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1 ila mutants known as the bang-sensitive (BS) paralytics.
2 fused in 56%, and 74% were receiving medical paralytics.
3 st common types of new-onset strabismus were paralytic (44.2% of cases), convergence insufficiency (1
4 of dsRNA targeted to the sodium ion channel paralytic A (TcNav) gene in Tribolium castaneum as a via
7 ocuronium is a commonly used nondepolarizing paralytic agent but its prolonged duration of action mus
8 n 3 and 13 days after discontinuation of the paralytic agent were 181 and 96 units/L, respectively.
9 pneumonia were aspiration (p < .001), use of paralytic agents (p = .002), and a high sedation level (
10 here was significant variation in the use of paralytic agents, seizure medications, induced hypotherm
12 We have isolated a temperature-sensitive paralytic allele of the Drosophila calcium channel alpha
13 revious work with temperature-sensitive (TS) paralytic alleles of comt has revealed a function for dN
16 CSAS, DSiaT, and voltage-gated channel genes paralytic and seizure were consistent with the hypothesi
17 Amyotrophic lateral sclerosis (ALS) is a paralytic and usually fatal disorder caused by motor-neu
18 ween Na(+) channel defects and the long-term paralytic attacks experienced by patients with HyperKPP.
19 g the reduction in severity and incidence of paralytic autoimmune disease and the reduction in Th1 cy
20 enotype swimming-induced paralysis (Swip), a paralytic behavior observed in hermaphrodite worms with
21 utation exacerbating the bang-sensitive (BS) paralytic behavioral phenotypes of several seizure-sensi
22 te from the poliomyelitis case count and the paralytic case-to-infection ratio for type 2 wild poliov
23 which leads to different numbers of expected paralytic cases and risks of circulating vaccine-derived
24 nd intermittently in other areas without any paralytic cases as determined by intensified surveillanc
25 lence may have contributed to the absence of paralytic cases in the background of high population imm
26 Israeli response to WPV1 detection prevented paralytic cases; a more rapid response might have interr
27 le bond correlation) analysis identified the paralytic compound as quisqualic acid (C(5)H(7)N(3)O(5))
30 n produced by Clostridium tetani that causes paralytic death to hundreds of thousands of humans annua
31 TMEV led within 10-14 days to a rapid-onset paralytic demyelinating disease characterized by PLP139-
32 immunosuppressed C58 and AKR mice and cause paralytic disease (age-dependent poliomyelitis [ADPM]).
34 ibitor of TGF-beta signaling ameliorated the paralytic disease and reduced the accumulation of pathog
35 avirus FrCas(E) causes a rapidly progressive paralytic disease associated with spongiform neurodegene
36 tween March 1993 and April 1994, 74 cases of paralytic disease attributable to poliovirus type 3 were
37 linum neurotoxin, the causative agent of the paralytic disease botulism, is an endopeptidase composed
40 ophic lateral sclerosis (ALS), a progressive paralytic disease characterized by loss of motor neurons
41 virus induced a rapid-onset, nonprogressive paralytic disease characterized by potent activation of
42 When in vivo treatment with DON was stopped, paralytic disease developed along with the inflammatory
43 olio immunization resulted in a reduction of paralytic disease from an estimated annual prevaccine le
44 -derived HEK293 cells, the capacity to cause paralytic disease in both humans and PVR-Tg21 transgenic
45 -55 peptide (GMCSF-MOG) reversed established paralytic disease in both passive and active models of E
46 effectively prevented chronic, nonremitting, paralytic disease in myelin oligodendrocyte glycoprotein
47 cytokine IL-10, and in the absence of IL-10, paralytic disease occurred earlier and mice died faster.
49 Amyotrophic lateral sclerosis is a fatal paralytic disease that targets motor neurons, leading to
51 L/6 and WT mice developed chronic, sustained paralytic disease with average maximum clinical scores o
52 iovirus vaccine (IPV) is efficacious against paralytic disease, but its effect on mucosal immunity is
53 e 30% (95% CI 19-41) per dose against type 1 paralytic disease, compared with 11% (7-14) for the triv
58 s neurotoxin are the causative agents of the paralytic diseases botulism and tetanus, respectively.
59 idial neurotoxins (CNTs) responsible for the paralytic diseases tetanus and botulism, respectively.
60 re syndrome (GBS), an acute, immune-mediated paralytic disorder affecting the peripheral nervous syst
62 dismutase-1 (SOD1) cause a form of the fatal paralytic disorder amyotrophic lateral sclerosis (ALS),
63 tion can account for salient features of the paralytic disorder amyotrophic lateral sclerosis, includ
65 Amyotrophic lateral sclerosis (ALS) is a paralytic disorder caused by degeneration of motor neuro
67 AN) form of the Guillain-Barre syndrome is a paralytic disorder of abrupt onset characterized patholo
69 hic lateral sclerosis (ALS) is a progressive paralytic disorder resulting from the degeneration of mo
70 n, develop experimental allergic neuritis, a paralytic disorder with clinical, histologic, and electr
71 at altered splicing of the Drosophila Na(v) (paralytic, DmNa(v)) contributes to seizure-like behavior
73 ide was low in a rodent model, with a median paralytic dose of approximately 200 mg/kg body weight fo
75 protein and hoip mutant embryos are largely paralytic due to defects in myotube elongation and sarco
77 linical patterns, encephalitic (furious) and paralytic (dumb), have been recognized in human rabies.
79 ls (pSC) could indirectly contribute to this paralytic effect by influencing nerve terminal function
83 protocol can also be modified to follow the paralytic effects with other pharmacological reagents.
84 e excitotoxicity in fatal alphavirus-induced paralytic encephalomyelitis, we treated mice infected wi
85 on of OX-40L was found to be associated with paralytic episodes of EAE and was reduced or absent at d
86 diseases are typified by relapsing-remitting paralytic episodes, after CREAE induction by sensitizati
89 poses diagnostic problems, particularly the paralytic form, which closely resembles Guillain-Barre s
90 The botulinum neurotoxins (BoNTs) cause the paralytic human disease botulism and are one of the high
91 patients developed a major complication with paralytic ileus characterized by total inhibition of gas
92 rade 3 (fracture, muscle injury, laceration, paralytic ileus, pain, presyncope, urinary retention, an
98 for botulism among patients presenting with paralytic illness to facilitate early HBAT treatment bef
101 ditory function would be a useful adjunct to paralytic immobilization and would reduce any possible d
102 PC during the development of T cell-mediated paralytic inflammation in diseases such as experimental
103 9-TMEV-infected mice developed a rapid onset paralytic inflammatory, demyelinating disease paralleled
104 xpression of RpoN* protected C. elegans in a paralytic killing assay, whereas worms succumbed to para
107 entanyl equivalent/kg; 95% CI, 0.90-16), and paralytic medications (odds ratio, 2.3; 95% CI, 0.79-80)
111 rosophila identified a temperature-sensitive paralytic mutant of the voltage-gated calcium channel al
112 identified on the basis of a bang-sensitive paralytic mutant phenotype in a sensitized genetic backg
113 nwk (nervous wreck), a temperature-sensitive paralytic mutant that causes excessive growth of larval
116 tigated clamping properties in the syx(3-69) paralytic mutant, which has a single-point mutation in t
118 llection of Drosophila temperature-sensitive paralytic mutants for those exhibiting shortened lifespa
119 rvations explain why screens for conditional paralytic mutants in Drosophila inevitably recover ts al
120 isolated a Drosophila temperature-sensitive paralytic mutation in syntaxin that rapidly blocks synap
123 , as first revealed by temperature-sensitive paralytic mutations in the Drosophila dynamin gene, shib
124 ateral sclerosis (ALS), an adult-onset fatal paralytic neurodegenerative disease with both upper and
125 Miller Fisher syndrome (MFS) variant of the paralytic neuropathy, Guillain-Barre syndrome, and are b
126 ome is the most common and most severe acute paralytic neuropathy, with about 100,000 people developi
128 misalignment owing to congenital or acquired paralytic or comitant strabismus and 17 healthy voluntee
129 s and genetic interactions characteristic of paralytic (para) and maleless (mle) mutations that cause
130 hannel of unknown function homologous to the paralytic (para) sodium channel, which mediates neuronal
131 seizure-like behaviors, as an allele of the paralytic (para) voltage-gated Na(+) (Na(V)) channel gen
132 transmission, as well as cacophony (cac) and paralytic (para), voltage-gated ion channels central to
137 tion of reaching and grasping movements by a paralytic person or an amputee would greatly facilitate
138 tions of which cause a temperature-sensitive paralytic phenotype associated with hyperactivity in the
145 w rapid and reversible temperature-sensitive paralytic phenotypes hitherto only described for the ts
149 mitigate against risk of vaccine-associated paralytic polio and circulating vaccine-derived poliovir
151 ad to wider circulation of LPVs and cases of paralytic polio in Amish communities if an importation o
152 have studied this important risk factor for paralytic polio in an animal system for poliomyelitis an
155 us, 1 of 3 wild poliovirus serotypes causing paralytic polio since the beginning of recorded history.
156 preventing rare cases of vaccine-associated paralytic polio, financially sustaining IPV introduction
157 during 2005-2007, resulting in >200 cases of paralytic polio, whereas the second, which began in 2013
159 nodeficient patients with vaccine-associated paralytic poliomyelitis (iVAPP), cases reported in the U
160 are and sporadic cases of vaccine-associated paralytic poliomyelitis (VAPP) and the emergence of gene
161 records of patients with vaccine-associated paralytic poliomyelitis (VAPP) in Hungary during 1961-19
162 ause of the rare cases of vaccine-associated paralytic poliomyelitis (VAPP) in OPV recipients and the
164 an average of 9 cases of vaccine-associated paralytic poliomyelitis (VAPP) were confirmed each year
168 n of poliomyelitis due to vaccine-associated paralytic poliomyelitis and circulating vaccine-derived
169 rmed VAPP case was defined as a diagnosis of paralytic poliomyelitis and residual paralysis at 60 day
170 binding to the PV receptor (PVR) and causes paralytic poliomyelitis by replicating within motor neur
172 llion could lead to roughly 200 000 expected paralytic poliomyelitis cases every year in low-income c
175 conducted to detect poliovirus infections or paralytic poliomyelitis in Amish communities in Minnesot
176 ncrease the likelihood of vaccine-associated paralytic poliomyelitis in recipients of live attenuated
177 rrent challenges to the final eradication of paralytic poliomyelitis include the continued transmissi
179 en November 1991 and March 1992, 37 cases of paralytic poliomyelitis occurred in Jordan, where none h
182 ur isolates from cases of vaccine-associated paralytic poliomyelitis related to the CHAT vaccine reve
184 alent oral poliovirus vaccine against type 1 paralytic poliomyelitis were 67% (95% confidence interva
191 f both clinical and pathological features in paralytic rabies and axonal Guillain-Barre syndrome.
192 ncephalitic rabies and from 2 human cases of paralytic rabies demonstrated only minor nucleotide diff
194 nical and pathological features of a case of paralytic rabies with acute axonal neuropathy that close
195 is (EAE), can be induced to develop repeated paralytic relapses with a graded reduction in clinical s
196 Mutants lacking RIG-3 have an exaggerated paralytic response to a cholinesterase inhibitor, aldica
200 e (SPR) biosensor assay for the detection of paralytic shellfish poisoning (PSP) toxins in shellfish
202 xins exert the toxic effects associated with paralytic shellfish poisoning and allow for their detect
204 ic mechanisms of certain metabolites such as paralytic shellfish poisoning toxins and polyether toxin
207 , we describe the de novo synthesis of three paralytic shellfish poisons, gonyautoxin 2, gonyautoxin
209 ped and validated for the rapid screening of paralytic shellfish toxins (PSTs) from a variety of shel
211 ell known producers of the potent neurotoxic paralytic shellfish toxins that can enter the food web a
212 ssay format uses a high affinity antibody to paralytic shellfish toxins with a detection signal gener
218 (DRS) is the most common form of congenital paralytic strabismus in humans and can result from alpha
224 cTCR is administered during ongoing disease, paralytic symptoms become exacerbated and the majority o
225 pressing the human G85R SOD1 variant develop paralytic symptoms concomitant with the appearance of SO
226 onotoxin SIVA, causes characteristic spastic paralytic symptoms when injected into fish, and in frog
227 Tg mice were found to develop a lethal early paralytic syndrome induced by a CD8 T cell-dependent aut
231 infecting mice with either a demyelinating, paralytic (V-1) or nonpathogenic (V-2) variant of a neur
232 revealed by class I tetramer technology the paralytic variant was superior in inducing specific CD8+
233 Drosophila mutants, the Bang-sensitive (BS) paralytics, which are 3-10 times more susceptible to sei
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