ライフサイエンスコーパス: neurologic

1 lastic, congenital, other neurologic, or non-neurologic.

2 ed into five broad categories as follows: 1) neurologic, 2) respiratory, 3) cardiovascular, 4) renal

3 p for development of blinatumomab-associated neurologic adverse events and suggests interfering with

4 ld be the basis of mitigation strategies for neurologic adverse events associated with blinatumomab t

5 t of B-cell malignancies, is associated with neurologic adverse events in a subgroup of patients.

6 or a two-step process for the development of neurologic adverse events in response to blinatumomab: (

7 Neurologic adverse events occurred in 65% of patients; a

8 istribution and the early occurrence of most neurologic adverse events, (ii) T-cell transmigration th

9 and cytokine release to potentially trigger neurologic adverse events.

10 and laboratory factors and acute and chronic neurologic and cognitive outcomes.

11 )) were generated and examined for lifespan, neurologic and hepatic functions, as well as liver histo

12 drug target for the treatment of a number of neurologic and inflammatory disorders.

13 in Npc1(-/-) mice not only does not reverse neurologic and motor dysfunction, but further worsens ov

14 gin of network alternations underlying human neurologic and neuropsychiatric diseases.

15 icular enlargement, a key feature of several neurologic and psychiatric diseases, is mediated by unkn

16 CNS physiology and function that manifest as neurologic and psychiatric diseases.

17 elp to better understand the role of SEZ6 in neurologic and psychiatric diseases.

18 d to the development of viable therapies for neurologic and psychiatric disorders.

19 ncephalopathy, encompass a broad spectrum of neurologic and psychiatric features, but the pathogenesi

20 ncept that celiac disease is associated with neurologic and psychological features.

21 re measured by wrist actigraphy, severity of neurologic and systemic illness by Glasgow Coma Scale an

22 The risks for cCMV and related sequelae (neurologic and/or hearing loss) following a maternal inf

23 present as a severe systemic and often fatal neurologic and/or respiratory disease.

24 49 abdominal, 45 orthopedic, 34 vascular, 8 neurologic, and 4 genitourinary surgical procedures, or

25 ICUs included medical/surgical, trauma, neurologic, and cardiac care units.

26 ers is associated with numerous psychiatric, neurologic, and neurodegenerative conditions.

27 The proportion of cutaneous, neurologic, and other complications was 6.40% (95% CI:1.

28 Proportions of cutaneous, neurologic, and other complications were 6.40% (95% CI,1

29 1.03; p < 0.001) with hematological, sepsis, neurologic, and pulmonary disease categories having the

30 ean time between admission and tracheostomy, neurologic assessment at admission, confirmed ventilator

31 ported a high prevalence of musculoskeletal, neurologic, auditory, and visual complications among Ebo

32 ported a high prevalence of musculoskeletal, neurologic, auditory, and visual complications among Ebo

33 We conclude that neurologic autoantibodies do not cross disease barriers

34 The finding of mildly increased neurologic autoantibodies in SLE may be consistent with

35 = 49, HD n = 33), and 4) a control cohort of neurologic autoimmunity (relapsing-remitting multiple sc

36 een cognitive processes and their underlying neurologic bases during development.SIGNIFICANCE STATEME

37 Here, we examined the impact of VEGF-A on neurologic changes that underly HSK using a mouse model

38 IV-associated sensory neuropathy is a common neurologic comorbidity of HIV infection and prevails in

39 Hepatic encephalopathy (HE) is a serious neurologic complication in patients with liver cirrhosis

40 l, 27% (95% CI, 0.17-0.39%) had at least one neurologic complication, 23% (95% CI, 0.14-0.32%) hypoxi

41 The MHCA + SACP group had lower rate of neurologic complications (3/61 vs 10/53 for DHCA; p < 0.

42 outcomes will depend on better defining the neurologic complications and underlying pathophysiology

43 Background Neurologic complications in coronavirus disease 2019 (CO

44 prevalence, predictors of and survival from neurologic complications in patients who have undergone

45 intraoperative rupture are the most frequent neurologic complications of intracranial aneurysm coilin

46 ient understanding of the pathophysiology of neurologic complications prevents us from addressing the

47 These outbreaks have been associated with neurologic complications that include congenital abnorma

48 Rates of neurologic complications were analyzed, and associated f

49 al membrane oxygenation were associated with neurologic complications.

50 over 24 hours were associated with important neurologic complications: intracranial hemorrhage, ische

51 ndrome of the trephine (SoT) is a reversible neurologic condition that often occurs following DC as a

52 (AS), previously associated with an acquired neurologic condition, the paraneoplastic opsoclonus-myoc

53 lammation and cell death which drive various neurologic conditions including Alzheimer's disease, ALS

54 ncreased risk for the development of several neurologic conditions including progressive multiple scl

55 ses and plays a harmful role in cancer, many neurologic conditions, and chronic viral infections.

56 Age is a critical risk factor for many neurologic conditions, including progressive multiple sc

57 d potential therapeutic targets for multiple neurologic conditions, including those affecting the per

58 In many neurologic conditions, the distal axon experiences energ

59 ation (DBS) is used to treat a wide array of neurologic conditions.

60 may also play a role in cell death in other neurologic conditions.

61 with comparison groups of chronic pain and a neurologic control (Alzheimer's disease).

62 Neurologic damage following cardiac arrest remains a maj

63 ditional carbon monoxide application reduces neurologic damage.

64 bjects, and for intubated subjects excluding neurologic deaths also demonstrated good discrimination

65 d miscalibrated, whereas the model excluding neurologic deaths showed perfect calibration.

66 y distress syndrome (including and excluding neurologic deaths) had excellent discrimination (both ar

67 Models excluding neurologic deaths, for intubated subjects, and for intub

68 e Version 1 cohort, for the cohort excluding neurologic deaths, for intubated subjects, and for intub

69 bjects, and for intubated subjects excluding neurologic deaths.

70 Liver damage, neurologic decline, and molecular analyses of TSP-1 and

71 (-/-) AOM-treated mice had a reduced rate of neurologic decline, less cerebral edema, and a decrease

72 mmunodeficiency, sino-pulmonary disease, and neurologic decline.

73 2 knockout mice (Sac2KO) do not have obvious neurologic defects.

74 ses of neurological pathology and congenital neurologic defects.

75 of 0 to 2, signifying an absence of or minor neurologic deficit, was 35.1% in the thrombectomy group

76 nflammatory response may still contribute to neurologic deficits after reperfused stroke by using tar

77 hether axonal injury is related to long-term neurologic deficits and cognitive impairment in children

78 hildren with CM is associated with long-term neurologic deficits and cognitive impairment.

79 ile the associated neuroinflammation and the neurologic deficits are dramatically exacerbated.

80 rations were associated with the presence of neurologic deficits at hospital discharge, and at 6, 12,

81 We assessed neurologic deficits by neurobehavioral tests and blood-b

82 n after intracerebral hemorrhage, but severe neurologic deficits may confound its assessment and lead

83 ons in multiple brain regions and results in neurologic deficits such as seizures.

84 sessment Method for the ICU in patients with neurologic deficits, but novel tools designed for such p

85 t CNS axons is abortive, causing devastating neurologic deficits.

86 tly influence the severity of CHS-associated neurologic deficits.

87 tubated cognitively intact and without focal neurologic deficits.

88 entangling delirium symptoms from underlying neurologic deficits.

89 escue thrombectomy for patients with LVO and neurologic deterioration).

90 ion or haemorrhagic complications, and early neurologic deterioration.

91 ng for confounding variables such as age and neurologic diagnosis, both coefficient of variation of r

92 sclerosis (PMS) causes slow accumulation of neurologic disability and has been refractory to treatme

93 ominent at 7.0 T and independently predicted neurologic disability progression.

94 in and latterly neurons leading to permanent neurologic disability.

95 matter lesion load and cortical thickness to neurologic disability.

96 ility Status Scale (EDSS) was used to assess neurologic disability.

97 sified as having either hepatic (n = 711) or neurologic disease (n = 461).

98 subtype dysfunction is a key contributor to neurologic disease circuits, but identifying associated

99 g severe and often lethal respiratory and/or neurologic disease in animals and humans.

100 Multiple sclerosis (MS) is a common cause of neurologic disease in young adults that is primarily tre

101 nd in the brain, and it is hypothesized that neurologic disease leads to the production of autoantibo

102 Patients with a prior history of neurologic disease were excluded.

103 Excluded were children with systemic neurologic disease, optic nerve or retinal disease (even

104 ease cases were identified; none experienced neurologic disease.

105 o control of viral replication as well as to neurologic disease.

106 tering disease that is often associated with neurologic disease.

107 relapsing-remitting MS (RRMS; n = 12), other neurologic diseases (ONDs; n = 1), and healthy controls

108 17 [standard deviation]; 113 women) with 35 neurologic diseases and normal brain MRI scans obtained

109 ide unique insights into the pathogenesis of neurologic diseases, and identify potential targets for

110 seases including inflammatory bowel disease, neurologic diseases, cardiovascular disorders, and cance

111 ion is a key pathologic hallmark of numerous neurologic diseases, however, its exact role in vivo is

112 e therapeutic benefit of a ketogenic diet in neurologic diseases, including epilepsy.

113 Neural activity in the pallidum goes awry in neurologic diseases, such as Parkinson's disease.

114 prove the treatment, diagnosis, and study of neurologic diseases.

115 s have identified genetic variants linked to neurologic diseases.

116 sclerosis (FSGS), as well as to cases of the neurologic disorder Charcot-Marie-Tooth disease that are

117 ICANCE STATEMENT Epilepsy is a heterogeneous neurologic disorder commonly associated with comorbid em

118 EMENT Tinnitus, or ringing in the ears, is a neurologic disorder that affects 15% of the general popu

119 Episodic cluster headache is a disabling neurologic disorder that is characterized by daily heada

120 Chronic subdural hematoma is a common neurologic disorder that is especially prevalent among o

121 Autism is a common and complex neurologic disorder whose scientific underpinnings have

122 ) and its ability to expose axonal damage in neurologic disorders have solicited a considerable amoun

123 of node assembly and the pathophysiology of neurologic disorders in which impaired paranodal functio

124 Defects in cell polarity are associated with neurologic disorders including autism and microcephaly.

125 For the constellation of neurologic disorders known as chemotherapy-induced perip

126 optica spectrum disorders n = 15; and other neurologic disorders n = 26).

127 n.SIGNIFICANCE STATEMENT Monogenic causes of neurologic disorders, although rare, can provide opportu

128 renal disease, coronary artery disease, and neurologic disorders, but not pulmonary disease, immunoc

129 brain, and their dysfunction underlies many neurologic disorders, especially epilepsy.

130 n is involved in the pathogenesis of several neurologic disorders, including epilepsy.

131 endritic architectures are hallmarks of many neurologic disorders, including stroke-induced damage ca

132 anganese is an environmental risk factor for neurologic disorders, such as a Parkinson's disease-like

133 of dendritic structures accompanies numerous neurologic disorders, such as schizophrenia and autism.

134 entions, i.e. mirror therapy, in people with neurologic disorders.

135 to increased risk of developing age-related neurologic disorders.

136 ral dysmotility, inflammatory, hormonal, and neurologic disorders.

137 as a potential strategy for the treatment of neurologic disorders.

138 determine their therapeutic applications in neurologic disorders.

139 with neuroinflammation in epilepsy and other neurologic disorders.SIGNIFICANCE STATEMENT Neuroinflamm

140 role in clinical diagnosis and treatment of neurologic disorders.Supplemental material is available

141 ator protein (CTMP) in Akt-signaling related neurologic dysfunction and skeletal muscle metabolism.

142 nth surveillance: no overt constitutional or neurologic dysfunction was noted for any study animals.

143 ients with cancer, often leading to malaise, neurologic dysfunction, or death.

144 s in the LYST gene that involves progressive neurologic dysfunction.

145 To examine the neurologic effects of infection in the absence of other

146 T) of the head is used worldwide to diagnose neurologic emergencies.

147 ), other cardiac (aOR: 12.8; p < 0.001), and neurologic etiologies (aOR: 8.72; p < 0.001) were also a

148 Detailed cardiologic and neurologic evaluation at study enrollment and for a medi

149 de 3 or higher cytokine release syndrome and neurologic events occurred in 15% and 31% of patients, r

150 mediated complications such as thrombotic or neurologic events.

151 that captures motor abnormalities on routine neurologic examination and which is associated with cogn

152 She remained intubated with a limited neurologic examination due to sedative medications until

153 Certain components of the neurologic examination may be overvalued, such as absent

154 Neurologic examination was notable for drowsiness, right

155 measures of mood, cognitive performance, and neurologic examination, with elective cerebrospinal flui

156 help neurologists in understanding the many neurologic facets of COVID-19.

157 were no differences in median mood scores or neurologic findings and cognitive performance improved m

158 measures were perinatal history, visual and neurologic findings, and magnetic resonance (MR) imaging

159 eater than 90 mm Hg was associated with good neurologic function (adjusted relative risk, 2.46; 95% C

160 The primary outcome was favorable neurologic function at 6 months (Glasgow Outcome Scale-E

161 Good neurologic function at hospital discharge occurred in 30

162 rrest was independently associated with good neurologic function at hospital discharge.

163 ticus termination for no return to premorbid neurologic function were estimated by Poisson regression

164 Sleep's impact on neurologic function, and cognitive endurance affect capa

165 e secondary damage and preserve anatomic and neurologic function.

166 abolic state of the brain can greatly impact neurologic function.

167 iteria included prematurity and pre-existing neurologic, genetic, metabolic, or intraocular pathology

168 increased the risk for gastrointestinal and neurologic harms (all moderate-certainty evidence).

169 e genetic boundaries between psychiatric and neurologic illness?

170 ocellular injury, hyperglycemia and ketosis, neurologic illnesses, ocular symptoms, and dermatologic

171 had acute neurologic symptoms necessitating neurologic imaging.

172 animal models, but human variants leading to neurologic impairment have not been described.

173 ammatory disease of the CNS characterized by neurologic impairment resulting from primary demyelinati

174 pnea or cyanosis during the present illness, neurologic impairment, and presence of an enteral feedin

175 th birth defects, including microcephaly and neurologic impairment.

176 hat causes immobilizing pain and significant neurologic impairment.

177 Cause of death was neurologic in 60.0% and multiple organ failure in 34.3%

178 ratory distress syndrome nonsurvivors versus neurologic in 85.4% of nonsurvivors without pediatric ac

179 re reported in 10 studies and were primarily neurologic in nature, with two cases of coma-one resulti

180 ngitis or encephalitis improved diagnosis of neurologic infections and provided actionable informatio

181 with mounting concern about new and emerging neurologic infections.

182 s associated with differential mortality and neurologic injury in intensive care and cardiac arrest p

183 on and change over 24 hours on mortality and neurologic injury in patients undergoing venoarterial ex

184 spontaneous circulation and proportional to neurologic injury representing a promising novel biomark

185 dies examined neuroimaging results and found neurologic injury to be more frequent in venoarterial ve

186 d postresuscitation success rates, degree of neurologic injury, and severity of myocardial dysfunctio

187 on and infectious cause of fetal anomaly and neurologic injury.

188 egulation (CA) plays a key role in secondary neurologic injury.

189 vascular illness (P < 0.001) and severity of neurologic insult (P = 0.02) were higher in neonates wit

190 nts with a diagnosis of aSAH admitted to the neurologic intensive care unit of a regional referral ho

191 Neurologic involvement of HIV remains an important conce

192 y aid in the assessment of disease severity, neurologic involvement, or prognostication.

193 ver, are tick-borne infections with frequent neurologic involvement.

194 onavirus 2 (SARS-CoV-2) infection with acute neurologic manifestations and referral for brain MRI.

195 However, the mechanisms underlying the neurologic manifestations in Ebola patients are not know

196 eview the MRI findings associated with acute neurologic manifestations in patients with COVID-19.

197 The number of recognized neurologic manifestations of SARS-CoV-2 infection is rap

198 ithout ischemic infarcts had a wide range of neurologic manifestations that were associated with abno

199 The most common neurologic manifestations were alteration of consciousne

200 for hospitalization and oxygen therapy, (c) neurologic manifestations, and (d) abnormal brain MRI fi

201 disease 2019 (COVID-19) and presenting with neurologic manifestations.

202 Further research with a systematic neurologic monitoring is necessary to define the timing

203 led data argue for CANOMAD to be included in neurologic monoclonal gammopathy of clinical significanc

204 test were upper respiratory (n=32, 68%) and neurologic (n=30, 64%); fever was not commonly reported

205 cessive syndrome characterized by a distinct neurologic, ophthalmologic, and facial phenotype.

206 High rates of any neurologic, ophthalmologic, and hearing abnormalities we

207 of these patients will have life-threatening neurologic or cardiologic conditions.

208 on = -2.66, 95% CI = -4.85 to -0.47) but not neurologic or quality of life outcomes.

209 19 patients, finding association with either neurologic or thrombotic complications.

210 m as vascular, neoplastic, congenital, other neurologic, or non-neurologic.

211 esponsible for unexplained gastrointestinal, neurologic, or skin disorders.

212 -4.83; p = 0.025) and survive with favorable neurologic outcome (adjusted odds ratio, 2.21; 95% CI, 1

213 To identify plasma biomarkers for poor neurologic outcome (Cerebral Performance Categories scor

214 We modeled associations between dichotomized neurologic outcome (good vs poor) and quantitative elect

215 The primary outcomes were favorable neurologic outcome (swine Cerebral Performance Category

216 d mean arterial blood pressure would improve neurologic outcome after cardiac arrest.

217 hypothermia may increase survival with good neurologic outcome after cardiac arrest.

218 Pooled results showed no difference of good neurologic outcome among survivors between the two treat

219 We defined a favorable neurologic outcome as a CPC score of 1 or 2.

220 lacebo did not significantly improve 6-month neurologic outcome as measured by the Glasgow Outcome Sc

221 he Oxford Visual Geometry Group), to predict neurologic outcome at 12 and 24 hours after cardiac arre

222 Survival with good neurologic outcome at 180 days was not different between

223 ge of patients who survived with a favorable neurologic outcome at day 90 than was observed with targ

224 h higher mortality and no difference in good neurologic outcome compared with normothermia in critica

225 novel biomarkers for the prediction of poor neurologic outcome in out-of-hospital cardiac arrest sur

226 me, resulted in a significant improvement of neurologic outcome prediction (C-index, 0.70; explained

227 Neurologic outcome prediction in out-of-hospital cardiac

228 entified risk factors significantly improved neurologic outcome prediction.

229 tation was 29% (95% CI, 0.26-0.33%) and good neurologic outcome was achieved in 24% (95% CI, 0.21-0.2

230 Neurologic outcome was assessed by the Cerebral Performa

231 Favorable neurologic outcome was more likely with hemodynamic-dire

232 agement 33 degrees C survived with favorable neurologic outcome, compared with 30% in the targeted te

233 The primary outcome was survival with good neurologic outcome, defined as Cerebral Performance Cate

234 ose-response increase in probability of good neurologic outcome, with mean arterial blood pressure gr

235 Sixty-three patients (66%) had a poor neurologic outcome.

236 lmonary resuscitation patients achieved good neurologic outcome.

237 71 kDa protein as novel biomarkers for poor neurologic outcome.

238 n arterial blood pressure is associated with neurologic outcome.

239 ogic recovery to improve early prediction of neurologic outcome.

240 othermia is currently recommended to improve neurologic outcomes in adults with persistent coma after

241 pinephrine improved overall survival but not neurologic outcomes in out-of-hospital cardiac arrest pa

242 ospital discharge and survive with favorable neurologic outcomes than patients with pulseless arrests

243 pulmonary resuscitation myocardial function, neurologic outcomes, and survival.

244 r has beneficially improved both hearing and neurologic outcomes, both fundamental advances for these

245 ved survival at 30 days and 3 months but not neurologic outcomes, standard dose of epinephrine decrea

246 established multivariate brain measure, the Neurologic Pain Signature (NPS), as a common nociceptive

247 In contrast, the neurologic pain signature, a neuromarker sensitive and s

248 Ps; two females), in three noncallosotomized neurologic patients (NPs; two females), and in a sample

249 ale behavioral and neuroanatomical data from neurologic patients with focal brain lesions can be leve

250 ared to wild-type controls but show no overt neurologic phenotype.

251 common in females (male/female: 328/383) and neurologic presentation in males (259/202; P < 0.001).

252 essure over 20 mm Hg is associated with poor neurologic prognosis, but measuring intracranial pressur

253 ing definitive recommendations based on poor neurologic prognosis, most physicians seem to wait until

254 Neurologic prognostication was not a part of any of the

255 cell transplant (HCT) has been shown to halt neurologic progression, although the mechanism of diseas

256 up that developed adverse events showed less neurologic recovery (odds ratio, 0.55; 95% CI, 0.32-0.96

257 Brain mitochondrial dysfunction limits neurologic recovery after cardiac arrest.

258 process of raising the promise of long-term neurologic recovery during the management of stroke.

259 Electroencephalogram features predict neurologic recovery following cardiac arrest.

260 study aimed to identify novel biomarkers of neurologic recovery to improve early prediction of neuro

261 ary angiography that was delayed until after neurologic recovery.

262 CACH/VWM), a leukodystrophy characterized by neurologic regression in the setting of febrile illness

263 ICU admission diagnosis (especially sepsis-, neurologic-, respiratory-, and cardiovascular-related),

264 continuous electroencephalography and absent neurologic responses were independently associated with

265 However, the neurologic role of TREM2 in normal aging is poorly under

266 portion of sensorineural hearing loss and/or neurologic sequelae were 32.4% (95% confidence interval

267 0-1.04), p = 0.003; and any acute pathologic neurologic sign/event, 5.04 (2.15-12.01), p < 0.001 were

268 ic fixation, and 6 children had cognitive or neurologic signs at the time of diagnosis (75%).

269 ew lesions, escalating steroids, progressive neurologic signs or symptoms, or non-CNS progression.

270 resuscitation, and appearance of pathologic neurologic signs were associated with adverse outcomes i

271 The potential neurologic sparing, possibly via reduced volume of chron

272 the Repeatable Battery for the Assessment of Neurologic Status and executive function with the Trail

273 measures of survival to discharge, favorable neurologic status at discharge (Cerebral Performance Cat

274 istration and dysglycemia were correlated to neurologic status at discharge defined by disability gra

275 ent therapy, time to target temperature, and neurologic status at discharge from the intensive care u

276 y was to test whether autoantibodies against neurologic surface Ags are found in nonneurologic autoim

277 Autoantibodies against neurologic surface Ags were not observed in RA and T1D p

278 describe a subpopulation of individuals with neurologic symptomatic cryptococcal antigenemia but nega

279 The second most common reason was focal neurologic symptoms (16%); only 16% of these studies sho

280 Many patients with an LMNA mutation have neurologic symptoms by their 30s and develop progressive

281 and using imputed data, less interference of neurologic symptoms in daily activities (P = .008) and f

282 oronavirus disease 2019, 108 (15%) had acute neurologic symptoms necessitating neurologic imaging.

283 9 D-CAA mutation carriers (M(+) ; 13 without neurologic symptoms, 6 with prior lobar intracerebral he

284 Of 308 patients with acute neurologic symptoms, 73 met the inclusion criteria and w

285 erum levels of ferritin peaked with onset of neurologic symptoms, and higher ferritin levels were ass

286 Manganese exposure produces Parkinson's-like neurologic symptoms, suggesting a selective dysregulatio

287 ts, or gastrointestinal, musculoskeletal, or neurologic symptoms.

288 ialosyl epitopes in the context of evocating neurologic symptoms.

289 primary nonrespiratory (gastrointestinal or neurologic) symptoms, had lung parenchymal findings susp

290 The onset of the neurologic syndrome preceded the diagnosis of seminoma i

291 route and is known for causing outbreaks of neurologic syndromes and abortion storms.

292 are highly prevalent, presenting with severe neurologic syndromes and associated with high risk of re

293 ome, pulmonary, cardiac, renal, hepatic, and neurologic toxicities, hemophagocytic lymphohistiocytosi

294 ells, which could explain the lower level of neurologic toxicity associated with Hu19-CD828Z.

295 inhibit dopamine receptor D2, a mediator of neurologic toxicity induced by perphenazine and related

296 However, severe neurologic toxicity occurred in only 5% of patients who

297 Neurologic toxicity was evaluated during an 8-month surv

298 No neurologic toxicity was observed.

299 eatment for B-cell lymphoma, but often cause neurologic toxicity.

300 even at low doses devoid of hematological or neurologic toxicity.