ライフサイエンスコーパス: paralytic

1 n the flexor carpi radialis (FCR), which was paralytic.

2 ila mutants known as the bang-sensitive (BS) paralytics.

3 fused in 56%, and 74% were receiving medical paralytics.

4 The most frequent etiologies were paralytic (27.9%), adult-onset esotropia (19.0%), and th

5 st common types of new-onset strabismus were paralytic (44.2% of cases), convergence insufficiency (1

6 of dsRNA targeted to the sodium ion channel paralytic A (TcNav) gene in Tribolium castaneum as a via

7 alpha-Conotoxin GIC shows no paralytic activity in fish or mice.

8 ngth RoIA analog exhibits delayed but potent paralytic activity when administered to mice and fish; t

9 The paralytic agent (+)-saxitoxin (STX), most commonly assoc

10 ocuronium is a commonly used nondepolarizing paralytic agent but its prolonged duration of action mus

11 n 3 and 13 days after discontinuation of the paralytic agent were 181 and 96 units/L, respectively.

12 pneumonia were aspiration (p < .001), use of paralytic agents (p = .002), and a high sedation level (

13 , although the comparative efficacy of these paralytic agents for achieving successful intubation in

14 here was significant variation in the use of paralytic agents, seizure medications, induced hypotherm

15 One of these mutations is a TS paralytic allele of the calcium channel alpha1-subunit g

16 We have isolated a temperature-sensitive paralytic allele of the Drosophila calcium channel alpha

17 revious work with temperature-sensitive (TS) paralytic alleles of comt has revealed a function for dN

18 ogy, pathophysiology, and natural history of paralytic and incomitant strabismus.

19 Mutations in the genes paralytic and Scutoid cause olfactory defects, as do mut

20 CSAS, DSiaT, and voltage-gated channel genes paralytic and seizure were consistent with the hypothesi

21 Amyotrophic lateral sclerosis (ALS) is a paralytic and usually fatal disorder caused by motor-neu

22 re any strabismus and its subtypes including paralytic and vertical strabismus, esotropia, and exotro

23 ween Na(+) channel defects and the long-term paralytic attacks experienced by patients with HyperKPP.

24 g the reduction in severity and incidence of paralytic autoimmune disease and the reduction in Th1 cy

25 als' true first choice requires the use of a paralytic (azide) to trap the worms at their initial cho

26 enotype swimming-induced paralysis (Swip), a paralytic behavior observed in hermaphrodite worms with

27 utation exacerbating the bang-sensitive (BS) paralytic behavioral phenotypes of several seizure-sensi

28 irst IPV dose administration to mitigate the paralytic burden caused by poliovirus type 2.

29 te from the poliomyelitis case count and the paralytic case-to-infection ratio for type 2 wild poliov

30 ype 2 was identified in 0.5% (181/35 724) of paralytic cases and 11% (298/2804) of sewage wastewater

31 A total of 35 724 paralytic cases and 2804 sewage wastewater samples colle

32 which leads to different numbers of expected paralytic cases and risks of circulating vaccine-derived

33 on, often detecting circulating virus before paralytic cases are reported.

34 nd intermittently in other areas without any paralytic cases as determined by intensified surveillanc

35 ly allowing circulation without detection of paralytic cases for long periods of time.

36 ne-derived poliovirus (VDPV2) and associated paralytic cases in several continents represent a threat

37 lence may have contributed to the absence of paralytic cases in the background of high population imm

38 ) in 2022, the expected number of additional paralytic cases in years 2023 and beyond is small (less

39 estimates of polio incidence and numbers of paralytic cases prevented.

40 type 2 (cVDPV2) establishment and associated paralytic cases, oral polio vaccine 2 was globally withd

41 Israeli response to WPV1 detection prevented paralytic cases; a more rapid response might have interr

42 found that 88% of WPV1 strains isolated from paralytic children belonged to a single antigenic lineag

43 le bond correlation) analysis identified the paralytic compound as quisqualic acid (C(5)H(7)N(3)O(5))

44 se mice via the intramuscular route causes a paralytic condition consistent with poliomyelitis.

45 litis (R-EAE) displays a relapsing-remitting paralytic course in female SJL mice.

46 n produced by Clostridium tetani that causes paralytic death to hundreds of thousands of humans annua

47 TMEV led within 10-14 days to a rapid-onset paralytic demyelinating disease characterized by PLP139-

48 immunosuppressed C58 and AKR mice and cause paralytic disease (age-dependent poliomyelitis [ADPM]).

49 D1 variant containing both mutations develop paralytic disease akin to ALS.

50 ibitor of TGF-beta signaling ameliorated the paralytic disease and reduced the accumulation of pathog

51 avirus FrCas(E) causes a rapidly progressive paralytic disease associated with spongiform neurodegene

52 tween March 1993 and April 1994, 74 cases of paralytic disease attributable to poliovirus type 3 were

53 linum neurotoxin, the causative agent of the paralytic disease botulism, is an endopeptidase composed

54 block neurotransmitter release, and cause a paralytic disease botulism.

55 ciated with severe respiratory illness and a paralytic disease called acute flaccid myelitis in infan

56 Botulism is a rare and potentially fatal paralytic disease caused by botulinum neurotoxin (BoNT).

57 Botulism is a potentially fatal paralytic disease caused by the action of botulinum neur

58 Botulism is a potentially lethal paralytic disease caused primarily by toxins of the anae

59 ophic lateral sclerosis (ALS), a progressive paralytic disease characterized by loss of motor neurons

60 virus induced a rapid-onset, nonprogressive paralytic disease characterized by potent activation of

61 When in vivo treatment with DON was stopped, paralytic disease developed along with the inflammatory

62 Botulism is a paralytic disease due to the inhibition of acetylcholine

63 olio immunization resulted in a reduction of paralytic disease from an estimated annual prevaccine le

64 -derived HEK293 cells, the capacity to cause paralytic disease in both humans and PVR-Tg21 transgenic

65 -55 peptide (GMCSF-MOG) reversed established paralytic disease in both passive and active models of E

66 piratory virus and causative agent of severe paralytic disease in children, by the Erasmus group show

67 effectively prevented chronic, nonremitting, paralytic disease in myelin oligodendrocyte glycoprotein

68 in children and can result in a debilitating paralytic disease known as acute flaccid myelitis.

69 cytokine IL-10, and in the absence of IL-10, paralytic disease occurred earlier and mice died faster.

70 Avian botulism, a paralytic disease of birds, often occurs on a yearly cyc

71 Amyotrophic lateral sclerosis is a fatal paralytic disease that targets motor neurons, leading to

72 No paralytic disease was found in the community, and no pol

73 L/6 and WT mice developed chronic, sustained paralytic disease with average maximum clinical scores o

74 iovirus vaccine (IPV) is efficacious against paralytic disease, but its effect on mucosal immunity is

75 e 30% (95% CI 19-41) per dose against type 1 paralytic disease, compared with 11% (7-14) for the triv

76 nt on glycolipids mediate the postinfectious paralytic disease, Guillain-Barre syndrome (GBS).

77 smutase 1 (SOD1) provokes noncell autonomous paralytic disease.

78 from those of wild poliovirus and can cause paralytic disease.

79 ain-Barre syndrome (GBS), a life-threatening paralytic disease.

80 s neurotoxin are the causative agents of the paralytic diseases botulism and tetanus, respectively.

81 ome enteroviruses are responsible for severe paralytic diseases such as poliomyelitis or acute flacci

82 idial neurotoxins (CNTs) responsible for the paralytic diseases tetanus and botulism, respectively.

83 tion, which causes childhood respiratory and paralytic diseases worldwide.

84 re syndrome (GBS), an acute, immune-mediated paralytic disorder affecting the peripheral nervous syst

85 SOD1 is a cause of the fatal, paralytic disorder ALS.

86 dismutase-1 (SOD1) cause a form of the fatal paralytic disorder amyotrophic lateral sclerosis (ALS),

87 tion can account for salient features of the paralytic disorder amyotrophic lateral sclerosis, includ

88 peroxide dismutase-1 is a cause of the fatal paralytic disorder amyotrophic lateral sclerosis.

89 Amyotrophic lateral sclerosis (ALS) is a paralytic disorder caused by degeneration of motor neuro

90 ALS is a fatal paralytic disorder characterized by a progressive loss o

91 AN) form of the Guillain-Barre syndrome is a paralytic disorder of abrupt onset characterized patholo

92 Amyotrophic lateral sclerosis is a fatal paralytic disorder of unknown cause.

93 hic lateral sclerosis (ALS) is a progressive paralytic disorder resulting from the degeneration of mo

94 n, develop experimental allergic neuritis, a paralytic disorder with clinical, histologic, and electr

95 lerosis (ALS) is the most common adult-onset paralytic disorder, characterized mainly by a loss of mo

96 at altered splicing of the Drosophila Na(v) (paralytic, DmNa(v)) contributes to seizure-like behavior

97 olates were neurovirulent (50% intramuscular paralytic dose in Tg21-PVR mice: log10(7.0)).

98 ide was low in a rodent model, with a median paralytic dose of approximately 200 mg/kg body weight fo

99 isqualic acid demonstrated the same positive paralytic dose-response.

100 protein and hoip mutant embryos are largely paralytic due to defects in myotube elongation and sarco

101 manifest in either encephalitic (furious) or paralytic (dumb) forms.

102 linical patterns, encephalitic (furious) and paralytic (dumb), have been recognized in human rabies.

103 + T cells with sufficient potency to reverse paralytic EAE.

104 ls (pSC) could indirectly contribute to this paralytic effect by influencing nerve terminal function

105 Because the paralytic effect of BoNT is a consequence of its enzymat

106 sk to public health safety due to its severe paralytic effects after ingestion.

107 The mutants are insensitive to the paralytic effects of ryanodine, and lack detectable ryan

108 At a molecular level, BoNT exerts its paralytic effects through intracellular cleavage of vesi

109 protocol can also be modified to follow the paralytic effects with other pharmacological reagents.

110 e excitotoxicity in fatal alphavirus-induced paralytic encephalomyelitis, we treated mice infected wi

111 on of OX-40L was found to be associated with paralytic episodes of EAE and was reduced or absent at d

112 diseases are typified by relapsing-remitting paralytic episodes, after CREAE induction by sensitizati

113 nting with severe myotonia without fulminant paralytic episodes.

114 re phenotype Cav1.1-R1239H, with up to daily paralytic episodes.

115 Paralytic esotropia may be caused by lateral rectus supe

116 poses diagnostic problems, particularly the paralytic form, which closely resembles Guillain-Barre s

117 The botulinum neurotoxins (BoNTs) cause the paralytic human disease botulism and are one of the high

118 patients developed a major complication with paralytic ileus characterized by total inhibition of gas

119 testinal hemorrhage, intestinal obstruction, paralytic ileus, gastrointestinal ulceration, gastrointe

120 otransmission, and endocrine system, causing paralytic ileus, hyperkalemia, oliguria, pulmonary edema

121 rade 3 (fracture, muscle injury, laceration, paralytic ileus, pain, presyncope, urinary retention, an

122 intestinal dysmotility which can progress to paralytic ileus.

123 thin the intestinal muscularis, resulting in paralytic ileus.

124 n in mortality, return of flatus, or risk of paralytic ileus.

125 ospital stay is bowel complication including paralytic ileus.

126 Botulism is a rare, potentially fatal paralytic illness caused by neurotoxins.

127 nd 2018 have resulted in over 600 cases of a paralytic illness that is known as AFM.

128 for botulism among patients presenting with paralytic illness to facilitate early HBAT treatment bef

129 Botulism is a rare, life-threatening paralytic illness.

130 yelitis (AFM), which is a poliomyelitis-like paralytic illness.

131 encing acute neurological progression of his paralytic illness.

132 ditory function would be a useful adjunct to paralytic immobilization and would reduce any possible d

133 PC during the development of T cell-mediated paralytic inflammation in diseases such as experimental

134 9-TMEV-infected mice developed a rapid onset paralytic inflammatory, demyelinating disease paralleled

135 xpression of RpoN* protected C. elegans in a paralytic killing assay, whereas worms succumbed to para

136 al mediators of innate immunity against fast paralytic killing by Pseudomonas.

137 ent to confer resistance to Pseudomonas fast paralytic killing.

138 entanyl equivalent/kg; 95% CI, 0.90-16), and paralytic medications (odds ratio, 2.3; 95% CI, 0.79-80)

139 Benzodiazepines, opioids, and paralytic medications are possible risk factors for infe

140 However, paralytic, muscular dysgenic mutant chick embryos also e

141 ave isolated a SNAP-25 temperature-sensitive paralytic mutant in Drosophila, SNAP-25(ts).

142 rosophila identified a temperature-sensitive paralytic mutant of the voltage-gated calcium channel al

143 identified on the basis of a bang-sensitive paralytic mutant phenotype in a sensitized genetic backg

144 nwk (nervous wreck), a temperature-sensitive paralytic mutant that causes excessive growth of larval

145 Physiological analysis of two lines of paralytic mutant zebrafish, relaxed and sofa potato, rev

146 A novel paralytic mutant, nubian, was identified in a behavioral

147 tigated clamping properties in the syx(3-69) paralytic mutant, which has a single-point mutation in t

148 rosophila melanogaster "bang-sensitive" (BS) paralytic mutant.

149 llection of Drosophila temperature-sensitive paralytic mutants for those exhibiting shortened lifespa

150 rvations explain why screens for conditional paralytic mutants in Drosophila inevitably recover ts al

151 isolated a Drosophila temperature-sensitive paralytic mutation in syntaxin that rapidly blocks synap

152 This paralytic mutation specifically and selectively decrease

153 Temperature-sensitive paralytic mutations in NSF (comatose) also block synapti

154 , as first revealed by temperature-sensitive paralytic mutations in the Drosophila dynamin gene, shib

155 ateral sclerosis (ALS), an adult-onset fatal paralytic neurodegenerative disease with both upper and

156 Konzo is a neglected paralytic neurological disease associated with food (cas

157 Miller Fisher syndrome (MFS) variant of the paralytic neuropathy, Guillain-Barre syndrome, and are b

158 ome is the most common and most severe acute paralytic neuropathy, with about 100,000 people developi

159 is marked by a specific form of restrictive paralytic ophthalmoplegia with or without ptosis.

160 misalignment owing to congenital or acquired paralytic or comitant strabismus and 17 healthy voluntee

161 s and genetic interactions characteristic of paralytic (para) and maleless (mle) mutations that cause

162 hannel of unknown function homologous to the paralytic (para) sodium channel, which mediates neuronal

163 seizure-like behaviors, as an allele of the paralytic (para) voltage-gated Na(+) (Na(V)) channel gen

164 Loss of paralytic (para), the sole gene that encodes Drosophila

165 transmission, as well as cacophony (cac) and paralytic (para), voltage-gated ion channels central to

166 : hangover, CG9947, CG4420, eIF2a, Rbp2, and paralytic (para).

167 the Drosophila voltage-gated sodium channel paralytic (para).

168 We have purified a novel paralytic peptide with 32 AA and a single disulfide bond

169 A paralytic peptide, psi-conotoxin Piiie has been purified

170 tion of reaching and grasping movements by a paralytic person or an amputee would greatly facilitate

171 tions of which cause a temperature-sensitive paralytic phenotype associated with hyperactivity in the

172 re responsible for the temperature-sensitive paralytic phenotype in comatose (comt) mutants.

173 iral vector expressing VPS35 exacerbates the paralytic phenotype in Tg SOD1(G93A) mice.

174 mutant alleles with a temperature-sensitive paralytic phenotype were analyzed.

175 required in order to rescue the kcc(DHS1) BS paralytic phenotype.

176 produce a dominant, X-linked, cold-sensitive paralytic phenotype.

177 olate new mutations that modify the cac(TS2) paralytic phenotype.

178 ure potassium channels in adults rescues the paralytic phenotype.

179 w rapid and reversible temperature-sensitive paralytic phenotypes hitherto only described for the ts

180 ginally isolated on the basis of conditional paralytic phenotypes.

181 heart rate, as well as genes associated with paralytic phenotypes.

182 We estimated the risk of vaccine-associated paralytic polio (VAPP) in LAC for 1992-2011.

183 mitigate against risk of vaccine-associated paralytic polio and circulating vaccine-derived poliovir

184 story about my uncle Charlie, who contracted paralytic polio at an early age, and the remembrances on

185 e protection of the world population against paralytic polio cannot be achieved simply by stopping th

186 Uttar Pradesh reported the highest number of paralytic polio cases in India during 2001-2007.

187 uggest GPEI prevented 2.5-6 million cases of paralytic polio compared to counterfactual worlds withou

188 polio vaccines prevented 5 million cases of paralytic polio for 1960-1987 and 24 million cases world

189 ad to wider circulation of LPVs and cases of paralytic polio in Amish communities if an importation o

190 have studied this important risk factor for paralytic polio in an animal system for poliomyelitis an

191 022, New York State (NYS) reported a case of paralytic polio in an unvaccinated young adult, and subs

192 Paralytic polio once afflicted almost half a million chi

193 al for host-parasite evolution, for example, paralytic polio or viral cancer.

194 us, 1 of 3 wild poliovirus serotypes causing paralytic polio since the beginning of recorded history.

195 ) have resulted in substantial reductions in paralytic polio worldwide.

196 preventing rare cases of vaccine-associated paralytic polio, financially sustaining IPV introduction

197 during 2005-2007, resulting in >200 cases of paralytic polio, whereas the second, which began in 2013

198 cine-derived polioviruses (iVDPVs) and cause paralytic polio.

199 nodeficient patients with vaccine-associated paralytic poliomyelitis (iVAPP), cases reported in the U

200 are and sporadic cases of vaccine-associated paralytic poliomyelitis (VAPP) and the emergence of gene

201 records of patients with vaccine-associated paralytic poliomyelitis (VAPP) in Hungary during 1961-19

202 ause of the rare cases of vaccine-associated paralytic poliomyelitis (VAPP) in OPV recipients and the

203 Vaccine-associated paralytic poliomyelitis (VAPP) is a rare adverse event a

204 an average of 9 cases of vaccine-associated paralytic poliomyelitis (VAPP) were confirmed each year

205 int mutations, leading to vaccine-associated paralytic poliomyelitis (VAPP).

206 tes to the development of vaccine-associated paralytic poliomyelitis (VAPP).

207 found in conjunction with vaccine-associated paralytic poliomyelitis (VAPP).

208 n of poliomyelitis due to vaccine-associated paralytic poliomyelitis and circulating vaccine-derived

209 rmed VAPP case was defined as a diagnosis of paralytic poliomyelitis and residual paralysis at 60 day

210 binding to the PV receptor (PVR) and causes paralytic poliomyelitis by replicating within motor neur

211 nd for emergency protection of contacts of a paralytic poliomyelitis case.

212 llion could lead to roughly 200 000 expected paralytic poliomyelitis cases every year in low-income c

213 hly investigated; none has been confirmed as paralytic poliomyelitis due to wild poliovirus.

214 d type 2 polioviruses and vaccine-associated paralytic poliomyelitis from Sabin oral poliovirus vacci

215 The number of cases of paralytic poliomyelitis has declined in Nigeria since th

216 conducted to detect poliovirus infections or paralytic poliomyelitis in Amish communities in Minnesot

217 ncrease the likelihood of vaccine-associated paralytic poliomyelitis in recipients of live attenuated

218 rrent challenges to the final eradication of paralytic poliomyelitis include the continued transmissi

219 mbinant from a child with vaccine-associated paralytic poliomyelitis is described.

220 en November 1991 and March 1992, 37 cases of paralytic poliomyelitis occurred in Jordan, where none h

221 An outbreak of paralytic poliomyelitis occurred in the Dominican Republ

222 A paralytic poliomyelitis outbreak occurred in Namibia in

223 ur isolates from cases of vaccine-associated paralytic poliomyelitis related to the CHAT vaccine reve

224 alent oral poliovirus vaccine against type 3 paralytic poliomyelitis was 18% (95% CI, 9 to 26).

225 alent oral poliovirus vaccine against type 1 paralytic poliomyelitis were 67% (95% confidence interva

226 No cases of vaccine-associated paralytic poliomyelitis were detected.

227 From 1990 through 1999, 61 cases of paralytic poliomyelitis were reported; 59 (97%) of these

228 During 1976-1995, 48 outbreaks of paralytic poliomyelitis with a cumulative total of appro

229 rome, 5400 cases (95% UI, 0-26 300 cases) of paralytic poliomyelitis, 10.3 million hospitalizations (

230 gical sequelae, congenital rubella syndrome, paralytic poliomyelitis, hospitalization, and death) and

231 (OPV) can revert to neurovirulence and cause paralytic poliomyelitis.

232 ly increasing the risk of vaccine-associated paralytic poliomyelitis.

233 king natural oral human infection leading to paralytic poliomyelitis.

234 emonstration of safety in primate models for paralytic poliomyelitis.

235 f both clinical and pathological features in paralytic rabies and axonal Guillain-Barre syndrome.

236 ncephalitic rabies and from 2 human cases of paralytic rabies demonstrated only minor nucleotide diff

237 Patients with paralytic rabies had longer survival times than those wi

238 nical and pathological features of a case of paralytic rabies with acute axonal neuropathy that close

239 is (EAE), can be induced to develop repeated paralytic relapses with a graded reduction in clinical s

240 tio, 1.01; 1.01-1.03; p = 0.017), and use of paralytics (relative risk, 1.54; 1.26-1.90, p < 0.001).

241 Mutants lacking RIG-3 have an exaggerated paralytic response to a cholinesterase inhibitor, aldica

242 In EAE, improvement in paralytic scores was seen when the drug was given prior

243 An asymmetric synthesis of the paralytic shellfish poison (PSP), (+)-gonyautoxin 3, is

244 ethal bis-guanidinium neurotoxin that causes paralytic shellfish poisoning (PSP) by blocking voltage-

245 Paralytic shellfish poisoning (PSP) is a serious human i

246 Paralytic shellfish poisoning (PSP) toxin monitoring in

247 e (SPR) biosensor assay for the detection of paralytic shellfish poisoning (PSP) toxins in shellfish

248 The presence of paralytic shellfish poisoning (PSP), diarrheic shellfish

249 nsuming seafood carrying these toxins causes paralytic shellfish poisoning (PSP).

250 xins exert the toxic effects associated with paralytic shellfish poisoning and allow for their detect

251 1, or A. fundyense) is the leading cause of Paralytic Shellfish Poisoning in North and South America

252 Paralytic shellfish poisoning is a toxic syndrome descri

253 ic mechanisms of certain metabolites such as paralytic shellfish poisoning toxins and polyether toxin

254 groups: amnesic shellfish poisoning toxins, paralytic shellfish poisoning toxins, and diarrhetic she

255 ent infamously associated with red tides and paralytic shellfish poisoning, is described.

256 f algae that is responsible for red tide and paralytic shellfish poisoning.

257 The paralytic shellfish poisons are a collection of guanidin

258 , we describe the de novo synthesis of three paralytic shellfish poisons, gonyautoxin 2, gonyautoxin

259 ve been evaluated as visible sensors for the paralytic shellfish toxin saxitoxin.

260 of A.catenella via sxtA, a gene involved in Paralytic Shellfish Toxin synthesis, may be a promising

261 ped and validated for the rapid screening of paralytic shellfish toxins (PSTs) from a variety of shel

262 Paralytic shellfish toxins (PSTs) produced by marine din

263 The periodate oxidation of paralytic shellfish toxins (PSTs) was demonstrated, over

264 nooxygenases involved in the biosynthesis of paralytic shellfish toxins (PSTs), SxtT and GxtA, adding

265 ell known producers of the potent neurotoxic paralytic shellfish toxins that can enter the food web a

266 ssay format uses a high affinity antibody to paralytic shellfish toxins with a detection signal gener

267 orptions in testing of shellfish samples for paralytic shellfish toxins.

268 th up to a 20-fold increase in production of paralytic shellfish toxins.

269 These mechanisms culminate in reduction of paralytic signs of EAE.

270 was given prior to or following the onset of paralytic signs.

271 itive paralysis with kinetics reminiscent of paralytic sodium-channel mutants.

272 exotropia (21.8%), hypertropia (13.5%), and paralytic strabismus (16.1%).

273 lgia (aOR, 4.81), optic atrophy (aOR, 3.74), paralytic strabismus (aOR, 2.36), and psoriasis (aOR, 1.

274 Each represents a specific form of paralytic strabismus characterized by congenital restric

275 gistic regression models, beneficiaries with paralytic strabismus had a 78% increased odds of POAG (O

276 (DRS) is the most common form of congenital paralytic strabismus in humans and can result from alpha

277 Unraveling the genetics of the paralytic strabismus syndromes known as congenital crani

278 Paralytic strabismus was the most common subtype of new-

279 requent as exotropia, and 2 participants had paralytic strabismus.

280 nction and improve cosmesis in patients with paralytic strabismus.

281 e evaluation and management of patients with paralytic strabismus.

282 ren had strabismus; only 1 was microvascular paralytic strabismus.

283 cTCR is administered during ongoing disease, paralytic symptoms become exacerbated and the majority o

284 pressing the human G85R SOD1 variant develop paralytic symptoms concomitant with the appearance of SO

285 onotoxin SIVA, causes characteristic spastic paralytic symptoms when injected into fish, and in frog

286 resulting in aggressive T-cell lymphomas and paralytic symptoms.

287 Tg mice were found to develop a lethal early paralytic syndrome induced by a CD8 T cell-dependent aut

288 ype neurotransmitter release at restrictive (paralytic) temperatures.

289 The toxin is paralytic to mice and fish, consistent with its nearly i

290 ither monophasic with general anesthesia and paralytics to minimize muscle contraction, or biphasic w

291 ation sites within the endogenous Drosophila paralytic transcript.

292 infecting mice with either a demyelinating, paralytic (V-1) or nonpathogenic (V-2) variant of a neur

293 revealed by class I tetramer technology the paralytic variant was superior in inducing specific CD8+

294 hat using monovalent OPV2 is generating more paralytic VDPV2 outbreaks with the potential for establi

295 All peptides were highly paralytic when injected into adult zebrafish and bath-ap

296 Drosophila mutants, the Bang-sensitive (BS) paralytics, which are 3-10 times more susceptible to sei