ライフサイエンスコーパス: convulsion

1 ts presented at 4 months with a hypoglycemic convulsion.

2 acterized by speech arrest and a generalized convulsion.

3 imals but are anxiogenic and can precipitate convulsions.

4 susceptibility to pharmacologically induced convulsions.

5 QA was associated with a history of convulsions.

6 cated in a familial form of juvenile febrile convulsions.

7 ases in rCBF precede the onset of O2-induced convulsions.

8 diate genetic sensitivity to cocaine-induced convulsions.

9 epileptic syndrome, benign neonatal familial convulsions.

10 reater severity of pentylenetetrazol-induced convulsions.

11 KC also have a history of infantile afebrile convulsions.

12 ween oral automatisms and generalized clonic convulsions.

13 of the 'benign' nature of early-life febrile convulsions.

14 even in mice that had no visible evidence of convulsions.

15 antly, short stature, mental retardation and convulsions.

16 go, headaches, and deafness to blindness and convulsions.

17 there were clear behavioral and EEG signs of convulsions.

18 initiation and maintenance of soman-induced convulsions.

19 ibility to drug-naive and ethanol withdrawal convulsions.

20 g domoic acid administration with or without convulsions.

21 ous system aberrations, such as seizures and convulsions.

22 an antiepileptic drug rescued the prolonged convulsions.

23 ts may be limited by side effects, including convulsions.

24 09 with at least 1 diagnosis code of febrile convulsions.

25 red only admissions for febrile and afebrile convulsions.

26 ns did not affect pentylenetetrazol-enhanced convulsions.

27 51 of 304 seizures progressed to generalized convulsions.

28 nfluences alcohol and barbiturate withdrawal convulsions.

29 rawal severity, measured by handling-induced convulsions.

30 seizures that do not progress to generalized convulsions.

31 , influences SB242084- and baclofen-enhanced convulsions.

32 etetrazole (PTZ) exposure paradigm to induce convulsions.

33 es that often cause adverse effects, such as convulsions.

34 eastfeed, 317/2,340 (13.6%) with two or more convulsions, 1,057/2,340 (45.2%) with severe anaemia, an

35 , 317/2340 (13.6%) had experienced 2 or more convulsions, 1057/2340 (45.2%) had severe anemia, and 44

36 on (6.0%) in the bevacizumab-alone group and convulsion (13.9%), neutropenia (8.9%), and fatigue (8.9

37 on (6.0%) in the bevacizumab-alone group and convulsion (13.9%), neutropenia (8.9%), and fatigue (8.9

38 [9%]), leucopenia (18 [7%] vs 20 [8%]), and convulsion (14 [5%] vs 15 [6%]).

39 .4-4.7; p<0.0001), family history of febrile convulsions (14.6, 6.3-34.1; p<0.0001), history of both

40 susceptibility to pentylenetetrazole-induced convulsions 15 weeks after TBI.

41 roup), stomatitis (24 [31%] vs eight [21%]), convulsion (18 [23%] vs ten [26%]), and pyrexia (17 [22%

42 egarding histories of epilepsy, seizures, or convulsions 3 or more years prior to diagnosis (odds rat

43 rtial seizures without secondary generalized convulsions, 34.8% of seizures had desaturations below 9

44 common of which were hypertension (8.3%) and convulsion (6.0%) in the bevacizumab-alone group and con

45 common of which were hypertension (8.3%) and convulsion (6.0%) in the bevacizumab-alone group and con

46 g (68% vs. 50%, p = 0.17) or death following convulsions (74% vs. 44%, p = 0.02).

47 bunit KCNQ2 lead to benign familial neonatal convulsions, a dominantly inherited form of generalized

48 and Scn1b(+/+) mice to hyperthermia-induced convulsions, a model of pediatric febrile seizures.

49 as death, danger signs (inability to drink, convulsions, abnormally sleepy), fever (>/=38 degrees C)

50 difference in sensitivity to cocaine-induced convulsions across C57BL/6J (6J) and C57BL/6ByJ (6ByJ) m

51 d HR, 23.6; 95% CI, 20.6-27.1), and neonatal convulsions (adjusted HR, 33.5; 95% CI, 30.1-37.4).

52 Domoic acid-induced convulsions affects limbic structures such as hippocampu

53 More than one-third of patients treated had convulsions, altered consciousness, or coma.

54 BLLs (97%, > 45 microg/dL), and incidence of convulsions among children before death (82%) suggest th

55 sitional candidate gene for familial febrile convulsion and Cayman type cerebellar ataxia.

56 tual protection of mice from acute toxicity (convulsion and lethality) of a lethal dose of cocaine (1

57 ed during the study: one case of intrapartum convulsion and one case of disseminated intravascular co

58 n II, and H-Dmt-Tic-NH-CH2-Bid could produce convulsions and antidepressant-like effects in the force

59 ch as norfloxacin exhibit a low incidence of convulsions and anxiety.

60 These data suggest that the convulsions and ataxia observed in opt mice may be cause

61 bility to block maximal electroshock-induced convulsions and ATPA-induced rigidity in mice.

62 ive cholinergic activity elicits generalized convulsions and brain lesions.

63 ic dyskinesia (38.7%; n = 560) and infantile convulsions and choreoathetosis (14.3%; n = 206) constit

64 enign familial infantile epilepsy, infantile convulsions and choreoathetosis and paroxysmal kinesigen

65 aths in children following prolonged febrile convulsions and idiopathic convulsive status epilepticus

66 ported progressive volume loss after febrile convulsions and in active epilepsy.

67 ssing its ability to prevent cocaine-induced convulsions and lethality in the rat.

68 ently protected mice against cocaine-induced convulsions and lethality.

69 Analogies between benign familial neonatal convulsions and other channelopathies of skeletal and ca

70 ing to its neurotoxic effects, which include convulsions and other chronic issues.

71 Cannabis has been used to treat convulsions and other disorders since ancient times.

72 D), and their combination-known as infantile convulsions and paroxysmal choreoathetosis (ICCA)-are re

73 containing a gene responsible for 'infantile convulsions and paroxysmal choreoathetosis' (ICCA).

74 receptor antagonist scopolamine blocked the convulsions and prevented increased Fos and GFAP stainin

75 atures (37 degrees), cac flies show frequent convulsions and pronounced locomotor defects.

76 gs characterize glyphosate's exacerbation of convulsions and propose the GABA-A receptor as a neurolo

77 antagonist CGP 35348 prevented tonic-clonic convulsions and significantly enhanced survival of the m

78 nd codeine are involved in the modulation of convulsions and that morphine and/or codeine may act as

79 -1 complexes exist at different stages after convulsions and that they regulate ensembles of differen

80 .c., 30 min before DFP) prevents DFP-induced convulsions and the associated neuronal damage and morta

81 site severe neonatal morbidity (eg, neonatal convulsions) and perinatal mortality (ie, stillbirths an

82 izures, 1.11 (95% CI, 1.06-1.17) for febrile convulsions, and 1.04 (95% CI, 0.97-1.13) for epilepsy.

83 te caused episodes of prolonged akinesia and convulsions, and major damage to pyramidal neurons of th

84 in-5-glucoside cause poisoning, tonic-clonic convulsions, and neurotoxic effects.

85 hypothermia, movement only when stimulated, convulsions, and poor feeding.

86 after vaccination, mainly pneumonia, febrile convulsions, and salmonella sepsis.

87 ntidepressant-like effects without producing convulsions, and some peptidic agonists can increase BDN

88 affects discrete brain circuits by inducing convulsions, and that domoic acid-induced convulsions ca

89 t start extracorporeal membrane oxygenation, convulsions, and use of antiepileptics.

90 Cocaine-induced convulsions appear to be mediated by serotonin (5-HT) ne

91 Febrile convulsions are a common form of childhood seizure.

92 Here, we demonstrate that handling-induced convulsions are less severe in congenic vs. background s

93 rosis often have histories of severe febrile convulsions as infants.

94 and was found to induce cholinergic AEs and convulsion at therapeutic indices similar to previous co

95 Only JOM-13 produced convulsions at doses required for antidepressant-like ef

96 trains that are susceptible to sound-induced convulsions (audiogenic seizures, or AGSs).

97 een 2 and 5% of children will have a febrile convulsion before the age of 5.

98 eceptor, acr-2(gf), causes an epileptic-like convulsion behavior.

99 putative mechanisms accounting for observed convulsion behaviors.

100 pilepsy syndrome of benign familial neonatal convulsions (BFNC) exhibits the remarkable feature of cl

101 Benign familial neonatal convulsions (BFNC) is a rare autosomal dominant generali

102 Benign familial neonatal convulsions (BFNC), a class of idiopathic generalized ep

103 One type is benign familial neonatal convulsions (BFNC), a dominantly inherited disorder of n

104 inherited epilepsy, benign familial neonatal convulsions (BFNC), has also been localized to chromosom

105 an seizure disorder benign familial neonatal convulsions (BFNC), presumably by reducing IK(M) functio

106 of inheritance: the benign familial neonatal convulsions (BFNC; refs 2,3).

107 Benign familial neonatal convulsion (BNFC) is a neurological disorder caused by m

108 xposed to Roundup did not recover from their convulsions, but drug treatment resulted in full recover

109 and posterior to the lesion, suggesting that convulsions can arise independently from distinct subset

110 ife-threatening emergency, because recurrent convulsions can cause death or injury.

111 ation of GABA falls below a threshold level, convulsions can occur.

112 ng convulsions, and that domoic acid-induced convulsions cause chronic effects on brain function that

113 ng (MRI) was performed after complex febrile convulsions (CFCs) in 27 infants.

114 seline (prostration, impaired consciousness, convulsions, coma), and malaria status were not related

115 P) compounds cause toxic symptoms, including convulsions, coma, and death, as the result of irreversi

116 pisodes with altered consciousness, coma, or convulsions constituted 36.6% of all episodes in treated

117 Fear of brain damage, coma, convulsions, death and dehydration was high across many

118 Domoic acid, in the absence of convulsions, decreased relative [14C]AA incorporation in

119 Since 6ByJ mice are less sensitive to convulsions despite the fact that they have more 5-HT(2)

120 the ETX seizure network in generating tonic convulsions during AGS.

121 nvestigate if seizures affect sensitivity to convulsions during subsequent exposure to HBO(2) and to

122 events in the lower-threshold group included convulsions (during normoglycemia) in one newborn and on

123 ileptogenic sites, we examined soman-induced convulsion effects on CNS TRH.

124 onvulsion susceptibility and discovered that convulsion effects were significantly enhanced when LIS-

125 ich 5 (base deficit, impaired consciousness, convulsions, elevated blood urea, and underlying chronic

126 uding alcohol and barbiturate withdrawal and convulsions elicited by chemical and audiogenic stimuli.

127 ions of 6J and 6ByJ mice and cocaine-induced convulsions following pretreatment with the 5-HT reuptak

128 sities across these mice and cocaine-induced convulsions following pretreatment with the 5-HT(2) anta

129 -1, CDK-5, and CDKA-1) exhibited significant convulsions following PTZ and RNAi treatment.

130 oups were tested hourly for handling-induced convulsions for 10 hr and at Hours 24 and 25.

131 f epilepsy known as benign familial neonatal convulsions, for the first time enabled insight into the

132 4 nested algorithms for identifying febrile convulsions from the administrative databases of 10 Fren

133 diate genetic sensitivity to cocaine-induced convulsions, further supporting the role of these sites

134 n aged 2-8 years (10 postvaccination febrile convulsions +/- gastroenteritis and 7 fever and/or gastr

135 age of a putative autosomal dominant febrile convulsion gene to chromosome 8q13-21.

136 d family members indicates that this febrile convulsion gene, which we call FEB2 , can be localized t

137 and/or by management of frequent spontaneous convulsions (>1 per hour) with anticonvulsants.

138 stage 6 seizure or generalized tonic-clonic convulsion (GTC).

139 Subjects whose convulsions had persisted for more than 5 minutes and wh

140 of mice were evaluated for handling-induced convulsions (HIC) or abnormal EEG (high-voltage "brief s

141 or alcohol withdrawal using handling-induced convulsions (HICs) following both acute and chronic alco

142 ch is increased severity of handling induced convulsions (HICs).

143 erential ethanol withdrawal handling-induced convulsions (HICs).

144 tly prognostic across meta-analyses: febrile convulsions, hippocampal sclerosis, focal abnormal MRI,

145 sociated with impaired or aberrant movement, convulsions, history of hearing problems, other conditio

146 lethally challenged mice included seizures, convulsions, hyperexcitability, and/or depression.

147 Febrile seizures (FSs) are the most common convulsion in infancy and childhood.

148 The doses producing convulsions in 50% (CD(50)) and 97% (CD(97)) of animals

149 ed a greater facilitation of cocaine-induced convulsions in 6ByJ relative to 6J mice, suggesting that

150 these ablations to investigate the source of convulsions in a gain-of-function mutant for the acetylc

151 elegans offers an opportunity to study such convulsions in a simple animal with a defined nervous sy

152 mg/kg i.p., caused stereotyped behavior and convulsions in approximately 60% of rats which received

153 e studies of neuronal networks that subserve convulsions in closely-related epilepsy models are revea

154 ffects of 15 daily pentylenetetrazol-induced convulsions in immature rats beginning at postnatal day

155 This compound did not cause tonic-clonic convulsions in mice, had a good pharmacokinetic profile,

156 rotective against pentylenetetrazole-induced convulsions in rats without the motor impairment associa

157 hose required for analgesic activity produce convulsions in rodents and nonhuman primates.

158 induces epileptiform activity and behavioral convulsions in rodents.

159 e toxicity studies, we observed tonic-clonic convulsions in several mice at high doses.

160 here were 12 perinatal deaths and 5 neonatal convulsions in the control group compared with 3 perinat

161 ared with 3 perinatal deaths and no neonatal convulsions in the DHA group (P = 0.03 in both cases).

162 nd continued to have persistent or recurrent convulsions in the emergency department for at least 5 m

163 ing genetic susceptibilities to seizure-like convulsions in vivo.

164 Postvaccination febrile convulsions in young children were rare but not previous

165 these mutants or the antagonist alone caused convulsions, indicating a threshold was exceeded in resp

166 ncies of flumazenil and zolpidem in blocking convulsions induced by 9 and DMCM, respectively, indicat

167 g assay and in vivo potency by inhibition of convulsions induced by N-methyl-D-aspartate (NMDA) in mi

168 This indole derivative inhibited convulsions induced by NMDA in mice, when administered b

169 terized by peak susceptibility to 'provoked' convulsions--induces severe, age-dependent seizures.

170 frequent progression of elicited generalized convulsions into a prolonged (> 8 min) postictal convuls

171 e to 6J mice, suggesting that sensitivity to convulsions is mediated postsynaptically.

172 inherited, such as benign familial neonatal convulsions, juvenile myoclonic epilepsy, as well as ben

173 Additionally, PTZ-induced convulsions led to alterations in protein structures obt

174 breastfeeding/drinking, vomiting everything, convulsions, lethargy, unconsciousness, or head nodding)

175 genetic variance in acute alcohol withdrawal convulsion liability to a >35 centimorgan (cM) interval

176 port here another autosomal dominant febrile convulsion locus on chromosome 19p.

177 f C. tetani infection, control of spasms and convulsions, maintenance of the airway, and management o

178 aging have shown that very prolonged febrile convulsions may produce hippocampal injury and that foca

179 s may play a role in the etiology of febrile convulsions, mesial temporal sclerosis, and temporal lob

180 Here we show that convulsions mimicking epilepsy can be induced by a mutat

181 ice variant showed a parallel propensity for convulsions, miR-211 decreases, and miR-134 elevation.

182 ations more quickly, and produce generalized convulsions more frequently.

183 In addition, cinanserin attenuated convulsions more potently in 6J relative to 6ByJ mice.

184 hyxia (n=3), septicaemia (n=1), and neonatal convulsion (n=1).

185 hoea (n=31 [19%]), fatigue (n=21 [13%]), and convulsion (n=18 [11%]).

186 , dizziness (n = 16), headache (n = 11), and convulsions (n = 11).

187 inhibitor of cholinesterase, causes intense convulsions, neuropathology and, ultimately, death.

188 sponse is inadequate, and anticonvulsants if convulsions occur.

189 creased with a family history of non-febrile convulsions (odds ratio 3.3, 95% CI 2.4-4.7; p<0.0001),

190 times from active treatment to cessation of convulsions of 3.3 minutes and 1.6 minutes.

191 id tonic firing during the generalized tonic convulsions of AGS.

192 Two had short febrile convulsions, one had PFC and one had non-febrile seizure

193 romolar range, there was no association with convulsions or depth of coma.

194 e duration of epilepsy, a history of febrile convulsions or of generalized seizures.

195 leton (OR, 0.27; 95% CI, 0.11-0.60), febrile convulsions (OR, 0.39; 95% CI, 0.21-0.67), viral intesti

196 ticus (defined as easily visible generalized convulsions) or subtle status epilepticus (indicated by

197 with MTS have a history of prolonged febrile convulsion (PFC) in childhood.

198 uding 21 with a history of prolonged febrile convulsion (PFC), underwent qualitative and quantitative

199 rotein termed synaptobrevin, exhibit similar convulsion phenotypes following chemical induction.

200 izure behaviors manifest in various types of convulsions, potentially including human epilepsy.

201 bipolar disorder and could contribute to the convulsions produced by excessive doses of this drug.

202 In the presence of convulsions, relative [14C]AA incorporation was decrease

203 that are mutated in benign familial neonatal convulsions represent an important new target for anti-e

204 ces the risk of perinatal death and neonatal convulsions requires further investigation.

205 ospitalization, deterioration in coma score, convulsions, respiratory distress, and pneumonia were mo

206 backgrounds to create a sensitized state for convulsion susceptibility and discovered that convulsion

207 pha,3beta-isomers were more toxic (death and convulsions) than the 2 beta,3beta- and 2 beta,3 alpha-i

208 al from chronic alcohol exposure can produce convulsions that are likely due to ethanol (EtOH) neuroa

209 ntraniliprole and M. anisopliae relieved the convulsions that normally accompany M. anisopliae infect

210 Severing the ventral nerve cord caused convulsions to occur independently anterior and posterio

211 selected lines that display severe and mild convulsions upon removal from chronic EtOH exposure.

212 ctive surveillance of aseptic meningitis and convulsion was established to evaluate the risk associat

213 An elevated relative incidence of convulsion was found in the 6- to 11-day period after re

214 A prior history of febrile convulsions was obtained in 13 HTS patients (81.3%) but

215 Seizures and convulsions were considered severe symptoms but were oft

216 disease rapidly improved under treatment and convulsions were either completely suppressed or substan

217 Identical convulsions were obtained using C. elegans mutants defec

218 However, convulsions were often seen in children, and abortions a

219 lonic epilepsy, absence epilepsy, or febrile convulsions were screened by conformation-sensitive gel

220 s manifested by (1) generalized tonic-clonic convulsions with multiple failings, which were elicited

221 ell-known adverse events of fever, rash, and convulsions within the first 14 days.

222 elected for resistance to ethanol withdrawal convulsions (WSR).