ライフサイエンスコーパス: convulsion

1 ts presented at 4 months with a hypoglycemic convulsion.

2 susceptibility to pharmacologically induced convulsions.

3 QA was associated with a history of convulsions.

4 cated in a familial form of juvenile febrile convulsions.

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

6 diate genetic sensitivity to cocaine-induced convulsions.

7 epileptic syndrome, benign neonatal familial convulsions.

8 reater severity of pentylenetetrazol-induced convulsions.

9 KC also have a history of infantile afebrile convulsions.

10 ween oral automatisms and generalized clonic convulsions.

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

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

13 antly, short stature, mental retardation and convulsions.

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

15 there were clear behavioral and EEG signs of convulsions.

16 initiation and maintenance of soman-induced convulsions.

17 ibility to drug-naive and ethanol withdrawal convulsions.

18 g domoic acid administration with or without convulsions.

19 ous system aberrations, such as seizures and convulsions.

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

21 09 with at least 1 diagnosis code of febrile convulsions.

22 red only admissions for febrile and afebrile convulsions.

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

24 ns did not affect pentylenetetrazol-enhanced convulsions.

25 51 of 304 seizures progressed to generalized convulsions.

26 nfluences alcohol and barbiturate withdrawal convulsions.

27 rawal severity, measured by handling-induced convulsions.

28 seizures that do not progress to generalized convulsions.

29 , influences SB242084- and baclofen-enhanced convulsions.

30 etetrazole (PTZ) exposure paradigm to induce convulsions.

31 imals but are anxiogenic and can precipitate convulsions.

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

33 [9%]), leucopenia (18 [7%] vs 20 [8%]), and convulsion (14 [5%] vs 15 [6%]).

34 .4-4.7; p<0.0001), family history of febrile convulsions (14.6, 6.3-34.1; p<0.0001), history of both

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 ive cholinergic activity elicits generalized convulsions and brain lesions.

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

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

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

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

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

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

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

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

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

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

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

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

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

70 -1 complexes exist at different stages after convulsions and that they regulate ensembles of differen

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

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

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

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

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

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

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

78 Febrile convulsions are a common form of childhood seizure.

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

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

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

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

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

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

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

86 putative mechanisms accounting for observed convulsion behaviors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 -1, CDK-5, and CDKA-1) exhibited significant convulsions following PTZ and RNAi treatment.

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

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

115 4 nested algorithms for identifying febrile convulsions from the administrative databases of 10 Fren

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 induces epileptiform activity and behavioral convulsions in rodents.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 Seizures and convulsions were considered severe symptoms but were oft

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

190 Identical convulsions were obtained using C. elegans mutants defec

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

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

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

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

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