Aim To investigate the effect of Salidroside on the focal celebral ischemia/reperfusion injury in rats and its underlying mechanism. Methods Adult male Sprague-Dawley rats, weighing 260-300 g, were ran-domly divided into three groups: sham, MCAO, MCAO+salidroside ( Sal ) groups. The rats were sub-jected to local celebral ischemia reperfusion with su-
ture-occluded method. The rats of MCAO +Sal group were treated intraperitoneally with salidroside ( 50 mg ·kg-1 ) for 6 days. Neurological deficit testing was performed with Longa’ s Scale. The mRNA expressions of Neun,Nogo-A,and NgR were detected by RT-qPCR in ischemic brain. The protein expressions of Neun, NGF , BDNF , Nogo-A and NgR were determined by
Western blot. Results Compared with MCAO group, salidroside significantly improved the neurological defi-cit,promoted the expressions of Bcl-2,Neun,NGF,BD-NF, and inhibited the expressions of Nogo-A, NgR. Conclusion Salidroside can reduce neurological defi-cit, increase the number of Nissl’ s Body and the ex-pression of Neun, and protect rats against focal cele-
bral ischemia/reperfusion injury,which may be accom-plished by increasing the expressions of Bcl-2, NGF, BDNF, and inhibiting the expressions of Nogo-A, NgR.

Aim To investigate glucose uptake effects and mechanism of emodin in 3T3-L1 adipocytes. Methods LPS-induced differentiated 3 T3-L1 adipo-cytes were divided into control group and emodin ( 1 , 10, 50 μmol · L-1 ) groups. Then, 6-NBDG uptake and the expression of cell surface GLUT4 , PPARγ, AMPKα1/2 , p-AMPKα1/2 , IRS-1 , p-IRS-1 , Adi-ponectin, chREBP-α and chREBP-β were detected. The ability of 6-NBDG uptake in LPS-induced 3 T3-L1 adipocytes was also evaluated following interference with AMPK inhibitor and PPARγinhibitor, respective-ly. Meanwhile, STZ-induced diabetic rats were ran-domly divided into control group and emodin treatment group. The mRNA expression of Adiponectin and pro-tein expression of cell surface GLUT4 , AMPKα1/2 , p-AMPKα1/2 were measured. Results Compared with the control group, emodin improved the mRNA expres-sion of cell surface GLUT4, Adiponectin, chREBP-αand chREBP-β, and protein expression of cell surface GLUT4 , PPARγ, IRS-1 , p-IRS-1 , AMPKα1/2 and p-AMPKα1/2 in 3T3-L1 adipocytes(P<0. 05). Emodin enhanced 6-NBDG uptake and the uptake of emodin group was both decreased following interference with AMPK inhibitor and PPARγ inhibitor, respectively ( P<0. 05 ) . Emodin also increased the mRNA expression of Adiponectin and protein expression of cell surface GLUT4 , AMPKα1/2 and p-AMPKα1/2 in adipose tis-sue of T2 DM rats ( P <0. 05 ) . Conclusion Emodin can enhance glucose uptake in 3 T3-L1 adipocytes and the mechanism is probably associated with activating Adiponectin and IRS-1 , thereby activating AMPK and PPARγ.

Aim To investigate the neuroprotective effect of salidroside in MCAO rats. Methods The rats were subjected to middle cerebral artery occlusion with suture-occluded method, and the neurologic injury and infarct size of rats were evaluated. According to the gene chip detected, the protein expressions of caspase-3 , cleaved caspase-3 were determined and the mRNA expressions of IL-6, Vgf, Hba-a2, Hbb-b1, Hbb, CD44, Pnpla2, Slc6a5 and Slc5a7 were tested. Re-sults Compared with MCAO group, salidroside signif-icantly improved the neurological deficit, reduced the infarct sizes, inhibited the expressions of cleaved caspase-3 protein and IL-6 mRNA, promoted the ex-pressions of Vgf, Hba-a2, Hbb-b1, Hbb, and reduced the expressions of CD44 , Pnpla2 , Slc6 a5 and Slc5 a7 . Conclusions Salidroside can reduce the neurological deficit and infarct size, and protect rats against focal cerebral ischemia-reperfusion injury, which may be ac-complished by increasing the expressions of Vgf, Hba-a2, Hbb-b1, and Hbb, and decreasing the expressions of cleaved caspase-3 , IL-6 , CD44 , Pnpla2 , Slc6 a5 and Slc5 a7 .

Objective To know the contents and changes situation of trace elements among children aged 0-6 years old in Chengdu are‐a .Methods The BH5100T atomic absorption spectrometry was adopted to detect the levels of trace elements Cu ,Zn ,Ca ,Mg ,Fe in 786 children aged 0-6 years old undergoing the physical examination in our hospital from April 2015 to November 2015 .The detection results were statistically analyzed .Results The deficiency rates of Cu ,Zn ,Ca ,Mg and Fe in Chengdu area were 0 .4% ,5 .0% ,18 .1% ,9 .5% and 8 .3% respectively ,in which the deficiency rates of Ca in children aged <1 ,1 ,2 ,3 ,≥ 4 years old were 47 .4% ,27 .5% ,12 .6% ,9 .9% and 11 .9% respectively ,indicating that the Ca deficiency rate in children < 1 years old was higher .The Ca deficiency rate had statistical differ‐ence among different age groups(P<0 .05) ,and there were no statistically significant differences in the deficiency rates of several trace ele‐ments among different age groups of male and female children .Conclusion The abnormality rate of trace elements among children aged 0-6 years old in Chengdu area is higher ,in which the Ca deficiency rate is highest ,meanwhile the Mg and Fe were lack too .The trace element content in children is closely related with the feeding habit .The 0-6 years old children in this area should pay attention to the supplement of trace elements ,especially supplement of Ca ,meanw hile breastfeeding is advocated .

Objective To discuss the application value of modified Hodge test(MHT) for screening carbapenemase-producing Enterobacteriaceae.Methods The 24 Enterobacteriaceae reduced susceptibility to carbapenems were detected by MHT.At the same time,polymerase chain reaction(PCR) was used to detect carbapenemase genes of KPC,NDM,IMP,SIM and VIM.PCR products were sequenced and the results were compared with the sequences of Gen Bank database.Comprehensive analysis the application value of MHT and PCR to detect carbapenemase.Results Among these 24 strains,13 stains appeared to produce carbapenemase by MHT,5 positive strains were found to carry carbapenemase genes by PCR.By comparing with the sequences of Gen Bank database 1 strain were confirmed to KPC-2 and 4 strains were confirmed to IMP-4.We found that 4 strains of Enterobacteriaceae,detected carbapenemase by MHT and PCR at the same time.9 strains of MHT were positive,but we couldn′t detect the carbapenemase genes.1 strain of MHT was negative,but carbapenemase gene was found in the strain.Conclusion The value of MHT to screen carbapenemase-producing Enterobacteriaceae is necessary to further study.

Objective To establish protein fingerprinting identification model of Pseudomonas aeruginosa (P. aeruginosa) and to lay a foundation for rapid identification of P. aeruginosa by proteinchip golden array. Methods Sixty-four P. aeruginosa and one hundred and ninety-nine control bacteria identified in our laboratory were collected and divided into training and testing group. Surface enhanced laser desorption ionization time of flight mass spectrometry (SELDI-TOF-MS) and proteinchip golden array were used to detect the protein profiling of the bacteria. Data were automatically collected by Ciphergen Proteinchip Software and protein markers of P. aeruginosa were screened by BioMarker Wizard Software. Classification tree model was developed and validated by BioMarker Patterns Software. The model was blindly tested with twenty-nine P. aeruginosa and sixty-four control bacteria. Results Eighty protein peaks were detected between 3000 and 20 000, among which fifty-eight ones showed significantly difference between P. aeruginosa and the control bacteria (P＜0.01). By BioMarker Patterns Software, one protein peak ( M/Z at 14 045.2) was chosen to develop a classification tree model. The results exhibited with sensitivity of 96. 55% and specificity of 100%. Conclusion Proteinchip golden array has the potential for rapid identification of P. aeruginosa.

AIM: To observe the expression of fractalkine, and its receptor, CX3CR1, in renal tissues of patients with diffuse proliferative lupus glomerulonephritis (WHO class IV), minimal glomerular abnormalities, and normal kidney. Meanwhile, the correlation among the expression of fractalkine, CX3CR1 and CD68-positive macrophages was investigated, and the role of fractalkine and CX3CR1 in the pathogenesis of lupus nephritis was discussed. METHODS: The expressions of fractalkine, CX3CR1 and CD68 were detected immunohistochemically in kidney tissue sections obtained from twenty-one patients with WHO class IV lupus nephritis, eighteen cases with minimal glomerular abnormalities, and eight normal kidneys which were no abnormality under light microscope. RESULTS: (1) Fractalkine was generally indistinguishable in tissue sections from normal kidney and minimal glomerular abnormalities. CX3CR1-positive cells and CD68-positive macrophages were sparsely detected in the glomeruli and in the cortical interstitium. (2) There were considerable CX3CR1-positive cells and macrophages in both the glomeruli and the interstitium in sections from class IV lupus nephritis. The number of CX3CR1-positive cells significantly correlated with the number of macrophages in the glomeruli and in the interstitium respectively (r=0.956, P

Objective To establish protein fingerprints of common bacteria in clinics and to lay a foundation for rapid identification of bacteria.Methods Strains of Escherichia coli,Klebsiella pneumoniae,Pseudomonas aeruginosa and Staphylococcus aureus were detected by surface enhanced laser desorption and ionization time-of-flight mass spectrometry (SELDI-TOF MS).Stable expression protein peaks were screened and the data was input into the self-constructed Fingerwave software for identification of target bacteria by protein fingerprint comparison.Two hundred and fifty-six clinical isolates,including E.coli,K.pneumoniae,P.aeruginosa and S.aureus were detected and the data was compared with constructed database to evaluate its diagnostic value.Results The protein fingerprints including four common bacteia was used to identify the target bacteria with identification rate of 93.1％ (54/58) for E.coli,87.2％ (75/86) for K.pneumoniae,96.2％ (60/63) for P.aeruginosa and 96.2％ (51/53) for S.aureus,respectively.Conclusion Common bacteria can be rapidly identified by using the protein fingerprint comparison,which provides a powerful tool for bacterial identification.

Objective To investigate the mechanism of one carbapenems resistant Raoultella planticola( R.planticola) isolate.Methods This is an experimental study.R.planticola was isolated from a patient′s drainage fluid from orthopedic department in November 2010 in Sichuan Provincial People′s Hospital.Minimum inhibitory concentration of R.planticola to 13 antibiotics was determined by using the agar dilution method.Modified Hodge test was used to detect carbapenemase .EDTA synergistic test was performed to research metallo-beta-lactamase.The genes coded the β-lactamase were amplified by polymerase chain reaction ( PCR ) , including class A carbapenemase ( KPC ) , class B carbapenemases (NDM, IMP, VIM, SIM), extended spectrum beta-lactamases[ESBL(CTX, TEM, SHV)], and AmpCβ-lactamases ( FOX, EBC, ACC, DHA, CIT, MOX).Results The susceptibility test showed that R.planticola was resistant to 9 antibiotics.MIC value of meropenem for R.planticola was up to 32 mg/L.R.planticola kept intermediary to imipenem , whereas it was susceptible to cefepime , amikacin and polymyxin B.Modified Hodge test and EDTA synergistic test were positive in R.planticola.Class B carbapenemase (IMP) gene and two extended spectrum β-lactamases(CTX, SHV) genes were positive by PCR.The genes were conformed as IMP-4, CTX-M3 and SHV-12 by sequencing and compared with GenBank.Other resistant genes were negative.Conclusion IMP-4 was identified in R.planticola, the combined produce IMP-4 and ESBLs might be the main mechanism of R.planticola resistant to carbapenems.

Objective:To investigate the role of microRNA (miR)-155 in hydrogen peroxide (H 2O 2)-induced oxidative stress injury in lens epithelial cells (LECs) and its mechanism regulating silent information regulator factor related enzymes 1 (SIRT1). Methods:The HLE-B3 at the logarithmic growth phase was taken and cultured for 24 hours under different concentrations of H 2O 2 (0, 50, 100, 200, 400, 800 μmol/L), and the cell viability was detected by MTT assay to determine the optimal concentration of H 2O 2 for establishing an oxidative stress injury model.HLE-B3 cells were divided into 6 groups, untreated blank control group, model control group cultured with 100 μmol/L H 2O 2, miR-155 mimics group transfected with miR-155 mimics, miR-155 mimics negative control group transfected with miR-155 mimics negative control, miR-155 inhibitor group transfected with miR-155 inhibitor, and miR-155 inhibitor negative control group transfected with miR-155 inhibitor negative control.Transfected cells were cultured with 100 μmol/L H 2O 2.Cells in various groups were cultured for 24 hours, and cell morphology was observed under an inverted microscope.The relative expression of miR-155 and SIRT1 mRNA in cells was assayed by fluorescent quantitative PCR.Cell apoptosis rates were detected by flow cytometry.Reactive oxygen species (ROS) content was identified by 2', 7'-dichlorofluorescein diacetate (DCFH-DA) fluorescent probe method.Superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration were measured by ELISA method.The targeting of SIRT1 by miR-155 was tested by dual luciferase reporter gene system.Expressions of SIRT1, B-cell lymphoma/leukemia-2 gene (bcl-2), bcl-2 associated X protein (bax), cleaved-cysteine aspartase 3 (cleaved-Caspase-3) proteins were determined by Western blot. Results:With the increase of H 2O 2 concentration, the cell viability gradually decreased, and the differences in cell viability among different concentrations were statistically significant (all at P<0.05), and 100 μmol/L was selected as the experimental concentration.Cells in blank control group grew well adherently.The number of cells in model control group decreased, and the morphology of some surviving cells changed, and their boundaries were blurred.There were fewer cells in miR-155 mimics group than model control group, and the cell morphology changed.There were more cells in miR-155 inhibitor group than model control group, and the cells grew well.Compared with model control group, the relative expression level of miR-155, the apoptosis rate, ROS content, MDA concentration, as well as the relative expression levels of bax and cleaved-Caspase-3 proteins were increased, and the relative expression level of SIRT1 mRNA, the SOD activity, the relative expression of SIRT1 and bcl-2 proteins, as well as bcl-2/bax were decreased in miR-155 mimics group, and the differences were statistically significant (all at P<0.05). Compared with model control group, the relative expression of miR-155, the apoptosis rate, ROS content, MDA concentration, as well as the relative expression levels of bax and cleaved-Caspase-3 proteins were decreased, and the relative expression level of SIRT1 mRNA, SOD activity, the relative expression levels of SIRT1 and bcl-2 protein, as well as bcl-2/bax were significantly increased in miR-155 inhibitor group, and the differences were statistically significant (all at P<0.05). The relative luciferase activity of wild-type SIRT1 in cells transfected with miR-155 mimics was 0.41±0.07, which was significantly weaker than 1.00±0.11 in cells transfected with miR-155 mimics negative control, and the relative luciferase activity of wild-type SIRT1 in cells transfected with miR-155 inhibitor was 1.98±0.17, which was significantly higher than 1.00±0.12 in cells transfected with miR-155 inhibitor negative control, showing statistically significant differences ( t=7.838, 8.157; both at P<0.05). No obvious effect on the relative luciferase activity of mutant SIRT1 was found in transfected cells. Conclusions:miR-155 is involved in H 2O 2-induced oxidative damage of LECs, and its overexpression can target the expression of SIRT1 and play a role in cell injury.