To observe its proliferation and cytolytic activity in vitro induced by autologous soluble tumor antigen and IL-2, PBMC costimulated with TSA extracted from gastric tumor by biochemical procedure and IL-2 was cultured. The proliferation and cytotoxicity were evaluated by MTT method and the phenotype was analysed by APAAP method. TSA alone did not induce PBMC proliferation while TSA (10?g/ml) with IL-2 presented syngenic stimulating effect which was time and concentration dependent. The cytolytic unit of PBMC induced with IL-2/TSA was 86.3% vs 48.6% with IL-2 alone. The phenotypic measurement demonstrated that TSA enhanced CD25 and CD8 expression significantly. The observation offered experimental data for further research work about tumor activated killer(TAK) cells. The results indicated that TAK cells would be a new type of immunoactive cells in adoptive immunotherapy against tumor.

Glial cell line-derived neurotrophic factor(GDNF) is a kind of protein factor which can regulate the enteric nervous system in survival,differentiation,colonization and injury repair.It has been confirmed in the disorders of the enteric nervous system,such as hirschsprung and anorectal malformations,but the specific mechanism in regulation of this factor is still unknown.Studies have found that GDNF/GFRa1/RET and GDNF/GFRa1 / NCAM pathway may be involved in the growth and maturation of the enteric nervous system,the disorders of those pathways above may lead to diseases by affecting the differentiation,proliferation and migration of intestinal neural stem cells,causing dysfunctions in the anatomical structure and function of the intestinal neurons.

Ras-related C3 botulinum toxin substrate 1 (Rac1) is a member of the small Rho guanosine triphosphatase (GTPase) family, having GTPase activity and serving as a " molecular switch" in a variety of cell signal transduction processes.It is involved in cell migration, adhesion, proliferation and apoptosis.Rac1 can affect the migration of neural crest cells through regulating the actin polymerization of neural crest cells and the formation of membrane protrusions, possibly leading to disorders related to abnormal neural crest migration, such as congenital megacolon and cardiac outflow tract defects.In this article, the main biological functions of Rac1 and its role in the mechanism of ente-ric neural crest cell development were described.

Regulatory non -coding RNA is a kind of non -ncoding RNA which has regulatory effect,play an important role in the development and plasticity of the human nervous system,and related to the pathogenesis of nervous system diseases.Hirschsprung′s disease(HD)is the the most common diseases associated with digestive tract pediatric deformity,at present the causes are not clear,generally considered the etiology of HD is the enteric nervous system (ENS)abnormal development of embryonic period,through the in -depth research of regulatory non -coding RNA in human nervous system development,finding that there is a close relationship between the regulatory non -coding RNA and nosogenesis of HD.This provides a basis for studying of the pathogenesis of HD.In this paper,research progress on regulatory non -coding RNA in the pathogenesis of HD are reviewed and this paper explore the role of RNA in HD,it provides a new target in the early diagnosis and treatment of HD.

China has entered a new economic and social development,public hospitals have to face the further deepening of the medical system reform,public welfare and welfare,and to face the fierce market competition in the field of social capital into the medical field.It is necessary to build a public hospital management accounting system.The significance of the construction of public hospital management accounting system is expounded,the problems of the construction of public hospital management accounting system are found out,and the corresponding countermeasures are put forward.

AIM:To investigate the role of p38 MAPK/ATF-2 pathway in C-relative protein ( CRP)-induced endothelial cell activation.METHODS:Human coronary artery endothelial cells ( HCAEC) were cultured and were used between passages 3 and 7.CRP served as a stimulus for endothelial cell activation.Western blotting was performed to de-termine the expression and phosphorylation of eNOS, p38 and ATF2.ELISA was carried out to detect the levels of ICAM-1, VCAM-1 and MCP-1 released from HCAEC.Pharmacological p38 inhibitors SB203580 and SB202190 were used to de-termine the effect of p38/ATF-2 pathway.RESULTS:CRP reduced the p-eNOS level in a concentration-dependent man-ner and induced the release of ICAM-1, VCAM-1 and MCP-1.The p38/ATF-2 pathway was activated by CRP treatment. SB203580 and SB202190 partially rescued p-eNOS level and suppressed the secretion of ICAM-1, VCAM-1 and MCP-1. CONCLUSION:p38MAPK/ATF-2 pathway participates in CRP-induced endothelial activation.

Objective To analyze the possible prognostic factors of thoracic-esophageal cancer patients with lymph node (LN) metastasis after esophagectomy plus three-field lymphadenectomy.Methods 590 esophageal cancer patients with LN metastasis after esophagectomy plus three-field lymphadenectomy were recruited from Jan.1993 to Mar.2007,and the prognostic factors and causes of postoperative failure were analyzed.Results Five-year survival in the whole sample was 29.6％.While the 5-year survival in different subgroups with 1-2,3-6 or ＞ 7 metastatic LNs were 41.2％,22.2％ and 7.0％ (x2 =62.158,P ＜0.0001),respectively.Univariate analysis showed that tumor site,disease length,T stage,number of metastatic LN and the seventh edition of AJCC staging system were prognostic factors.Multivariate analysis indicated that tumor site and number of metastatic LN were two independent prognostic factors.Conclusion Tumor site and number of metastatic LN were independent prognostic factors influencing the outcome of esophageal cancer.

Objective To evaluate the effect of oxycodone pretreatment on autophagy during renal ischemia-reperfusion (I/R) in rats.Methods Thirty-six SPF healthy adult male Wistar rats,aged 6-9 weeks,weighing 180-220 g,were divided into 3 groups (n=12 each) using a random number table:sham operation group (Sham group),I/R group and oxycodone pretreatment group (Oxy group).The left renal pedicles were clamped with atraumatic microclips for 45 min followed by reperfusion to establish the model of renal I/R injury in I/R and Oxy groups.Oxycodone 0.5 mg/kg was injected via the caudal vein at 15 min before ischemia in group Oxy,and the equal volume of normal saline was given instead in I/R and Sham groups.At 24 h of reperfusion,blood samples were collected from hearts for measurement of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations.The animals were then sacrificed and left renal tissues were obtained for examination of pathological changes (with a light microscope) and for determination of Bcl-2 and Beclin-1 expression (by immunohistochemistry).Results Compared with Sham group,the concentrations of serum Cr and BUN were significantly increased,and the expression of Bcl-2 and Beclin-1 in renal tissues was up-regulated at 24 h of reperfusion in I/R and Oxy groups (P<0.05).Compared with I/R group,the concentrations of serum Cr and BUN were significantly decreased,the expression of Bcl-2 in renal tissues was up-regulated,and the expression of Beclin-1 in renal tissues was down-regulated at 24 h of reperfusion (P<0.05),and the pathological changes were significantly attenuated in Oxy group.Conclusion Oxycodone pretreatment inhibits autophagy through up-regulating the expression of Bcl-2 and down-regulating the expression of Beclin-1,thus attenuating renal I/R injury in rats.

AIM:To investigate the effect of liraglutide ( LG) on the expression of fibronectin type Ⅲdomain-containing protein 5 (FNDC5) in the C2C12 myotubes.METHODS:The C2C12 mouse myoblast cell line was induced to differentiation.Differentiated cells were stimulated with gradient concentrations (1 ~1000 nmol/L) of LG for different time (0 ~24 h).The effects of LG on the expression of FNDC5 and the activation of adenosine 5'-monophosphate ( AMP)-activated protein kinase ( AMPK) signaling pathway were determined .After pretreated with glucagon-like peptide-1 ( GLP-1 ) receptor antagonist exendin 9-39 , the inhibitor of Ca 2+/calmodulin-dependent protein kinase kinase 2 (CAMKK2), STO609, or the inhibitor of AMPK, Compound C, the LG-induced FNDC5 expression in C2C12 myotubes was examined.The expression of FNDC5 and the activation of AMPK were determined by Western blot .RESULTS: In C2C12 myotubes, LG promoted the expression of FNDC5 in a dose-and time-dependent manner .LG also activated AMPK signaling pathway .These effects of LG were partly abolished by exendin 9-39 , STO609 and Compound C .CONCLUSION:LG promotes the expression of FNDC5 via GLP-1 receptor in the C2C12 myotubes possibly through activation of the CAMKK2/AMPK signaling pathways .

[ ABSTRACT] AIM:To investigate the role of hydrogen sulfide ( H2 S) on impaired wound healing in ob/ob mice and the underlying mechanism.METHODS:The ob/ob mice were randomly divided into 3 groups, including vehicle, in-sulin and NaHS for treatment.C57BL/6 mice were treated with vehicle as control.Full-thickness punch biopsy wounds were created on the mice.Firstly, H2 S concentrations in the skins and granulation tissues were measured.The mRNA ex-pression of cystathionineγ-lyase ( CSE) was detected by RT-qPCR.The protein expression of CSE and MMP-9 were deter-mined by Western blot.The neutrophil and monocyte/macrophage infiltration was analyzed by immunohistochemistry me-thod.The levels of tumor necrosis factor (TNF)-αand interleukin (IL)-6 were measured by ELISA.Collagen formation was measured by Masson staining.RESULTS:The H2 S levels in the skin and granulation were significantly decreased in ob/ob mice and increased in the NaHS-treated mice ( P<0.05 ) .CSE expression at mRNA and protein levels was significantly decreased in ob/ob mice compared with the control mice (P<0.05).The wound healing period was significantly shorter in NaHS group than that in vehicle-treated ob/ob mice group (P<0.05), in which the insulin group had no difference with vehicle ob/ob mice group.The neutrophil and monocyte/macrophage infiltration, and TNF-αand IL-6 levels were signifi-cantly increased in ob/ob groups, but were decreased in NaHS group ( P<0.01 or P<0.05 ) .Meanwhile, NaHS in-creased collagen formation in the granulation tissues of ob/ob mice.CONCLUSION:H2 S/CSE down-regulation contributes
to impaired wound healing in diabetes, which is alleviated by exogenous H2 S possibly through anti-inflammation.