic studies indicate that deficits in these pathways are implicated in neurodegene

221 GFP rescues the behavioral and physiological deficits in tmc triple mutants.

222 6 in muscle lamin A/C-KO mice diminishes the deficits in trabecular bone mass but not muscle.

223 By relating deficits in value-based decision-making to region-specif

224 in medical and academic settings because of deficits in various EF domains.

225 ion, we found that SC inhibition also caused deficits in visual target selection.

226 observe partially discriminable but similar deficits in well myelinated mice in which glial cells ca

227 5b prevented subtle gait deficits in WT alphaS mice and the PD-like resting tremo

228 ie some of the symptoms, including cognitive deficits, in LD.

229 ounterregulatory responses (CRRs) to glucose deficit, including increased feeding and elevation of ci

230 li to exacerbate alphaSyn-induced behavioral deficits, including intestinal and motor impairments.

231 ocular dominance plasticity, and can rescue deficits induced by prolonged monocular deprivation.

232 ae pathovar tomato strain DC3118 (coronatine deficit)-induced stomatal closure.

233 velopment of multivariate methods for lesion-deficit inferences.

234 Regulated deficit irrigation (RDI) is a viticultural practice know

235 ng muscle-derived IL-6 (mIL-6), and why this deficit is correctable by osteocalcin but not by IL-6.

236 ism(s) involved with persistent neurological deficits is not fully known, mitochondrial dysfunction i

237 calization in cognitive neuroscience, lesion-deficit mapping is in practice distorted by unmodelled n

238 focal cortical impairments, we derive lesion-deficit maps of a broad range of psychological subdomain

239 racerebral hemorrhage, but severe neurologic deficits may confound its assessment and lead to underdi

240 uggests that age-related temporal processing deficits may develop more central to the auditory nerve,

241 anding the network effects of these cellular deficits may help predict epileptogenesis.

242 olumes (p < 0.001) and worsened neurological deficits (median score = 9 vs 5 with vehicle, p = 0.008)

243 es and rods (low-luminance VA, low-luminance deficit, mesopic light sensitivity), or rods (scotopic l

244 t, increased sociability, learning and motor deficits, mimicking several of the human symptoms.

245 entified miRNAs to demonstrate their role in deficit moisture stress tolerance mechanism of horsegram

246 centric learning and caused reference memory deficits (Morris water maze), but did not affect proxima

247 ffective countermeasure against the skeletal deficits observed in astronauts during spaceflight.

248 ongst food-borne pathogens has led to severe deficit of available therapeutics and requires novel int

249 Our synthesis highlights a deficit of information on this topic, and we outline a v

250 s (GPe) are critically involved in the motor deficits of dopamine-depleted mouse models of Parkinson'

251 ng beta-catenin expression is able to rescue deficits of Nae1 mutant mice.

252 rebral hemisphere may result in a variety of deficits, often affecting the domain of spatial cognitio

253 We additionally noted a selective deficit on an object location memory task, which require

254 for repression of root development by water deficit or ABA.

255 or this dissociation in DP could be that the deficit originates in the early perceptual encoding of f

256 intake in addiction, and document that these deficits persist at least one month after detoxification

257 138 cases (82.1%) had developed neurological deficits preoperatively with the average tumor size of 4

258 Outcomes included time to resolution of base deficit, product volumes transfused, and INR after resus

259 with NVLD relative to those without spatial deficits (RD and TD).

260 COMT on root growth and adaptation to water deficit remain unexplored.

261 centriole duplication, but the cause of this deficit remains unknown.

262 es may relate to the cognitive and affective deficits remains to be determined with a large cohort of

263 2(dp/+)) and identified social and cognitive deficits reminiscent of ASD and ID phenotypes.

264 ses and EEG abnormalities, improve cognitive deficits, revert autistic-like behaviors and protect aga

265 Global deficit score improved 25% in coinfection with the visua

266 cal motor networks independent of individual deficit severity.

267 ally, targeted lesioning of modules produced deficits similar to those observed in lesion studies of

268 NT mice and neuropathological and behavioral deficits similar to those shown by Liu et al.

269 nglia neuron type-specific pathology and the deficits stemming from them in male heterozygous Q175 mi

270 resulting in increased attenuation of water-deficit stress.

271 apeutic strategy for conditions of cognitive deficit such as neurodegeneration.

272 mmation is implicated in auditory processing deficits such as impairment in gap detection.

273 rom initial models centered on neurochemical deficits, such as the monoamine hypothesis, research tow

274 ic blockade of Kcnn2 improves these learning deficits, suggesting Kcnn2 blockers as a new interventio

275 ere are equally likely to result in language deficits, suggesting that language is distributed symmet

276 n improved both cognitive and P50 inhibition deficits, suggesting that longer term treatment with alp

277 Water deficits that coincide with flowering result in leaf wil

278 aine-induced CBF reductions lead to neuronal deficits that contribute to hypofrontality and to compul

279 caling and intrinsic homeostatic plasticity, deficits that could be rescued by treatment with lithium

280 the adult: adolescent stress led to circuit deficits that recapitulates schizophrenia, whereas adult

281 e lines, this novel model shows pathological deficits throughout the CNS including accumulation of ly

282 ere, we relate patterns of brain damage with deficits to the content and structure of spontaneous con

283 Mean PMDs improved over 6 months in deficit-trained patients (mean change in the right eye,

284 limb placement emerged as a novel behavioral deficit unpredicted by our previous study of chemotherap

285 ng in an exponential climb in vapor pressure deficit (VPD).

286 DAT deficit was defined as less than 65% of putamen striatal

287 A rotarod deficit was not present in Q175 mice until 18 months, bu

288 On the neural level, this outgroup deficit was reflected in the activation of the inferior

289 To address this deficit, we developed a fully-automated robotic screenin

290 ment and neurodegeneration caused by ATP6V1A deficit were improved by a repositioned compound, NCH-51

291 In addition, visual search deficits were associated with modifications of FC betwee

292 Mbp mRNA transport deficits were confirmed by single molecule RNA FISH.

293 ction and impaired working memory, and these deficits were prevented by global IL-1R1 knockout.

294 0-ms period caused a contralateral detection deficit, whereas inhibition immediately before or after

295 inflammation, ischemia, trauma, and genetic deficits, which are characterized by retinal ganglion ce

296 h abnormal gamma oscillations and behavioral deficits with high correlation by pharmacological and ge

297 matoxylin and Eosin staining, and behavioral deficits with open field activity.

298 ddition, these mice developed motor and gait deficits with underlying muscle atrophy, similar to that

299 eeks post-stroke despite recovery from motor deficits, with hypertensive animals showing some symptom

300 ncrease in the magnitude of both surplus and deficit years.