ライフサイエンスコーパス: paralysis

1 rve finding that was unilateral or ascending paralysis).

2 l prostheses being developed for people with paralysis.

3 d during mechanical ventilation after muscle paralysis.

4 ucilia cuprina) induced rapid but reversible paralysis.

5 people worldwide living with the effects of paralysis.

6 show delayed onset and a shorter duration of paralysis.

7 thus restored grasping abilities after hand paralysis.

8 l-established cause of myotonia and periodic paralysis.

9 ce showed decreased neural invasion and less paralysis.

10 H2O airway pressure under heavy sedation or paralysis.

11 this recruitment translates into more severe paralysis.

12 cause susceptibility to myotonia or periodic paralysis.

13 sure resulted in temporary functional T-cell paralysis.

14 mulus relation, without evidence of periodic paralysis.

15 , Caenorhabditis elegans exhibits reversible paralysis.

16 lted in CNS alphaS pathology associated with paralysis.

17 ons in the spinal cord and subsequent muscle paralysis.

18 ys receiving 10(8) or 10(9) TCID50 developed paralysis.

19 ession, even when started after the onset of paralysis.

20 igated during surveillance for acute flaccid paralysis.

21 etylcholine binding to its receptor, causing paralysis.

22 cal symptoms including tremors and hind-limb paralysis.

23 ly, we noted no events of vaccine-associated paralysis.

24 perexpression promotes immune exhaustion and paralysis.

25 otor neuron degeneration, muscle wasting and paralysis.

26 of motor function and the onset of hindlimb paralysis.

27 (SCI) can cause neurological dysfunction and paralysis.

28 mouse models of ALS, leading to progressive paralysis.

29 ntral nervous system (CNS) to elicit spastic paralysis.

30 zed mice were protected against WPV1-induced paralysis.

31 g acute unilateral lower motor neuron facial paralysis.

32 f this disease is motoneuron dysfunction and paralysis.

33 e extracellular level and cannot reverse the paralysis.

34 loss of voluntary motor function and muscle paralysis.

35 rve, the spinal cord, and the brain, causing paralysis.

36 sorder with loss of motor neurons and muscle paralysis.

37 and protected mice from TeNT-induced spastic paralysis.

38 and that are associated with fatal hind limb paralysis.

39 f inflammation and may be involved in immune paralysis.

40 and spinal cord that leads to blindness and paralysis.

41 proteins showed signs of neurotoxin-induced paralysis.

42 ue level and ultimately in hind limb/segment paralysis.

43 years of age with sudden onset of fever and paralysis.

44 s a pathomechanism for hypokalaemic periodic paralysis.

45 luding non-dystrophic myotonias and periodic paralysis.

46 strated partial protection from the onset of paralysis.

47 nervous system was impaired, thus preventing paralysis.

48 generalized weakness was described more than paralysis.

49 on only one side, the one not afflicted with paralysis.

50 rly 2014 in the absence of any acute flaccid paralysis.

51 as hyperphagia, increased weight, and leaden paralysis.

52 f magnitude through minimization of detector paralysis.

53 ns leading to spasticity, muscle atrophy and paralysis.

54 s that can potentially assist in the case of paralysis.

55 an ex vivo assay for BoNT/A-mediated muscle paralysis.

56 ve emotions trigger these episodes of muscle paralysis.

57 as a consequence, instigates ZIKV-associated paralysis.

58 channels (NaV) of nerve and muscle, causing paralysis.

59 st-developmental expression caused age-onset paralysis.

60 infected, and many of the monkeys developed paralysis.

61 motor function and accelerated the onset of paralysis.

62 onnections, resulting in movement defects or paralysis.

63 ed by three clinical trial participants with paralysis.

64 and an almost complete elimination of muscle paralysis.

65 r restoration of reaching and grasping after paralysis.

66 S fibril muscle injected mice that developed paralysis.

67 ust alphaS pathology and in some cases cause paralysis.

68 o restore function to people with upper-limb paralysis.

69 edies of millions of children with permanent paralysis.

70 everity, resulting in recovery from hindlimb paralysis.

71 inently featuring motor neuron (MN) loss and paralysis.

72 tore complex movements in people living with paralysis.

73 f full-length tau isoforms did not result in paralysis.

74 uncertain relation to hypokalaemic periodic paralysis.

75 PP was defined as any AFP case with residual paralysis 60 days following onset that did not have a cl

76 Most had no fever (99%), descending paralysis (93%), no mental status change (91%), at least

77 er rate of reporting non-polio acute flaccid paralysis (AFP) (OR = 1.13, 95% CI 1.02-1.26 for a 1-uni

78 Surveillance for acute flaccid paralysis (AFP) is a fundamental cornerstone of the glob

79 old identified with non-polio acute flaccid paralysis (AFP) reported through polio surveillance, inf

80 We used acute flaccid paralysis (AFP) surveillance data from Nigeria collected

81 ES complements clinical acute flaccid paralysis (AFP) surveillance for possible polio cases.

82 Gaps in acute flaccid paralysis (AFP) surveillance have been consistently docu

83 oviruses (NPEVs) isolated from acute flaccid paralysis (AFP) surveillance in Shandong Province, China

84 es collected information about acute flaccid paralysis (AFP) surveillance resources, training, data m

85 es were identified using LAC's acute flaccid paralysis (AFP) surveillance system.

86 uring July 2009 to support the acute flaccid paralysis (AFP) surveillance system.

87 ews the epidemiology of polio, acute flaccid paralysis (AFP) surveillance, and the implementation of

88 ess indicators associated with acute flaccid paralysis (AFP) surveillance, routine immunization, and

89 n activity that can complement acute flaccid paralysis (AFP) surveillance.

90 A case of acute flaccid paralysis (AFP) was defined as a child <15 years of age

91 only 57% and surveillance for acute flaccid paralysis (AFP) was suboptimal (AFP rate<1 per 100,000 p

92 es obtained from patients with acute flaccid paralysis (AFP) were compared by nucleotide sequencing o

93 ase was defined as any case of acute flaccid paralysis (AFP) with virological confirmation of WPV1.

94 , directly addressing the burden and cost of paralysis after stroke.

95 Loss of LSD1 leads to paralysis, along with widespread hippocampus and cortex

96 stained muscle contractions that can lead to paralysis and abnormal posture.

97 ared with mechanical ventilation with muscle paralysis and absence of diaphragmatic activity.

98 ckout mice suffer from progressive hind limb paralysis and ataxia and die around 6 weeks after birth.

99 regated alphaS in M83(+/-) mice also induced paralysis and CNS alphaS pathology, although less effici

100 om patients with MS and reversed established paralysis and CNS inflammation in four different EAE mod

101 din-3-yl)phenol (PHTPP) reversed established paralysis and CNS inflammation, characterized by a drama

102 ess a cluster of children with acute flaccid paralysis and cranial nerve dysfunction geographically a

103 temporally defined cluster of acute flaccid paralysis and cranial nerve dysfunction in children asso

104 rized by motor neuron loss and that leads to paralysis and death 2-5 years after disease onset.

105 omyelitis mouse model with complete hindlimb paralysis and death by 30 d after induction of QKI delet

106 uired for neurotransmission, causing flaccid paralysis and death by asphyxiation.

107 brain inflammation, and protected mice from paralysis and death during treatment.

108 erative motor neuron disease, causing muscle paralysis and death from respiratory failure.

109 It reduced paralysis and death in an acute pulmonary thrombosis mod

110 ic killing assay, whereas worms succumbed to paralysis and death in its absence.

111 hibitor of ferroptosis, delayed the onset of paralysis and death induced by Gpx4 ablation.

112 progressive loss of motor neurons leading to paralysis and death typically within 3-5 years of onset.

113 tor neuron dysfunction disease that leads to paralysis and death.

114 beginning at 16 days, followed by hind-limb paralysis and death.

115 m the time of infection delayed the onset of paralysis and death.

116 mitant progressive muscle weakness ending in paralysis and death.

117 ALS begins focally but disseminates to cause paralysis and death.

118 e resulted in rapid onset and progression of paralysis and death.

119 rons in the brain and spinal cord leading to paralysis and death.

120 urred, virus was cleared, and mice developed paralysis and died.

121 tigators that highlighted persistent flaccid paralysis and electrophysiological evidence of axonal lo

122 used by the loss of motor neurons leading to paralysis and eventually death.

123 and loss cause progressive muscle weakness, paralysis and eventually premature death of afflicted in

124 genous GM3 significantly slowed the onset of paralysis and increased survival.

125 autoimmune encephalomyelitis (EAE), reducing paralysis and inflammation, while inducing several pathw

126 It can result in paralysis and may be fatal.

127 ) to that found in the patient with periodic paralysis and myotonia.

128 nce that loss of LSD1 in adult mice leads to paralysis and neurodegeneration in the hippocampus and c

129 cks in mouse models of hypokalaemic periodic paralysis and now needs to be tested in patients.

130 th soluble, nonaggregated alphaS resulted in paralysis and pathology in only a subset of mice, wherea

131 severity ranging from progressive infantile paralysis and premature death (type I) to limited motor

132 e expression of TDP-43 in motoneurons led to paralysis and premature lethality.

133 lar Ca(2+) ([Ca(2+)]i) rescued age-dependent paralysis and prevented the neurodegeneration of GABAerg

134 tched to WPV1 cases by age, date of onset of paralysis and region; and asymptomatic "neighborhood con

135 Using acute flaccid paralysis and routine, monthly countrywide environmental

136 id movements, dysarthria, dysphagia, spastic paralysis, and behavioral dementia in descendants of a 6

137 Neuroinvasion, paralysis, and death occurred for all mice infected with

138 s, resulting in progressive muscle weakness, paralysis, and death within 5 years of diagnosis.

139 osis (ALS) causes motor neuron degeneration, paralysis, and death.

140 progressively, resulting in muscle wasting, paralysis, and death.

141 and spinal ventral horn, motor dysfunction, paralysis, and death.

142 degeneration, progressive motor dysfunction, paralysis, and death.

143 e associated with myositis, atrophy, paresis/paralysis, and death.

144 is, dilated cardiomyopathy, type I diabetes, paralysis, and even death.

145 it problems, muscle denervation and atrophy, paralysis, and have diminished life expectancy.

146 roencephalogram and complete skeletal muscle paralysis, and is associated with vivid dreams.

147 eparanase 2 caused embryonic skeletal muscle paralysis, and morphant motor neurons had aberrant morph

148 <10 or >29, flail chest, hemo/pneumothorax, paralysis, and multisystem trauma.

149 accine (OPV), surveillance for acute flaccid paralysis, and OPV "mop-up" campaigns.

150 and found that these larvae exhibit episodic paralysis, and their astrocytes poorly infiltrate the CN

151 s transient ischemic attacks, migraine, Todd paralysis, and Uhthoff phenomenon.

152 ucing symptoms such as loss of coordination, paralysis, and violent spasms.

153 motor disorder (FMD) including weakness and paralysis are commonly referred to physiotherapists.

154 sponse, arguing against a generalized T cell paralysis as a major cause of protracted immune suppress

155 e used to assess early disease onset, before paralysis, as well as disease progression in diverse mou

156 set and protects from the development of the paralysis associated with a murine model of multiple scl

157 res of the increasing cases of acute flaccid paralysis associated with anterior myelitis noted in the

158 Ps, and drugs for the treatment of diaphragm paralysis associated with high cervical spinal cord inju

159 e results in progressive ataxia and hindlimb paralysis associated with motor neuron degeneration, sev

160 A subset of Cu-V103Z mice developed paralysis between 500 and 730 days.

161 le for persons suffering from complete motor paralysis but intact cognitive and emotional processing,

162 can prevent attacks of hypokalaemic periodic paralysis, but this has not yet been tested in patient t

163 LeTx is one of the toxins causing immune paralysis by cleaving and inactivating the mitogen-activ

164 ne interfaces (BMIs) aim to help people with paralysis by decoding movement-related neural signals in

165 rove the quality of life of individuals with paralysis by directly mapping neural activity to limb- a

166 ighly potent neurotoxin that elicits flaccid paralysis by enzymatic cleavage of the exocytic machiner

167 extensive nerve cell dysfunction and severe paralysis by the age of 3 weeks.

168 iovirus isolates from Nigerian acute flaccid paralysis cases obtained from routine surveillance.

169 th received several reports of acute flaccid paralysis cases of unknown etiology.

170 the N-DRC, drc3 does not suppress flagellar paralysis caused by loss of radial spokes.

171 Cases of paralysis caused by poliovirus have decreased by >99% si

172 h genetically confirmed hypokalemic periodic paralysis (Cav1.1-R1239H mutation, n = 5; Cav1.1-R528H m

173 ream mentation combined with skeletal muscle paralysis characterizes rapid eye movement sleep.

174 glycoprotein-induced EAE resulted in reduced paralysis, CNS pathology, and incidence of relapses.

175 tween 2009 and 2014, using the acute flaccid paralysis database at the World Health Organization Nige

176 of toxic organophosphates that induce human paralysis due to severe axonopathy of large neurons.

177 for improving motor function in humans with paralysis due to spinal cord injury.

178 id not, however, cause exacerbated ascending paralysis during experimental autoimmune encephalomyelit

179 immunometabolic conditions, including immune paralysis during septic shock.

180 n uncontrollable onset of muscle weakness or paralysis during wakefulness.

181 The paralysis efficiency was independent of predator:prey si

182 tion groups, and surveillance (acute flaccid paralysis, enterovirus, and environmental) needs further

183 tory disease and is associated with cases of paralysis, especially among children.

184 diagnostic criteria for other acute flaccid paralysis etiologies were excluded.

185 untary movement in individuals with complete paralysis even years after injury.

186 eurological decline resulting in generalized paralysis, extreme emaciation and death.

187 ted varying efficacy in transiently reducing paralysis following BoNT poisoning, the precise mechanis

188 enefits of spontaneous breathing over muscle paralysis have been proven mainly in mild lung injury; n

189 Joining the Miami Project to Cure Paralysis in 1989 brought the opportunity to use this kn

190 35%), encephalitis in 6 (11%), acute flaccid paralysis in 4 (7%), and autonomic dysregulation with pu

191 d malformation of astrocytes and episodes of paralysis in a Drosophila model.

192 es for the ability to reduce the severity of paralysis in a mouse model of EV-D68 infection: (1) huma

193 A4(1) demonstrated partial protection from paralysis in a murine model of poliomyelitis.

194 ns such as hypoparathyroidism and vocal cord paralysis in a small proportion of patients.

195 t strain of Sindbis virus (NSV) causes fatal paralysis in adult C57BL/6 mice during clearance of infe

196 studying and eventually treating progressive paralysis in ALS patients.

197 death of motor neurons leads to progressive paralysis in amyotrophic lateral sclerosis (ALS).

198 s a bilateral, symmetric, descending flaccid paralysis in an afebrile and alert patient without senso

199 fests with cranial nerve palsies and flaccid paralysis in children and adults.

200 n, a process contributing to immunometabolic paralysis in human and mouse sepsis monocytes, can be re

201 ulinum (Clb), the causative agent of flaccid paralysis in humans that can be fatal in 5 to 10% of cas

202 d neutralizing antibodies to EV-D68, reduced paralysis in infected mice and decreased spinal cord vir

203 an 2014 EV-D68 isolate that reliably induces paralysis in mice due to infection and loss of spinal co

204 We observed modestly decreased time to paralysis in mice transgenic for human A53T alphaS (line

205 VAMP4 in cultured neurons and causes flaccid paralysis in mice.

206 been limited surveillance for acute flaccid paralysis in North America since the regional eradicatio

207 indicate that the cytopathology and episodic paralysis in our Drosophila EA6 model stem from a gain-o

208 Case series of acute flaccid paralysis in patients with radiological or neurophysiolo

209 ant from AQP4(-/-), but not WT, mice induced paralysis in recipient WT and B-cell-deficient mice.

210 y was conducted among cases of acute flaccid paralysis in the 25 high-polio-incidence districts of we

211 virulence, measured as the ability to cause paralysis in the cPVR mouse model.

212 Muscle paralysis increased the number of Hh-responsive cells in

213 tment was also effective in reducing ongoing paralysis induced by adoptive transfer of either pathoge

214 , the dramatic motor neuron degeneration and paralysis induced by Gpx4 ablation suggest that ferropto

215 Motor paralysis is among the most disabling aspects of injury

216 Hypokalaemic periodic paralysis is typically associated with mutations of volt

217 88V) in a patient with myotonia and periodic paralysis, located within the S1 segment of the second d

218 ion during mechanical ventilation and muscle paralysis may be a contributing factor to unsuccessful r

219 orf72 ALS/FTD that shows decreased survival, paralysis, muscle denervation, motor neuron loss, anxiet

220 other conditions than high heel wear such as paralysis, muscular atrophy, and muscular dystrophy.

221 d S4 translocation for hypokalaemic periodic paralysis mutations at arginine residues located below t

222 entified in patients with myotonia, periodic paralysis, myasthenia, or congenital myopathy.

223 suppression of DC maturation and the "immune paralysis" observed during EBOV infections results from

224 ce the course of DSB repair, indicating that paralysis of meiotic chromosome mobility in a genotoxic

225 botulism, a fatal illness caused by flaccid paralysis of muscles due to botulinum neurotoxin (BoNT)

226 NT/A application causes long-lasting flaccid paralysis of muscles through inhibiting the release of t

227 These events resulted in complete paralysis of primary CD4(+) T cell activation, affecting

228 I are respiratory complications secondary to paralysis of respiratory muscles.

229 ting motor neurons that leads to progressive paralysis of skeletal muscle.

230 urological disorder that is characterized by paralysis of the facial nerves and variable other congen

231 our individuals diagnosed as having complete paralysis of the legs.

232 usually involving some degree of progressive paralysis of the upper and/or lower extremities.

233 wild poliovirus caused thousands of cases of paralysis often in countries where poliomyelitis had not

234 ome, 50% were found to have bilateral facial paralysis on examination.

235 ipient VAPP cases were defined as those with paralysis onset 4-40 days following OPV; cases meeting t

236 ividuals who received 0 doses, or those with paralysis onset outside the 4-40-day interval.

237 Paralysis or amputation of an arm results in the loss of

238 Clusters of acute flaccid paralysis or cranial nerve dysfunction in children are u

239 No gross signs of paralysis or paresis were also observed.

240 Patients initially seen with acute flaccid paralysis or pulmonary edema had significantly greater f

241 Removal of loading via microgravity, paralysis, or bed rest leads to rapid loss of muscle mas

242 because the neurological evaluation excluded paralysis, our final diagnosis was ACC type VII.

243 myotonia congenita and hyperkalemic periodic paralysis, our study exemplifies how variations within t

244 mTORC1 paralysis protects multiple myeloma cells against DEPTOR

245 ts in spinal cord inflammation and ascending paralysis, referred to as conventional experimental auto

246 OPV after the switch would risk outbreaks of paralysis related to type 2-circulating vaccine-derived

247 omparable inflation of dependent lung during paralysis required almost threefold greater driving pres

248 rapy for the treatment of respiratory muscle paralysis resulted from cervical SCI.

249 bital-induced sleep and zoxazolamine-induced paralysis, secondary to decreased expression and activit

250 V103Z SOD1 moderately accelerated the age to paralysis, similar in magnitude to WT/L126Z mice.

251 omuscular disorders with features of ataxia, paralysis, skeletal muscle wasting, and degeneration.

252 Besides obvious motor and sensory paralysis, spinal cord injury also induces a functional

253 y also induces a functional SCI-IDS ('immune paralysis'), sufficient to propagate clinically relevant

254 KccB also caused astroglial malformation and paralysis, supporting the idea that the EAAT1(P>R) mutat

255 portance of maintaining strong acute flaccid paralysis surveillance even in adults, and the need to m

256 cted a retrospective review of acute flaccid paralysis surveillance in the security-compromised state

257 ong cases reported through the acute flaccid paralysis surveillance system between November 2008 and

258 A robust acute flaccid paralysis surveillance system, including a multitiered p

259 ntary immunization activities, acute flaccid paralysis surveillance, and routine immunization with th

260 human resources and strengthen acute flaccid paralysis surveillance.

261 teams, (3) field work, and (4) acute flaccid paralysis surveillance.

262 gans based on the phenotype swimming-induced paralysis (Swip), a paralytic behavior observed in herma

263 ay dopamine (DA)-dependent, Swimming-Induced Paralysis (Swip), we identified a novel gene, swip-10, t

264 worldwide suffer from diseases that lead to paralysis through disruption of signal pathways between

265 routine immunization offers protection from paralysis to successfully vaccinated recipients, but it

266 b was transected at postnatal day 8 to cause paralysis to that limb.

267 anxiety, for example, tremor, paraesthesiae, paralysis, to that of a physical illness.

268 ronic sleepiness and cataplexy-sudden muscle paralysis triggered by strong, positive emotions.

269 900S, R1239H) linked to hypokalemic periodic paralysis type 1 and of CaV1.3-R3 (R990H) identified in

270 h genetically confirmed hypokalemic periodic paralysis underwent calf muscle imaging.

271 ein thrombosis, major procedure, spinal cord paralysis, venous injury, lower extremity fracture, pelv

272 In patients with hypokalemic periodic paralysis versus healthy volunteers, Cl(-) and Na(+) con

273 after DCV infection, but also after cricket paralysis virus (CrPV) and flock house virus (FHV) infec

274 The cricket paralysis virus (CrPV) uses an internal ribosomal entry

275 The intergenic IRES of Cricket Paralysis Virus (CrPV-IRES) forms a tight complex with 8

276 of the honey bee dicistrovirus Israeli acute paralysis virus (IAPV) IRES PKI domain can uncouple 0 an

277 rus (DWV)] and dicistrovirids [Israeli acute paralysis virus (IAPV), black queen cell virus (BQCV)] i

278 Many of them, including slow bee paralysis virus (SBPV), cause lethal diseases in honeybe

279 that MV is most closely related to Slow bee paralysis virus (SBPV), which is highly virulent in hone

280 study, we identify the dicistrovirus cricket paralysis virus 1A (CrPV-1A) protein that functions to i

281 The dicistrovirus Cricket Paralysis virus contains a unique dicistronic RNA genome

282 acterized at high resolution how the Cricket Paralysis Virus Internal Ribosomal Entry Site (CrPV-IRES

283 The cricket paralysis virus internal ribosome entry site (CrPV-IRES)

284 Using the cricket paralysis virus internal ribosome entry site element, co

285 ed CrPV-1A, within the dicistrovirus cricket paralysis virus that can inhibit host transcription, mod

286 Consistent with this idea, swip-10 paralysis was blunted in mutants deficient in either ves

287 ugh the effect of pifk-1 mutation on time to paralysis was considerably delayed.

288 Diaphragmatic paralysis was higher (3.5% vs. 0.6%; p = 0.05), but PV s

289 n Hughlings Jackson, his work on aphasia and paralysis was highly regarded by contemporaries.

290 Unilateral diaphragm paralysis was identified in 3 infants.

291 ing these criteria but with unknown residual paralysis were added.

292 Botulism is characterized by flaccid paralysis, which can be caused by intoxication with any

293 displayed tremor that progressed to hindlimb paralysis, which correlated with diminished numbers of m

294 cally within motor neurons to elicit flaccid paralysis, while retrograde TeNT traffics to inhibitory

295 Options for people with severe paralysis who have lost the ability to communicate orall

296 rare but distinct syndrome of acute flaccid paralysis with evidence of spinal motor neuron involveme

297 lation using PLP-CreERT resulted in hindlimb paralysis with immobility at approximately 30 d after 4-

298 olorado (Aurora, CO, USA) with acute flaccid paralysis with spinal-cord lesions involving mainly grey

299 median survival by 50% and delayed hindlimb paralysis, with animals remaining ambulatory until the h

300 S) is the most common cause of acute flaccid paralysis worldwide, and is thought to be immune-mediate