Objective To investigate the clinical effects of phacoemulsification combined with goniosynechialysis on the treatment of primary angle-closure glaucoma (PACG) with cataract. Methods The retrospective review included 71 patients (98 eyes) with PACG and cataract treated in Tianjin Huanghe Hospital. Patients were underwent phacoemulsification and intraocular lens implantation combined goniosynechialysis. Among these patients, there were 21 males (30 eyes) and 50 females (68 eyes). Patients ranged in age from 53 to 94 years old, everage (73.94 ± 6.43) years old. They were divided into acute angle-closure glaucoma with cataract group (47 patients, 64 eyes) and chronic angle-closure glaucoma with cataract group (24 patients, 34 eyes). The visual acuity, intraocular pressure (IOP), anterior chamber angle, anterior chamber depth (CCT), topical and oral medications and surgical complications were observed before and after surgery in two groups. All the patients were followed up for 6 months. Results At the end of follow-up, postoperative visual acuity, IOP, CCT, anterior chamber angle and IOP-lowing medicine (topical and oral medications) were all improved in the two groups compared with those of preoperative levels (all P < 0.01). There were no statistical differences in preoperative or postoperative average visual acuity, IOP and anterior chamber angle between two groups (all P > 0.05). Values of CCT were significantly higher before and after operation in chronic angle-closure glaucoma with cataract group than those of acute angle-closure glaucoma with cataract group (P < 0.05). No drug-control rate of intraocular pressure was 76.5% (26/34) for chronic angle-closure glaucoma with cataract group than that of acute angle-closure glaucoma with cataract group (100%, 64/64). There was no need on topical medication in acute angle-closure glaucoma with cataract group. There were 14 eyes had corneal edema and 8 eyes appeared iris fibrous exudation in two groups, while no other serious complications. Conclusion For patients with PACG and cataract, the combined surgery of phacoemulsification and goniosynechialysis is a safe and effective therapy that can improve visual acuity and reduce IOP with fewer complications.

AIM: To determine the effect of rapamycin on the progression of passive Heymann nephritis (PHN), and whether autophagy is involved in this process .METHODS:Male Sprague-Dawley rats (n=24) were ran-domly divided into 3 groups:control group , PHN group and rapamycin treatment group .The rat PHN model was induced by injection of anti-Fx1A serum through penile vein , and all rats were sacrificed on day 21.Automatic biochemical analyzer was used to detect 24 h urine protein , blood urea nitrogen and serum creatinine .Renal damage was observed through per-iodic acid-silver methenamine staining .The number of podocyte was estimated by Weibel-Gomez method .The glomerular deposition of C5b-9, the expression of caspase-3 and expression of autophagy marker LC 3 in glomeruli were examined by immunofluorescence staining , immunohistochemical staining and Western blotting , respectively.RESULTS: Rapamycin significantly reduced proteinuria in the PHN rats (P<0.05), while the renal functions in 3 groups were normal, without significant difference .Although rapamycin limited weight gain in the rats , the health of the rats during drug treatment was not affected .Rapamycin retarded glomerular basement membrane thickening in the PHN rats .Rapamycin significantly re-duced the podocyte deletion by preventing podocyte apoptosis .Rapamycin enhanced the level of autophagy of glomerular in-herent cells .CONCLUSION:In the disease process of PHN , appropriate strength of autophagy plays a protective role . Rapamycin appropriately enhances autophagy and prevents podocyte apoptosis , thus reducing nephropathy and proteinuria . This may be one of the important mechanisms of rapamycin to slow down the progress of PHN .

Objective To investigate the role of autophagy in podocyte damage,and the intracellular mechanism of autophagy activation through passive Heymann nephritis (PHN) animal model.Methods Male Sprague-Dawley rats (n=40) were studied on day 0,2,4,7,and 21 after induction of PHN by injection of anti-Fx1A.Podocyte morphology and autophagosomes were observed by transmission electron microscopy.Podocyte numerical density was estimated by Weibel-Gomez =method.Cell apoptosis was detected by TUNEL assay and caspase-3 immunohistochemical staining.Expressions of autophagy markers and endoplasmic reticulum stress (ERS)-associated proteins were analyzed by Western blotting.Results (1) In PHN rats,immunohistochemical staining showed that C5b-9 deposited along glomerular basement membrane on day 4 to day 21.Small subepithelial electron -dense deposits and a part of foot process fusion were detected in the glomerulus of PHN rats on day 4 by transmission electron microscope,and podocyte damage was aggravated on day 21.Furthermore,compared with control,the urinary protein levels of PHN rats began to increase on day 3,and reached the top on day 21 [(50.6±6.0) mg/24 h].(2) The number of podocytes significantly decreased in PHN rats compared with control group on day 21(P ＜ 0.05).(3) In PHN rats,apoptotic podocytes were found by caspase-3 immunohistochemical staining and TUNEL assay on day 21.(4) The expression of autophagy marker LC3 Ⅱ was markedly increased on day 7 and 21,but down-regulated on day 21 compared with day 7.Moreover,accumulated autophagosomes in podocytes were detected on day 7 and 21 by transmission electron microscope.(5) The level of GRP78 was significantly increased on day 2 and 7 but reduced to baseline on day 21.At the same time,the downstream pathways (ATF6α,p-PERK and p-JNK) of unfolded protein response were also up-regulated in the early process of PHN and down-regulated later.Conclusions Autophagy is an important way to protect against immunemediated podocyte injury in membranous nephropathy.Autophagy activation is mainly related to endoplasmic reticulum stress induced by complement attack.This provides an important basis for a thorough understanding of the role of autophagy in the process of podocyte damage and the pathogenesis of membranous nephropathy.

AIM:In podocytes , autophagy occurs at a high basal level and dysregulated autophagy is associa -ted with a variety of podocytopathies .This paper is to investigate the role of autophagy in sublytic C 5b-9-induced podocyte injury.METHODS: Sublytic complement C5b-9 stimulation was used as an in vitro model.Autophagosomes were con-firmed using monodansylcadaverine (MDC) staining.Immunoblotting was used to measure the change of autophagy-related markers.Cellular morphological changes were observed by Wright-Giemsa staining.Immunofluorescence staining and con-focal microscopy were used to detect the expression and distribution of nephrin .The cell viability was assessed by methylth-iazol tetrazolium (MTT) assay.The cell apoptosis was assessed by Annexin V-fluorescein isothiocyanate/PI staining.RE-SULTS:For ensuring sublytic complement injury , the maximal amounts of anti-podocyte antiserum and 160 ×-diluted nor-mal human serum were used without inducing cell lysis (defined as >5%LDH release).Sublytic C5b-9 promoted autoph-agy of podocytes in vitro.The proautophagic effect of sublytic C 5b-9 manifested in the form of accumulated MDC-labeled vesicles and enhanced the expression of LC 3-Ⅱ.Autophagy inhibitor 3-methyladenosine (3-MA) promoted sublytic C5b-9-induced podocyte morphological abnormalities .Compared with the sublytic C5b-9-injured podocytes, 3-MA exposure further decreased the expression of nephrin .3-MA enhanced sublytic C5b-9-induced podocyte apoptosis .CONCLUSION: Sub-lytic C5b-9 attack induces autophagy , which may play a protective role against complement-mediated podocyte injury .

Objective To determine the effect of rapamycin on sublytic C5b-9-induced podocyte adhesion damage,and whether autophagy is involved in this progression.Methods Sublytic complement C5b-9 stimulation was used in vitro.Autophagosomes were viewed using electron microscopy.Western blotting was used to measure the change of autophagy-related markers.Attachment assay was used to assess the adhesion of podocyte.Confocal microscopy was used to explore the expression patterns of cytoskeletal protein F-actin.Flow cytometry was used to measure the level of adhesion-associated protein integrin α3.Results (1) For ensuring sublytic complement injury,the maximal amounts of anti-podocyte antiserum and 160×-diluted normal human serum were used without inducing cell lysis (defined as ＞ 5％ LDH release).(2) Sublytic C5b-9 promoted autophagy in podocyte in vitro.The proautophagic effect of sublytic C5b-9 manifested in the form of accumulated autophagosomes and enhanced expression of LC3-lⅡ.(3) Inhibition of autophagy by 3-methyadenine enhanced the effect of sublytic C5b-9-induced podocyte injury,including serious cytoskeleton damage and markedly reduced adhesion of podocyte.(4) Rapamycin treatment significantly improved the above lesions.(5) Rapamycin enhanced autophagy induced by sublytic C5b-9 in podocyte.Conclusions In summary,rapamycin can improve sublytic CSb-9-induced podocyte adhesion damage by appropriate autophagy activation.These findings provide important information for the development of appropriate protocols for the application of mTOR (mammalian target of rapamycin) inhibitors in podocytopathy.

ObjectiveTo study the role of L-arginine/nitric oxide (NO) pathway in the antidepressant effects of ketamine.MethodsForty two male Wistar rats (200-250 g) were equally randomized into 7 groups ( n =6 ):control group ( C group ),L-Arginine ( a precursor of NO ) group ( LA group),L-NAME ( an non-selectivity inhibitor of NO synthase) group ( LN group),ketamine 3 mg/kg group ( K3 group),ketamine 10 mg/kg group (K10 group),L-Arginine + ketamine 10 mg/kg group(LAK10 group),L-NAME + ketamine 3 mg/kg group (LNK3 group).The forced swimming test (FST) of 15 min (pre-test session) was used to establish a rat depression model,then twenty-four hours later FST (test session) was carried out of 6 min and the immobility time in last 5 min was recorded. All the groups were pretreated with saline 1.0 ml,L-arginine 750 mg/kg or L-NAME 30 mg/kg 90 min before FST.Saline 1.0 ml,ketamine 3.0 mg/kg or ketamine 10.0 mg/kg were injected 60 min before FST.The content of hippocampal NO was detected immediately after ethology measurement.ResultsCompared with C group (immobility time:( 139.0 ± 27.6)s),the immobility time decreased significantly (( 85.5 ± 34.2),(91.3 ±31.6)s) in K10 group and LNK3 group (P＜0.05),K3 group,LA group,LAK10 group and LN group had no significant difference (P＞0.05) ;compared with C group ( (0.61 ±0.21 ) μmol/gProt),the content of NO increased in LA group ( ( 1.09 ±0.39) μmol/gProt) and decreased in K10 group and LNK3 group significantly( (0.28 ± 0.12),(0.31 ± 0.14 ) μmol/gProt) (P ＜ 0.05 ),K3 group,LAK10 group and LN group had no significant difference (P ＞ 0.05).ConclusionThe antidepressant effects of ketamine are related to the suppression of L-arginine/nitric oxide pathway.

Objective To investigate the mechanism of carbapenem-resistant in Enterobacteriaceae strains isolated from Fuyang First People′s Hospital and to analyze their epidemiological features. Methods The Enterobacteriaceae strains with reduced ertapenem susceptibility were isolated from the Fuy-ang First People′s Hospital during January 2013 to August 2014.K-B disk diffusion and E-test were per-formed to detect the antimicrobial susceptibilities of those strains.The modified Hodge test, ethylenediami-netetraacetic acid ( EDTA) disk synergy test and extended-spectrumβ-lactamases ( ESBLs) confirmation test were used to screen out the carbapenem-resistant phenotypes.PCR analysis and gene sequencing were used to analyze drug resistance genes, genetic structures surrounding the blaKPC-2 gene and seven house-keeping genes of Klebsiella pneumonia ( K.pneumoniae) strains.The sequences of the seven house-keeping genes were analyzed with multilocus sequence typing ( MLST) .Pulsed field gel electrophoresis ( PFGE) was per-formed for homology analysis within the same species.S1-PFGE in combination with Southern blot analysis was used to determine the location of carbapenem resistance genes.Results A total of 19 Enterobacteriace-ae isolates with reduced susceptibility to ertapenem were screened out.Each of them was resistant to multiple antibiotics and harbored several resistance genes.Seven genes including the blaKPC-2 , blaIMP-4 , blaSHV-1 , blaCTX-M-65 , blaCTX-M-15 , blaTEM-1 and rmtB genes were the prevalent drug resistance genes.Fourteen out of the nineteen strains were identified as K.pneumoniae strains, mainly belonged to the ST11 type according to the results of MLST.Among the nineteen strains, eleven K.pneumoniae isolates and one Escherichia coli isolate carried the blaKPC-2 gene, located on plasmids varying in size (95 kb, 140 kb, 200 kb and 240 kb) .The ge-netic structures of all isolates were ISKpn8, blaKPC-2 and ISKpn6-like from upstream to downstream.The blaIMP-4 gene was detected in one Klebsiella oxytoca isolate and one K.pneumoniae isolate, located on a plas-mid about 300 kb in size.Conclusion Carbapenemases KPC-2 and IMP-4 were closely related to the car-bapenem resistance in carbapenem-resistant Enterobacteriaceae strains isolated form the Fuyang First People′s Hospital.No predominant clone was found in those carbapenem-resistant K.pneumoniae isolates.

Background/Aims: Interleukin-22 (IL-22) is an important cytokine maintaining homeostasis at barrier surfaces. In this study, the role of IL-22 in acute pancreatitis-associated intestinal injury was further explored. Methods: Severe acute pancreatitis (SAP) was induced by administration of L-arginine in Balb/c mice at different time gradients. Histopathological examinations were made in both the pancreas and small intestine. Furthermore, recombinant murine IL-22 (rIL-22) was administrated to L-arginine-induced SAP mice by intraperitoneal injection. The mRNA levels of IL-22R1, Reg-IIIβ,Reg-IIIγ, Bcl-2, and Bcl-xL were detected in the small intestine by real-time polymerase chain reaction, and protein levels of total and phosphorylated STAT3 were assessed via Western blot. Results: Compared with normal control group, 72 hours of L-arginine exposure induced the most characteristic histopathological changes of SAP, evidenced by pathological changes and serum amylase levels. Meanwhile, significant pancreatitis-associated intestinal mucosa injury was also observed. The gene expression levels of antimicrobial proteins Reg-IIIβ, Reg-IIIγ and anti-apoptosis proteins Bcl-2, Bcl-xL were downregulated in small intestine. Furthermore, Larginine-induced SAP was attenuated by rIL-22 treatment. Importantly, pancreatitis-associated intestinal mucosa injury was also ameliorated, reflected by improved pathological changes and significant increase in gene expression levels of Reg-IIIβ, Reg-IIIγ, Bcl-2 and Bcl-xL. Consistently, serum amylase levels and mortality were decreased in mice treated with rIL-22. Mechanistically, the upregulated expressions of these protective genes were achieved by activating STAT3. Conclusions Exogenous rIL-22 attenuates L-arginine-induced acute pancreatitis and intestinal mucosa injury in mice, via activating STAT3 signaling pathway and enhancing the expression of antimicrobial peptides and antiapoptotic genes.

Background/Aims: Interleukin-22 (IL-22) is an important cytokine maintaining homeostasis at barrier surfaces. In this study, the role of IL-22 in acute pancreatitis-associated intestinal injury was further explored. Methods: Severe acute pancreatitis (SAP) was induced by administration of L-arginine in Balb/c mice at different time gradients. Histopathological examinations were made in both the pancreas and small intestine. Furthermore, recombinant murine IL-22 (rIL-22) was administrated to L-arginine-induced SAP mice by intraperitoneal injection. The mRNA levels of IL-22R1, Reg-IIIβ,Reg-IIIγ, Bcl-2, and Bcl-xL were detected in the small intestine by real-time polymerase chain reaction, and protein levels of total and phosphorylated STAT3 were assessed via Western blot. Results: Compared with normal control group, 72 hours of L-arginine exposure induced the most characteristic histopathological changes of SAP, evidenced by pathological changes and serum amylase levels. Meanwhile, significant pancreatitis-associated intestinal mucosa injury was also observed. The gene expression levels of antimicrobial proteins Reg-IIIβ, Reg-IIIγ and anti-apoptosis proteins Bcl-2, Bcl-xL were downregulated in small intestine. Furthermore, Larginine-induced SAP was attenuated by rIL-22 treatment. Importantly, pancreatitis-associated intestinal mucosa injury was also ameliorated, reflected by improved pathological changes and significant increase in gene expression levels of Reg-IIIβ, Reg-IIIγ, Bcl-2 and Bcl-xL. Consistently, serum amylase levels and mortality were decreased in mice treated with rIL-22. Mechanistically, the upregulated expressions of these protective genes were achieved by activating STAT3. Conclusions Exogenous rIL-22 attenuates L-arginine-induced acute pancreatitis and intestinal mucosa injury in mice, via activating STAT3 signaling pathway and enhancing the expression of antimicrobial peptides and antiapoptotic genes.

OBJECTIVETo explore the optimal surgical approach for Siewert II and III adenocarcinoma of esophagogastric junction (AEG).

METHODSClinical data of 135 patients with Siewert II and III AEG treated in our hospital from August 2007 to August 2012 were analyzed retrospectively. Of 135 patients, 57 received transthoracic path for the stomach and proximal gastrectomy, second station lymph node resection (transthoracic group), and 78 cases received transabdominal hiatal approach (transabdominal group). The intraoperative lymph node harvested, postoperative complications and 5-year survival rate were compared between the two groups.

RESULTSThere were no significant differences in the residual tumor positive margin and anastomotic leakage rate between the two groups (both P>0.05). Compared with transthoracic group, transabdominal group had more lymph node dissected (11.1±0.2 vs. 10.4±0.3, P=0.033], less postoperative cardiac [2.6% (2/78) vs. 19.3% (11/57), P<0.01] and pulmonary [7.7% (6/78) vs. 21.1% (12/57), P<0.05] morbidity, and short postoperative hospital stay [(13.4±0.1) d vs. (16.4±0.3) d, P<0.01]. A total of 128 cases were followed up for median 38 months (6 to 72 months). The 5-year survival rate in transthoracic group and transabdominal group was 29.8% and 34.6% respectively, without significant difference (P>0.05).

CONCLUSIONFor the treatment of patients with Siewert II and III AEG, transabdominal hiatal approach can remove more lymph nodes, reduce postoperative cardiopulmonary morbidity and shorten hospital stay.

Adenocarcinoma ; surgery ; Esophageal Neoplasms ; surgery ; Esophagogastric Junction ; pathology ; Gastrectomy ; Humans ; Lymph Node Excision ; Lymph Nodes ; pathology ; Postoperative Complications ; Retrospective Studies ; Stomach Neoplasms ; surgery ; Survival Rate