コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 y but that long-term IGF-1 treatment was pro-epileptic.
2 observed, including confusion (3 patients), epileptic (1 patient), amnestic (1 patient), and a sever
3 observed, including confusion (12 patients), epileptic (1 patient), amnestic (3 patients), and fulmin
5 important to explain the slow propagation of epileptic activity and other normal propagations at simi
6 iation has therapeutic implications, because epileptic activity can occur at early disease stages and
7 al lobe and fusiform gyrus may be related to epileptic activity in IGE patients with absence seizures
24 g analysis in a mouse model of TLE using 100 epileptic and 100 control hippocampi shows the proconvul
27 (EMG) for differentiation between convulsive epileptic and psychogenic nonepileptic seizures (PNESs).
28 human astrocytes along with astrocytes from epileptic and tumor foci and compared these to human neu
30 and rescue behavioral deficits in a chronic epileptic animal model more than 6 months after treatmen
31 ticus, late electrocorticography to identify epileptic animals and post-mortem immunohistochemistry t
32 r previously reported impaired inhibition in epileptic animals at basket cell-to-granule cell (BC-->G
33 Furthermore, activating granule cells in non-epileptic animals evoked acute seizures of increasing se
37 on revealed consistent downregulation in the epileptic brain in heterogeneous forms of epilepsy inclu
38 ctal epileptiform discharges (IEDs) identify epileptic brain regions and can impair memory, but the m
39 ifically target adult-born DGCs arise in the epileptic brain, whereas axons of interneurons and pyram
43 nduced decrease of neuron recruitment during epileptic bursts can lead to an increase in burst freque
47 d, epileptiform spikes were more frequent in epileptic compared with nonepileptic rodents; however, t
50 ic database, we may find that apart from the epileptic conditions, Intermittent Head Drops have been
52 alas and hippocampi were conducted in 50 non-epileptic controls (age 7-79 years) and 50 patients with
54 gest that only limited subsets of neurons in epileptic depth regions initiate the seizure-onset and t
55 gain-of-function) seizures and corresponding epileptic discharges with prominent sleep activation in
57 linked to developmental defects in mice and epileptic disorders in humans, little is known about its
58 sociated with a wide spectrum of early-onset epileptic disorders ranging from benign familial neonata
59 ther neuronal hyperexcitation, a hallmark of epileptic disorders, could accelerate this conversion.
60 made in understanding the pathophysiology of epileptic disorders, seizures remain poorly controlled i
62 ons with levetiracetam, an FDA-approved anti-epileptic drug, enhanced survival of chemotherapy drug-t
63 research is to reconcile the effects of anti-epileptic drugs (AEDs) on individual neurons with their
66 y.SIGNIFICANCE STATEMENT The effects of anti-epileptic drugs on individual neurons are difficult to s
67 n of status epilepticus and efficacy of anti-epileptic drugs will be important to improve outcomes.
68 r than additional trials of second-line anti-epileptic drugs, to avoid neuronal injury and pharmaco-r
70 east 10 years of age (7367 artefact-free non-epileptic electrodes), whereas a younger group included
71 e beta1 subunit gene GABRB1 in children with epileptic encephalopathies (EEs) Lennox-Gastaut syndrome
72 tations in the etiology of developmental and epileptic encephalopathies (EEs), highlighting their gen
73 2 channels are also strongly associated with epileptic encephalopathies and intellectual disability i
74 v7.3 (R230C) recently found in patients with epileptic encephalopathies and/or intellectual disabilit
78 s (IS) and Lennox-Gastaut syndrome (LGS) are epileptic encephalopathies characterized by early onset,
79 de novo CHD2 mutations, but is also seen in epileptic encephalopathies due to other gene mutations.
82 argeted resequencing of 644 individuals with epileptic encephalopathies led to the identification of
84 ht to identify genetic causes of early onset epileptic encephalopathies with burst suppression (Ohtah
85 basis for how these mutations contribute to epileptic encephalopathies, we compared the effects of t
93 nd epileptic phenotypes, including infantile epileptic encephalopathy (EIEE), suggestive of a gain of
95 RB3) identified in patients with early-onset epileptic encephalopathy (EOEE) and profound development
97 nt publication described a distinct neonatal epileptic encephalopathy (MIM 615905) caused by autosoma
98 rane-fusion machinery, cause infantile early epileptic encephalopathy (Ohtahara syndrome), but it is
99 channel KV1.2, in six isolated patients with epileptic encephalopathy (one mutation recurred three ti
100 SCN8A encephalopathy, or early infantile epileptic encephalopathy 13 (EIEE13), is caused predomin
102 ynonymous de novo mutations in patients with epileptic encephalopathy and for common susceptibility v
103 RHOBTB2 as causative for a developmental and epileptic encephalopathy and have elucidated the role of
105 3 patients (eight previously described) with epileptic encephalopathy carrying either novel or known
106 /Q390X) KI mice are associated with a severe epileptic encephalopathy due to a dominant negative effe
107 Photosensitivity is prominent in a very rare epileptic encephalopathy due to de novo CHD2 mutations,
110 on sequencing on patients with a spectrum of epileptic encephalopathy phenotypes, and we identified f
112 spasms are seizures associated with a severe epileptic encephalopathy presenting in the first 2 years
113 ssense mutation p.Asn1768Asp in a child with epileptic encephalopathy that included seizures, ataxia,
114 Scn8a(N1768D) mutant mice provide a model of epileptic encephalopathy that will be valuable for study
115 lepsy was common, with severity ranging from epileptic encephalopathy to well-controlled seizures.
116 ibed here, however, cause a severe infantile epileptic encephalopathy with a central myelin defect an
117 ON: We characterize the genetic landscape of epileptic encephalopathy with burst suppression, without
118 d epilepsy syndrome (FIRES) is a devastating epileptic encephalopathy with limited treatment options
121 unrelated individual) with severe infantile epileptic encephalopathy, clubfoot, absent deep tendon r
123 hiatric disorders: autism spectrum disorder, epileptic encephalopathy, intellectual disability and sc
124 al disorders, and 14 patients with infantile epileptic encephalopathy, of which 13 had severe neurode
125 hiatric disorders: autism spectrum disorder, epileptic encephalopathy, schizophrenia, and severe inte
126 y leads to potentially fatal early infantile epileptic encephalopathy, severe developmental delay, an
127 developed a model of a severe human genetic epileptic encephalopathy, the Gabrg2(+/Q390X) knock-in m
129 have recently been recognized as a cause of epileptic encephalopathy, which is characterized by refr
137 to three real exome sequencing data sets of epileptic encephalophathies and intellectual disability
138 pically, the term has mainly been related to epileptic episodes, but the spectrum of clinical conditi
139 ay identify features more consistent with an epileptic event and laboratory studies and brain imaging
141 res (encephalopathy, psychiatric, cognitive, epileptic, extrapyramidal and inflammatory cerebrospinal
142 ing can be used to infer the localisation of epileptic foci and assist in the design of intracranial
143 increased tryptophan uptake and trapping in epileptic foci and brain tumors, but the short half-life
144 ve astrocytes are commonly found in putative epileptic foci and have been hypothesized to be disease
145 itability, with many distinctive features of epileptic foci, including high-frequency oscillations wi
146 ic activity (i.e. synaptic noise) within the epileptic focus is one endogenous method of ictogenesis.
147 ll, among all patients with AE and a defined epileptic focus, 7 had predominant increased volume ipsi
152 is preserved across-species, specific to the epileptic hippocampus and upregulated in chronic epileps
153 ipple-like oscillations (150-250Hz) in human epileptic hippocampus are associated with 2 distinct pop
154 gest a potential role for RNA editing in the epileptic hippocampus in the occurrence and severity of
155 ility to sustain recurrent excitation in the epileptic hippocampus, which raises questions about the
156 ells to hippocampal hyperexcitability in the epileptic hippocampus.SIGNIFICANCE STATEMENT In the hipp
158 fects of both the KD and KB in spontaneously epileptic Kcna1-null mice using a combination of behavio
160 lthough carbamazepine (CBZ) has a known anti-epileptic mechanism, paradoxically, it has also been rep
161 we show that feeding levetiracetam, an anti-epileptic medication, to Abeta-expressing flies suppress
162 ippocampal slices at 270 DAT, was reduced in epileptic mice but restored to naive levels in epileptic
163 The degree of differential RNA editing in epileptic mice correlated with frequency of seizures, an
164 ranscribing P2rx7 in hippocampal slices from epileptic mice displayed enhanced agonist-evoked P2X7 re
165 eduction in seizure activity was observed in epileptic mice receiving intrahippocampal CGE progenitor
167 enitors transplanted into the hippocampus of epileptic mice rescued handling and open field deficits
168 apillary constrictions in the hippocampus of epileptic mice than in that of normal mice, in addition
172 d epilepsy progression relative to untreated epileptic mice; the latter showing a significant and dra
175 method to identify cellular changes in human epileptic neocortex using transcriptional clustering.
184 ly temporally precise cross-area analyses of epileptic neuronal networks and find a feed-forward prop
186 amplitude and HCN1 surface expression under epileptic or normal physiological conditions are poorly
188 We demonstrate the capacity to predict the epileptic outcome in five different models of PIE, highl
189 esulted in a 90% clinical improvement in non-epileptic paroxysmal manifestations and a normalised bra
193 CTA" was significantly less frequent in male epileptic patients (0.173) than in normal males (0.305).
194 econd, we tested 20 refractory temporal lobe epileptic patients (11 women) with unilateral hippocampa
198 ha 1 subunit gene, SCN1A, were identified in epileptic patients and confirmed as causative factors of
199 y of numerous antiepileptic drugs, 20-30% of epileptic patients are pharmacoresistant with seizures n
203 btained from the laser-microdissected GCL of epileptic patients, identifying several miRNAs (miR-21-5
204 the human motor cortex in pharmacoresistant epileptic patients, we report a pattern of electroenceph
211 us mutations cause developmental defects and epileptic phenotypes, including infantile epileptic ence
214 transmission failures at BC-->GC synapses in epileptic pilocarpine-treated rats are not attributable
216 es using slices from healthy and chronically epileptic rats and find that epileptiform activity is as
218 oximal locations, i.e., closer to CA3; while epileptic rats exhibited stronger interactions at distal
220 impaired transmission at BC-->GC synapses in epileptic rats is attributable to later steps in exocyto
222 graded in this condition, we used normal and epileptic rats to examine theta activity accompanying ac
223 cholinergic fiber varicosities was higher in epileptic rats versus control rats in the inner and oute
231 her addition of cannabidiol to existing anti-epileptic regimens would be safe, tolerated, and efficac
232 of p39 and p35 in synaptic Cdk5 function and epileptic responses, arguing that cooperation between Cd
233 sal cavity and poor water solubility of anti-epileptics restrict absorption, leading to insufficient
234 monstrate the spontaneous transition between epileptic seizure and spreading depression states as the
235 d neurosurgeons using simulated and recorded epileptic seizure data to demonstrate our system's effec
238 ulti-unit computational neural mass model of epileptic seizure termination and postictal recovery was
239 tor cells causes mice to develop progressive epileptic seizure, and dramatically reduces basal synapt
246 gy and explosive dynamical transitions as in epileptic seizures and their propagations in the brain.
248 igate the brain amino acid metabolism during epileptic seizures by (18)F-FET PET and to elucidate the
250 e and fertile, and they did not manifest the epileptic seizures characteristic of the Alpl(-/-) model
252 in the development of hyperexcitability and epileptic seizures following traumatic brain injury (TBI
253 he galanin neuropeptide in the regulation of epileptic seizures has been established in animal models
254 RY ON THIS ARTICLE : Accurate forecasting of epileptic seizures has the potential to transform clinic
258 euronal death induced by proneurotrophins or epileptic seizures was assessed and compared with respon
259 ailable antagonist, JNJ-47965567, suppressed epileptic seizures well beyond the time of treatment and
260 pomas, higher incidence of pharmacoresistant epileptic seizures, and more severe neuropsychiatric dis
261 fected tissues, and in plasma in response to epileptic seizures, and point to it as biomarker of hipp
262 ing to severe neurological symptoms, such as epileptic seizures, but no specific treatment is availab
263 id 10 significantly reduced the incidence of epileptic seizures, cortical amyloid burden, and neuroin
265 e comprising severe retardation, early onset epileptic seizures, optic nerve/cerebellar atrophy, peda
266 neurodevelopmental disorder characterized by epileptic seizures, severe intellectual disability, and
267 nd manifests in an altered susceptibility to epileptic seizures, underscoring the importance of FGF-d
268 e a possible mechanism for the recurrence of epileptic seizures, which are known to be the results of
282 n that docosahexaenoic acid (DHA) attenuates epileptic seizures; however, the molecular mechanism by
284 re score (P = 0.003), and a higher number of epileptic 'spike' events (P = 0.023) than the control mi
287 tients tend to transit from non-epileptic to epileptic states more often than controls in the model.
290 h mild to severe ID, long-lasting hypotonia, epileptic susceptibility, frontal bossing, mild hypertel
291 equencing in Finnish individuals with severe epileptic syndromes, we identified pathogenic compound h
292 er a promising new avenue for effective anti-epileptic therapy for intractable pediatric epilepsy pat
293 galanin have antiepileptic actions in human epileptic tissue as well, we applied these neuropeptides
294 gical therapeutic approach, whereby resected epileptic tissue from temporal lobes of pharmacoresistan
295 iomarkers of the transformation of normal to epileptic tissue would help to stratify patients at risk
297 at, first, patients tend to transit from non-epileptic to epileptic states more often than controls i
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。