Dynamic changes of TrkB gene expression in Streptococcus pneumoniae meningitis after treatment with antibiotics and dexamethasone.

Background: Although more and more new potent antibiotics have been used, the incidence of neurological sequelae of Streptococcus pneumoniae meningitis has not improved in children over the last decade. The expression of TrkB mRNA, a receptor of brain-derived neurotrophic factor, is associated with the incidence of neurological sequelae of Streptococcus pneumoniae meningitis.

Methods: Rats of 3 weeks old were used to construct a model of Streptococcus pneumoniae meningitis and served as normal controls.

Novel chloride channel gene mutations in two unrelated Chinese families with myotonia congenita.

Myotonia congenita (MC) is a genetic disease characterized by mutations in the muscle chloride channel gene (CLCN1). To date, approximately 130 different mutations on the CLCN1 gene have been identified. However, most of the studies have focused on Caucasians, and reports on CLCN1 mutations in Chinese population are rare.

The role of an Ommaya reservoir in the management of children with cryptococcal meningitis.

Cryptococcal meningitis is the most common life-threatening fungal infection and is associated with high mortality in children. Amphotericin B plus flucytosine and fluconazole is the optimal current therapy. Implantation of an Ommaya reservoir for intraventricular infusion of medication and aspiration of cerebrospinal fluid (CSF) for the treatment of increased intracranial pressure (ICP) has been reported.

Wilson disease: identification of two novel mutations and clinical correlation in Eastern Chinese patients.

Aim: To study mutations in the P-type ATPase (ATP7B) gene responsible for Wilson disease (WD) in the Eastern Chinese population, and the possible correlation of specific mutations with clinical characteristics.

Methods: Mutations of the ATP7B gene were sought by means of direct sequencing in 50 Eastern Chinese WD patients of Han ethnic origin.

Results: Two novel mutations, Asp96Gly and Asp196Glu, were first identified.

Brain-derived neurotrophic factor rescues neurons from bacterial meningitis.

Mortality and neurologic deficits still occurs frequently following bacterial meningitis in children, despite antibiotic treatment. We investigated the neuroprotective effects of brain-derived neurotrophic factor (BDNF) on brain neurons in bacterial meningitis. The rat model of bacterial meningitis and a normal rat model were developed.

Neuroprotective effects of brain-derived neurotrophic factor (BDNF) on hearing in experimental pneumococcal meningitis.

Bacterial meningitis is still one of the most common causes of acquired profound sensorineural deafness in children despite antibiotic treatment. We investigated the neuroprotective effects of brain-derived neurotrophic factor on hearing function in experimental bacterial meningitis. We implanted stainless steel tubes into both cerebral ventricles of Sprague-Dawley rats aged 21 days.

Activation of ATP-sensitive potassium channels prevents the cleavage of cytosolic mu-calpain and abrogates the elevation of nuclear c-Fos and c-Jun expressions after hypoxic-ischemia in neonatal rat brain.

The purpose of this study was to determine whether activation of ATP-sensitive K+ (KATP) channels with diazoxide (DIZ) is able to prevent the cleavage of cytosolic mu-calpain and abrogate the elevation of nuclear c-Fos and c-Jun protein (c-Fos, c-Jun) expressions after hypoxic-ischemia (HI) in brain. The model of hypoxic-ischemic brain injury (HIBI) was made in the 7-day-old Sprague-Dawley (SD) rats by left carotid arterial ligation and hypoxia (8% oxygen). DIZ was injected into the left lateral ventricle (5 microl, 1 mg/ml) before or post-hypoxic-ischemia (HI) insults.

Effect of diazoxide on regulation of vesicular and plasma membrane GABA transporter genes and proteins in hippocampus of rats subjected to picrotoxin-induced kindling.

Epileptiform discharges and behavioral seizures may be the consequences of excess excitation from inadequate inhibitory effects associated with gamma-aminobutyric acid (GABA). GABA is taken up and accumulated in synaptic vesicles by the action of vesicular GABA transporter (VGAT) before its release into the synaptic cleft, and removed from synaptic regions by the action of transporter proteins GABA transporter-1 (GAT-1) and GABA transporter-3 (GAT-3). In this experiment, the effects of diazoxide (DIZ) on the VGAT, GAT-1 and GAT-3 mRNA and protein levels in hippocampus, and on the seizure activities of picrotoxin (PTX)-induced kindling rats were observed.

[Time-course of mu-calpain activation, c-Fos, c-Jun, HSP70 and HSP27 expression in hypoxic-ischemic neonatal rat brain].

Objective: The cascade of physiological events underlying hypoxic-ischemic brain damage (HIBD) remains to be fully established. The perinatal brain shows both an increased tolerance to hypoxic-ischemic (HI) injury and a faster and more complete recovery than the adult. It is, therefore, important to understand the sequence of events following hypoxia and ischemia in young animals.

Regulation of brain-derived neurotrophic factor (BDNF) expression following antibiotic treatment of experimental bacterial meningitis.

Although more and more new potent antibiotics have been used, mortality and neurologic deficits still occur frequently following bacterial meningitis in children. In this article, the expression of brain-derived neurotrophic factor messenger ribonucleic acid (RNA) and its production in the brains of rats were investigated during the course of experimental bacterial meningitis and after treatment with an antibiotic plus dexamethasone. In the brains of Streptococcus pneumoniae-inoculated rats, brain-derived neurotrophic factor (BDNF) messenger RNA was obviously up-regulated after inoculation for 24 hours (P < .

Electro-acupuncture preconditioning abrogates the elevation of c-Fos and c-Jun expression in neonatal hypoxic-ischemic rat brains induced by glibenclamide, an ATP-sensitive potassium channel blocker.

This study aimed to clarify the neuroprotective mechanism of electro-acupuncture (EA) preconditioning on hypoxic-ischemic brain injury (HIBI). Using Western blot, the expression of c-fos protein (c-Fos) and c-jun protein (c-Jun) induced by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker was examined from cerebral cortical and hippocampal samples in neonatal hypoxic-ischemic rats, with or without EA preconditioning. EA was performed on Hegu (LI4), a well-known acupoint commonly used in Oriental medicine for the treatment of neuronal injury resulting from hypoxia-ischemia (HI).

[Possible mechanism of electroacupuncture preconditioning for hypoxia/ischemic brain injury protection effect in neonatal rats].

Objective: To explore the possible mechanism of electroacupuncture preconditioning (EAPC) and combined with ATP-sensitive potassium channel (KATP) blocker preconditioning for hypoxia/ischemic brain injury protection by observing the changes of the immediate genes (c-fos and c-jun protein content) in brain at the early stage after cerebral hypoxia/ischemic injury, and the effect of EAPC on these changes.

Methods: Integrated density (ID) of c-fos and c-jun expression was measured by Western blot and computerized image processing.

Results: Hypoxia/ischemia could induce c-fos and c-jun protein in both cerebral cortex and hippocampus simultaneously, with the peak appearing 2-4 hrs later, and the expression in hyppocampus was higher than that in cortex.

[Expression of brain-derived neurotrophic factor at acute inflammatory injury of the brain].

Objective: To investigate the expression of brain-derived neurotrophic factor (BDNF) mRNA and immunoreactivity in experimental acute inflammatory brain injury.

Methods: Ten rats were inoculated with pneumococcus to establish the model of bacterial inflammatory brain injury and other 6 rats were used as normal controls. At 24 h after inoculating, the expression of BDNF mRNA and BDNF protein in brain tissue was detected by in situ hybridization and immunohistochemical methods, respectively.

[A case-control study of risk factors for childhood cerebal palsy].

OBJECTIVE: To identify possible risk factors for cerebral palsy (CP) in children. METHODS: A Population-based survey was conducted (including 92 CP cases) in 66 townships of 15 cities of Zhejiang Province from October to November, 1998. 184 of matched controls were selected for comparison.