Animals ; Antibodies, Helminth ; blood ; cerebrospinal fluid ; Child, Preschool ; Eosinophilia ; cerebrospinal fluid ; diagnosis ; etiology ; Female ; Humans ; Meningitis ; cerebrospinal fluid ; diagnosis ; etiology ; Neurocysticercosis ; complications ; drug therapy ; parasitology ; Taenia ; immunology

Objective To determine if there is an early developmental resistance to seizure-induced hi ppocampal damage. Methods Five daily pentylenetetrazol-indu ced convulsions in immature rats beginning at postnatal day P10,P60 groups.In b oth groups, the latency of seizure, the latency of Ⅳ/Ⅴ grade, the lasting time of seizure and mortality of rats after seizure were used to measure sensitivity of seizure or the resistance to brain damage. Conventional histopathological me thod was utilized to observe morpbological changes and cell counting of dentate granule cells, CA 3,CA 1 and hilar neurnns. Timm histochemical technique was a dopted to study mossy fiber sprou- ting.Results 1.In the both groups(P10,P60),there were significant differences in the latency of seizure (1.07?0.55 vs 8.27?1.48 P

Objective Study the ideal drug to treat age depen de nt epileptic ncephalopathy (ADEE) in earlier period. Methods fi fty-four patients with ADEE were studyed.21 cases used with single topiramate(T PM) as initial treatment and 27 cases used with TPM and antiepileptic drug(AEDs ) .Results Seizure was fully controlled in 11 patients with TPM m onotherapy and in 4 patients with TPM as adjunction.The differences was signif icant(P

Adult ; Aged ; Cervical Intraepithelial Neoplasia ; pathology ; surgery ; Cervix Uteri ; pathology ; surgery ; Conization ; methods ; Female ; Follow-Up Studies ; Humans ; Hysterectomy ; methods ; Middle Aged ; Neoplasm Recurrence, Local ; Neoplasm, Residual ; pathology ; surgery ; Uterine Cervical Neoplasms ; pathology ; surgery

Arsenic Poisoning ; diagnosis ; Humans ; Occupational Diseases ; diagnosis ; Occupational Exposure ; adverse effects

OBJECTIVETo explore the effect of Shenxiong Huayu Capsule (SHC) on the cerebral ischemia-reperfusion (IR) injury and the expression of growth associated protein 43 (GAP43) after total cerebral IR in the hippocampal CA1 region of rats.

METHODSTotally 100 male adult SD rats were randomly divided into five groups, i.e., the control group, the model group, the group A (by taking SHC once daily), the group B (by taking SHC twice daily), and the group C (by taking SHC thrice daily), 20 in each group. The total IR model was prepared by improved Pulsinelli's 4-vessel occlusion method. Morphological changes of the hippocampal CA1 region were observed by HE staining at day 1, 3, 7, and 14. The expression of GAP43 in the hippocampal CA1 region was detected using immunohistochemical assay at day 1, 3, 7, and 14. Meanwhile, the behavioral score was determined. The expression of GAP43 in the hippocampal CA1 region was detected using Western blot at day 14.

RESULTSCompared with the control group, the expression of GAP43 increased in the model group, the behavioral score was elevated, degenerated neurons increased, and survival neurons decreased in the model group (all P < 0.05). Compared with the model group, the expression of GAP-43 increased (with the most significant difference seen in the group C, P < 0.01), the behavioral score significantly decreased, degenerated neurons decreased, and survival neurons increased in each HSC group (all P < 0.05). Survival neurons obviously increased at day 14, of which, most number of survival neurons and highest contents of GAP43 protein could be seen in the group C, showing statistical difference when compared with those of the group A and the group B (P < 0.01).

CONCLUSIONSHC had protective effect on total cerebral IR in the hippocampal CA1, which might be associated with increased expression of GAP43.

Animals ; Brain Ischemia ; metabolism ; CA1 Region, Hippocampal ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; GAP-43 Protein ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism

This study is to investigate the effects of sophoridine on NF-kappaB signaling pathway in kidney tissue of endotoxemia mice and the mechanism involved. BALB/c mice were challenged with lipopolysaccharide (LPS) caudal vein injection, then sophoridine was administered by intraperitoneal injection. Totally 50 mice were divided into 5 groups: control group, LPS model group, sophoridine treatment 12 mg x kg(-1) group, 6 mg x kg(-1) group and 3 mg x kg(-1) group. All animals were sacrificed at 6 hours after treatment. Kidney and blood samples were harvested. IKKbeta mRNA and TNF-alpha mRNA expression of renal tissue was measured by the reverse transcription polymerase chain reaction (RT-PCR), and phosphorylation IKKbeta protein (pIKKbeta) was detected by immunohistochemistry. NF-kappaB P65 protein expression and distribution of renal tissue were observed by Western blotting and immunofluorescence laser confocal microscopy. Serum TNF-alpha level was detected by radioimmunoassay. The results showed that the sophoridine significantly reduced the expression of IKKbeta mRNA and pIKKbeta protein, and inhibited the expression of NF-kappaB P65 protein and decreased the entry nuclear rate of NF-kappaB P65 in the renal tissue of endotoxemia mice. Thereby the renal TNF-alpha mRNA expression and serum TNF-alpha level were significantly reduced. These results suggest that sophoridine could inhibit inflammatory reaction induced by LPS through inhibiting activation of NF-kappaB signaling pathway.

Objective To observe age-dependent feature of damage of hippocampus to different maturational stages rats after kindling repeated seizures.Methods The effects of 5 daily pentylenetetrazol-induced convulsions in different rats beginning at postnatal day 10,20,60(P10,P20,P60)were evaluated.In the 3 groups,Thionin staining method was utilized to observe morphological changes and cell counting of dentate granule cells,CA3,CA1,and hilar neurons.Timm's method of silver sulfide staining was adopted to observe the mossy fiber sprouting.Results 1.Cell counting of CA1,CA3 and hilar neurons in P10 and P20 groups demonstrated no differences from controls in rats,whereas P60 with daily seizures had a significant decrease in CA1,CA3 neurons(8.22?1.88,5.62?1.68 vs 6.31?1.50,3.62?1.40)(t=2.246,2.587 Pa

Humanities education in military medical university must have military feature in mind.According to special military demand, this education should combine teaching with military historical tradition, historical task, construction of curricula set-up system, and the reality of military campus culture construction to make this education have pertinence.

OBJECTIVETo evaluate the effects of prenatal stress on neurological functions after middle cerebral artery occlusion (MCAO) in adult offspring rats.

METHODSPregnant rats were randomly assigned to prenatal stress treatment, which was exposed to restraint three times daily in the last week of pregnancy, and no prenatal stress treatment. Adult male offspring rats were subjected to transient focal cerebral ischemia by MCAO. They were randomly divided into four groups: sham group, prenatal stress + sham group, MCAO group and prenatal stress + MCAO group (n = 10). After 24 hours of reperfusion, the neurological deficits were evaluated. The infarct size, cell apoptosis and expression of Caspase 3, cleaved Caspase 3 and Bcl-2 were detected.

RESULTSCompared with MCAO group, the neurological deficits, infarct size and apoptotic cells in prenatal stress + MCAO group were increased significantly (all P < 0.05). The expressions of Caspase 3 and cleaved Caspase 3 were much greater in prenatal stress + MCAO group than those of MCAO group, while the expression of Bcl-2 was significantly decreased in prenatal stress + MCAO group compared with MCAO group (all P < 0.05).

CONCLUSIONPrenatal stress might exacerbate neuroloeical deficits in the offspring rats after MCAO by increasing cell apoptosis.

Animals ; Apoptosis ; Caspase 3 ; metabolism ; Female ; Infarction, Middle Cerebral Artery ; physiopathology ; Ischemic Attack, Transient ; physiopathology ; Male ; Pregnancy ; Prenatal Exposure Delayed Effects ; physiopathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stress, Physiological