Objective To investigate the effects of normobaric hyperoxia intervention on learning and memory abilities of valproic acid(VPA) autism model rats and the morphology of pyramidal cells in hippocampus CA1 area.Methods Animal model groups of autism were obtained in male offspring of the Wistar rats that received intraperitoneal injection of 600 mg/kg VPA at the 12.5 day after pregnancy.According to the eye opening time,behavior,weaning weight and the learning and memory abilities which were evaluated by the Y electricity maze test at the 28th day after birth,40 male VPA autism model rats were randomly selected 20 only and divided into normobaric hyperoxia model group (group A,n =10),atmospheric air model group (group B,n =10).Normal control groups were obtained in male offspring of Wistar rats that received intraperitoneal injection of equivalent physiological saline at the same period pregnancy.(group C,n =10).Rats in group A were treated with oxygen for 1 h per day and lasted 1 week;group B and C were treated with normal air.The learning and memory abilities of three groups were assessed at the 35th day after birth.The immunohistochemistry methods and image analysis were used to observe the pyramidal cells of autism model rats in hippocampal CA1 region.The effect of normobaric hyperoxia therapy on pyramidal cell of autism model rats in hippocampal CA1 region were evaluated by HE staining technique.Results The trying times of group A after treatment were less than those before treatment (31.15 ± 0.99 vs 31.54 ± 0.97,t =2.739,P =0.018).The memory times were more than those before treatment (3.00± 0.58 vs 2.69 ± 0.48,t =-2.309,P =0.040).The trying times of group A after treatment were less than those in group B after treatment (P =0.016).The memory times of group A were not different from that in group B after treatment(P=0.810).The morphology of pyramidal cells in hippocampal CA1 region showed that the pyramidal cells of the autism model rats had apoptosised.The number of apoptotic cells reduced and the number of normal form cells increased after the normobaric hyperoxia intervention compared with the autism model rats.Conclusion Normobaric hyperoxia intervention can improve the learning and memory abilities of the autism model rats.The apoptosis of the pyramidal neurons in hippocampal CA1 might be reduced after the normobaric hyperoxia intervention.

Objective To compare clinical Pseudomonas aeruginosa different sources of β-lactamase-resistant phenotype differences,as to provide theoretical basis for guiding clinical rational use of antibiotics.Methods Isolation of 478 strains of Pseudomonas aeruginosa were collected from clinical specimens in the First Affiliated Hospital of Xi'an Jiaotong University from January to December 2015,by VITEK 2 Compact bacteria identification and drug sensitivity analysis of advanced expert system for β-lactamase-resistant phenotype,statistical analysis of drug resistance phenotype and antibiotic resistance.Results 478 strains of Pseudomonas aeruginosa were mainly composed of phenotype 5 and phenotype 3.Sputum,drainage fluid and bile duct bile specimens of Pseudomonas aeruginosa were based on phenotype 5,accounted for 31.08％,34.71％ and 38.46％.Multiple comparison x2 were 3.893,4.071 and 5.595,There was no statistical difference between groups compare significance (P＞0.05).Urine,secretions and whole blood samples of Pseudomonas aeruginosa were phenotype 3,accounted for 34.88 ％,27.78 ％,45.45 ％;Multiple comparison x2 were 6.654,9.956 and 9.852.There was no statistical difference between groups compare significance (P＞0.05).Sputum,drainage of liquid,bile duct bile and urine,secretion,whole blood specimens respectively source of Pseudomonas aeruginosa resistant phenotype distribution of two comparative difference was statistically significant (x2 =15.056～22.050,P＜0.05).Comparing the resistance of different β-lactamase-resistant phenotypes in Pseudomonas aeruginosa isolates from different sources:the sputum specimen source in imipenem,meropenem,piperacillin and piperacillin/tazobactam had significant difference (x2 =22.225～39.025,P＜0.05).There was statistical significance in department of hepatobiliary surgery only ceftazidime and meropenem differences (x2 =21.890～22.872,P＜0.05).Conclusion The phenotypic analysis of β-lactamase-resistant phenotypes of Pseudomonas aeruginosa from different specimens was different,which provided a theoretical basis for guiding the clinical application of antibiotics and the control of nosocomial infection of Pseudomonas aeruginosa.

Objective To observe the clinical effect of monosialotetrahexosyl ganglioside sodium injection (GM1) on spastic cerebral palsy. Methods 98 children with spastic cerebral palsy were randomly divided into control group (n=50) and treatment group (n=48). Both groups received Bobath approach, and the treatment group received GM1 in addition. They were assessed with Functional Independence Measure for Children (WeeFIM), Gross Motor Function Measure (GMFM) and Gesell Development Schedule (GDS) before and after 90 days of treatment. Results The scores of WeeFIM, all the dimensions of GMFM and the gross motor, fine motor, personal-social and adaption of the GDS improved in both groups after treatment (P<0.05), and improved more in the treatment group than in the control group (P< 0.05). Conclusion GM1 may further improve the recovery of function for children with spastic cerebral palsy.

We investigated the pathogen of an outbreak of lung infection with unknown causes.By epidemiological analysis,we used real-time PCR,ELISA,gold dipstick,VITEK2 and MALDI-TOF-MS to identify suspicious bacteria.We made use of serum plate agglutination test to confirm the suspicious bacteria and the patient serum.We isolated 2 strains of Cryptococcus albidus from environmental samples.There has been specific agglutination between suspicious bacteria and patient serum.This pneumonia may be related to the infection of Ccryptococcus albidus.

Betulinic acid (BA), a pentacyclic lupane-type triterpene, has a wide range of bioactivities. The main objective of this work was to evaluate the hepatoprotective activity of BA and the potential mechanism underlying the ability of this compound to prevent liver damage induced by alcohol in vivo. Mice were given oral doses of BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and induced liver injury by feeding 50% alcohol orally at the dosage of 10 ml/kg after 1 h last administration of BA. BA pretreatment significantly reduced the serum levels of alanine transaminase, aspartate transaminase, total cholesterol, and triacylglycerides in a dose-dependent manner in the mice administered alcohol. Hepatic levels of glutathione, superoxide dismutase, glutathione peroxidase, and catalase were remarkably increased, while malondialdehyde contents and microvesicular steatosis in the liver were decreased by BA in a dose-dependent manner after alcohol-induced liver injury. These findings suggest that the mechanism underlying the hepatoprotective effects of BA might be due to increased antioxidant capacity, mainly through improvement of the tissue redox system, maintenance of the antioxidant system, and decreased lipid peroxidation in the liver.
Animals ; Antioxidants/pharmacology ; Blood Chemical Analysis ; Enzymes/blood ; Ethanol/*toxicity ; Lipid Peroxidation/drug effects ; Liver/*drug effects/enzymology/metabolism/pathology ; Male ; Mice ; Random Allocation ; Triterpenes/*pharmacology

To investigate the effects of gossypol acetic acid (GA) on proliferation and apoptosis of the macrophage cell line RAW264.7 and further understand the possible underlying mechanism responsible for GA-induced cell apoptosis, RAW264.7 cells were treated with GA (25~35 micromol/L) for 24 h and the cytotoxicity was determined by MTT assay, while apoptotic cells were identified by TUNEL assay, acridine orange/ethidium bromide staining and flow cytometry. Moreover, mitochondrial membrane potential (DeltaPsi(m)) with Rhodamine 123 and reactive oxygen species (ROS) with DCFH-DA were analyzed by fluorescence spectrofluorometry. In addition, the expression of caspase-3 and caspase-9 was assessed by Western Blot assay. Finally, the GA-induced cell apoptosis was evaluated by flow cytometry in the present of caspase inhibitors Z-VAD-FMK and Ac-LEHD-FMK, respectively. GA significantly inhibited the proliferation of RAW264.7 cells in a dose-dependent manner, and caused obvious cell apoptosis and a loss of DeltaPsi(m) in RAW264.7 cells. Moreover, the ROS production in cells was elevated, and the levels of activated caspase-3 and caspase-9 were up-regulated in a dose-dependent manner. Notably, GA-induced cell apoptosis was markedly inhibited by caspase inhibitors. These results suggest that GA-induced RAW264.7 cell apoptosis may be mediated via a caspase-dependent mitochondrial signaling pathway.
Animals ; Antineoplastic Agents, Phytogenic/*pharmacology ; Apoptosis/*drug effects ; Cell Line ; Cell Proliferation/*drug effects ; Dose-Response Relationship, Drug ; Gossypol/*analogs & derivatives/pharmacology ; Membrane Potential, Mitochondrial/*drug effects ; Mice ; Mice, Inbred BALB C ; Reactive Oxygen Species/*metabolism ; Signal Transduction/*drug effects