Indonesian
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
Halaman 1 dari 23 hasil
Inhibition of aconitase in astrocytes increases the sensitivity to chemical convulsants.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Although there is evidence that astrocytes support neuronal function, the contribution of astrocytes to seizure onset and termination is not known. To determine whether there are changes in seizure susceptibility or neuronal damage when the ability of astrocytes to generate ATP is reduced, 0.5 nmol
Infantile cerebellar-retinal degeneration associated with a mutation in mitochondrial aconitase, ACO2.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Degeneration of the cerebrum, cerebellum, and retina in infancy is part of the clinical spectrum of lysosomal storage disorders, mitochondrial respiratory chain defects, carbohydrate glycosylation defects, and infantile neuroaxonal dystrophy. We studied eight individuals from two unrelated families
Mitochondrial complex I inhibition in cerebral cortex of immature rats following homocysteic acid-induced seizures.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
The major finding of the present study concerns the marked decrease of respiratory chain complex I activity in the cerebral cortex of immature rats following seizures induced by bilateral intracerebroventricular infusion of dl-homocysteic acid (600 nmol/side). This decrease was already evident
Age dependence of seizure-induced oxidative stress.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
The mechanisms underlying the decreased vulnerability of the immature brain to seizure-induced neuronal death remain unknown. We asked whether oxidative stress plays a role in the resistance of immature animals to seizure-induced brain damage. Mitochondrial aconitase inactivation and
Fluorocitrate-mediated astroglial dysfunction causes seizures.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
A role for astroglia in epileptogenesis has been hypothesised but is not established. Low doses of fluorocitrate specifically and reversibly disrupt astroglial metabolism by blocking aconitase, an enzyme integral to the tricarboxylic acid cycle. We used cerebral cortex injections of fluorocitrate,
Enhanced hippocampal F2-isoprostane formation following kainate-induced seizures.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
We attempted to obtain evidence for the occurrence of oxidant injury following seizure activity by measuring hippocampal F2-isoprostanes (F2-IsoPs), a reliable marker of free radical-induced lipid peroxidation. Formation of F2-IsoPs esterified in hippocampal phospholipids was correlated with
Mitochondrial dysfunction and oxidative stress: cause and consequence of epileptic seizures.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Mitochondrial dysfunction has been implicated as a contributing factor in diverse acute and chronic neurological disorders. However, its role in the epilepsies has only recently emerged. Animal studies show that epileptic seizures result in free radical production and oxidative damage to cellular
Mitochondrial oxidative stress and increased seizure susceptibility in Sod2(-/+) mice.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Epileptic seizures can occur as a result of mitochondrial dysfunction. Mitochondria have vital functions such as energy generation, control of cell death, neurotransmitter synthesis, and free radical production. Which of these critical mitochondrial functions contributes to epileptic seizures is
The role of astrocytes in seizure generation: insights from a novel in vitro seizure model based on mitochondrial dysfunction.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Approximately one-quarter of patients with mitochondrial disease experience epilepsy. Their epilepsy is often severe and resistant towards conventional antiepileptic drugs. Despite the severity of this epilepsy, there are currently no animal models available to provide a mechanistic understanding of
Mitochondrial dysfunction associated with neuronal death following status epilepticus in rat.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Status epilepticus (SE) in humans and animal models results in significant cerebral damage and an increased risk of subsequent seizures, associated with a characteristic pattern of neuronal loss particularly affecting the hippocampus. Seizure related cell death is considered to be excitotoxic, but
Calcium gluconate and sodium succinate for therapy of sodium fluoroacetate experimental intoxication in cats: clinical and electrocardiographic evaluation.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Sodium fluoroacetate (SFAC) or Compound 1080 is a potent rodenticide, largely used after 1946 for rodent and home pest control. The toxic effects of SFAC are caused by fluorocitrate action, a toxic metabolite, which has a competitive action with aconitase enzyme, leading to citrate accumulation and
Levetiracetam: antiepileptic properties and protective effects on mitochondrial dysfunction in experimental status epilepticus.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
OBJECTIVE
To assess the anticonvulsant activity of the novel antiepileptic drug, levetiracetam (LEV) in a model of self-sustaining limbic status epilepticus, and to measure the consequence of LEV treatment on the pattern of mitochondrial dysfunction known to occur after status epilepticus
The expanding clinical spectrum of mitochondrial diseases.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
The mitochondrion is the only extranuclear organelle containing DNA (mtDNA). As such, genetically determined mitochondrial diseases may result from a molecular defect involving the mitochondrial or the nuclear genome. The first is characterized by maternal inheritance and the second by Mendelian
Clinical, radiological, and genetic characteristics of 16 patients with ACO2 gene defects: Delineation of an emerging neurometabolic syndrome.
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Mitochondrial aconitase is the second enzyme in the tricarboxylic acid (TCA) cycle catalyzing the interconversion of citrate into isocitrate and encoded by the nuclear gene ACO2. A homozygous pathogenic variant in the ACO2 gene was initially described in 2012 resulting in a novel disorder termed
Expanding the clinical and phenotypic heterogeneity associated with biallelic variants in ACO2
Hanya pengguna terdaftar yang dapat menerjemahkan artikel
Masuk daftar
Objective: We describe the clinical characteristics and genetic etiology of several new cases within the ACO2-related disease spectrum. Mitochondrial aconitase (ACO2) is a nuclear-encoded tricarboxylic acid cycle enzyme. Homozygous
Database tanaman obat terlengkap yang didukung oleh sains
- Bekerja dalam 55 bahasa
- Pengobatan herbal didukung oleh sains
- Pengenalan herbal melalui gambar
- Peta GPS interaktif - beri tag herba di lokasi (segera hadir)
- Baca publikasi ilmiah yang terkait dengan pencarian Anda
- Cari tanaman obat berdasarkan efeknya
- Atur minat Anda dan ikuti perkembangan berita, uji klinis, dan paten
Ketikkan gejala atau penyakit dan baca tentang jamu yang mungkin membantu, ketik jamu dan lihat penyakit dan gejala yang digunakan untuk melawannya.
* Semua informasi didasarkan pada penelitian ilmiah yang dipublikasikan
