Objective To observe the effects of electro-acupuncture on the expression and inhibition of DNA binding protein 2 (Id2) and myelin basic protein (MBP),and to explore the mechanism of remyelinization after compressive spinal cord injury (CSCI) in rats.Methods Fifty-four SD rats were randomly divided into a control group and a treatment group,and each was further subdivided into 3 time point subgroups:3,7 and 14 days.There were 9 rats in each subgroup.The CSCI models were made with a self-designed method.The acupuncture points Jiaji (EX-B2),bilateral Zusanli (ST36) and Taixi (KI3) were selected for treatment.Electro-acupuncture (continuous wave,2 Hz,1.5 V)was applied to the bilateral Zusanli (ST36) and Taixi (KI3) points.The control group received the injury but no treatment.The changes in the ultrastucture of the nerve fibers＇ white matter were de-termined by transmission electron microscopy (TEM).The alterations in the expression of MBP and Id2 were observed by double labeled immunofluorescence and Western blotting on the 3rd,7th and 14th day after the injury.Results TEM showed that the myelin sheaths in the control group had degenerated,swollen,and even broken down after CSCI.Changes to the myelin sheaths in the treatment group were milder than those in the control group.The immunofluorescence results showed the amount of Id2-immunoreactive oligodendrocytes in the control group to be (20 ±2) on the 3rd day after CSCI,becoming (16 ± 1) on the 14th day.The differences among the 3 control subgroups were not statistically significant.The amount of Id2-immunoreactive oligodendrocytes in the treatment group was (13 ± 1) on the 3rd day,reaching a minimum the 14th day.The differences among the 3 treatment groups were statistically significant.The differences compared with the control group at the same time points were also statistically significant.Western blotting showed that the expression of Id2 in the contrast and treatment groups was (1.12 ±0.12) and (0.67 ±0.01) respectively on the 3rd day after CSCI,and both decreased with time.The expression of Id2 in both groups reached their minima ((0.86 ±0.02) and (0.25 ±0.01) respectively) on the 14th day.The difference between the treatment groups and the contrast group was statistically significant at each time point.The expression of MBP in the contrast and treatment groups at day 3 was (0.44 ± 0.02) and (0.67 ± 0.04) respectively,and these increased with time.The expression of MBP in both groups peaked at the 14th day (at (0.95 ± 0.04) and (1.74 ± 0.09) respectively).These differences were again statistically significant.Conclusion Electro-acupuncture can regulate the expression of Id2 and MBP after CSCI.The down-regulation of Id2 which controls MBP negatively and the up-regulation of MBP may contribute to remyelination in the injured spinal cord.

Objective To evaluate the changes of GRP78 expression in the Spinal Cord of Ischemia/Reperfusion Injuried Rat.Methods Fifty five adult Wistar rats(250～300 g)were randomly divided into 2 groups as control group(n=5)and operation group(n=50).The spinal cord SCII model was established.The expression of GRP78 was detected in spinal cord tissue through immunohistochemistry(IHC)and Western blot analysis,and the neuronal apoptosis was detected through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)methods.Results The GRP78 expression was increased at 30 min of reperfusion,and peaked at 7 h,but began to decline at 11 h post-reperfusion,and reduced significantly at 23 h.The number of GRP78 positive neurons at 0.5,3,7,11 and 23 h groups was(19.4?1.34),(42.6?2.30),(82.4?2.07),(40.0?1.58)and(18.8?0.83),respectively and significantly higher than that of control group(P

0.05).The grade of antibiotics tended to decline with the increase in of dressing change freqnency so it could decrease the expenditure of antibiotics.The rate of fungal infection lowered while hospitalization did not appear to be prolonged.CONCLUSIONS After the analysis of the use of antibacterials for burn patients,we find that the proper use of antibiotics and the increase in dressing change would lower the grade of antibiotics and expenditure,at the same time they do not increase the rate of bacterial infection and fungal infection,and do not prolong the duration of patients hospitalization time.

Objective To investigate the effect of RNAi-mediated sTAT3 gene silencing on the invasiveness of human pancreatic cancer cells. Methods STAT3 shRNA expression vector was stably transfected to SW1990 cells.STAT3 mRNA and protein expression were examined using reverse transcription polymerase chain reaction(RT-PCR)and Western blot,respectively.The invasion ability of SW1990 cells was determined by cell invasion assay in vitro.RT-PCR and Westem blot were performed to detect the mRNA and protein expression of the MMP-2 and VEGF,respectively. Results mRNA and protein expression of STAT3 were inhibited significantly by stable transfection of STAT3 shRNA expressing vectors.STAT3 silence with RNAi significantly inhibited the invasion ability of SW1990 cells decreasing protein and mRNA expression of MMP-2 and VEGF in SWl990 cells. Conciusion STAT3 silence with RNAi significantly inhibits the invasion ability of pancreatic cancer cells through down-regulating MMP-2 and VEGF.

Objective To evaluate the screening effect of osteoporosis self-assessment tool for Asians (OSTA) in middle aged and elderly healthy men in Chengdu.Methods A total of 4042 healthy men aged 40 to 106 years received dual energy X-ray absorptiometry (DXA) assay,and OSTA index evaluation.Measurement sites included lumbar spine (L1-4),left femoral neck,trochanter,Ward's area,total hip and femoral shaft.All persons were classified into highosteoporosis-group (OSTA≤-4),mediumosteoporosis-group (-4 ＜ OSTA≤≤-1),low osteoporosis-group (OSTA＞-1),or the low risk-group (OSTA＞-1) and high risk-group (OSTA≤-1) by OSTA scores.T-scores were compared between different measurement sites detected by DXA.The sensitivity,specificity,Kappa value and the area under receiver operating characteristic (ROC) curve (AUC) of OSTA in screening osteoporosis were evaluated.Results The prevalence of osteopenia and osteoporosis in lumbar spine,proximal femur were gradually increased along with aging.The detection rate of osteoporosis in lumbar spine and proximal femur were 16.2％ and 24.0％ respectively in subjects aged over 80 years.OSTA index in low-risk,medium-risk group,high-risk group were 85.0％,11.0％,4.0％ respectively.The detection rate of osteoporosis in lumbar spine and proximal femur were 2.6％ and 1.6％ in low-risk group,10.4％ and 10.4％ in medium-risk group,and 29.3％ and 30.5％ in high-risk group,respectively.Taking OSTA ≤-1 as the cut-off value,the sensitivity and specificity of OSTA in screening osteoporosis in lumbar spine and femur by T-score＜-1 were 28.1％,28.7 ％,89.0％ and 92.4％ respectively,and by T-score≤-2.5 were 51.6％,63.2％,86.7％ and 86.8％ respectively.The consistency of diagnosis result between T-score and OSTA index according to the three versus two risk levels was 0.153 and 0.197 versus 0.195 and 0.243 Kappa value,respectively.The AUC of OSTA index for lumbar spine and femur by T-score＜-1 and T-score≤-2.5 were 0.689 and 0.823,and for different age groups and different measurement sites were 0.639 and 0.899 (all P＜0.001).Conclusions OSTA index has a certain ability in screening osteoporosis in men aged over 50 years.There are different screening results on osteoporosis among the different age groups.

Objective To investigate the effect and mechanism of RNAi-mediated STAT3 gene silence on human pancreatic cancer cells growth in vivo. Methods STAT3 shRNA expression vector was stably transfected to SW1990 cells. STAT3 and p-STAT3 protein was examined using Western blot. The growth ability of SW1990 cells in vivo was determined in a subcutaneous tumor model of nude mice. Western blot was performed to detect the protein expression of Bcl-xL and cyclin D1. Results The protein expression of STAT3 and p-STAT3 decreased by 90% and 92% by stable transfection of STAT3 shRNA expressing vectors(P ＜0. 05). Inhibition of STAT3 with RNAi significantly inhibited the growth ability of SW1990 cells in vivo( P ＜ 0. 05 ). The tumor weight significantly decreased( P ＜ 0. 05 ). Moreover, the relative Bcl-xL and cyclinD1 protein expression in SW1990-RNAi cells reduced by 56% and 50% compared with that of the parental SW1990 cells, respectively (P ＜ 0. 05). Conclusions Inhibition of STAT3 with RNAi significantly inhibits the growth ability of pancreatic cancer cells through down-regulating Bcl-xL and cyclin D1.

Objective: In order to investigate the effects of activating and blocking Stat3 signaling pathway on invasion ability of human pancreatic cancer cells and explore its action mechanism.Methods:Human pancreatic cancer Capan-2 cells were treated with IL-6. SW1990 human pancreatic cancer cells were treated with AG490. Cell proliferation was measured by MTT assay. Western blotting and immunocytochemistry were performed to detect expression of phosphorylated Stat3 (p-Stat3) protein. Real-time fluorogentic quantitative PCR (RFQ-PCR) and Western blotting were used to detect the mRNA and protein expression of VEGF and MMP-2 mRNA, respectively. The invasion abilities of SW1990 and Capan-2 cells were determined by cell invasion assay in vitro. Results:IL-6 stimulated the proliferation of Capan-2 cells (P<0.05), elevated the expression of p-Stat3, increased the mRNA and protein expressions of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 2 (MMP-2) (P<0.05), and enhanced the invasion ability of Capan-2 cells. AG490 inhibited the proliferation of SW1990 cells (P<0.05), down-regulated the expression of p-Stat3, markedly decreased the mRNA and protein expression of VEGF and MMP-2 (P<0.05), and weakened the invasion ability of SW1990 cells. Conclusion:Stat 3 signaling pathway plays an important role in the invasion and metastasis of pancreatic cancer. Stat 3 signaling transduction pathway may provide a novel therapeutic target for the treatment of pancreatic cancer.

Objective To investigate the expression of miRNA-301a-3p in pancreatic cancer and to correlate the expression on invasion , migration and colony formation of pancreatic cancer cells .Methods The expression of miRNA-301a-3p in 20 paired pancreatic cancer tissues and matched adjacent tissues , and pancreatic cancer cell lines and normal pancreatic ductal cells were detected by real -time PCR.miRNA-301a-3p mimics or inhibitors were used to up-regulate or down-regulate the miRNA-301a-3p level in pancre-atic cancer cell lines in order to figure out the effects of miRNA-301a-3p on cell invasion, migration and col-ony formation of pancreatic cancer cells , respectively .Results In pancreatic cancer tissues and cell lines , miRNA-301a-3p was significantly up-regulated when compared with the matched adjacent tissues ( P <0.05) and normal pancreatic ductal cells (P<0.05), respectively.Overexpression or downexpression of miRNA-301a-3p enhanced or suppressed colony formation , invasion and migration abilities of pancreatic cancer cells in vitro.Upregulation of miRNA-301a-3p promoted tumorigenesis in vivo.Conclusion miR-NA-301a-3p might function as an oncogene to promote tumorigenesis in pancreatic cancer .

Objective To investigate the role of demyelination and the alteration of chondrotin sulfate proteoglycan (CSPG,NG2) expression after compression injury of the spinal cord (CSCI).Methods Seventy-five adult Sprague-Dawley rats were randomly divided into a normal group,a sham-operation group,a CSCI 1 day group,a CSCI 3 day group,and a CSCI 7 day group.There were 15 rats in each group.The injuries in the CSCI groups were inflicted using a technique devised in our laboratory.Basso-Beattie-Bresnahan (BBB) neurological function assessment was used to assess the rats' motor function,osmic acid staining and transmission electronic microscopy (TEM)were used to observe any pathological changes of myelinated nerve fibers in the white matter at 1,3 and 7 days after CSCI.The amount of myelinated nerve fibers in the posterior funiculus of the spinal cord and the ratio of myelin sheath thickness to axon diameter (the G-ratio) were calculated.Any alteration in NG2 expression was observed by Western blotting.Results The average neurological function assessment scores in the CSCI groups were (1.23 ±0.45),(0.65 ± 0.35) and (0.00 ± 0.00) respectively.Compared with the normal group (21.00 ± 0.00) and the sham operation group (21.00 ± 0.00),the differences were all statistically significant.The rats' motor function deteriorated gradually with time after the CSCI.Osmic acid staining showed that the white matter was intact in the normal and sham groups.After being compressed the myelinated nerve fibers became swollen,degenerated and broke down.The amount of myelinated nerve fibers in the normal group,the sham operation group and the three CSCI groups was (2771 ± 108),(2675 ± 199),(2403 ± 161),(1708 ± 70) and (8 10 ± 95) respectively.The amount of myelinated nerve fibers decreased in the CSCI groups and reached a minimum on the 7th day.The difference was statistically significant.The TEM quantity analysis showed that the G-ratios in the normal,sham operation,and CSCI 1 day,3 day and7 day groups were (18.10±0.4),(17.70±1.0),(6.69 ±0.8),(5.73 ±0.4) and (4.95 ±0.5) respectively.Compared with the normal and sham operation groups,the G-ratios in the 3 CSCI groups were lower and reached their minimum on the 7th day after injury.The difference was statistically significant.TEM observation showed that the axons and myelin sheaths were intact in the normal and sham groups.After CSCI the axons became swollen and cell organelles in the axoplasm degenerated and decreased.The layers of myelin sheath shrank,folded and even wrinkled,which had an onion-like appearance.The oligodendrocytes exhibited chromatin condensation.Macrophages showed infiltration.Western blotting showed that the expression of NG2 in the CSCI groups reached a maximum on the 1st day after injury and then decreased with time.The expression of NG2 in the CSCI groups was higher than in the normal and sham groups,and the difference was statistically significant.Conclusion Demyelination occurs after CSCI-the amount of myelinated nerve fibers decreases and neurological deficits increase with time.The expression of NG2 was associated with changes in the myelin sheaths after CSCI and contributed to recovery of the myelin sheath through proliferation and differentiation to oligodendrocytes and perhaps other kinds of cells.

Objective To investigate correlation between demyelination and caspase-12 expression alteration after compressed spinal cord injury (CSCI) so as to discuss mechanism of demyelinating lesion after CSCI.Methods Seventy-five adult SD rats were randomly divided into five groups,ie,normal group,control group,compression 1 d,3 d and 7 d groups,with 15 rats per group.Models of spinal cord compression were established with a self-made device.Ultrastructure of the demyelinated nerve fibers was observed by electronic microscope and oligodendrocyte apoptosis was detected by TUNEL staining and double labeling immunofluorescence.Immunoblotting was used to defect caspase-12 that was related to cell apoptosis.Results Demyelination of nerve fiber occurred after CSCI and was aggravated with time.Apoptosis of oligodendrocytes was found after CSCI,and showed significant difference between compression 7 d group and normal group (P ＜ 0.05).Caspase-12 was also upregulated with extension of compression time.Conclusion Caspase-12 mediating oligodendrocyte apoptosis is one of the mechanisms of nerve fiber demyelination after CSCI.