ライフサイエンスコーパス: neurological

1 tartle reflex), severe postnatal progressive neurological abnormalities (including abnormal neonatal

2 nderstudied despite the emerging evidence of neurological abnormalities induced by dystrophin loss.

3 Disruption of mTOR signaling can result in neurological abnormalities.

4 The diagnosis and treatment of neurological ailments always remain an utmost challenge

5 action, which is a common feature of various neurological and age-related pathologies, making this pa

6 The most common reasons for readmission were neurological and cardiac events; readmission reasons var

7 edications are of limited efficacy and cause neurological and cardiovascular side effects because the

8 of human variation that is characterised by neurological and cognitive differences.

9 entially have a positive long-term impact on neurological and functional recovery.

10 Many neurological and musculoskeletal diseases impair movemen

11 g tasks has been observed in a wide range of neurological and neuropsychiatric disorders.

12 an endocannabinoid ligand, mediates several neurological and physiological processes, which are term

13 immunity, cardiovascular health, as well as neurological and psychiatric conditions.

14 r of common genetic variants associated with neurological and psychiatric disease risk.

15 vary with age and cognitive function, and in neurological and psychiatric diseases.

16 in genes associated with monogenic forms of neurological and psychiatric disorders in individuals wi

17 who is 43 years old, continues to be without neurological and psychiatric symptomatology.

18 mild to severe disease, and sometimes fatal neurological and respiratory manifestations.

19 pendent pathologies, including inflammatory, neurological, and immune diseases.

20 this enzymatic activity with cardiovascular, neurological, and oncological disorders.

21 lications as the chief symptom, however, the neurological aspect of the disease is also becoming incr

22 ica spectrum disorders (NMOSD) are a type of neurological autoimmune disease characterized by attacks

23 point mutation, identified in patients with neurological but no endocrine defects, we show that the

24 , we show that NDP expression is enriched in neurological cancers, including GBM, and its levels posi

25 ation (ASIA), or International Standards for Neurological Classification of Spinal Cord Injury (ISNCS

26 A cross-sectional analysis of the Neurological, cOgnitive and VIsual performance in hiv-in

27 Similar to other neurological cohorts, GA and PCI may be important parame

28 Pa(CO(2)) was independently associated with neurological complications after controlling for previou

29 atients suffered more frequently from severe neurological complications in comparison to all control

30 is associated with an increased incidence of neurological complications in patients with respiratory

31 f Zika virus (ZIKV) and its association with neurological complications necessitates studies on the m

32 endemic regions or for the treatment of the neurological complications of Zika virus infection.

33 eak in South America, substantial numbers of neurological complications, such as Guillain-Barre syndr

34 patients and causes frequent thrombotic and neurological complications.

35 t against HIV-1 infection and HIV-associated neurological complications.

36 ly associated with an increased incidence of neurological complications.

37 fluid features of 31 COVID-19 patients with neurological complications.

38 he brain and its duplication leads to severe neurological conditions as well.

39 possibility of studying a broad spectrum of neurological conditions in vivo.

40 ls or that show promise for the treatment of neurological conditions that respond poorly to existing

41 of neuroinflammation to the pathogenesis of neurological conditions, including infection, traumatic

42 accelerate similar progress in a spectrum of neurological conditions, with more than 50 clinical tria

43 enesis and have been associated with various neurological conditions.

44 for FND are distinct from therapy for other neurological conditions.

45 mendous potential to improve function across neurological conditions.

46 otein that has been associated with numerous neurological conditions.

47 is (MS) (n=69), optic neuritis (n=5) and non-neurological controls (n=37).

48 a majority of candidate blood biomarkers for neurological damage that are studied today are proteins

49 sly unexplored candidate blood biomarkers of neurological damage with possible clinical utility, many

50 ing experimental stroke resulting in reduced neurological damage.

51 vivirus, is linked to microcephaly and other neurological defects in neonates and Guillain-Barre synd

52 Affected subjects exhibit signs of severe neurological defects.

53 ation in cerebral ischemia, and in improving neurological deficit after stroke.

54 led infarct volumes (p < 0.001) and worsened neurological deficits (median score = 9 vs 5 with vehicl

55 farct risk and volumes, collateral flow, and neurological deficits after pretreatment with olcegepant

56 Axon regeneration failure causes neurological deficits and long-term disability after spi

57 Animals developed contralateral neurological deficits but were ambulatory.

58 al morbidities are associated with long term neurological deficits in life and have also been associa

59 gh the mechanism(s) involved with persistent neurological deficits is not fully known, mitochondrial

60 And 138 cases (82.1%) had developed neurological deficits preoperatively with the average tu

61 enetrated perihematoma brain tissue, reduced neurological deficits, and improved hematoma clearance,

62 ion imbalance, as well as a range of chronic neurological deficits.

63 y and secondary brain injuries and permanent neurological deficits.

64 region may provide a mechanism for transient neurological deficits.

65 ry macrophages may lead to tissue damage and neurological deficits.

66 diagnoses of ADRD, cognitive impairment, or neurological degeneration, who developed appendicitis be

67 cal and pathological processes, ranging from neurological development to disease progression.

68 2 in 21 patients affected by disturbances in neurological development.

69 We recruited 20 patients with common neurological diagnoses and 10 controls (i.e. patients wi

70 ted as "functional connections" for maps and neurological diagnostics.

71 ction is a leading cause of hearing loss and neurological disabilities in children, with the disease

72 infant birth defects, resulting in permanent neurological disability for one newborn child every hour

73 , brain MRI, and associations with death and neurological disability in prospective cohorts of Malawi

74 Secondary outcomes were measures of neurological disability, functional independence in acti

75 , dizziness and falls, is a leading cause of neurological disability.

76 (WMMS) that separates severe from attenuated neurological disease (p = 1.2 e-5).

77 ertiary-level hospital, with suspected acute neurological disease and a history of suspected arbovira

78 Recognition of neurological disease associated with SARS-CoV-2 in patie

79 Temporal lobe epilepsy is a complex neurological disease caused by imbalance of excitation a

80 ) infection can cause severe respiratory and neurological disease in humans.

81 le sclerosis (MS), the most common disabling neurological disease in young adults.

82 Sex is a key modifier of neurological disease outcomes.

83 of how abnormalities in this process lead to neurological disease remains very superficial.

84 significant obstacle for the development of neurological disease therapies.

85 rocesses may occur in human cells, and cause neurological disease when impaired.

86 Multiple sclerosis (MS) is a neurological disease with a substantial genetic componen

87 0 controls (i.e. patients without structural neurological disease).

88 etabolic dysfunction are often implicated in neurological disease, but effective mechanism-based ther

89 abies virus (RABV) causes a severe and fatal neurological disease, but morbidity is vaccine preventab

90 nscriptomic differences in the expression of neurological disease-risk genes in microglia.

91 ndrome (CANVAS) is a progressive late-onset, neurological disease.

92 pportunistic infection that can cause severe neurological disease.

93 ebrile illness, which can progress to severe neurological disease.

94 tandem repeat expansions are known to cause neurological disease.

95 l function and its disruption contributes to neurological disease.

96 increases in immune-mediated and infectious neurological disease.

97 hrough which altered mTOR signaling leads to neurological disease.

98 Microglia are implicated in neurological diseases and modulated by microRNAs, but it

99 Many neurodegenerative and neurological diseases are rooted in dysfunction of the n

100 Chronic neurological diseases are the leading cause of disabilit

101 translational CRISPR-based approach to treat neurological diseases characterized by abnormal circuit

102 Genome-wide association studies of neurological diseases have identified thousands of varia

103 ent, and behavior, as well as modeling human neurological diseases like neuropathic pain.

104 Neurological diseases owing to the existence of the BBB

105 Many neurological diseases present with substantial genetic a

106 ells as well as early diagnosis of different neurological diseases related to abnormal levels of dopa

107 ide repeats that are responsible for causing neurological diseases such as myotonic dystrophy type 1,

108 into astrocytes are of interest for specific neurological diseases, creating a need for approaches th

109 implicated in the pathogenesis of almost all neurological diseases, including Alzheimer's disease (AD

110 , and high mortality rates for patients with neurological diseases, including brain cancers and neuro

111 rant network excitability in psychiatric and neurological diseases, such as epilepsy.

112 ibute to increased susceptibility to several neurological diseases, such as multiple sclerosis and Pa

113 This is relevant in aging and age-related neurological diseases, where neuroinflammation contribut

114 tablishes mutations in CLCN6 associated with neurological diseases, whose spectrum of clinical featur

115 scular disease, cancer, diabetes and chronic neurological diseases.

116 eir therapeutic efficacy in animal models of neurological diseases.

117 stem-cell-derived cells for the treatment of neurological diseases.

118 pansions within genes is associated with >30 neurological diseases.

119 compound associated with cardiovascular and neurological diseases.

120 isease mechanisms and therapeutic targets in neurological diseases.

121 (hMGL) offers a novel approach for treating neurological diseases.

122 osphorylation has been implicated in several neurological diseases.

123 to study normal human brain development and neurological diseases.

124 ron-glial interaction and its alterations in neurological diseases.

125 ng by pharmacological means for treatment of neurological diseases.

126 ausal variants of sQTLs and their associated neurological diseases.

127 People with functional neurological disorder (FND) are commonly seen by occupat

128 present a predisposing factor for functional neurological disorder (FND) but previous research has yi

129 l temporal lobe epilepsy (MTLE) is a chronic neurological disorder affecting almost 40% of adult pati

130 Huntington's disease (HD) is a neurological disorder characterized by motor disturbance

131 Dystonia is a neurological disorder characterized by sustained or inte

132 .SIGNIFICANCE STATEMENT Epilepsy is a common neurological disorder defined by recurrent, unprovoked s

133 Functional neurological disorder is a common and phenomenologically

134 Isolated dystonia is a neurological disorder of heterogeneous pathophysiology,

135 Diagnosis of neurological disorder or cognitive impairment were exclu

136 aumatic brain injury (TBI) is a debilitating neurological disorder that can seriously impact the pati

137 , and 14.7% (n = 5141) were diagnosed with a neurological disorder, equivalent to a suicide rate of 4

138 ualized as a cognitive variant of functional neurological disorder, termed functional cognitive disor

139 l in understanding the long-term progressive neurological disorder.

140 years among individuals not diagnosed with a neurological disorder.

141 embolism), one of whom died; (iv) peripheral neurological disorders (n = 8), seven with Guillain-Barr

142 ychotic drug chlorpromazine for treatment of neurological disorders and cancer.

143 ibute to the pathogenesis of some autoimmune neurological disorders and could even contribute to neur

144 n(11-14) and mutations in NALCN cause severe neurological disorders and early death(15,16).

145 c morphology is a common theme among several neurological disorders and is thought to precede neurode

146 Visuomotor impairments characterize numerous neurological disorders and neurogenetic syndromes, such

147 National Institute of Neurological Disorders and Stroke for the randomisation

148 National Institute of Neurological Disorders and Stroke, National Institutes o

149 vances in prevention and management of major neurological disorders are not sufficiently effective to

150 arget for treatment of Mn toxicity and other neurological disorders associated with dysregulation of

151 Prion diseases are rare, neurological disorders caused by the misfolding of the c

152 Epilepsies are a group of neurological disorders characterised by recurrent epilep

153 Neurological disorders have been linked to suicide, but

154 ew possibilities for probing psychiatric and neurological disorders impacted by insular cortex dysfun

155 oirs, thereby reducing neuroinflammation and neurological disorders in HIV-infected individuals.

156 , which contributes to neuroinflammation and neurological disorders in HIV-infected patients.

157 cine-305 was previously linked to paroxysmal neurological disorders in humans.

158 ption factor implicated as a drug target for neurological disorders including Alzheimer's and Parkins

159 BBB dysfunction, however, is evident in many neurological disorders including ischemic stroke, trauma

160 nd efficacy towards the treatment of various neurological disorders like AD, PD, schizophrenia, epile

161 ance to grand challenges in the treatment of neurological disorders motivate continued growth of this

162 ide, but the risk across a broad spectrum of neurological disorders remains to be assessed.

163 initially discussed the global statistics of neurological disorders reported by WHO and other reputed

164 Patients with sialidosis present various neurological disorders such as: myoclonic epilepsy and h

165 ain models that reconstruct aspects of major neurological disorders under static or dynamic condition

166 Neurological disorders with IgG antibodies against myeli

167 the study of the physiology and aetiology of neurological disorders, and to the development of person

168 In humans, mutant aaRS cause a diversity of neurological disorders, but their molecular aetiologies

169 y offer a therapeutic strategy in cancer and neurological disorders, in which pericyte dysfunction co

170 iagnosed with a variety of acute and chronic neurological disorders, including ischemic stroke, hemor

171 ings have implications for the management of neurological disorders, such as autism and intellectual

172 uronal development is frequently impaired in neurological disorders, such as autism and schizophrenia

173 lled BAF complexes) in both human cancer and neurological disorders, suggesting new mechanisms and ac

174 Aberrant metabolism is a key factor in many neurological disorders.

175 cardiovascular, metabolic, inflammatory and neurological disorders.

176 l and applied to animal models of a range of neurological disorders.

177 ous system development and are implicated in neurological disorders.

178 and diseases processes, including cancer and neurological disorders.

179 ompositions and contributes to metabolic and neurological disorders.

180 in particular, are increasingly the focus of neurological disorders.

181 have been associated with many metabolic and neurological disorders.

182 eat expansion is the molecular basis for ~40 neurological disorders.

183 communities have been implicated in several neurological disorders.

184 cts of early dopamine-replacement therapy in neurological disorders.

185 s immune dysregulation in the development of neurological disorders.

186 affective behaviors that could contribute to neurological disorders.

187 rature implicating these proteins in various neurological disorders.

188 ted DBS leads was validated in patients with neurological disorders.

189 pathways may provide therapeutic targets for neurological disorders.

190 ) tract, and it is associated with different neurological disorders.

191 of the E/I ratio is associated with numerous neurological disorders.

192 research to tackle the growing challenge of neurological disorders.

193 ssue concentration is elevated in cancer and neurological disorders.

194 ist of drugs from other therapeutic classes (neurological drugs, anticancer agents, and many others),

195 ne phosphoribosyltransferase [HGprt]-related neurological dysfunction and HGprt-related hyperuricemia

196 (PLP), result in failure of myelination and neurological dysfunction in the X-chromosome-linked leuk

197 pread transcriptional alterations and severe neurological dysfunction than MeCP2 loss.

198 neurological problems (LND and HGprt-related neurological dysfunction).

199 L (LAS1-like) gene have been associated with neurological dysfunction.

200 not been possible to determine any potential neurological dysfunction.

201 In particular, potential neurological effects are one of the most poorly understo

202 entional and electronic cigarettes, produces neurological effects that drive addiction and may damage

203 opic disorder with a unique constellation of neurological, endocrine, exocrine, and haematological fi

204 , acute respiratory distress syndrome (25%), neurological events (25%), arrhythmias (22%), and venous

205 count <300 cells/mm3 underwent standardized neurological examination and functional status assessmen

206 ic assessment, clinical scales, physical and neurological examination, bedside cognitive tests, neuro

207 riable degree of intellectual disability and neurological features as the core symptoms.

208 of morphological, growth, developmental, and neurological findings and medical concerns expands the s

209 ies that reverse CNS damage and restore lost neurological function across a spectrum of diseases.

210 ered to oligodendrocytes in vivo to modulate neurological function and lifespan, establishing a new p

211 stinal bacteria to the brain that can affect neurological function and/or neurodevelopmental and neur

212 anges in the photoreceptor to the underlying neurological function of transducing light into electric

213 Neurological function was normal after next-day recovery

214 Relative risk of mortality or poor neurological function was significantly reduced in UMN-E

215 Myelin plasticity is critical for neurological function, including learning and memory.

216 ulation results in long-term improvements in neurological function, suppression of neuroinflammatory

217 embryogenesis, stem cell fate, fertility and neurological functions in Drosophila.

218 ize <=20 mum), affecting fish behavioral and neurological functions, intestinal permeability, metabol

219 TM variants are associated with the familiar neurological HIDEA syndrome, but how these variants migh

220 ic differences were observed in the signs of neurological illness, time to disease onset, morphology

221 accurate diagnosis and timely management of neurological immune-related adverse events (irAE-N).

222 pose of the present study is to characterize neurological impairment following TBI in rats with an un

223 h KCNA2 mutations, the proband exhibits mild neurological impairment, more characteristic of patients

224 port a model by which Tip60 protects against neurological impairments in different NDs via similar mo

225 change from baseline at 90 days; substantial neurological improvement at 3 days; symptomatic intracra

226 isorder that is characterized by progressive neurological injury culminating in death, typically by 3

227 ion is a common consequence of many forms of neurological injury, including stroke and nerve damage.

228 increase recovery of sensory function after neurological injury.

229 bility limitations undertaking aged care and neurological inpatient rehabilitation.

230 Non-cancerous acute neurological insults also induced significant thymic inv

231 Mid stage, congenital defects and neurological lesions in foetuses like haemorrhages, diff

232 ght into molecular mechanisms underlying the neurological manifestation of diseases associated with i

233 e purine pathway, is characterized by severe neurological manifestations and uric acid overproduction

234 al presentation is with respiratory disease, neurological manifestations are being recognised increas

235 reports and series describe a wide array of neurological manifestations in 901 patients, but many ha

236 The spectrum of neurological manifestations linked to these viruses, and

237 These disorders have other neurological manifestations of central/peripheral hypere

238 Recent studies in brain science and neurological medicine paid a particular attention to dev

239 g of multiple disease-modifying medicines in neurological medicine.

240 ryptophan metabolism are reported in several neurological, metabolic, psychiatric, and intestinal dis

241 Neurological morbidities were assessed with longitudinal

242 bone metastasis is the most common source of neurological morbidity in cancer patients.

243 d the number of individuals with age-related neurological movement disorders including Parkinson's Di

244 e safety endpoint included the major adverse neurological or cardiovascular system or procedure-relat

245 es only, we considered genes associated with neurological or psychiatric disorders as candidate genes

246 but not intraosseously, and favored improved neurological outcome at discharge.

247 The neurological outcome is extremely variable depending on

248 of the response to therapy and to subsequent neurological outcome.

249 orates the metastatic phenotype and improves neurological outcome.

250 Neurological outcomes were assessed by American Spinal I

251 nd their products can be deployed to improve neurological outcomes.

252 n ZDHHC genes, have been linked to different neurological pathologies and cancers, and there is growi

253 ny brain functions and implicated in several neurological pathologies.

254 potential to improve how we detect and treat neurological pathologies.

255 hologs responsible for some newly discovered neurological pathologies.

256 ignificant disease, with widespread cases of neurological pathology and congenital neurologic defects

257 Finally, we show that different neurological pathways are linked to each of these neurot

258 thy subjects (age range: 26-79 years) and 16 neurological patients who reported subjective memory imp

259 many people infected, the overall number of neurological patients, and their associated health burde

260 ile generally considered for its devastating neurological phenotype, disturbances in other organ syst

261 dominant disorder characterized by a complex neurological phenotype, with high prevalence of intellec

262 ate the effects of genetic variants on seven neurological phenotypes (Alzheimer disease, amyotrophic

263 d in western Kenya, resulting in the risk of neurological phenotypes in older children.

264 have emerged as responsible for a variety of neurological phenotypes.

265 We aimed to investigate whether neurological presentations differed according to the inf

266 is significantly increased in patients with neurological problems (LND and HGprt-related neurologica

267 ole in the development of many cognitive and neurological processes; however, epidemiological evidenc

268 however, the burden now lies with estimating neurological prognoses in a large number of patients who

269 also occur primarily in males, with notable neurological, psychiatric, medical, and lifespan associa

270 Angiogenesis promotes neurological recovery after stroke and is associated wit

271 ble CIS cases for steroid treatment to speed neurological recovery.

272 bility limitations admitted to aged care and neurological rehabilitation.

273 n be helpful in minimizing the perioperative neurological risk for individual patients.

274 concentration ratio (B(T) /A) as an index of neurological risk.

275 onatal circulation and protects against nHSV neurological sequela and mortality (C.

276 ting potential mechanisms of risk for common neurological sequelae (e.g., dementia).

277 e cases, might lead to craniosynostosis with neurological sequelae and facial hypoplasia.

278 Many people who survive PML are left with neurological sequelae and some with persistent, low-leve

279 rebrovascular function and contribute to the neurological sequelae associated with brain metastasis.

280 er, these patients might be left with severe neurological sequelae.

281 ty and risk of cancer and likely measures of neurological sequelae: neuropsychiatric morbidities, edu

282 ven that machine learning methods applied to neurological signals are being used in emerging diagnost

283 A total of 39 CHIKV-deaths presented with neurological signs and symptoms, and CHIKV-RNA was found

284 h the characteristics of ET, with additional neurological signs of uncertain clinical significance.

285 opmental disorder associated with a range of neurological, somatic, and behavioral symptoms.

286 time (P = 0.032) and improved the follow-up neurological status (P = 0.026).

287 val, and basic assessments of functional and neurological status.

288 eduction, without impacting on the patient's neurological status.

289 ith coexisting non-movement disorder-related neurological symptoms (100 [45%] of 222; excepting cases

290 identify carriers at risk before significant neurological symptoms are evident.

291 costeroids induced the complete remission of neurological symptoms in 4 of 5 patients.

292 This is readily evident in the neurological symptoms that accompany systemic acid/base

293 nt two patients with COVID-19 and concurrent neurological symptoms.

294 Patients with the neurological syndrome known as body integrity dysphoria

295 mal models are needed to demonstrate whether neurological syndromes are directly caused by specific d

296 which associate ocular features with severe neurological syndromes.

297 leads to severe skeletal, cardiovascular and neurological systems malformations as well as other medi

298 tween the evolution of the immunological and neurological systems.

299 re observed between sedentary behaviours and neurological traits, including education and body mass i

300 no adverse events and neither cognitive nor neurological worsening.