Objective To analyze the distribution and antimicrobial resistance of pathogenic strains in wound infec-tion,and provide scientific evidence for rational use of antimicrobial agents in treatment of wound infection as well as reducing the emergence of drug-resistant organisms.Methods Data about pathogenic strains isolated from wound specimens of patients with wound infection in a hospital between June 2011 and April 2014 were analyzed retrospectively.Results A total of 965 pathogenic strains were isolated from wound specimens,the main infection sites were limbs(50.47%);infected patients mainly distributed in department of orthopaedic surgery(44.97%);trauma and incisional wound infection were the major infection types(47.98%,36.48%,respectively).Among iso-lated pathogens,gram-positive bacteria,gram-negative bacteria,and fungi accounted for 37.20%,59.59%,and 3.21 % respectively.The main gram-positive bacteria were highly susceptible to vancomycin,teicoplanin,and linezolid,the main gram-negative bacteria were highly resistant to most commonly used antimicrobial agents except cefoperazone/sulbactam,piperacillin/ tazobactam,imipenem,and meropenem.Conclusion Patients with wound infection are mainly distributed in department of orthopedics,the main infection types are trauma and surgical site infection,antimicrobial resistant rates of the major gram-positive and gram-negative bacteria are both high.Sur-geons,especially orthopedics surgeons,should pay attention to the culture of pathogens and monitoring of antimi-crobial susceptibility,use antimicrobial agents rationally,and strengthen the prevention and control of surgical site infection,so as to reduce the infection incidence and occurrence of drug-resistant organisms.

Aim To investigate the effect of indirubin derivative PHⅡ-7 and TRAIL on proliferation in breast cancer cell MCF-7 and its MDR counterpart MCF-7/ADR and the mechanism.Methods Growth inhibition rate was examined respectively by MTT assay under treatment with TRAIL or PHⅡ-7 or in combination. Cell apoptosis and ROS production were examined by flow cytometry.The change of TRAIL receptors(DR4/DR5 )in mRNA was analysed by realtime PCR.Re-sults IC50 of PHⅡ-7 on MCF-7 and MCF-7/ADR was (4.49 ±1.55 ),(3.44 ±0.90 )μmol · L-1 respec-tively;MDA-MB-231 was TRAIL sensitive cell line, and apparently TRAIL induced apoptosis in MDA-MB-23 1 .Low concentration of PHⅡ-7 in combination with TRAIL could augment TRAIL-induced cytotoxic effect including apoptosis while TRAIL or PHⅡ-7 treatment alone had limited cytotoxity to those cells.Besides, PHⅡ-7 at this concentration had little toxicity to hu-man peripheral blood mononuclear cells even if in com-bination with TRAIL.PHⅡ-7 generated ROS produc-tion inside MCF-7 and MCF-7/ADR cells and up-regu-lated DR4/DR5 expression concentration dependently. Once upon ROS scavenger NAC involved,the effect of TRAIL receptors up-regualtion by expression was abro-gated.Conclusions PHⅡ-7 at low concentration could improve the sensitivities of breast cancer cell MCF-7 and MCF-7/ADR to TRAIL,the mechanism of which may be the ability of ROS production by PHⅡ-7 help up-regulated TRAIL receptor DR4,DR5 .Our re-search set a solid foundation for PHⅡ-7 in combination with TRAIL in future clinical application.

Aim To explore the anti-proliferation effects of curcumin trinicotinate ( CurTn ) on vascular smooth muscle cell ( VSMC ) and its mechanism. Methods The cells were cultured in DMEM supple-mented with 10% fetal bovine serum. MTT assay was used to examine cell proliferation. FCM was used to observe cell cycle. The expressions of PCNA, Cy-clinD1 and p-ERK1/2 were analyzed using Western blot. Results CurTn could inhibit the proliferation of VSMC and showed a certain amount-time relationship. What’ s more, CurTn could increase the G1 phase pro-portion of cell, decrease the S phase proportion and the expression level of PCNA protein. It was also found that CurTn significantly inhibit the protein expression of p-ERK1/2 and Cyclin D1 . Conclusion CurTn may inhibit the proliferation of VSMC via downregulating the expression of CyclinD1 and p-ERK1/2 .

Primary central nervous system germ cell tumors (CNS-GCTs) in children and adolescents have unique clinical features and methods of treatment compared with those in adults. There is little information about Chinese children and adolescents with CNS-GCTs. Therefore, in this study we retrospectively analyzed the clinical features and treatment outcome of Chinese children and adolescents with primary CNS-GCTs. Between January 2002 and December 2012, 57 untreated patients from a single institution were enrolled. They were diagnosed with CNS-GCTs after pathologic or clinical assessment. Of the 57 patients, 41 were males and 16 were females, with a median age of 12.8 years (range, 2.7 to 18.0 years) at diagnosis; 43 (75.4%) had non-germinomatous germ cell tumors (NGGCTs) and 14 (24.6%) had germinomas; 44 (77.2%) had localized disease and 13 (22.8%) had extensive lesions. Fifty-three patients completed the prescribed treatment, of which 18 underwent monotherapy of surgery, radiotherapy, or chemotherapy, and 35 underwent multimodality therapies that included radiotherapy combined with chemotherapy or surgery combined with chemotherapy and/or radiotherapy. PEB (cisplatin, etoposide, and bleomycin) protocol was the major chemotherapy regimen. The median follow-up time was 32.3 months (range, 1.2 to 139 months). Fourteen patients died of relapse or disease progression. The 3-year event-free survival (EFS) and overall survival rates for all patients were 72.2% and 73.8%, respectively. The 3-year EFS was 92.9% for germinomas and 64.8% for NGGCTs (P = 0.064). The 3-year EFS rates for patients with NGGCTs who underwent monotherapy and multimodality therapies were 50.6% and 73.5%, respectively (P = 0.042). Our results indicate that multimodality therapies including chemotherapy plus radiotherapy were better treatment option for children and adolescents with CNS-GCTs.
Adolescent ; Antineoplastic Agents ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Bleomycin ; administration & dosage ; Central Nervous System Neoplasms ; therapy ; Child ; Child, Preschool ; Cisplatin ; administration & dosage ; Combined Modality Therapy ; statistics & numerical data ; Disease-Free Survival ; Etoposide ; administration & dosage ; Female ; Humans ; Male ; Neoplasm Recurrence, Local ; Neoplasms, Germ Cell and Embryonal ; therapy ; Retrospective Studies ; Survival Rate ; Treatment Outcome

OBJECTIVETo design and develop a novel esophageal prosthesis by selecting appropriate biomaterials, developing special manufacturing techniques, and investigating the feasibility of replacement of cervical esophagus in mongrel dogs.

METHODSIn accordance with the requirements of ideal esophageal substitutes, we designed a new type of esophageal prostheses. The inner stent were made with polyurethane of medical grade, and the outer surface of the prosthesis was coated with collagen-chitosan sponge. The silicone tube was used as a control. Thirteen adult mongrel dogs that were divided into two groups were used to establish the experimental models.

RESULTSIn the experimental group (n = 8), the esophageal prostheses were completely incorporated with the native esophagus and adherent to the surrounding host connective tissues. Epithelial linings of varying degrees were formed on the luminal surface, and complete epithelization was seen in 1 month postoperatively. The granulation at the sites of the anastomosis in this group was less significant than that of the control group. One dog has been surviving for 12 months up to now without any complications. In the control group (n = 5), esophageal epithelial was not observed on the luminal surface, constriction of the regenerated esophagus progressed and all the dogs died within 2 months after operation.

CONCLUSIONThese observations suggest that this esophageal prosthesis made of composite biomaterials has high biocompatibility and potential for long-segment esophageal reconstruction, which is promising for the clinical repair of esophageal defects.

Absorbable Implants ; Animals ; Artificial Organs ; Biocompatible Materials ; Chitosan ; Collagen ; Dogs ; Esophagus ; Implants, Experimental ; Models, Animal ; Polyurethanes ; Prosthesis Design ; methods ; Prosthesis Implantation

OBJECTIVETo investigate the effect of adenovirus-mediated endostatin gene transfer on transplanted lung cancer in mice and its mechanism of action.

METHODSTransplant tumor model was induced by subcutaneous inoculation of 2 x 10(6) Lewis lung cancer (LLC) cells into the back of C57BL/6 mice. The mice were treated by intratumoral injection of 2 x 10(9) pfu Ad-mEndostatin. The expression of endostatin in situ and its maintaining time were detected by immunohistochemistry and Western Blot, respectively. The endostatin level in serum was determined by ELISA . The inhibition of tumor growth and changes of survival were recorded and the microvessel density (MVD) was determined by histochemical stainingwith CD31 and CD105 antibodies. The tumor apoptosis was observed by electron microscopy.

RESULTSIn comparison with controls, intratumoral injection of Ad-mEndostatin significantly inhibited the tumor growth and metastasis, and prolonged the survival rate of mice (P < 0.05). Strong positive expression of mEndostatin was seen in the tumor tissue after injection of Ad-mEndostatin, immunhistochemically ostained by mouse endostatin monoclonal antibody, while the control groups showed only very low expression or absence. Serum endostatin concentration was 1540 +/- 560 ng/ml at the second week of administration, the expression of endostatin diminished a month later. The microvessel density (MVD)) decreased from 42.4 +/- 4.8 to 10.5 +/- 3.2 per x 200 magnificetion microscopic field by CD10 staining and from 68.5 +/- 4.5 to 37.5 +/- 4.6 by CD31 staining, respectively (P < 0.05). More apoptotic tumor cells were seen under the transmission electron microscope.

CONCLUSIONEndostatin gene therapy mediated by adenoviral vector efficiently induces expression of endostatin in vivo, and inhibits the growth and metastasis of tumor. It is concluded that its action is targeted to tumor neovasculature and the mechanism is inhibition of tumor angiogenesis.

Adenoviridae ; genetics ; Angiogenesis Inhibitors ; genetics ; metabolism ; therapeutic use ; Animals ; Carcinoma, Lewis Lung ; metabolism ; pathology ; therapy ; Cell Line, Tumor ; Endostatins ; genetics ; metabolism ; therapeutic use ; Genetic Therapy ; Genetic Vectors ; Male ; Mice ; Mice, Inbred C57BL ; Microvessels ; pathology ; Neoplasm Transplantation ; Neovascularization, Pathologic ; pathology ; Random Allocation ; Transfection ; Tumor Burden

BACKGROUNDAdvanced oxidation protein products (AOPPs) are new uremic toxins reported by Witko-Sarsat in 1996, which are associated with the pathogenesis of atherosclerosis. However, the mechanisms by which AOPPs enhance atherosclerosis have not been fully understood. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine which stimulates migration of monocytes and plays a critical role in the development of atherosclerosis. In this study, we investigated the effect of AOPPs on MCP-1 expression in cultured vascular smooth muscle cells (VSMCs).

METHODSVSMCs were cultured and then co-incubated with AOPP (200 micromol/L, 400 micromol/L) for different times with or without pretreatment with specific p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580. RT-PCR and Western blott were used to detect MCP-1 mRNA and protein expression at different time points after AOPP stimulation in rat smooth muscle cells. Western blot was used to detect the expression of phosphorylated p38 MAPK.

RESULTSTreatment of VSMC with AOPPs resulted in a significant increase of the expression of MCP-1 mRNA and protein in time- and dose-dependent manner, and could activated p38 MAPK. Pretreatment of VSMCs with SB203580 resulted in a dose-dependent inhibition of AOPPs-induced MCP-1 mRNA and protein expression.

CONCLUSIONSAOPPs can stimulate MCP-1 expression via p38 MAPK in VSMCs. This suggests that AOPPs might contribute to the formation of atherosclerosis through this proinflammatory effect.

Animals ; Atherosclerosis ; etiology ; Cardiovascular Diseases ; etiology ; Cells, Cultured ; Chemokine CCL2 ; genetics ; Enzyme Activation ; Imidazoles ; pharmacology ; Kidney Failure, Chronic ; complications ; Male ; Muscle, Smooth, Vascular ; cytology ; metabolism ; Myocytes, Smooth Muscle ; metabolism ; Oxidation-Reduction ; Proteins ; metabolism ; Pyridines ; pharmacology ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; Uremia ; metabolism ; p38 Mitogen-Activated Protein Kinases ; physiology

OBJECTIVE To study the clinical curative effect of Qigui Yishen decoction in the treatment of patients with chronic kidney diseases of spleen and kidney deficiency.METHODS Patients with chronic kidney diseases met the diagnosis criteria were divided into two groups.Both groups were given the high quality low protein,low salt,low fat,low phosphorus diet,and also given basic treatments such as correcting water and electrolyte disorders,acidosis,anemia,lowering blood pres-sure,anticoagulation and regulating lipid.On the basis of this,the treatment group was also given Qigui Yishen decoction o-rally.Objective indexes including kidney function,serum plasminogen activator inhibitor-1(PAI-1),transforming growth fac-tor-β1(TGF-β1)and changes of TCM syndrome scores were observed after four weeks.RESULTS After the treatment,TCM syndrome scores in two groups decreased significantly compared with pre-treatment(P<0.05~0.01),and the treatment group was better than the control group(P<0.05~0.01).PAI-1,ALB/Cr,TGF-β1 and IL-6 levels in two groups decreased significantly after treatment(P<0.05~0.01),and the treatment group was better the control group(P<0.05~0.01). CONCLUSIONS Qigui Yishen decoction has definite curative effect on protecting renal function and alleviating the progress of renal fibrosis,and its therapeutic effect may be related to the improvement of blood coagulation and endothelial cell function.

OBJECTIVETo investigate the effect of adjuvant chemotherapy on the prognosis of patients with low-risk cervical cancer (without pelvic lymph node metastasis, parametrial involvement, positive surgical margin, primary tumor size > 4 cm, deep cervical stromal invasion, or lymph-vascular space invasion).

METHODSThe clinical data of 208 patients with low-risk cervical cancer were studied retrospectively to analyze the indications of adjuvant chemotherapy and its relationship with tumor recurrence and the patients' survival.

RESULTSThe median follow-up time of the cohort was 73 months. The overall tumor recurrence rate was 4.8% and the total 5-year survival rate of the patients was 96.0%. Sixty-nine of the patients received adjuvant chemotherapy (Taxol+Cisplatin) after the operation with a median of 2.5 (2-4) courses. Univariate analysis showed that the histological tumor grade was significantly associated with adjuvant chemotherapy (P<0.001). In the 114 grade III patients, 50 received adjuvant chemotherapy as compared with 19 in the 94 grade I-II patients. Among the grade III patients, no significant differences was found in the overall survival rate (97.0% vs 95.0%) or tumor recurrence rate (4.0% vs 4.7%) rate between the patients with adjuvant chemotherapy and those without. The tumor size (2 cm or less vs >2 cm) was significantly associated with tumor recurrence rate (1.1% vs 7.5%, P=0.034) and the overall 5-year survival rate (100.0% vs 93.0%, P=0.034) in the 208 patients. In the 139 patients receiving only surgical treatment, the tumor recurrence and 5-year survival rates were not significantly correlated with the histologic grade, age, FIGO staging, gross type, tumor size or histologic type.

CONCLUSIONB There has been no sufficient evidence to support the prescription of postoperative adjuvant chemotherapy for low-risk cervical cancer based on histological grading of the tumor, which may not help in reducing tumor recurrence or improving the long-term survival of the postoperative patients.

Adult ; Aged ; Chemotherapy, Adjuvant ; Female ; Humans ; Middle Aged ; Prognosis ; Retrospective Studies ; Survival Rate ; Treatment Outcome ; Uterine Cervical Neoplasms ; drug therapy ; mortality ; pathology ; Young Adult

Objective: To replace esophageal defects with artificially composed biodegradable materials and non-biodegradable materials. Met hods: A two-layered tube consisting of a collagen-chitosan sponge and an inner polyurethane stent was used to replace 5 cm esophageal segmental defect s in 15 dogs. The inner polyurethane stent was removed endoscopically at weekly intervals from 2 or 4 weeks. Results: Partial regeneration of es ophageal epithelia was observed in 5 dogs at week 2, and progressing constricti on occurred and the dogs became unable to swallow within 1 month. In the 10 dog s that the polyurethane stent was removed at week 4, regenerated esophageal tiss ue successfully replaced the defects, and complete epithelization was observed 1 month after surgery. Complete regeneration of esophageal mucosa structures, inc luding mucosal smooth muscle and mucosal glands were observed 3 months after surgery, and partial regeneration of esophageal muscle tissue was also observed 6 months after surgery. Conclusion: Our artificial prosthesis i n reconstruction of the cervical esophagus segment in dogs is feasible. Through temporary polyurethane tube, collagen-chitosan sponge provides a three-dimensi onal structure suitable for the regeneration and sufficient degradation time for the complete regeneration of esophagus.