[Characteristics of continuous spike-and-wave during slow wave sleep syndrome in children].

Objective: Continuous spike-and-wave during slow wave sleep (CSWS) syndrome is one of the presentations of electrical status epilepticus during sleep (ESES). The purpose of this study was to investigate the characteristics of CSWS syndrome in children.

Methods: Between 2007 and 2009, a total of 778 nocturnal long-term or 24-hr video-EEG records were included.

Roles of astrocytes and microglia in seizure-induced aberrant neurogenesis in the hippocampus of adult rats.

Recent evidence showed that epileptic seizures increase hippocampal neurogenesis in the adult rat, but prolonged seizures result in the aberrant hippocampal neurogenesis that often leads to a recurrent excitatory circuitry and thus contributes to epileptogenesis. However, the mechanism underlying the aberrant neurogenesis after prolonged seizures remains largely unclear. In this study, we examined the role of activated astrocytes and microglia in the aberrant hippocampal neurogenesis induced by status epilepticus.

Thirteen-year follow-up of patients with tri-ortho-cresyl phosphate poisoning in northern suburbs of Xi'an in China.

Based on reports published so far, organophosphorus (OP) compounds do remarkable harm to human health. In 1995 there was an outbreak of organophosphorus-ester induced delayed neuropathy (OPIDN) due to tri-ortho-cresyl phosphate (TOCP) poisoning in northern suburbs of Xi'an in China. The 74 affected patients were treated and followed up after definite diagnosis.

Heterogeneous expression of the voltage-gated calcium channel alpha2 subunit and the voltage-gated sodium channel alpha subunit in chicken spinal motoneurons.

The localization of the voltage-gated calcium channel (VGCC) alpha2 and the voltage-gated sodium channel (VGSC) alpha subunits was immunohistochemically investigated in chicken spinal motoneurons. Approximately 83% and 46% of spinal motoneurons were positive for VGCCalpha2 and VGSCalpha subunits, respectively. Almost all VGSCalpha subunit-positive motoneurons exhibited the VGCCalpha2 subunit immunoreactivity.

Erythropoietin pre-treatment prevents cognitive impairments following status epilepticus in rats.

Selective neuronal loss is closely associated with cognitive impairments that occur following status epilepticus (SE). Our previous study suggested that erythropoietin (Epo) pre-treatment suppressed hippocampal neuronal death in rats after 1 h of SE convulsions. However, the underlying protective mechanism remained unclear.

Up-regulation of D-serine might induce GABAergic neuronal degeneration in the cerebral cortex and hippocampus in the mouse pilocarpine model of epilepsy.

Epilepsy is a serious neurological disorder with neuronal loss and spontaneous recurrent seizures, but the neurochemical basis remains largely unclear. We hypothesize that D-serine, a newly identified endogenous co-agonist of N-methyl-D-aspartate (NMDA) receptor, may trigger excitotoxicity and neuronal damage in epileptogenesis. By using a mouse pilocarpine model, immunohistochemistry, Fluoro-Jade staining and double-labeling, the present study revealed up-regulation of D-serine expression in a proportion (41%) of neurons in the cerebral cortex and hippocampus.

Time-course of neuronal death in the mouse pilocarpine model of chronic epilepsy using Fluoro-Jade C staining.

Epilepsy is a serious neurological disorder in human beings and the long-term pathological events remain largely obscure. We are interested in elucidating long-term brain injury that may occur in the temporal lobe epilepsy, and time-course of neuronal death was examined in a mouse pilocarpine model of chronic epilepsy by Fluoro-Jade C (FJC) dye that can specifically stain the degenerative neurons in the central nervous system. The FJC stain combined with immunohistochemistry to neuronal nuclear specific protein revealed that pilocarpine-induced status epilepticus (SE) resulted in massive degenerative death of neuronal cells in brains with their dense distribution in the cerebral cortex and hippocampus.

Activation of cerebral peroxisome proliferator-activated receptors gamma exerts neuroprotection by inhibiting oxidative stress following pilocarpine-induced status epilepticus.

Status epilepticus (SE) can cause severe neuronal loss and oxidative damage. As peroxisome proliferator-activated receptor gamma (PPARgamma) agonists possess antioxidative activity, we hypothesize that rosiglitazone, a PPARgamma agonist, might protect the central nervous system (CNS) from oxidative damage in epileptic rats. Using a lithium-pilocarpine-induced SE model, we found that rosiglitazone significantly reduced hippocampal neuronal loss 1 week after SE, potently suppressed the production of reactive oxygen species (ROS) and lipid peroxidation.

Immunohistochemical demonstration of the calcium channel alpha2 subunit in the chicken dorsal root ganglion and spinal cord: a special reference to colocalization with calbindin-D28k in dorsal root ganglion neurons.

We used immunohistochemical methods to examine the distribution of the calcium channel alpha2 (CCalpha2) subunit in the chicken spinal cord and dorsal root ganglion (DRG) neurons and determine its relationship with calbindin-D28k (CB) in the DRG neurons. In the spinal cord, CCalpha2 subunit was detected in nerve terminals, which were observed as dot-like structures, and in laminae I, II, III and Lissauer's tract in the dorsal horn. In the DRG neurons, approximately 65% of the total neurons were CCalpha2 subunit positive, and most (86%) of these neurons were small to medium sized, suggesting that the CCalpha2 subunit and/or a complex of the CCalpha2 and delta subunits is possibly localized in a number of nociceptive neurons.

Topiramate reduced sweat secretion and aquaporin-5 expression in sweat glands of mice.

Decreased sweat secretion is a primary side effect of topiramate in pediatric patients, but the mechanism underlying this effect remains unclear. This study aimed to better understand how topiramate decreases sweat secretion by examining its effect on the expression of carbonic anhydrase (CA) II and aquaporin-5 (AQP5), total CA activity, as well as on tissue morphology of sweat glands in mice. Both developing and mature mice were treated with a low (20 mg/kg/day) and high dose (80 mg/kg/day) of topiramate for 4 weeks.

[Correlation between hippocampal mossy fiber sprouting and synaptic reorganization and mechanisms of temporal lobe epilepsy].

Objective: To explore the effects of the ultrastructural features of sprouted mossy fiber synapses in the mechanism of temporal lobe epilepsy. To explore the correlation between axon guidance molecule-netrin-1 gene expression and mossy fiber synaptic reorganization.

Methods: Sixty-one SD rats underwent intraperitoneal injection of lithium chloride and pilocarpine to establish models of status epilepticus characterized with temporal lobe epilepsy.

Postnatal expression and denervation induced up-regulation of aquaporin-5 protein in rat sweat gland.

The evolution of aquaporin-5 (AQP5) expression during postnatal development has not been defined in the sweat gland. Previous studies have suggested that AQP isoforms in several peripheral targets are regulated by a neural mechanism. We have examined, in rat sweat glands, the expression of AQP5 during postnatal development and the effects of denervation on AQP5 expression.

Erythropoietin preconditioning on hippocampus neuronal apoptosis following status epilepticus induced by Li-pilocarpine in rats through anti-caspase-3 expression.

Unlabelled: Selective neuronal loss following status epilepticus (SE) was first described just under 100 years ago. The acute pathology following SE was shown to be 'ischemic cell change' and was assumed to arise through hypoxia/ischemia. Recently, erythropoietin (Epo) has been shown to have potent anti-apoptosis activity in central nervous system neurons in animal models of ischaemic injury.

(-)-Epigallocatechin gallate inhibits lipopolysaccharide-induced microglial activation and protects against inflammation-mediated dopaminergic neuronal injury.

Microglial activation is believed to play a pivotal role in the selective neuronal injury associated with several neurodegenerative disorders, including Parkinson's disease (PD) and Alzheimer's disease. We provide evidence that (-)-epigallocatechin gallate (EGCG), a major monomer of green tea polyphenols, potently inhibits lipopolysaccharide (LPS)-activated microglial secretion of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) through the down-regulation of inducible NO synthase and TNF-alpha expression. In addition, EGCG exerted significant protection against microglial activation-induced neuronal injury both in the human dopaminergic cell line SH-SY5Y and in primary rat mesencephalic cultures.

Topiramate therapy for paroxysmal kinesigenic choreoathetosis.

We observed the clinical efficacy of topiramate for paroxysmal kinesigenic choreoathetosis (PKC). Topiramate was administered as a monotherapy with titrated dosages to 8 patients with PKC. Target daily dose of topiramate was 100 to 200 mg; the follow-up period ranged from 8 months to 2 years.

Effects of nitric oxide on dentate gyrus cell proliferation after seizures induced by pentylenetrazol in the adult rat brain.

Epileptic seizures have been shown to increase the proliferation of granule cell precursors in the adult brain, but the underlying mechanisms remain largely unknown. This study examined the effect of nitric oxide (NO) on the proliferation of granule cell precursors in adult rats after pentylenetrazol (PTZ)-induced generalized clonic seizures. Using systemic bromodeoxyuridine (BrdU) to label dividing cells, we found that injection of the neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (50 mg/kg i.

Ionotropic glutamate receptor antagonists inhibit the proliferation of granule cell precursors in the adult brain after seizures induced by pentylenetrazol.

Seizures have been shown to promote the proliferation of granule cell precursors in the adult brain, but the underlying mechanisms remain largely unknown. Using systemic bromodeoxyuridine (BrdU) to label dividing cells, we examined the effects of selective ionotropic glutamate receptor antagonists on granule cell precursor proliferation in adult rats after pentylenetrazol (PTZ)-induced generalized clonic seizures. We found that the NMDA receptor antagonist MK-801 significantly inhibited behavioral and EEG seizures and completely blocked seizure-induced increase in the number of BrdU-labeled cells in the dentate gyrus.

Dentate granule cell neurogenesis after seizures induced by pentylenetrazol in rats.

Epileptic seizures originating from the limbic system have been shown to stimulate the proliferation rate of granule cell precursors in the adult brain, but it is not clear if other type(s) of seizures have the similar effects. This study examined the effects of pentylenetrazol (PTZ)-induced generalized clonic seizures on dentate granule cell neurogenesis in adult rats. Using systemic bromodeoxyuridine (BrdU) to label dividing cells, we studied the proliferation rate of neural precursor cells in the dentate gyrus at various time points after PTZ-induced seizures.

[Assessment of autonomic nervous function during orthostatic stress in pilots with history of syncope].

Objective: To assess the role of autonomic nervous function during orthostatic tolerance tests (OTT) in pilots with history of G-induced loss of consciousness (G-LOC) or vasovagal syncope (VVS).

Method: The relation between heart rate variability (HRV) and outcome of OTT result were compared among 3 groups of cases: 1) 30 patients with history of syncope and positive OTT as patient group (PG); 2) 20 cases with history of syncope but negative OTT result as negative group (NG); 3) 15 age-, sex-, flight plane model-, flight time-matched healthy pilots as healthy control (HC). OTT results and HRV, heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) before and after OTT and their time and frequency domain were compared and analyzed among the three groups.