Comparison between uncut Roux-en-Y and Roux-en-Y reconstruction after distal gastrectomy for gastric cancer: A meta-analysis

AIM To compare uncut Roux-en-Y(U-RY) gastrojejunostomy with Roux-en-Y(RY) gastrojejunostomy after distal gastrectomy(DG) for gastric cancer.METHODS A literature search was conducted in Pubmed, Embase, Web of Science, Cochrane Library, Science Direct, Chinese National Knowledge Infrastructure, Wanfang, and China Science and Technology Journal Database to identify studies comparing U-RY with RY after DG for gastric cancer until the end of December 2017. Pooled odds ratio or weighted mean difference with 95% confidence interval was calculated using either fixed-or random-effects models. Perioperative outcomes such as operative time, intraoperative blood loss, and hospital stay; postoperative complications such as anastomotic bleeding, stricture and ulcer, reflux gastritis/esophagitis, delayed gastric emptying, and Roux stasis syndrome; and postoperative nutritional status(serum hemoglobin, total protein, and albumin levels) were the main outcomes assessed. Metaanalyses were performed using RevM an 5.3 software.RESULTS Two randomized controlled trials and four nonrandomized observational clinical studies involving 403 and 488 patients, respectively, were included. The results of the meta-analysis showed that operative time [weighted mean difference(WMD):-12.95; 95%CI:-22.29 to-3.61; P = 0.007] and incidence of reflux gastritis/esophagitis(OR: 0.40; 95%CI: 0.20-0.80; P = 0.009), delayed gastric emptying(OR: 0.29; 95%CI: 0.14-0.61; P = 0.001), and Roux stasis syndrome(OR: 0.14; 95%CI: 0.04-0.50; P = 0.002) were reduced; and the level of serum albumin(WMD: 0.71; 95%CI: 0.24-1.19; P = 0.003) was increased in patients undergoing U-RY reconstruction compared with those undergoing RY reconstruction. No differences were found with respect to intraoperative blood loss, hospital stay, anastomotic bleeding, anastomotic stricture, anastomotic ulcer, the levels of serum hemoglobin, and serum total protein. CONCLUSION U-RY reconstruction has some clinical advantages over RY reconstruction after DG.

Effect of ATF3-deletion on apoptosis of cultured retinal ganglion cells

AIM：To investigate the effect of activating transcription factor-3（ATF3）-deletion on apoptosis of cultured retinal ganglion cells（RGCs）.METHODS：Three ATF3 siR NA（ATF3-rat-651, ATF3-rat-319, ATF3-rat-520） were constructed, and were transiently transfected into RGC-5 cells. Quantitative real-time polymerase chain reaction（PCR） was used to examine ATF3 expression and the most effective ATF3 siR NA was selected for further studies. Flow cytometry was applied to investigate the effects of ATF3 deletion on RGC-5 apoptosis under elevated hydrostatic pressure. Quantitative realtime PCR and Western blot were performed to validate differentially expressed genes and proteins in ATF3-knockdown RGC-5 cells.RESULTS：ATF3 specific siR NA effectively down-regulated ATF3 expression and significantly inhibited cell apoptosis in RGC-5 cells. Quantitative real-time PCR and Western blot confirmed that ATF3 knockdown remarkably decreased Jun-B and increased c-Jun at both m RNA and protein levels in RGC-5 cells.CONCLUSION：ATF/cA MP-response element-binding family of transcription factors may be involved in the development of glaucoma and could be novel treatment targets for glaucoma.

Inhibition on Apoptosis Induced by Elevated Hydrostatic Pressure in Retinal Ganglion Cell-5 via Laminin Upregulating β1-integrin/Focal Adhesion Kinase/Protein Kinase B Signaling Pathway

Background：Glaucoma is a progressive optic neuropathy characterized by degeneration of neurons due to loss of retinal ganglion cells （RGCs）.High intraocular pressure （HIOP）,the main risk factor,causes the optic nerve damage.However,the precise mechanism of HIOP-induced RGC death is not yet completely understood.This study was conducted to determine apoptosis of RGC-5 cells induced by elevated hydrostatic pressures,explore whether laminin is associated with apoptosis under pressure,whether laminin can protect RGCs from apoptosis and affirm the mechanism that regulates the process of RGCs survival.Methods：RGC-5 cells were exposed to 0,20,40,and 60 mmHg in a pressurized incubator for 6,12,and 24 h,respectively.The effect of elevated hydrostatic pressure on RGC-5 cells was measured by Annexin V-fluorescein isothiocyanate/propidium iodide staining,3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay,and Western blotting of cleaved caspase-3 protein.Location and expression oflaminin were detected by immunofluorescence.The expression of β 1-integrin,phosphorylation of focal adhesion kinase （FAK） and protein kinase B （PKB,or AKT） were investigated with real-time polymerase chain reaction and Western blotting analysis.Results：Elevated hydrostatic pressure induced apoptosis in cultured RGC-5 cells.Pressure with 40 mmHg for 24 h induced a maximum apoptosis.Laminin was declined in RGC-5 cells after exposing to 40 mmHg for 24 h.After pretreating with laminin,RGC-5 cells survived from elevated pressure.Furthermore,β1-integrin and phosphorylation of FAK and AKT were increased compared to 40 mmHg group.Conclusions：The data show apoptosis tendency of RGC-5 cells with elevated hydrostatic pressure.Laminin can protect RGC-5 cells against high pressure via β 1-integrin/FAK/AKT signaling pathway.These results suggest that the decreased laminin of RGC-5 cells might be responsible for apoptosis induced by elevated hydrostatic pressure,and laminin or activating β1-integrin/FAK/AKT pathway might be potential treatments to prevent RGC loss in glaucomatous optic neuropathy.

Suppressive effect of Aurantii Fructus Immaturus and Atractylodis Macrocephalae Rhizoma on glutamic acid-induced autophagy of interstitial cells of Cajal

Objective:To investigate the effects of Aurantii Fructus Immaturus(Zhishi,ZS)and Atractylodis Macrocephalae Rhizoma(Baizhu,BZ)-containing serum on glutamate-induced autophagy in rat colonic interstitial cells of Cajal(ICCs)and to analyze the underlying mechanism.Methods:Rat colonic ICCs cultured in vitro were identified by fluorescence and then stimulated with glutamic acid(5 mmol/L)for 24 h to establish a cell model of autophagy.The cells were then treated with different concentrations of ZSBZ-containing serum or rat serum.The viability of the ICCs was detected with cell counting kit-8 assays,and cell apoptosis rates were examined with flow cytometry.The ultrastructure and autophagosomes in the ICCs were observed using transmission electron microscopy.The effects of ZSBZ-containing serum on apoptosis-associated mediators were assessed by Western blotting and real-time quantitative polymerase chain reaction.In addition,microtubule-associated protein light chain 3(LC3),p-phosphoinositide 3-kinase(p-PI3 K),p-Akt and p-mammalian target of rapamycin(pm TOR)expression was detected via Western blotting analysis.Results:Compared to those in the model group,ICC viability and apoptosis rates were significantly increased by ZSBZ-containing serum(P<0.05).In addition,the expression levels of Beclin-1,LC3,pPI3 K,p-Akt and p-mTOR were significantly lower(P<0.05)and Bcl-2 expression was higher in the ZSBZ-containing serum treatment groups than in the model group(P<0.05).Conclusion:Our findings demonstrated that ZSBZ protects glutamic acid-stimulated ICCs,and this beneficial effect may be mediated by a reduction in autophagy via inhibition of the PI3 K/Akt/mTOR pathway.