Objective:To study the effect of Vitamin E(VitE)and Sodium selenite on nonalcoholic fatty liver(NAFL).Methods:24 SD rats were randomly divided into 3 groups.The model group,treatment group and contrast group were respectively fed with high fat diet,interfering diet and normal diet.All animals were sacrificed at the end of the 5th week.The liver pathology was observed under the light microscope.Superoxide dismutase(SOD),malondialdehyde(MDA)were determined by biochemistry analysis.The expressions of nuclear factor kappa B(NF-kB)and tumor necrosis factor alpha(TNF-?)proteins in hepatocytes were examined by immunohistochemistry.Result:①compared with the contrast group,serum and liver SOD levels decreased in model group,while MDA were raised.The expressions of NF-kB and TNF-a proteins in liver tissue increased significantly in model group.②compared with the model group,serum and liver SOD level increased in treatment group,while MDA was lowered.The expression of NF-kB proteins in liver tissue was reduced in treatment group,and no significant changes occured in TNF-a protein expression.Conclusions:Combination of sufficient quantum of VitE and Sodium selenite can improve the SOD activities and reduce the expression of NF-kB proteins in liver tissue,which is possibly the important mechanism for VitE and Sodium selenite to prevent NAFL.

Objective To study the mutation of DNA fragment of rpoB gene in different degrees of rifampin-resistance in Mycobacterium tuberculosis.Methods DNA fragment of rpoB gene in Mycobacterium tuberculosis was sequenced,including 32 low-level (R50) rifampin-resistant strains (50?g/mL rifampin-resistant),22 high-level (R250) rifampin-resistant strains (250?g/mL rifampin-resistant),10 (R0)rifampin-sensative strains and 1 H 37 Rv strain.Results No mutation was detected in 10 rifampin-sensative strains and 1 H 37 Rv strain;25(78.1%)rifampin-resistant strains had mutations in R50 and 21(95.5%)rifampin-resistant strains had mutations in R250(P=0.170).The mutatione points were distributed disorderly in R50.The 531-Ser mutation(57.1%)and joint mutation(23.8%)were more in R250 than those in R50.Conclusion The frequency of mutation in the rpoB gene of rifampin-resistant strain is higher.The mutation points are distributed disorderly in R50.The 531-Ser mutation(57.1%)and joint mutation(23.8%)are major mutative characteristics in R250.

Objective To evaluate the clinical,epidemiological,and viral molecular biology features of 26 patients infected with H7N9 avian influenza A virus. Methods Clinical and epidemiological data of 26 patients with con-firmed avian influenza A (H7N9)infection in 2013 and 2014 were collected,virus isolated from human and poultry were identified and typed through sequencing.Results Of 26 patients,fever and cough were the most common symptoms,all patients had pneumonia;20 patients (76. 92% )developed acute respiratory distress syndrome (ARDS);25 patients (96.15% )had leucopenia or normal leukocytes at the initial diagnosis;treatment with antivi-ral drugs was initiated in 25 patients at a median of 10 days after the onset of illness;10 patients (38.46% )died. Gene sequencing indicated Gln226Leu and Gly186Val substitutions in human virus H7 gene and the PB2 Asp701Asn mutation. Conclusion Acute respiratory system damage is the main clinical manifestation of avian influenza (H7N9)virus infection in humans,live poultry exposure is an important risk factor for H7N9 infection in humans, adaptive mutation occurred at partial site of avian virus gene,which can be more easily be spread from birds to hu-man and cause serious diseases,it is necessary to strengthen the pathogen monitoring.

Objective To observe the level changes of serum interleukin-18(IL-18) and tumor necrosis factor-?(TNF-?) in alcohol liver disease of rats.Methods The dose of 56% alcohol [5～9 g/(kg?d)] was administeredvia gastrolavage once daily for 12 weeks in ALD model rats.The control rats were grven the same volume of saline.The rats were killed at the end of 4,8,12W.The pathological changes of liver were observed under light microscope after HE staining,and the levels of IL-18 and TNF-? in serum was determined with ELISA.Results The tissues of model rats showed various changes of chronic alcohol liver disease at the end of 4,8,12W,such as: fatty degeneration,inflammatory changes and fibrosis.The levels of ALT and AST in models were obviously higher than those of the controls(P

Objective To determine and compare the contents of oxypaeoniflorin and paeoniflorin of Paeoniae Radix,and to improve the quality standard of Radix Paeonia.Methods The contents of oxypaeoniflorin and paeoniflorin in different kind of White and Red Peony Root were successfully analyzed by HPLC.Results The content of oxypaeoniflorin in Red Peony Root is more than White Peony Root at 0.8361％ ;The content of paeoniflorin in White Peony Root is more than Red Peony Root at 0.2157％.The proportion of paeoniflorin and oxypaeoniflorin in White Peony Root is more than Red Peony Root.Conclusion With HPLC technology,quantitative analysis of active constituents in Paeoniae Radix was performed accurately.

P2X7 receptors,belonging to purinergic P2 receptor family,are ATP-gated cation channels,which can choose the bivalent cations freely.P2X7 receptors join in cell signal conduction and the excretion of the cytokines and other physical functions.In recent years,researchers have discovered P2X7 receptors mediate the cells to live and grow by increasing oxidation and phosphorylation and intracellular ATP reserve.In breast cancer,the P2X7 receptors express abnormally,and can activate the MAPK lied in cytoplasm.The phosphorylated MAPK enter the nucleus and activates a series of protein kinases,and then affects the genesis and development of breast cancer.

BACKGROUND: Traumatic brain injury generates a cascade of arachidonic acid metabolic events that mainly presented by the increment of prostaglandin and oxygen free radicals. Indomethacin can potently inhibit the activity of cyclooxygenase, decrease the synthesis of prostaglandins, and may decrease the production of oxygen free radical, and thus may attenuate the pathological changes of brain injury.OBJECTIVE: To observe the changes of prostaglandin in early brain injury and after indomethacin intervention, so as to explore the pharmacological mechanism of indomethacin.DESIGN: A randomized and controlled trial based on experimental animals.SETTING: Department of neurosurgery and department of cerebral surgery in a university hospital.MATERIALS: This study was carried out at the Laboratory of Neurosurgery Department, Medical College of Southeast University between March and September 2000. Thirty-six hybrid cats were randomly divided into normal control group, brain injury group and indometbacin intervention group, with 12 cats in each group.INTERVENTIONS: Brain injury was simulated according to previously reported grading mechanical traumatic animal model establishment; cats with medium brain injury were enrolled in this study. The ultimate concentrations of prostacyclin (PGI2) and thromboxane A (TXA2) to 6-keto-prostaglandin F 1 alpha(6-keto-PGF1α) and thromboxane B2(TXB2) in brain vein blood, as well as total brain superoxide dismutase(SOD) and cerebral water content were measured 6 hours after trauma.MAIN OUTCOME MEASURES: 6-keto-PGF1α, TXB2, SOD, and cerebral water content.RESULTS: Both 6-keto-PGF1α and TXB2 in brain vein blood remarkably increased in early brain injury[from(0.057±0.010) g/L to (0.264±0. 126) g/L, from(0. 060 ±0. 012) g/L to(0. 134 ±0. 048) g/L respectively], with the increment of the former higher than the latter, the ratio of TXB2/6-keto-PGF1α decreased from 1. 052 ±0. 145 to 0. 545 ±0. 184, and cerebral water content increased from(77.39 ± 0. 36)% to (78.06±0.41)% ; meanwhile, total brain SOD significantly decreased from (94. 869 ± 5. 418) μkat/g to(54. 368 ± 3. 417) μ kat/g( P ＜ 0.01) . In contrast to brain injury group, the concentrations of 6-keto-PGF1α and TXB2 in indomethacin intervention group significantly decreased, which were similar to those of control group, but the total SOD significantly increased from (54. 368 ±3. 417) pkat/g to (81. 433 ±7. 268) μkat/g (P ＜0. 01), and water content lightly decreased without statistical significance( P ＞ 0. 1 ).CONCLUSION: PGI2 and TXA2 increase in early brain injury in experimental cat model, accompanied by free radical synthesis, resulting in the exacerbation of brain injury. Indomethacin may be helpful to relieve posttraumatic secondary brain injury by regulating the imbalance of PGT2 / TXA2 and decreasing the production of free radical.

Objective To study the expression and significance of excision repair cross complementing genes 1 (ERCCI) in the tissue of nasopharyngeal carcinoma(NPC).Methods ERCC 1 proteins was assayed with immunohistochemical method in the tissue of 103 cases of NPC and 50 cases of chronic inflammation of nasopharyngeal epithelium(CINE).Results The expression rate of ERCC1 was 45.63％ in NPCs,which was significantly lower than that in CINE (70.00％) (χ2 =8.037,P ＜ 0.05).The expression rate of ERCC 1 in NPCs had relationship with T,N staging and clinical staging as well as the presence of recurrence and metastasis (χ2 =9.007,9.992,8.343,5.792,all P ＜ 0.05),while no relationship with age and gender(χ2 =0.026,0.871,all P ＞ 0.05).The expression of ERCC1 in group of recurrence and metastasis was significantly lower than those in group of no recurrence and metastasis.Conclusion The expression of ERCC1 was significantly decreased in NPCs.ERCC1 will probably become prognostic biological parameters of NPC.

Depression is a common mental and psychiatry disorder. Depression is easy to recur and hard to cure.These urgent problems origin from the limited understanding of this disease and the big heteroge-neity in its genology. Generalized from recent relative papers we discovered that the important onset and sus-taining basis of depression is neuroremodeling,which includes the persistent changes of histocytology,ultra-structure of synapse and abnormal expressions of gene and protein of neurons in key brain regions,and so on. These changes affect the correct dealing on the neural message which lead to depression and become the sus-taining biological basis. Therefore the key strategies to prevent and cure depression lie on preventing,individ-ual therapy and reversing neuroremodeling.