Publications by authors named "Zhao-fu Chi"

Sirtuin 1 (SIRT1) regulates numerous neuronal processes, including metabolism, antioxidation and aging, through activation of peroxisome proliferator-activated receptor coactivator 1-α (PGC-1α), an upstream regulator of mitochondrial biogenesis and function. However, the role of SIRT1 in the oxidative stress induced by seizures has yet to be elucidated. The present study aimed to investigate whether SIRT1 was involved in the activation of the PGC-1α/mitochondrial antioxidant system following status epilepticus (SE) in rats.

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Article Synopsis
  • * In a study with immature rats, kainic acid (KA) was used to induce SRS, resulting in learning and memory deficits, reduced anxiety, and increased movement compared to control groups.
  • * Analysis showed that specific proteins (synaptophysin, SNAP-25, and synaptotagmin 1) decreased in expression in rats with SRS, indicating a potential link between these changes and the observed behavioral deficits.*
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Background: Familial cerebral cavernous malformations (CCMs), characterized by hemorrhagic stroke, recurrent headache and epilepsy, are congenital vascular anomalies of the central nervous system. Familial CCMs is an autosomal dominant inherited disorder and three CCM genes have been identified. We report a Chinese family with CCMs and intend to explore clinical, pathological, magnetic resonance imaging (MRI) features and pathogenic gene mutation of this family.

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The aim of this study was to investigate the value of T(2) (*)-weighted gradient echo imaging (GRE T(2) (*)-WI) for the detection of familial cerebral cavernous malformation (FCCM). Twenty-six members of 2 families with FCCM were examined using computed tomography (CT), conventional magnetic resonance imaging (MRI) and GRE T(2) (*)-WI sequences. We identified 12 cases of FCCM using GRE T(2) (*)-WI sequences.

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Resveratrol is indicated to be involved in neuroprotection and anti-inflammation in epileptic rats. The molecular mechanism is still not fully understood. In this study, we investigated the role of resveratrol in nuclear factor-kappa B associated inflammatory responses induced by status epilepticus.

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"Baicalin, a major flavonoid compound isolated from the dry roots of Scutellaria baicalensis Georgi, has been shown to be neuroprotective after ischemic brain injury. However, little is known about its effects on brain injury following intracerebral hemorrhage (ICH). In this study, we evaluated the effects of baicalin on ICH-induced brain injury in an ICH rat model.

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Objective: Alternating hemiplegia of childhood (AHC) is a rare and intractable disorder. The etiology and standard therapy of AHC remain unknown. The long-term effects of flunarizine or topiramate on patients with AHC are still not clear.

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Background: Toll-like receptors 2 (TLR2) and TLR4 are involved in the microglia-mediated inflammatory response, Aβ plaque formation and Aβ clearance in Alzheimer's disease (AD). Our previous studies have shown that variants in the TLR2 and TLR4 genes are associated with the risk of AD. Therefore, we hypothesize that there may be significant changes in TLR2 and TLR4 expressions on peripheral blood mononuclear cells (PBMCs) from patients with AD when compared to healthy control subjects.

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Objectives: Diffuse brain injury (DBI) has been shown to increase the proliferation of granule cell precursors in the adult dentate gyrus (DG). However, the mechanism by which DBI-induced cell proliferation in the DG may enhance seizure susceptibility remains largely unknown.

Materials And Methods: Using bromodeoxyuridine (BrdU) immunohistochemistry, we examined the effects of group II metabotropic glutamate receptor (mGluR) agonist, 2R,4R-4-aminopyrrolidine-2,4-dicarboxylate (2R,4R-APDC), on cell proliferation in the DG after DBI.

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Apoptosis and autophagy are common physiological and pathological processes in the human body. Death-associated kinase protein 1 (DAPK1), which participates in the process of cell death, has attracted people's attention for its potential risk with late-onset Alzheimer's disease (LOAD). A recent study identified two single nucleotide polymorphisms (SNPs) in DAPK1 that show significant association with LOAD in Caucasians.

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Delayed encephalopathy following carbon monoxide poisoning is a serious complication. Here, we report a patient with delayed encephalopathy who suffered from cognitive disorders and urinary incontinence after a temporal normal period of 15 days after acute intoxication, and his cognitive function recovered gradually following donepezil hydrochloride treatment. Now, he can undertake slight farming work.

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Temporal lobe epilepsy (TLE), characterized by spontaneous recurrent seizure (SRS), is associated with behavioural problems, but the underlying molecular mechanisms have not been clearly identified. In the present study, kainic acid (KA) was administered systemically in adult male Wistar rats to induce SRS. Behavioural performance analyses at 2, 4, and 6 weeks post-status epilepticus (post-SE) showed spatial learning memory deficit, anxiety and increased locomotor activity in rats with long-term SRS compared with rats without SRS after normal saline (NS) or KA-valproate (KA-VPA) treatment.

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Objective: To observe the clinical effect and security of Sanqi Tongshu capsule in treating ischemic strkoe.

Method: A multicenter, no dummy, open labeled clincal trail was conducted. 1 753 patient were enrolled in this clinical trial.

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Carbon monoxide (CO)-induced delayed neuron damage is the serious complication, but the underlying mechanisms are poorly understood. This study was designed to investigate the time-dependent changes of the lipid peroxidation (malondialdehyde, MDA) and antioxidative status (glutathione, GSH; glutathione peroxidase, GSH-Px; glutathione reductase, GR; and anti-reactive oxygen species anti-ROS) in nerve tissues for the possible mechanisms exploration. Adult rats were treated with CO by peritoneal injection, and sacrificed after day 0, 1, 3, 7, 14 and 21 of treatment.

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Background: Glutathione S-transferases (GSTs) play an important role in metabolizing anti-epileptic drugs (AEDs) in liver. Expressions of GSTs in brain, which may result in poor efficacy of AEDs, have not been well studied. Using clinical cortex specimen from 32 intractable epileptic subjects and 8 non-epileptic controls, the present study investigated the correlation between GSTs and intractable epilepsy.

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Approximately 20-30% of patients with epilepsy continue to have seizures despite carefully monitored treatment with antiepileptic drugs. The mechanisms that underlie why some patients are responsive and others prove resistant to antiepileptic drugs are poorly understood. Increasing evidence supports a role for altered mitochondrial function in the pathogenesis of epilepsy.

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This study investigated the effects of group II metabotropic glutamate receptor agonist, 2R, 4R-4-aminopyrrolidine-2,4-dicarboxylate (2R, 4R-APDC), on cell proliferation in the dentate gyrus of adult rats. 2R, 4R-APDC at a dose of 1 and 10 nmol/day resulted in decreased bromodeoxyuridine immunoreactive cells in the dentate gyrus. In addition, we found that APDC treatment had no effect on the number of BrdU+ and GFAP(+)-labeled cells or BrdU+ and NeuN(+)-labeled cells compared with controls.

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3-Aminobenzamide (3-AB), an inhibitor of poly(ADP-ribose) polymerase (PARP), has been proved to have neuroprotective properties. In this study, we examined the role of 3-AB in rat hippocampal neuron death induced by seizures. Our data showed that the seizures resulted in PARP activation and translocation of the apoptosis-inducing factor from the mitochondria to the nucleus, leading to neuron death.

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Mitochondrial dysfunction has been implicated as a contributing factor in epileptic seizures. Present studies were carried out to decipher seizure-dependent changes in mitochondrial function and ultrastructure in the chronic condition of temporal lobe epilepsy (TLE) induced by pilocarpine in rat hippocampus. Enzyme assay revealed significant depression of the activity of mitochondrial- and nuclear-encoded cytochrome oxidase (COX).

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