ライフサイエンスコーパス: neurologic

1 letal or ambulation (532 residents [74.2%]), neurologic (505 [70.4%]), respiratory (361 [50.3%]), and

2 d to permanent, irreversible damage, such as neurologic (75%) and pituitary (72.9%) injuries.

3 l IL-8, which also predicted higher risks of neurologic abnormalities at 4 mo (OR = 7.67; CI = 4.05,

4 pregnancies had significantly higher risk of neurologic abnormalities at 4 mo [odds ratio (OR) = 4.61

5 advantage and their involvement in offspring neurologic abnormalities at 4 mo and 1 y of age.

6 adverse outcomes (microcephaly, major fetal neurologic abnormalities, and intrauterine fetal death).

7 To understand the neurologic abnormality, we investigated behavioral, bioc

8 The Neurologic Academic Research Consortium is an internatio

9 o additional mortality risk for persons with neurologic (aHR, 0.7 [95% CI, 0.4-1.3]) or mental/behavi

10 vivo studies using NADA have focused on its neurologic and behavioral roles.

11 All neurologic and extraneurologic data and treatments were

12 12 (cobalamin) deficiency may produce severe neurologic and hematologic manifestations.

13 merged as a therapeutic strategy for several neurologic and inflammatory disorders.

14 se the possibility that persistent or occult neurologic and lymphoid disease may occur following clea

15 cated in the pathogenesis of a wide range of neurologic and neuropsychiatric diseases.

16 aling defects could contribute to a range of neurologic and neuropsychiatric disorders.

17 Adult neurologic and neurosurgical 1,118 patients in the pre p

18 gnancy in patients with clinically suspected neurologic and nonneurologic paraneoplastic syndromes.

19 a lysosomal storage disease characterized by neurologic and ophthalmologic abnormalities.

20 in development, homeostasis and a variety of neurologic and psychiatric diseases.

21 arget for the treatment of several important neurologic and psychiatric disorders, such as Alzheimer

22 rain and potentially generate biomarkers for neurologic and psychiatric disorders.

23 ial utility in normal physiology, as well as neurologic and psychiatric pathologies in which abnormal

24 ions; chronic comorbid conditions, including neurologic and respiratory disorders; and device use, in

25 ing the levels of slincR resulted in altered neurologic and/or locomotor behavioral responses.

26 vely followed over 3 years with psychiatric, neurologic, and neuropsychological assessments of safety

27 s carry devastating potential for cognitive, neurologic, and socio-emotional disease, but no objectiv

28 a statin or ACEI/ARB within 30 days of first neurologic assessment (baseline), with assessments by NP

29 Neurologic assessment and conventional, diffusion-tensor

30 ologic function for clinical assessment, the Neurologic Assessment in Neuro-Oncology scale was drafte

31 and thus may allow more rapid extubation and neurologic assessment.

32 ndividual infectious diseases and individual neurologic, autoimmune, and behavioral conditions.

33 utoantibody profiles to aid the diagnosis of neurologic autoimmunity (and predict cancer likelihood).

34 To assess in-hospital neurologic (CNS) complications in adult patients undergo

35 for 6 years, with biannual visits including neurologic, cognitive, and gait assessments.

36 concern, particularly given the high risk of neurologic complications (including Guillain-Barre syndr

37 Results No intraoperative neurologic complications (n = 10 [95% confidence interva

38 C deficiency can produce the hematologic and neurologic complications after birth, whereas TCblR/CD32

39 n underscore possible concern for additional neurologic complications and nonarthropod-mediated trans

40 The detection of neurologic complications secondary to ZIKV infection.

41 Four hundred twenty-six neurologic complications were reported in 356 patients (

42 tion of extracorporeal membrane oxygenation, neurologic complications, and presence of more than thre

43 nt association between Zika virus (ZIKV) and neurologic complications, including Guillain-Barre syndr

44 Is) are associated with rare but devastating neurologic complications.

45 ploration of cathodal tDCS as a treatment of neurologic conditions characterized by aberrant regional

46 vide insight to the numerous psychiatric and neurologic conditions that have been associated with abe

47 utologous HSCT for this and other autoimmune neurologic conditions warrants prospective study.

48 s of abnormal respiratory mechanics in acute neurologic conditions, bedside judgment, interpretation

49 rders of consciousness, and 14 treated other neurologic conditions, including stroke, traumatic brain

50 organ support after declaration of death by neurologic criteria (outside of organ donation; range, 1

51 organ support after declaration of death by neurologic criteria and 2) explore potential interventio

52 organ support after declaration of death by neurologic criteria easier to handle.

53 gement and personal experience with death by neurologic criteria was distributed electronically to pe

54 continuation of organ support after death by neurologic criteria.

55 e be continued after declaration of death by neurologic criteria.

56 Forty-seven neurologic critical care units in 18 countries.

57 were acute renal failure 41%, bleeding 25%, neurologic damage in survivors 21%, sepsis/infections 21

58 uximab presented with progressive multifocal neurologic decline.

59 erebral demyelination and rapid, devastating neurologic decline.

60 a congenital nephrotic syndrome with eye and neurologic defects caused by mutations in laminin beta2

61 ies (ICF) syndrome, which is associated with neurologic deficiencies.

62 at XXMT treatment significantly improved the neurologic deficit and quality of life of acute ischemic

63 s drive the EAE pathogenesis to irreversible neurologic deficit.

64 WT) and DP1(-/-) mice were subjected ICH and neurologic deficits and hemorrhagic lesion outcomes were

65 The neurologic deficits do not necessarily correlate with bl

66 f MeCP2 expression in a mouse model reverses neurologic deficits in adult animals, reactivation of th

67 sient worsening of residual poststroke focal neurologic deficits or transient recurrence of prior str

68 Surgery resulted in anticipated neurologic deficits related to the region of brain resec

69 The neurologic deficits that characterize multiple sclerosis

70 iencing fevers, syncope or presyncope, focal neurologic deficits, chest pain, nausea, vomiting, unint

71 effects of Xueshuan Xinmai tablets (XXMT) on neurologic deficits, quality of life and brain functiona

72 ring early lesion formation and the onset of neurologic deficits.

73 owever, many survivors suffer from long-term neurologic deficits.

74 n microhemorrhages, white matter injury, and neurologic deficits.

75 e future opportunities to treat or alleviate neurologic deficits.

76 ascertainment is based on multiple sources (neurologic departments, hospital discharge archives, and

77 ients develop infantile-onset of progressive neurologic deterioration and death by 2 years of age, wh

78 mmonly in young adults and cause progressive neurologic deterioration and premature death.

79 Eleven women with botulism had progressive neurologic deterioration and respiratory failure, requir

80 The patient had progressive neurologic deterioration in the first month of life.

81 s, unfavorable outcomes, hematoma expansion, neurologic deterioration, and severe hypotension were no

82 h early retinal degeneration and progressive neurologic deterioration, but have recently also been id

83 One patient, who had had rapid neurologic deterioration, had died from disease progress

84 ocephaly, and devastating ophthalmologic and neurologic developmental abnormalities.

85 Given the low probability of a serious neurologic diagnosis in the ambulatory setting and highe

86 ckness, and association with the severity of neurologic disability as assessed by the Kurtzke Expande

87 open spina bifida, a common cause of severe neurologic disability in humans.

88 Lesions and neurologic disability in inflammatory CNS diseases such

89 the extent of chronic CNS tissue damage and neurologic disability.

90 h and arthritis, occasionally complicated by neurologic disease and chronic arthritis.

91 namics of brain physiology in the context of neurologic disease and therapeutic interventions, which

92 rare variants identified in individuals with neurologic disease had complex, and sometimes opposing,

93 ry systems, but the public health impact for neurologic disease of moderately low vitamin B-12 status

94 erlying pathology (such as cancer or serious neurologic disease) associated with urinary incontinence

95 ctions are associated with birth defects and neurologic disease, and that the virus can be sexually t

96 risk factors for reintubation included acute neurologic disease, lower aPiMax, postextubation upper a

97 clusions formed by FUS and other proteins in neurologic disease.

98 genome stability pathways that prevent human neurologic disease.

99 ents as early-onset progressive visceral and neurologic disease.

100 n reports, or investigations for undiagnosed neurologic disease.

101 ng on human disorders ranging from cancer to neurologic diseases and immunity.

102 rain atrophy is a common feature of numerous neurologic diseases in which the role of neuroinflammati

103 ce in healthy CNS, its role in BBB repair in neurologic diseases such as MS remains unclear.

104 preclinical and clinical studies of several neurologic diseases with varying degrees of success.

105 nflammation has been associated with various neurologic diseases, including Alzheimer disease (AD).

106 cruitment to the brain is a hallmark of many neurologic diseases.

107 ay provide a novel therapy for TBI and other neurologic diseases.

108 main (NTD) aims for the treatment of various neurologic diseases.

109 ntion of a broad spectrum of different human neurologic diseases.

110 nodeficiency virus, autoimmune diseases, and neurologic diseases.

111 s play a key role in pathophysiology of many neurologic diseases/trauma, but the effect of immune cel

112 2 deficiency causes megaloblastic anemia and neurologic disorder in humans.

113 , such as multiple sclerosis, HIV-associated neurologic disorder, and stroke.

114 ntral Research Register and for diagnoses of neurologic disorders (ICD-8 codes 320-359 and ICD-10 cod

115 ents are increasingly recognized to underlie neurologic disorders and are often accompanied by additi

116 Excitotoxicity occurs in multiple neurologic disorders and NAD(+) was shown to prevent neu

117 as well as Guillain-Barre syndrome and other neurologic disorders in adults.

118 examined the use of zolpidem for noninsomnia neurologic disorders in humans for all dates up to March

119 ancy has been linked to an increased risk of neurologic disorders in offspring, including attention d

120 protein aggregates, which are implicated in neurologic disorders including Alzheimer disease and tra

121 haracteristics with uncommon immune-mediated neurologic disorders reported in treated HIV patients, i

122 nt of therapeutic approaches associated with neurologic disorders such as Parkinson disease-associate

123 Patients with atypical TTS more often had neurologic disorders than those with typical TTS (81 of

124 liosides result in the development of severe neurologic disorders, including gangliosidoses manifesti

125 rved to transiently treat a large variety of neurologic disorders, most often related to movement dis

126 ts a potential treatment mechanism for other neurologic disorders.

127 nthesize studies that used zolpidem to treat neurologic disorders.

128 n of GDH leads to a variety of metabolic and neurologic disorders.

129 netic regulators are responsible for several neurologic disorders.

130 o self-reported ocular disease, diabetes, or neurologic disorders; visual acuity of >/=20/25; refract

131 Overt vitamin B-12 deficiency causes neurologic disturbances in peripheral and central motor

132 itory-vestibular-visual deficits (6%), focal neurologic dysfunction (7.1%), and severe headaches (5.3

133 Bilirubin-induced neurologic dysfunction (BIND) and kernicterus has been u

134 eficits (HR, 2.3; 95% CI, 1.3 to 4.0); focal neurologic dysfunction (HR, 4.9; 95% CI, 3.2 to 7.5); an

135 with neurotropic pathogens, post-infectious neurologic dysfunction has traditionally been attributed

136 has been used to describe moderate to severe neurologic dysfunction observed in children exposed to e

137 manifestations include fever, splenomegaly, neurologic dysfunction, coagulopathy, liver dysfunction,

138 tage of newborns can cause bilirubin-induced neurologic dysfunction, potentially leading to permanent

139 nt myelin or myelin loss, lead to a range of neurologic dysfunctions, and can result in early death.

140 There is growing concern about the long-term neurologic effects of prenatal exposure to maternal over

141 TORCH infections are recognized to have neurologic effects, such as ventriculomegaly, intraventr

142 n of different EVs with a variety of chronic neurologic, endocrine, and cardiac disorders.

143 up, and imaging were negative for cardiac or neurologic etiology.

144 imodal brain imaging, cognitive testing, and neurologic evaluation, and imaging measures were compare

145 d documentation for moderate- and high-level neurologic evaluations.

146 t-dose cohort was stopped because of grade 3 neurologic events in both patients.

147 de 3 or higher cytokine release syndrome and neurologic events occurred in 13% and 28% of the patient

148 Grade 3 neurologic events occurred in 22% of patients (no grade

149 Neurologic events were dose limiting, and 60 mug/m(2)/da

150 rade 1 or 2), and three patients had grade 3 neurologic events, one of which (aphasia) required tempo

151 pression, the cytokine release syndrome, and neurologic events.

152 There were no grade 4 or 5 neurologic events.

153 annual, standardized neuropsychological and neurologic examination findings, using criteria from the

154 C]PiB PET, magnetic resonance imaging (MRI), neurologic examination, and detailed cognitive testing u

155 sis of the clinical features in the history, neurologic examination, and neuroimaging studies led to

156 examination is an essential component of the neurologic examination.

157 5/8; p < 0.03), and all survivors had normal neurologic examinations.

158 Patients with obvious neurologic fields were excluded.

159 edge on the components of fundoscopy and key neurologic findings observed on fundoscopic examination.

160 ensor imaging in patients who are recovering neurologic function after decompression surgery.

161 Disease progression, which leads to loss of neurologic function and death, can be halted only with a

162 nctional disabilities, as well as changes in neurologic function and in the extent of lesions on MRI.

163 iciency results in clinical abnormalities in neurologic function as well as in skeletal and cardiac m

164 an effort to standardize the measurement of neurologic function for clinical assessment, the Neurolo

165 physiologic indexes of peripheral or central neurologic function in asymptomatic older people with mo

166 urologic function or any clinical markers of neurologic function in older people with moderately low

167 mation, prevent neuronal damage and preserve neurologic function in the experimental autoimmune encep

168 -12 status with either peripheral or central neurologic function or any clinical markers of neurologi

169 Good neurologic function was observed in 92%.

170 no reasonable expectation that the patient's neurologic function will improve sufficiently to allow t

171 Performance Status, extent of resection, and neurologic function) as the existing RTOG RPA.

172 nciple goals of pain relief, preservation of neurologic function, and improvement in quality of life.

173 al decline apart from their acute effects on neurologic function.

174 We aimed to prospectively evaluate survival, neurologic, functional, and HRQoL outcomes in patients w

175 Spetzler neurologic functions were assessed post-operatively, and

176 r AMD; other eye conditions; cardiovascular, neurologic, gastrointestinal, and endocrine disease; cog

177 admitted to the same two hospitals for a non-neurologic illness within seven days of the date of admi

178 he characteristic pathologic change of acute neurologic impairment and chronic traumatic encephalopat

179 ulation of the urea cycle are known to cause neurologic impairment.

180 tatus epilepticus often results in permanent neurologic impairment.

181 HFR deficiency results in homocystinuria and neurologic impairment.

182 Neurologic improvement followed treatment with high-dose

183 er been known to cause a chronic systemic or neurologic infection in humans.

184 nd also assess donors carefully for signs of neurologic infection that may have been misdiagnosed as

185 es from mild febrile illness to severe fatal neurologic infection.

186 ted flavivirus that causes potentially fatal neurologic infection.

187 ial extracorporeal membrane oxygenation with neurologic injury of the lower limbs.

188 mmune system in the development of secondary neurologic injury over the days and weeks following a TB

189 Neurologic injury was defined as brain death, seizures,

190 requent type, and survival for patients with neurologic injury was poor.

191 y enrolled pediatric patients, patients with neurologic injury, or healthy volunteers.

192 membrane oxygenation factors associated with neurologic injury.

193 d injury or other forms of traumatic, acute, neurologic injury.

194 rane oxygenation for respiratory failure had neurologic injury.

195 ation were associated with increased odds of neurologic injury.

196 otoxicity, neuroinflammation, and subsequent neurologic injury.

197 astating multisystem disorder with prominent neurologic involvement.

198 d for a 14-day course for treatment of early neurologic Lyme disease in ambulatory patients.

199 14-day course of oral doxycycline for early neurologic Lyme disease in ambulatory patients.

200 dies assessing the incidence and spectrum of neurologic manifestations secondary to Zika virus (ZIKV)

201 with hyponatremic encephalopathy exhibiting neurologic manifestations, a bolus of 100 mL of 3% salin

202 addition to the well-described anatomic and neurologic manifestations, clinicians are now describing

203 Purpose Little is known about neurologic morbidity attributable to cranial radiotherap

204 sed with a meningioma experience significant neurologic morbidity.

205 nistered to women in preterm labor to reduce neurologic morbidity.

206 The available evidence for neurologic, neurodevelopmental, neurobehavioral, auditor

207 essments of a patient's spine disease: NOMS (neurologic, oncologic, mechanical instability, and syste

208 with IV sedation although no differences in neurologic outcome (45% of patients with cerebral perfor

209 - and hypoglycemia were associated with poor neurologic outcome (p = 0.001 and p = 0.054).

210 9; p = 0.03) and a marginal deterioration of neurologic outcome (risk ratio, 0.90; 95% CI, 0.80-1.01;

211 .70-0.96; p = 0.01) and a 35% improvement in neurologic outcome (risk ratio, 1.35; 95% CI, 1.18-1.54;

212 Among survivors, 90% (26/29) had a favorable neurologic outcome after 1-3 minutes versus 89% (8/9) af

213 Primary outcome of this analysis was neurologic outcome after 6 months, referred to as "Cereb

214 cemic variability, were associated with poor neurologic outcome and death.

215 It also improved the neurologic outcome and inhibited neuroinflammation in mi

216 of prognostication when evaluating potential neurologic outcome and terminal cases.

217 demonstrated increasing risk of unfavorable neurologic outcome as more caudal structures were affect

218 The proportion of patients with a favorable neurologic outcome at 3 months was similar in both group

219 The primary end point was poor neurologic outcome at 6 months (cerebral performance cat

220 The primary outcome was a good neurologic outcome at 6 months after ICU admission, defi

221 [12] years), 304 patients (52.5%) had a poor neurologic outcome at 6 months.

222 Favorable neurologic outcome at discharge was comparable between t

223 hours did not significantly improve 6-month neurologic outcome compared with targeted temperature ma

224 Good neurologic outcome could be predicted with sensitivities

225 ood vessels have been associated with better neurologic outcome following acute ischemic stroke (AIS)

226 radycardia and lower mortality and favorable neurologic outcome in a large cohort of comatose out-of-

227 To identify prognostic factors of good neurologic outcome in patients admitted to an ICU with a

228 re exogenous administration of contrast, and neurologic outcome in patients after AIS.

229 -approved perampanel treatment might enhance neurologic outcome in premature infants with IVH.

230 erely the avoidance of fever mediates better neurologic outcome in resuscitated patients.

231 matomal edema is an independent predictor of neurologic outcome is controversial.

232 ciation between ASL collaterals and improved neurologic outcome may help guide prognosis and manageme

233 the infection could potentially improve the neurologic outcome of infants infected in utero with HCM

234 ase III randomized trial to assess impact on neurologic outcome of intracranial pressure plus brain t

235 0.97-3.01; P = 0.06) and survival with good neurologic outcome remained similar (38% vs. 43%; OR, 1.

236 Survival with a favorable neurologic outcome was defined as a cerebral performance

237 Independent factors of good neurologic outcome were early (</=8 d after ICU admissio

238 urately classify injury severity and predict neurologic outcome would represent a paradigm shift in t

239 The primary outcome was 6-month neurologic outcome, with a Cerebral Performance Categori

240 cus during ICU stay were not associated with neurologic outcome.

241 At 6 months, 57% of patients had a good neurologic outcome.

242 Our data argue against a major effect on neurologic outcome.

243 eaths from early WLST and survival with good neurologic outcome.

244 cluded return of spontaneous circulation and neurologic outcome.

245 p and ship), which may have an effect on the neurologic outcome.

246 antly associated with long-term survival and neurologic outcome.

247 tory response is essential for improving the neurologic outcome.

248 blinded clinical trial, compared the 6-month neurologic outcomes and survival of patients with cardia

249 Neurologic outcomes are better when HSCT occurs at an ea

250 rn of spontaneous circulation, survival, and neurologic outcomes at hospital discharge.

251 33 degrees C for 48 hours results in better neurologic outcomes compared with currently recommended,

252 sium sulphate or control treatment and where neurologic outcomes for the baby were reported were elig

253 4-3p level was significantly associated with neurologic outcomes in the univariable analysis (odds ra

254 centrations and glycemic variability and the neurologic outcomes of patients randomized to targeted t

255 s and children by analyzing mortality rates, neurologic outcomes, and adverse effects.

256 ted surgically in infancy to prevent adverse neurologic outcomes.

257 tients who might otherwise survive with good neurologic outcomes.

258 ischarge, and 89% of survivors had favorable neurologic outcomes.

259 of intracranial hemorrhage; 2) survival and neurologic outcomes; and 3) factors associated with intr

260 ysfunction of this process may contribute to neurologic pathologies.

261 0% at peak, a ratio higher than that of many neurologic pharmacotherapies already in clinical use.

262 s of EBF3 function might mediate a subset of neurologic phenotypes shared by ARX-related disorders, i

263 the most common transthyretin mutation, and neurologic phenotypic expression differs between wild-ty

264 ous system and is involved in many essential neurologic processes such as mood, social behavior, and

265 ST) (within 72 h) based on estimates of poor neurologic prognosis and (1b) no WLST between 72 hours a

266 ys in absence of clinical predictors of poor neurologic prognosis or (2) surviving beyond 7 days.

267 Predictions about neurologic prognosis that are based on early clinical fi

268 Rates of appropriate neurologic prognostication increased after the intervent

269 The primary outcome was appropriate neurologic prognostication, defined as (1a) no early wit

270 Although tafamidis has been shown to delay neurologic progression of transthyretin familial amyloid

271 , infertility in males, and development of a neurologic psychiatric disorder, manganism.

272 nd restores OPC maturation, myelination, and neurologic recovery in preterm newborns with IVH.

273 ed inflammation and restores myelination and neurologic recovery in preterm rabbits with IVH.

274 r all relapses and 28% (95% CI, 20%-38%) for neurologic relapses.

275 alic involvement was associated with shorter neurologic RFS (HR, 2.35; 95% CI, 1.44-3.83; P < .001).

276 uscle tone (group x age, P < .001) and total neurologic scores (group x age, P = .01) that normalized

277 aresis, larger infarct sizes, lower Spetzler neurologic scores and increased mortality compared to th

278 s, 20% (30 of 149) reported at least one new neurologic sequela, including seizures (8.3%), auditory-

279 eporting a meningioma had increased risks of neurologic sequelae > 5 years after primary cancer diagn

280 CIs to evaluate the factors associated with neurologic sequelae after subsequent meningioma.

281 rain regions that are usually related to the neurologic sequelae observed after severe hyperbilirubin

282 tudy, a diagnosis of meningioma and onset of neurologic sequelae were ascertained.

283 ied by a high mortality rate or long-lasting neurologic sequelae.

284 she could be discharged home with only minor neurologic sequelae.

285 ons, persistent infection in the testes, and neurologic sequelae.

286 rebral performance category score, 3 [severe neurologic sequelae], 4 [coma], or 5 [death]).

287 Only one pig developed clinical neurologic signs suggestive of prion disease.

288 emergency department arrival, and favorable neurologic status at discharge.

289 tes, and the secondary outcome was favorable neurologic status at hospital discharge.

290 sociated with risk-standardized survival and neurologic status by a test for trend.

291 ched with enterprise data on vital signs and neurologic status to calculate the EWS for each postoper

292 d measures of PBA and depression (Center for Neurologic Study-Lability Scale (CNS-LS) and Patient Hea

293 ar cardiac phenotype but a greater burden of neurologic symptoms (pain, numbness, tingling, and walki

294 100% had gastrointestinal symptoms, 34% had neurologic symptoms, 43% had hemorrhagic manifestations,

295 the gut, and it is also related to renal and neurologic symptoms.

296 o a highly overlapping phenotype without the neurologic symptoms.

297 e incidence of a diverse spectrum of serious neurologic syndromes.

298 espiratory, cardiovascular, coagulation, and neurologic systems by day 7 after surgery.

299 ty-five percent of patients had grade 3 or 4 neurologic toxicities that completely resolved.

300 A growing number of neurologic treatments rely on neural implants capable of