BACKGROUND:Exercises play an important role in the recovery of neurological function after stroke. Few studies concerned the amount of exercise in rats after stroke. Hippocampus is strongly associated with cognitive function, but no reports addressed the expression of repulsive guidance molecule A in the rat hippocampus after ischemia and reperfusion. OBJECTIVE:To explore the effects of exercise on repulsive guidance molecule A expression in the hippocampus on the ischemic side in rats after cerebral ischemia-reperfusion injury. METHODS:120 Sprague-Dawley rats were equal y and randomly divided into normal group, sham-operation group, and 7-, 14-, 28-day model groups. The model of right cerebral ischemia-reperfusion injury was induced by ligation with nylon monofilament in rats of 7-, 14-, 28-day model groups. Low exercise group received treadmil training of 5 m/min, 5 minutes;7 m/min, 5 minutes;9 m/min, 20 minutes. Moderate exercise group received treadmil training of 8 m/min, 5 minutes;10 m/min, 5 minutes;13 m/min, 20 minutes. High exercise group received treadmil training of 8 m/min, 5 minutes;11 m/min, 5 minutes;20 m/min, 20 minutes. RESULTS AND CONCLUSION:Repulsive guidance molecule A mRNA and protein expression was highest in the ischemic side of the hippocampus in the 7-day model group without excercise. Moreover, repulsive guidance molecule A relative expression gradual y reduced over time. Compared with non-exercise, repulsive guidance molecule A mRNA and protein expression significantly decreased in the 14-and 28-day model groups during moderate exercise (P<0.05), but repulsive guidance molecule A mRNA and protein expression increased during high exercise. Above data confirmed that moderate exercises could decrease repulsive guidance molecule A expression in the affected side of the hippocampus of rats with cerebral ischemia-reperfusion injury.

f fibrosis-related factors in LX-2cells were significantly increased after co-cultured with QSG7701-HBx cells, which proved that HBx could induce fibrogenesis in vitro.

[Objective]To study the effect of femoral offset and hip joint center on joint function after total hip replacement,radiographic measurements were taken postoperation.[Method]A series of 92 hip joints(87 patients)were followed up.The average follow up priod was 25 monthes.The femoral offset and the position of the prothesis head center were measured in the orthophoric hip joint X-ray photograph and were compared with anatomic Fo and HJC.H arris evaluation system was used to evaluate joint function in four groups.The results were statistically analyzed,with Fisher' exact probability and P value less than 0.05 indicating significant difference.[Result]The coincidence rate of group A(both FO and HJC,27 hips)was 29.35%,group B(only Fo,23 hips)25.00%,group C(only HJC,31 hips)33.70%,group D(neither FO nor HJC,11 hips)11.96%.93.0% patients got the Harris score more than 80 for group A,73.19%(group B),74.19%(group C),27.27%(group D).The difference of Harris evaluation between A and B,A and C,A and D was significant statistically.[Conclusion]Based on the results of the study,the recovery of femoral offset and hip joint center should be considered to contribute to the healing effect after total hip replacement directly.

Objective To investigate the value of soluble triggering receptor expressed on myeloid cells-1(sTREM-1) in the diagnosis of bacterial pleural effusion. Methods The levels of sTREM-1 in pleural effusion were determined in 30 patients with bacterial pleural effusion, 33 patients with malignant pleural effusion,31 patients with tuberculous pleural effusion and 28 patients with transudate by quantitative ELISA assay. The levels of CRP in pleural effusion were assayed using immunonephelometry method. The diagnostic value was assessed by receiver operating characteristic ROC curve analysis. Results The levels of sTREM-1［(1255.2±248.6)ng/L］ in bacterial pleural effusion were significantly higher than those in malignant ［（125.6±22.4）ng/L］, tuberculous［（184.5±36.5）ng/L］ and transudate groups［（92.5±20.8）ng/L］ (P＜0.05). For ROC curve, when the cut off value of sTREM-1 was set at 425 ng/L, the sensitivity , specificity ,accuracy, positive predictive value and negative value was 93.3%,90.3%,91.9%,93.2% and 93.3%, respectively. Conclusions Detection of sTREM-1 in pleural effusion is helpful to differentiate pleural effusion of bacterial origin from those with other etiologies.

Objective To investigate the value of Cytochrome P450 (CYP3A5) * 3 gene polymorphism in providing individualized administration for the use of tacrolimus (Tac) in renal transplantation recipients.Method Pyrophosphate sequencing method was used to determine the CYP3A5 * 3 genotype of renal transplant patients in the first day after surgery.Sixty recipients were divided into experiment group and control group.Both groups of patients were routinely given the initial dose of Tac-4.0 mg/day in the first day after surgery.The experiment group of patients were given different doses of Tac based on the different CYP3A5 * 3 genotypes at the third day after surgery [for AA:0.12 mg/(kg· day),and for GG:0.06 mg/(kg· day)],and the control group of patients were given different dosages of Tac according to drug concentration.Different parameters were compared between two groups of patients:percentage of patients reaching the target concentration (3-8 μg/L) at the fifth day after surgery,days required to reach the target concentration level,times needed to adjust the dosage of Tac within two weeks.Result The percentage of patients reaching the target concentration in experiment group and control group was 90％ and 46.67％,respectively (P＜ 0.05).Days required to reach the target concentration were (3.67 ± 1.32) and (7.57 ± 3.42) on average,respectively (P ＜ 0.05).Times of adjusting the Tac dose in experiment group was significantly less than those in the control group (P＜0.05).In the experiment group,the target concentration was obtained even without dosage adjustment (70％).Conclusion Individualized adjustment of Tac doses for patients according to recipients' different CYP3A5 * 3 genotypes is beneficial for reaching target concentration as soon as possible,which is superior to traditional dosage regimen.

Objective To study the clinical characteristics,antimicrobial restistance of bloodstream infections (bacteremia) caused by multidrug-resistant Acinetobacter and analyze the outcomes of antibacterial therapy.Methods The clinical data were reviewed retrospectively for 74 patients with bloodstream infection caused by multidrug-resistant Acinetobacter who were trea-ted in HuaShan hospital from January 2005 to December 2011 .Results During the 6-year period,74 patients were diagnosed with multidrug-resistant Acinetobacter bacteremia,73 of which were nosocomial infections.The remaining one was community-acquired. Primary bloodstream infection accounted for 51 .4% (38/74),and secondary infection 48.6% (36/74), mainly secondary to pulmonary infections (23.0%,17/74). Solid tumor was the most common underlying disease (24.3%,18/74).Prior corticosteroid therapy,indwelling deep venous catheter,surgery and invasive procedures were predisposing factors of bacteremia. Acinetobacter-related bloodstream infections were associated with higher white blood cell count,increased neutrophil percentage,higher APACHE II score and lower serum albumin level.The bloodstream infection was caused by Acinetobacter baumannii in 65 pa-tients,Acinetobacter lwoffi in 7 patients,both Acinetobacter baumannii and Acinetobacter junii in one patient.The all-cause mortality rate was 27.0% (20/74).In vitro susceptibility testing showed that 20.0% (15/75 )of the Acinetobacter isolates were resistant to cefoperazone-sulbactam,which was the lowest among all the antibiotics tested.About 40.0% to 42.7% of the isolates were resistant to carbapenems.The outcome was related to the antimicrobial restistance.Carbapenem non-suscepti-ble Acinetobacter was associated with poorer outcome compared with carbapenem-susceptible Acinetobacter (mortality 46.9%vs 11 .9%,P <0.05 ).Cefoperazone-sulbactam non-susceptible Acinetobacter was also associated with poorer outcome com-pared with cefoperazone-sulbactam susceptible Acinetobacter (mortality 40.0% vs 18.2%,P <0.05).Of the 32 patients who had infections with carbapenem-non-susceptible Acinetobacter,20 received sulbactam-containing antimicrobial agent.The mor-tality of these 20 patients was 20.0% (4/20),significantly lower than that of the 12 patients who did not receive sulbactam-containing antimicrobial agent (66.7%).Conclusions Majority of the bloodstream infections caused by multidrug-resistant Acinetobacter are nosocomial infections.Surgical operation and serious condition may predispose the patients to develop Acine-tobacter bacteremia.Acinetobacter isolates are highly resistant to commonly used antibiotics.The Acinetobacter isolates not susceptible to carbapenem or cefoperazone-sulbactam are associated with poorer outcome and higher mortality.More attention should be paid to prevention and control of Acinetobacter-related nosocomial infections.

Objective To investigate the expression of cytokeratin 34βE12 in esophageal squamous cell carcinoma (ESCC),and its mechanism of action in the process of occurrence and development of an ESCC.Methods Immunohistochemistry was used to analyze the expression of cytokeratin 34βE12 in 252 ESCC patients,66 patients with esophageal carcinoma in situ,and 106 patients with adjacent normal esophageal mucosa before the relationship between its expression and biological behavior was evaluated on the basis of complete clinical information.In addition,Western blotting was used to determine the expression of cytokeratin 34βE12 in 60 patients with esophageal cancer and adjacent normal esophageal tissues.Results (1)The positive rate of caveolin-1 in ESCC,carcinoma in situ,and adjacent normal tissues was 85.7％,54.5％,and 25.7％,respectively.The difference between them was statistically significant (P ＜0.01).(2)The positive rate of cytokeratin 34βE12 in stages Ⅰ,Ⅱ,Ⅲ of ESCC was 76.5％,84.7％,and 96.3％,respectively.The expression intensity of cytokeratin 34βE12 in carcinoma tissue was gradually increased with the advance of clinical stages with a statistically significant difference (P =0.038).The positive rate of cytokeratin 34βE12 with group of lymph node metastasis was significantly higher than those without lymph node metastasis (P ＜ 0.01).(3)Western blotting results further confirmed that the expression of cytokeratin 34βE12 in ESCC was significantly higher than that in adjacent normal esophageal tissue (P ＜0.01).Conclusions The high expression of caveolin-1 might be involved in the occurrence and development of esophageal cancer.The expression of cytokeratin 34βE12 was correlated with the clinical stage of esophageal cancer.cytokeratin 34βE12 was a potential therapeutic target and a valuable prognostic indicator of esophageal cancer progression.

Objective: To investigate the effects of human tissue inhibitor of matelloproteinase 4 (TIMP 4) on vascular smooth muscle cells (VSMCs) migration and the neointimal formation after balloon injury in rats. Methods: The cultured VSMCs were transfected with an adenoviral vector containing human TIMP 4 gene, AdTIMP 4. Effect of TIMP 4 on VSMC migration was investigated by monolayer cell scrape. AdTIMP 4, control adenoviral vector or PBS was transduced into the rat carotid artery from the adventitial after carotid artery injury. Cell number within the internal elastic lamina 4 days after gene transfer was counted and neointima/media area ratio 28 days after gene transfer was calculated. Results: The migration distance of VSMCs infected with AdTIMP 4 was inhibited markedly. Morphometric analysis demonstrated a statistically significant reduction in the number of cells migrated into neointima compared with controls [(32.5?4.8) cells per section, (33.8?7.0) cells per section and (8.2?2.4) cells per section for uninfected, AdGFP treated and AdTIMP 4 treated arteries, respectively]. There was a reduction of intima/media ratio of TIMP 4 treated group by 66.5% compared with control groups 28 days after gene transfer ( P

BACKGROUND: The mitofusin 2 (Mfn2) may affects vascular smooth muscle cell Ras protein and suppress cellular proliferation through inhibition of extracellular signal-regulated protein kinase signaling pathway, which plays an important role in pathogenesis of vascular disorders such as hypertension, atherosclerosis and post-angioplasty restenosis. Mfn-2 gene amino acid sequence of the first 442 serine serves as protein kinase A (PKA) phosphorylation site, which is closely related to its phosphorylation status and may be involved in its functional regulation.OBJECTIVE: To investigate the effect of Mfn2 gene with PKA phosphorylation site deletion[Mfn2-PKA (△)] on inhibiting the proliferation of vascular smooth muscle cells and related signaling pathway.METHODS: Vascular smooth muscle cells of rats infected by recombinational adenovirus carrying green fluorescent protein,Mfn2 gane and Mfn2-PKA (△), were subcultured for 3-10 passages and randomly divided into 4 groups: ① Control group without intervention. ② Control group infected with adenovirus carrying green fluorescent protein. ③ Experiment group infected with adenovirus carrying Mfn-2 gene.④ Experiment group infected with adenovirus carrying Mfn2-PKA (△). Laser confocal microscopy was used to observe the locations of Mfn2 gene with and without PKA in cells. The expressions of extracallular signal-regulated protein kinase, Mfn2 gone and Mfn2-PKA (△) were determined by Western blot analysis. The growth curve of the vascular smooth muscle cells was explored by MTT.RESULTS AND CONCLUSION: The Mfn-2 and Mfn2-PKA (△) both expressed protein-specific bands in vascular smooth muscle cells. Two kinds of gone expression products were mainly located at the out membrane of mitochondria. Compared with the control group and adenovirus carrying green fluorescent protein group, the absorbance values at 3, 4, 5, 6 days were significantly reduced in adenovirus carrying Mfn2 group (P ＜ 0.01), and no obvious changes were observed in adenovirus carrying Mfn2-PKA (△) group. Compared with the control group and adenovirus carrying green fluorescent protein group, the extracellular signal-regulated protein kinase expression was significantly reduced in adenovirus carrying Mfn2 group (P ＜ 0.01), and no obvious changes were observed in adenovirus carrying Mfn2-PKA (△) group. Mfn2-PKA (△) located at the out membrane of mitochondria, has no effect on suppressing the proliferation of vascular smooth muscle cells, and no inhibition effect on extracellular signal-regulated protein kinase signaling pathway.

Objective To detect the effect of olfactory bulb(OB)lesion on proliferation,migration and differentiation of the neural stem cells(NSCs)in the subventricular zone(SVZ).Methods Forty-two healthy female SD rats were enrolled and randomly divided into normal control group,isotonic saline group and OB lesion at day 3,at weeks 1,2,3 and 4 groups,six rats per group.OB lesion was induced by N-methyl-D-aspartic acid(NMDA)injection.Bromodeoxyuridine(BrdU)was injected intraperitoneally to label NSCs.Immunohistochemical staining was used to detect the proliferation of SVZ NSCs.In addition,another 18 rats were randomly divided into normal control group,isotonic saline group and lesion group,six rats per group.BrdU was injected intraperitoneally one week after OB lesion and then the animals were sacrificed four weeks after BrdU injection to detect the migration and differentiation of NSCs with immunohistochemistry and immunofluorescence.Results Three days after OB lesion,BrdU-positive cells in SVZ began to increase(26.33 ± 2.58,P ＜0.01),reached the maximum at week 1 (35.33 +3.01,P＜0.01)and still sustained a high level at week 4(19.50+ 2.26,P＞0.05).Five weeks after the OB lesion,the rostral migratory-stream(RMS)and the BrdU-positive cells in OB were significantly increased(86.50 + 5.09,P ＜ 0.01)and(52.83 + 3.87,P ＜ 0.01),respectively.By using fluorescence double staining,most of the BrdU-positive cells were co-localized with the neuronal nuclear antigen(Neun),with a portion of BrdU-positive cells expressing the glial fibrillary acidic protein (GFAP).Conclusions OB lesion can improve the proliferation of NSCs in SVZ and migration of NSCs to OB.The newborn cells can differentiate into not only neurons,but also gliocytes and may be involved in lesion repair.