Respiratory viral infections are the most common cause of infantile wheezing, as well as one of the major inducents of acute exacebarbations of chronic childhood asthma. Recent studies focus on the mechanism of virus-induced airway inflammatory response which is still not completely clear. Many new pathophysiologic mechanisms such as epigenetics are advanced to explain the association between viral respiratory infections and asthma attack. In the present reports, recent data on the role of early-life viral infections in the development and progression of childhood asthma are reviewed.

Objective To observe the characteristics of macular optical coherence tomography (OCT) changes before and after silicone oil removal in patients who had undergone pars plana vitrectomy with silicone oil tamponade for macula-off rhegmatogenous retinal detachment (RRD).Methods Thirty-nine eyes that underwent silicone oil removal were enrolled in this retrospective study.The patients included 24 males and 15 females,with an average age of (53.05±4.03) years,the duration of silicone oil tamponade ranged from 3 to 7 months.Best-corrected visual acuity,intraocular pressure,slit lamp microscope and prelens,indirect ophthalmoscopy and fourier domain OCT were measured for all patients before and at months 1,3 and 6 after silicone oil removal.The macular microstructure were observed before and after silicone oil removal.Results Submacular fluid was detected in 6 eyes (15.38％),at the last time of follow-up,submacular fluid resolved completely in 2 eyes with disrupted ellipsoid zone,and resolved partly in 2 eyes.Disrupted ellipsoid zone were observed before silicone oil removal in 16 eyes (41.02％),6 eyes showed simultaneous disrupted ellipsoid zone and disrupted external limiting membrane,and there were 2 eyes that external limiting membrane was not identified,at the last time of follow-up,disrupted ellipsoid zone restored in 2 eyes and the extent of disrupted ellipsoid zone became reduced in 4 eyes.Cystoids macular edema were found in 2 eyes (5.12％),it resolved completely in 1 eye and resolved partly in 1 eye at the last time of follow-up.Macular epiretinal membrane was detected in 10 eyes (25.64％),and macular epiretinal membrane was found before silicone oil removal in 5 eyes,at the last time of follow-up,the membrane became thickened in 2 eye;5 eyes developed macular epiretinal membrane after silicone oil removal,at the last time of follow-up,the membrane became thickened in 1 eye.Secondary macular hole were noted in 2 eyes.Microcystic macular changes were observed in 9 eyes (23.07％),it was observed in 7 eyes before silicone oil removal,and was observed in 2 eyes after silicone oil removal,at the last time of follow-up,the cysts reduced in 1 eye.Conclusion Submacular fluid,disrupted ellipsoid zone and microcystic macular are the main macular ultrastructural changes that developed in patients with RRD before and after silicone oil removal.

Objective To evaluate the effect of dexmedetomidine on the activity of glycogen synthase kinase-3 beta (GSK-3β) during propofol-induced apoptosis in hippocampal nerve cells of newborn rats.Methods Sixty male 7-day-old Sprague-Dawley rats,weighing 10-15 g,were divided into 6 groups (n=10 each) using a random number table:normal saline group (group NS),fat emulsion group (group F),propofol group (group P) and different doses of dexmedetomindine groups (group D25,group D50 and group D75).Normal saline and fat emulsion 100 μl were injected intraperitoneally in group NS and group F,respectively.In group P,propofol 50 mg/kg was intraperitoneally injected,and an increment of propofol 50 mg/kg was added after righting reflex completely recovered,with the total amount of 100 mg/kg.In group D25,group D50 and group D75,dexmedetomidine 25,50 and 75 μg/kg were intraperitoneally injected,respectively,and 30 min later propofol 100 mg/kg was administered.At 2 h after emergence,the rats were sacrificed,their brains were removed for determination of apoptosis in hippocampal nerve cells (by TUNEL),and the hippocampi were isolated for detection of the expression of GSK-3β and phosphorylated GSK-3β (p-GSK-3β) by Western blot analysis.The apoptosis index (AI) and ratio of p-GSK-3β/GSK-3β were calculated.Results Compared with group NS,AI was significantly increased,the expression of p-GSK-3β was down-regulated,and the p-GSK-3β/GSK-3β ratio was decreased in P,D25,D50 and D75 groups (P＜0.05).Compared with group P,AI was significantly decreased,the expression of p-GSK-3β was up-regulated,and the p-GSK-3β/GSK-3β ratio was increased in D25,D50 and D75 groups (P＜0.05).Compared with group D25,AI was significantly decreased (P＜0.05),and no significant change was found in the expression of p-GSK-3β or ratio of p-GSK-3β/GSK-3β in D50 and D75 groups (P＞0.05).Compared with group D50,AI was significantly decreased (P＜0.05),and no significant change was found in the expression of p-GSK-3β or ratio of p-GSK-3β/GSK-3β in group D75 (P＞0.05).Conclusion The mechanism by which dexmedetomidine attenuates propofol-induced apoptosis in hippocampal nerve cells may be related to inhibition of GSK-3β activity in newborn rats.

Objective To evaluate the effects of dexmedetomidine on the expression of phosphor-cAMP response element binding protein (p-CREB) in isoloated hippocampal neurons of fetal rats.Methods SpragueDawley rats on 16-18 days of gestation were sacrificed and the fetal rats were obtained.The hippocampi of fetal rats were isolated and hippocampal neurons were seeded in culture medium for 8 days.The cells were then divided into 4 groups (n =12 each) using a random number table:control group (group C),dexmedetomidine 0.001 μmol/L group (group D1),dexmedetomidine 0.010 μmol/L group (group D2),and dexmedetomidine 0.100μmol/L group (group D3).In D1.3 groups,dexmedetomidine with the final concentrations of 0.001 μmol/L,0.010 μmol/L,and 0.100 μmol/L was added to the culture medium,respectively,and then the cells were incubated for 3.5 h.The apoptosis in hippocampal neurons was detected by flow cytometry.The expression of p-CREB in hippocampal neurons was determined by RT-PCR and Western blot.Results Compared with group C,apoptosis rate was significantly decreased and the expression of p-CREB was up-regulated in D1.3 groups.Conclusion Dexmedetomidine inhibits apoptosis in isolated hippocampal neurons of fetal rats by up-regulating the expression of p-CREB.

Objective To explore the effect of dexmedetomidine on phosphoinositide 3-kinase/protein kinase B (PI3K/Akt ) pathway in hippocampus of propofol anesthetized neonatal rats. Methods Eighty Sprague-Dawley male rats,aged 7 days,weighing 10-1 5 g,were randomly divided into 8 groups (n= 10 each):normal saline group (group N),DMSO group (group D),intralipid group (group I),propofol group (group P),dexmedetomidine 25 μg/kg,50 μg/kg and 75 μg/kg +propofol 100 mg/kg groups (groups PD25 ,PD50 and PD7 5 ),LY294002 25 μg + dexmedetomidine 75μg/kg + propofol 100 mg/kg group (group LYPD).The hippocampus of rats in all groups were taken 2 h after the animals fully awake.The ultrastructure of hippocampal neurons was observed by transmission electron microscope.The pAkt-(ser473 )protein and Akt protein in the hippocampus were evaluated by Western blot analysis.Results There was no significant difference in the expression of Akt protein among the eight groups.Compared with group N,the expression of pAkt (ser473)protein was significantly down-regulated in groups P,PD25 ,PD50 ,PD7 5 and LYPD (P <0.05).Compared with group P,the expression of pAkt (ser473)protein was increased significantly in groups PD7 5 and LYPD (P <0.05).Compared with group PD7 5 ,the expression of pAkt (ser473) protein was significantly down-regulated in group LYPD (P <0.05 ).The structure of hippocampal neurons was normal in groups N,I and D.Nuclear nuclei swelling,chromatin decreasing and mito-chondrion vacuolar degeneration were observed in group P while improved gradually with dexmedeto-midine in a dose-dependent manner in groups PD25 ,PD50 and PD7 5 .Neurons karyopyknosis,partial dissolution of nuclear membrane,chromatin condensation,mitochondria vacuolar degeneration were observed in group LYPD.Conclusion Dexmedetomidine pretreatment provides neuroprotection against propofol-induced hippocampal destruction by preserving PI3K/Akt pathway activity in the de-veloping brains.

Background and purpose:It has beenreported that miR-1284 is associated with gastric cancer lymph node metastasis in the research of microRNA microarray in human gastric cancer tissues. But the specific role of miR-1284 in gastric cancer has not been reported. The aim of this study was to investigate the effect of miR-1284 over-expression on the gene expression profiling and invasion/metastasis of human gastric cancer SGC-7901 cells. Methods:Gastric cancer SGC-7901 cells of LV-miR-1284 group were transfected with lentiviral vectors of miR-1284, cells of LV-NC-GFP group were transfected with lentiviral vectors without miR-1284, and cells of control group were not transfected with lentiviral vectors. The expression of miR-1284 was detected by the real-time fluorescent quantitative PCR. Differential expression genes were detected by the microRNA chip. Target genes of miR-1284 were predicted by the bioinformatics. Invasive ability was detected by the Transwell invasion assay. Metastasis ability was detected by subcutane-ously transplanted tumor model of nude mice.Results:Compared with LV-NC-GFP and control groups, the expressions of miR-1284 and 20 genes were up-regulated, and the expression of 17 genes was down-regulated in LV-miR-1284 group. One hundred and thirty-eight target genes of miR-1284 were predicted by the bioinformatics website. Compared with invasive cell number of LV-NC-GFP group (168.67±4.55) and control group (170.33±3.08), the ability of invasion ofcells was weakened in LV-miR-1284 group (70.00±2.37). Compared with the liver metastasis rate of LV-NC-GFP group (85.71%) and control group (85.71%), the ability of metastasis of cells was weakened in LV-miR-1284 group (14.29%). Conclusion:The ability of invasion and metastasis of SGC-7901 cells is suppressed by over-expression of miR-1284. The mechanism may be related to regulating the expression ofSUMO1 andJUNgenes.

AIM:To study the effect and the molecular mechanism of CDX 2 over-expression on the prolifera-tion, growth and cell cycle of human gastric cancer cell line SGC-7901.METHODS:The SGC-7901 cells in LV-CDX2-GFP group were transfected with the recombinant lentivirus vector LV-CDX2-GFP, the cells in LV-GFP group were trans-fected with the negative control lentiviral vector for the negative control , and the cells in blank control group were without any treatment.The cell proliferation was detected by CCK-8 assay.The cell cycle distribution was analyzed by flow cytome-try.The expression of CDX2, Bax, Bcl-2, cyclin D1 and survivin was determined by semi-quantitative RT-PCR and Wes-tern blotting .RESULTS:Compared with LV-GFP group and blank control group , the proliferation activity of the SGC-7901 cells was significantly lower (P<0.05), the G0/G1 phase proportion increased (P<0.05), the mRNA and protein levels of Bcl-2, cyclin D1 and survivin were reduced (P<0.05), and the mRNA and protein levels of Bax were up-regula-ted (P<0.05) in LV-CDX2-GFP group.No statistically significant difference of the above indexes was observed (P>0.05) between LV-GFP group and blank control group .CONCLUSION:Over-expression of CDX2 mediated by lentivirus inhibits the proliferation and growth of human gastric cancer SGC-7901 cells and arrestes the cell cycle at G 0/G1 phase, which may be related to down-regulation of Bcl-2, cyclin D1 and survivin and up-regulation of Bax .

Erythropoietin (EPO),which is routinely used in clinic to treat anemia,has been implicated in a wide range of activities on diverse tissues.Recently,accumulating evidence shows that EPO has antidepressant-like effects and may be a po-tential drug candidate for treating mood symptoms and memory dysfunction in depression.This review summarizes the current progress on EPO’s antidepressant-like effects,and explores its potential mechanism and clinical application in the future,provi-ding a general view of the research and application status of EPO in depression.

AIM:To evaluate the correlation between microRNA-1284 (miR-1284) and gastric cancer, and to investigate the underlying mechanism.METHODS: The expression of miR-1284 was examined by real-time PCR in 63 gastric cancer ( GC) tissue samples and 63 non-malignant adjacent tissue samples.The correlation between miR-1284 and the clinicopathological feature of GC was analyzed.Lentiviral vector containing miR-1284 was constructed and transfected into GC SGC-7901 cells.After transfection, the expression of miR-1284 was examined by real-time PCR.The cell activity was evaluated by CCK-8 assay.The cell cycle and apoptosis were determined by flow cytometry.The ability of cell migra-tion was measured by wound-healing assay.The potential target gene of miR-1284 was predicted by online bioinformatic softwares.The expression of JAG1 mRNA was examined by real-time PCR.The protein levels of JAG1, Notch1 and NF-κB were analyzed by Western blotting.RESULTS:Compared with non-malignant adjacent tissue samples, the results of real-time PCR showed significant downregulation of miR-1284 in 42 GC tissue samples ( P<0.05 ) .The expression level of miR-1284 was not significantly associated with age and gender of the patients, tumor size, TNM staging and lymph node metastases (P>0.05), but significantly associated with histologic grading (P<0.05).Compared with LV-NC-GFP group and control group, after transfection of miR-1284 in LV-miR-1284 group, the expression of miR-1284 was significantly in-creased (P<0.05), the percentages of apoptotic cells and the cells in G0/G1 phase were significantly increased (P<0.05), the cells activity and ability of migration were significantly decreased (P<0.05), and the expression of JAG1, Notch1 and NF-κB was significantly decreased (P<0.05).CONCLUSION:The inhibitory effect of miR-1284 on gastric cancer may be associated with the regulation of its targeting gene JAG1.

Objective To investigate the operation process,extent of resection,protection function,the tumor recurrence and clicical value of neuronavigation with intraoperative ultrasound for treating functional glioma;signifi-cance of intraoperative ultrasound for correcting brain shift.Methods We analyzed the cliclical materical of 24 case of functional gliomas which were resected by neuronavigation with intraoperative ultrasound.Results The accuracy of localization of functional glioma was 100%.The distance of brain shift was 2 to 10mm,with an average 4.7mm.After 24 hours MRI confirmed that total removal of function glioma was achieved in 21 cases,subtotal in 3 cases.After oper-ation function improve was 20 cases,invalid of 2 cases,hemiplegia happened in 2 cases and no death in all the patients.Conclusion Neuronavigation with intraoperative ultrasound can correct brain shift and improve the accuracy of localization of functional glioma,to improve extent of function glioma and decrease dysfunction.Neuronavigation with intraoperative ultrasound is important to functional glioma.