ライフサイエンスコーパス: neurological

1 mol/L) and mortality at day 21 attributed to neurological (181 vs. 90 mumol/L) and all causes (114 vs

2 Fever (73%), neurological (72%), gastrointestinal (41%), and cardiac

3 Survivors without neurological abnormalities before CSE have favourable ou

4 y, but primarily in those who have epilepsy, neurological abnormalities, or both before the episode o

5 Both vascular and neurological aetiologies of this pain have been suggeste

6 c oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a po

7 All patients underwent detailed neurological and electrophysiological examinations.

8 at 1 month post-injury were associated with neurological and functional recovery at 1-year follow-up

9 tc19(?/?) mouse model that shows progressive neurological and metabolic decline, decreased complex II

10 arct size, and this correlated with improved neurological and motor function, as well as with preserv

11 tissue damage, and what mechanisms underlie neurological and muscular pathologies that toxoplasmosis

12 Neurological and neurocognitive events were similar amon

13 role of GDNF are relevant in the context of neurological and neurodegenerative diseases that involve

14 of short nucleotide repeats produce several neurological and neuromuscular disorders including Hunti

15 Rescuing executive functions in people with neurological and neuropsychiatric disorders has been a m

16 ticity, the type of neuropathy and the other neurological and non-neurological features of the syndro

17 ffects elicited by D2R blockers when used in neurological and psychiatric conditions, including schiz

18 nt to the aetiology and treatment of diverse neurological and psychiatric diseases that are character

19 dysfunction of which contributes to various neurological and psychiatric diseases.

20 MDAR dysfunction is involved in a variety of neurological and psychiatric diseases; however, the mech

21 cause of its possible implication in several neurological and psychiatric disorders, including cognit

22 arning, and are associated with a variety of neurological and psychiatric disorders.

23 n, and working memory is impaired in several neurological and psychiatric disorders.

24 ch as mood and cognition, and influence many neurological and psychiatric illnesses.

25 cterized by variable expression of skeletal, neurological, and immunological abnormalities.

26 nd involves using neuroimaging, standardized neurological, and standardized motor assessments that in

27 tent BK channel peptide modulator is open to neurological applications, such as preventing audiogenic

28 Before and after the treatment, the neurological assessment and functional magnetic resonanc

29 We collected data from structured clinical neurological assessment, neurocognitive assessment (Wech

30 urodegeneration, and decreasing visceral and neurological cholesterol burden.

31 s who are at an increased risk of developing neurological cognitive comorbidities, and may extend to

32 ON: Myelopathy is considered the most common neurological complication of copper deficiency.

33 Neurological complications after transcatheter aortic va

34 , ranging from mild rash and fever to severe neurological complications and congenital malformations.

35 Patients with neurological complications directly attributable to meta

36 s potential underpinnings of ZIKV-associated neurological complications in humans.

37 izes the current evidence on ZIKV-associated neurological complications in the adults.

38 Neurological complications occurred after a median of 5.

39 rrence of respiratory, cardiac, allergic, or neurological complications requiring immediate intervent

40 llain-Barre syndrome(2,3) as ZIKV-associated neurological complications.

41 t human brain and is associated with serious neurological complications.

42 nctive pharmacology have an inherent risk of neurological complications.

43 No participant had current or past neurological conditions or major medical conditions.

44 the molecular study of psychiatric and other neurological conditions particularly challenging compare

45 A method for capturing gait signatures in neurological conditions that allows comparison of human

46 otball may be at increased risk of long-term neurological conditions, particularly chronic traumatic

47 A proposed neurological coupling-from the potential source of NO, e

48 ctive imaging biomarkers of inflammation and neurological damage in HIV- subjects with CNS cryptococc

49 al disorders and is traditionally related to neurological damage.

50 ection and Guillain-Barre syndrome and fetal neurological defects, including microcephaly, has prompt

51 ially forestall the appearance of HD-related neurological defects.

52 cular dystrophies associated with pronounced neurological defects.

53 Transgenic mice showed less neurological deficit compared with wild-type mice (n=6).

54 insult reduced brain infarct percentage and neurological deficit scores in C57BL/6 J mice, these eff

55 performance category score of 1 (mild or no neurological deficit) or 2 (moderate cerebral disability

56 iated with AVF were recorded: heart failure, neurological deficit/seizure, and hemorrhage.

57 rometabolic disease with patients developing neurological deficits and cardiomyopathy in the long-ter

58 However, neurological deficits are abundant under hypoxic conditi

59 uximab, but some die or acquire irreversible neurological deficits before they can respond, and relap

60 WMI) caused by hypoxia is a leading cause of neurological deficits following premature birth.

61 utcomes for patients include coma, permanent neurological deficits, and death.

62 a result of the irreversible accumulation of neurological deficits.

63 tural substrates accounting for these common neurological deficits.

64 CMS) in our clinic who developed progressive neurological deterioration (encephalopathy) and we wishe

65 entation could prevent hypoxia and secondary neurological deterioration and thus has the potential to

66 In comparison with other neurological diagnoses, subarachnoid hemorrhage patients

67 l presenting complaint prior to a definitive neurological diagnosis or more commonly with disease pro

68 ne transporter (DAT) gene, leading to severe neurological disabilities in children and adults.

69 (TBI) is set to become the leading cause of neurological disability across all age groups.

70 Multiple sclerosis is a major cause of neurological disability, which accrues predominantly dur

71 nal studies of seasonal influenza-associated neurological disease (IAND) and none from the Southern H

72 ould be considered even for patients without neurological disease (neuro-disease).

73 s associated with an unprecedented burden of neurological disease among adults.

74 % at distances greater than 26 km for severe neurological disease and at distances greater than 7 km

75 normobaric 11% O2 from an early age prevents neurological disease and dramatically improves survival

76 suggest a role for astrocyte dysfunction in neurological disease and identify key regions of infecti

77 using mTORC1 inhibitors to treat cancer and neurological disease and, potentially, to improve health

78 nt in the brain tissue of individuals before neurological disease becomes overt or serious.IMPORTANCE

79 Neurological disease drives symptoms through pathologica

80 ed by the ZIKV epidemic, but the spectrum of neurological disease in the adults appears broader as ca

81 cause hereditary spastic paraplegia (HSP), a neurological disease involving dying-back degeneration o

82 brain tissue of HIV patients without serious neurological disease is consistent with their emergence

83 </=4 years; less than half had pre-existing neurological disease or other risk factors for severe in

84 tingtin with an expanded polyQ and develop a neurological disease resembling Huntington disease.

85 Migraine is a widespread neurological disease with negative effects on quality of

86 ge encephalopathy reverses their established neurological disease, evidenced by improved behavior, ci

87 Epilepsy is a common neurological disease, manifested in unprovoked recurrent

88 iously associated with behavioral processes, neurological disease, psychological disorders, cancer, o

89 in extended lifespan and improved markers of neurological disease, via an unknown mechanism.

90 e of two diagnosis categories, RRMS or other neurological disease, with 87% accuracy by leave-one-out

91 anism through which many gene variants cause neurological disease.

92 tative diagnosis and systematic treatment of neurological disease.

93 ta-gut-brain communication during health and neurological disease.

94 g-AD-H and human AD cortices correlated with neurological disease.

95 on of RNAs could be a contributing factor to neurological disease.

96 with an estimated 14% of cases resulting in neurological disease.

97 it is a frequent cause of seizures and other neurological disease.

98 suggest that the TF protein is critical for neurological disease.

99 might explain a breakdown of the DMN in many neurological diseases characterized by declined cognitiv

100 ross the central nervous system (CNS) during neurological diseases do not address the heterogeneity o

101 ided by contrasting these changes with other neurological diseases in which there is also BBB malfunc

102 in the brain accompanies several high-impact neurological diseases including multiple sclerosis (MS),

103 ic targets for acute stroke injury and other neurological diseases involving capillary flow impairmen

104 biogenic amine signaling contribute to human neurological diseases of mood, appetite, and movement.

105 s of iron homeostasis in the brain linked to neurological diseases ranging from rare syndromes to mor

106 uggest that single gene mutations that cause neurological diseases such as epilepsy may affect a surp

107 it excitability associated with Gp1 mGluR in neurological diseases such as FXS.

108 long-standing interest for the treatment of neurological diseases such as glioblastoma.

109 l biological functions and are implicated in neurological diseases, including ataxias, amyotrophic la

110 ction contributes to various psychiatric and neurological diseases, including drug addiction and Park

111 Spasticity occurs in a wide range of neurological diseases, including neurodegenerative disea

112 nal ER dysfunction is implicated in numerous neurological diseases, its role at nerve terminals is po

113 tiated from iPSCs to study their function in neurological diseases, like Alzheimer's disease (AD).

114 While neurological diseases, such as Huntington disease and Al

115 revious evidence of mtDNA variation in other neurological diseases.

116 amental properties of the nervous system and neurological diseases.

117 anding brain function and the development of neurological diseases.

118 athological conditions, including cancer and neurological diseases.

119 s microRNAs that may serve as biomarkers for neurological diseases.

120 brain have a close relationship with typical neurological diseases.

121 calable, in vivo studies of neurobiology and neurological diseases.

122 ging as attractive therapeutic strategies in neurological diseases.

123 nervous system and potential aberrations in neurological diseases.

124 otransmission and are implicated in numerous neurological diseases.

125 lthy control subjects and other inflammatory neurological diseases.

126 sed as a core factor in the etiology of many neurological diseases.

127 or-mediated signalling is linked to numerous neurological diseases.

128 anipulations could lead to new treatments of neurological diseases.

129 d in healthy controls or patients with other neurological diseases.

130 ated for increasing drug or gene delivery in neurological diseases.

131 otein 2 (MeCP2) cause Rett syndrome (RTT), a neurological disorder affecting cognitive development, r

132 DGRG1 (G1; also known as GPR56) underlie the neurological disorder bilateral frontoparietal polymicro

133 Rett syndrome (RTT) is a debilitating neurological disorder caused by mutations in the gene en

134 Epilepsy is a common neurological disorder occurring in 3% of the US adult po

135 estless legs syndrome is a prevalent chronic neurological disorder with potentially severe mental and

136 an abnormal cortical event that underlies a neurological disorder.

137 Epilepsy is a serious and common neurological disorder.

138 represents a novel target in paraneoplastic neurological disorders and has high predictive value for

139 ptors are also implicated in psychiatric and neurological disorders and have received considerable at

140 tive and behavioral symptoms associated with neurological disorders and neuropsychiatric disease.

141 are promising drug targets to manage several neurological disorders and nicotine addiction.

142 the emerging idea of a systemic influence to neurological disorders and point to the need for future

143 useful source of primary cells for modeling neurological disorders at the molecular level.

144 spongiform encephalopathies (TSEs) are fatal neurological disorders caused by prions, which are compo

145 ic roles of genes influencing both sleep and neurological disorders could lead to new treatment strat

146 s an essential factor in the pathogenesis of neurological disorders following acute systemic inflamma

147 may extend to multiple neuropsychiatric and neurological disorders in which RELN deficiency is a com

148 with sleep disorders are also implicated in neurological disorders in which sleep abnormalities are

149 ka virus (ZIKV) infection is associated with neurological disorders of both the CNS and peripheral ne

150 emerging as a critical mechanism underlying neurological disorders of various etiologies, yet its ro

151 Thus, pericyte degeneration as seen in neurological disorders such as Alzheimer's disease may c

152 eteriorates, and these defects can result in neurological disorders such as hereditary spastic parapl

153 gy as well as in the pathogenesis of several neurological disorders such as stroke, spinal cord injur

154 thus reveal a novel therapeutic strategy for neurological disorders that are accompanied by Kv2.1-fac

155 native splicing and is implicated in several neurological disorders with developmental origins.

156 ptor (NMDAR) activity contributes to several neurological disorders, but direct antagonism is poorly

157 a central factor in the development of many neurological disorders, but much less is known about the

158 m HAART still develop various HIV-associated neurological disorders, even when the viral load is low.

159 such as arthritis, cardiovascular diseases, neurological disorders, fibrosis, and cancers.

160 V), a re-emerging flavivirus associated with neurological disorders, has spread rapidly to more than

161 and synapse impairments are features of many neurological disorders, including autism spectrum disord

162 undergo important phenotypic changes in many neurological disorders, including strokes, trauma, infla

163 s mutations in glypicans are associated with neurological disorders, such as autism and schizophrenia

164 ment observed in a number of psychiatric and neurological disorders, such as schizophrenia and Alzhei

165 modalities for the treatment of cancers and neurological disorders.

166 diting as a potential therapy to treat human neurological disorders.

167 tive ubiquitination is implicated in several neurological disorders.

168 (FDA) licensure 2005-2012 inclusive in seven neurological disorders.

169 in neuronal positioning lead to a variety of neurological disorders.

170 source of cells for regenerative medicine in neurological disorders.

171 blood-brain barrier (BBB) for treating many neurological disorders.

172 bunits have been associated with an array of neurological disorders.

173 mportant therapeutic target for a variety of neurological disorders.

174 and, potentially, selective vulnerability in neurological disorders.

175 nds as interesting approach for treatment of neurological disorders.

176 ssociated with numerous diseases, especially neurological disorders.

177 roles in brain development, homeostasis, and neurological disorders.

178 lvement in diseases as diverse as cancer and neurological disorders.

179 nociception and are implicated in a range of neurological disorders.

180 ts association with microcephaly and serious neurological disorders.

181 nesis and may shed light on MAP7 function in neurological disorders.SIGNIFICANCE STATEMENT Neurons co

182 and are associated with the presentation of neurological disturbances independently of disease stage

183 n unpublished trials of licensed and stalled neurological drugs, respectively.

184 to the vascular component of other forms of neurological dysfunction and degeneration.

185 d with amyloid cerebrovascular pathology and neurological dysfunction.

186 c focal retrograde amnesia following a minor neurological episode; and (iv) patients with gaps in the

187 2.82 to 10.8, p<0.0001) and transient focal neurological episodes (OR 11.7; 95% CI 2.70 to 50.6, p=0

188 as having had CED or a combined end point of neurological-etiology death or survival.

189 g, thromboembolic event, pump thrombosis, or neurological event) in the short-term cohort (as-treated

190 analysed all CT scans, echocardiograms, and neurological events in a masked fashion.

191 association with the combined outcome of new neurological events or death (HR, 1.58 [95% CI, 1.11-2.2

192 omechanical simulation results to supplement neurological evidence for similarities between the two b

193 resonance imaging and the Hammersmith Infant Neurological Examination may be helpful in assisting cli

194 ing-remitting multiple sclerosis, a complete neurological examination, a baseline brain and spinal co

195 rooke's Cognitive Examination (ACE-R), had a neurological examination, clinical diagnostics and multi

196 ribution underwent standard and quantitative neurological examination, including disability status, v

197 europathy and the other neurological and non-neurological features of the syndrome.

198 developmental disorder with some overlapping neurological features to Dup15q.

199 elin plasticity, with broad implications for neurological function in health and disease.

200 e inhibitors, A-33 and D159687, in mediating neurological function in mice.

201 Performance Status, extent of resection, and neurological function) were incorporated into a new mode

202 n gasping and 1-year survival with favorable neurological function, defined as a Cerebral Performance

203 We hypothesized that neurological function, which also depends on intracellul

204 ng cells that influence myelin structure and neurological function.

205 s important for genetic integrity and normal neurological function.

206 trophysiology to assess nBMP2 expression and neurological function.

207 -resident macrophage development and affects neurological function.

208 d to the injured parenchyma and improved the neurological function.

209 s, one with agranulocytosis), and decline in neurological functioning (one event, likely due to natur

210 the blood-brain-barrier, and improvement of neurological functions after ICH.

211 However, neurological functions of POMTs remain poorly understood

212 s to be identified and their contribution to neurological health to be examined.

213 ious and non-infectious causes of this acute neurological illness.

214 t on expression can be found in degenerative neurological illnesses, such as Alzheimer's disease.

215 licated in a number of human psychiatric and neurological illnesses.

216 Left untreated, jaundice can lead to neurological impairment and death.

217 l thickening that result in seizures, severe neurological impairment and developmental delay.

218 neonatal transition and may cause permanent neurological impairment, but optimal intervention thresh

219 of age and have disrupted AIS and many other neurological impairments including seizures, disrupted c

220 The devastating neurological impairments that result from blasts are sig

221 e incidence of cerebral palsy or other major neurological impairments was not significantly different

222 Many of these diseases are neurological in nature revealing critical roles for this

223 To date, targets of neurological infection and disease have not been investi

224 We examined biomarkers of neurological injury (neuromarkers) and inflammation in p

225 he presence of AEF may result in significant neurological injury resulting from air embolism.

226 BDG group) or carbon dioxide reactivity with neurological injury.

227 ected, averaged, and transformed to Montreal Neurological Institute (MNI) space.

228 s with researchers and staff at the Montreal Neurological Institute and Hospital during the developme

229 Images were spatially normalized to Montreal Neurological Institute template space.

230 ssociated with preterm birth may result from neurological insults that begin in utero.

231 rtant traumatic brain injury [TBI], need for neurological intervention, and clinically significant in

232 Through characterization of this neurological intracellular trafficking disorder, we esta

233 Central nervous system (CNS) infection and neurological involvement have also been reported in CCHF

234 he associated phenotypes range from isolated neurological involvement to JS with retinal dystrophy, a

235 linking de novo dominant EEF1A2 mutations to neurological issues in humans.

236 ecal HPbetaCD to participants with NPC1 with neurological manifestation at the National Institutes of

237 gnitive disorder (HAND) remains an important neurological manifestation that adversely affects a pati

238 Development of treatments for the neurological manifestations of MPS has been hindered by

239 se (AD), it also occurs in aging and various neurological, medical, and psychiatric conditions.

240 n comparison with 21 consecutively recruited neurological memory-disordered patients and 14 healthy c

241 CSE is associated with substantial long-term neurological morbidity, but primarily in those who have

242 Dystonia is a neurological movement disorder that forces the body into

243 on score of 26 or higher) with no history of neurological or psychiatric disorders, and had completed

244 mation from deep sequencing of patients with neurological or psychiatric disorders, we investigated m

245 .2-2.6; P=0.007) and survival with favorable neurological outcome (adjusted relative risk, 1.6; 95% c

246 To test serum tau as a predictor of neurological outcome after cardiac arrest.

247 promising novel biomarker for prediction of neurological outcome in patients with cardiac arrest.

248 kely target for therapies aimed at improving neurological outcome in preterm neonates with hypoxia-in

249 urvival to hospital discharge with favorable neurological outcome, defined as Pediatric Cerebral Perf

250 spital discharge and survival with favorable neurological outcome.

251 and 43% survived to discharge with favorable neurological outcome.

252 ying how viral infection can cause different neurological outcomes depending on host genetic backgrou

253 n of resuscitation efforts with survival and neurological outcomes from 2010 through 2014.

254 f cardiopulmonary resuscitation elements and neurological outcomes reporting have advanced substantia

255 on measurement of quality of resuscitation, neurological outcomes, and deletion of data that have pr

256 participants and their parents to determine neurological outcomes, with adverse outcome defined as p

257 ac arrest and 1-year survival with favorable neurological outcomes.

258 tion and their association with survival and neurological outcomes.

259 te that Gnal-haplodeficient mice have a mild neurological phenotype and display vulnerability to deve

260 Among patients presenting with diverse neurological problems, CSF discordance or escape was obs

261 d escape in patients presenting with diverse neurological problems.

262 ent predominantly abdominal, orthopedic, and neurological procedures.

263 wed significantly greater likelihood of full neurological recovery (mRS 0-1) at day 90 (OR 7.6, 95% C

264 injury and that uPA binding to uPAR promotes neurological recovery after an acute ischemic stroke.

265 antitative automated pupillometry to predict neurological recovery after CA.

266 Long-term data on the functional trajectory, neurological recovery, psychological sequelae, and the p

267 resented larger brain infarct size, worsened neurological scores, and reduced sensorimotor functions.

268 es of epilepsy in the world is produced as a neurological sequela in survivors of cerebral malaria.

269 ES has a favourable prognosis generally, but neurological sequelae and even fatalities can occur, esp

270 long-term follow-up, 1 of whom had permanent neurological sequelae.

271 of mice was aged until each mouse developed neurological signs as determined by trained animal techn

272 ed memory deficits, abrogated development of neurological signs, prevented neurodegeneration and sign

273 ification of genes influencing risk for some neurological sleep disorders.

274 reflect the specificity of the task and the neurological states.

275 y, otolaryngology-head and neck surgery, and neurological surgery (n = 63).

276 The median delay from neurological symptom debut to first hospital contact was

277 ions with self-report measures of functional neurological symptom severity or childhood abuse.

278 with time, peaking during the height of the neurological symptoms (1.5E copies/mL).

279 n stress-related neuroplasticity, functional neurological symptoms and reduced insular volume was ide

280 diseases and provides an explanation for the neurological symptoms observed in some patients with SLE

281 attack, which is clinically defined as focal neurological symptoms of ischaemic origin resolving spon

282 Patients with development of neurological symptoms within 12 months of anti-PD-1 ther

283 ions with self-report measures of functional neurological symptoms, adverse life events and PTSD symp

284 ical characteristics, time to development of neurological symptoms, and modified Rankin Scale (mRS) s

285 tration of Cu(II)(atsm) delayed the onset of neurological symptoms, improved locomotive capacity and

286 ond phase of the disease, after the onset of neurological symptoms, magnetic resonance imaging (MRI)

287 w dysfunction in their absence underlies FXS neurological symptoms.

288 sorder characterized by immunodeficiency and neurological symptoms.

289 activity were observed, even after onset of neurological symptoms.

290 with failure to thrive, immunodeficiency and neurological symptoms.

291 erature comparing PNES with other functional neurological symptoms.

292 wn etiological mechanisms of psychiatric and neurological synaptopathies.

293 sing key questions including the predominant neurological syndrome associated with the neuropathy, fo

294 arcts and leukoencephalopathy (CADASIL) is a neurological syndrome characterized by small vessel dise

295 riteria, is associated with a characteristic neurological syndrome.

296 ations compared to four other lesion-induced neurological syndromes (P < 0.0001).

297 Mechanisms for ZIKV-GBS and other neurological syndromes have been hypothesized, such as a

298 ctors, such as metals, interact to determine neurological traits.

299 tive behavior, supporting partial coincident neurological underpinnings for compulsive overeating and

300 prevalence of cerebral metastases in NENs, a neurological work-up should be performed.