OBJECTIVE:To standardize periooperative prophylactic application of antibiotics. METHODS:According to the characteristics of orthopaedic and parenchyma surgery,classifying evaluation table of typeⅠincision infection risk was designed sci-entifically and rationally. The individual application of antibiotics in surgery patients had been achieved through infection risk evalua-tion. High risk typeⅠincision patients used antibiotics rationally and low risk patients seldom used or didn’t use at all. RESULTS:Through using infection risks classifying table,the rate of antibiotics prophylactic application in typeⅠincision drops from 74.10%to 28.68%,and and the per capita duration of antibiotics prophylactic application shortened from 4.23 d to 2.21 d. The postopera-tive infection rate remained the same. CONCLUSIONS:Through infection risk classifying evaluation,individual application of anti-biotics can be achieved in surgery patients,so as to promote rational use of antibiotics for prophylactic use,reduce antibiotics dos-age and antibiotics abuse under the condition of controllable surgery infection.

Objective To compare the effect of different partition of nucleic acid protein complex on the affinity of enriched library in systematic evolution of ligands by exponential enrichment (SELEX). Methods Two protocols were adopted to select the enriched library to transforming growth factor ? receptor Ⅱ(TGF ? RⅡ). Protocol 1: protein was absorbed on the surface of 96 well plate; then, selection was carried out; the binding nucleotide acids were eluted from the supporter directly. Protocol 2: selection was done in solution; nucleotide acid protein complex was captured in nitrocellulose membrane; the binding nucleotide acids were obtained from membrane. Filter biding assay and gel shift assay were performed to detect the affinity of the enriched ssDNA library from different protocols. Results After 4 rounds of selection, the affinity to TGF ? RⅡ was obviously improved in the enriched library from protocol 2 compared with the initial library, while no such improvement was found in the enriched library from protocol 1. Conclusion In the SELEX experiment, the way of selection in solution, then partition of the binding nucleotide acids in filter is easier to enrich the binding fragment from initial ssDNA random library, compared with the way of fixation of target protein to solid supporter, then selection between the solid phase and liquid phase and elution of the binding nucleotide acids from supporter.

Objective To explore the correlation of S100 protein with the prognosis of patients with primary retroperitoneal liposarcoma. Methods Analyzed the clinical data about 108 patients with primary retroperitoneal liposarcoma managed with surgery from January 2009 to June 2014. All patients were followed up. Patients were divided into S100-positive group(58 patients) and S100-negative group (50 patients) according to the immunohistochemical staining results. The overall survival time and all clinical data between two group were compared. Results All patients with primary retroperitoneal liposarcoma received radical surgical resection for the first time. The overall 5-year recurrence rate were 88.9%(96/108), and the median recurrence time was 32.7 months. The 1-year, 2-year, and 5-year recurrence rates of the S100- positive group were 25.9% (15/58), 53.4% (31/58), 96.6% (56/58), respectively, and the median recurrence time were 26.2 mouths. The 1-year, 2-year, and 5-year recurrence rates of the S100-negative group were 10.0%(5/50), 36%(18/50), 80.0%(40/50) and the median recurrence time were 40.0 mouths. Log-rank test showed that S100 protein expression was significantly associated with postoperative recurrence rates (c2=9.931, P=0.002) and survival time (c2=4.571, P = 0.033). The difference between gender, age, removal of the joint organs and tumor size showed no statistical significance on disease special survival (P>0.05). Cox regression analysis showed that S100 protein expression (OR=1.582, 95%CI:1.005-2.491) and histologic subtype (OR=1.531, 95%CI: 1.254-1.870) were independent risk factors of the prognosis of primary retroperitoneal liposarcoma patients. Conclusions S100 protein played a critical role in retroperitoneal liposarcoma carcinogenesis and its expression may be used as a potential survival predictor in patients with primary retroperitoneal liposarcoma.

Objective To set up a method of rapid culture,drug susceptibility testing and identification for Mycobacterium Tuberculosis.Methods Using the method by ourselves made and examined the standard strains and clinical strains of mycobacterium,research to the culture, the drug susceptibility testing and the identification of group in mycobacterium by this method compared with the method of Lowenstein-Jensen (L-J) method. To make sure the characteristic identification of group in mycobacterium.Results Detection time of culture of this method was 19.13 d earlier than that of L-J method. The positive rate of the method was higher than that of the L-J method. The applied concentration of each drug was: INH:0.1 ?g/ml, RFP:1 ?g/ml, EB:2 ?g/ml, AMK:2 ?g/ml、LVFX:2 ?g/ml、PNB 200 ?g/ml、TCH 2.5 ?g/ml respectively. The report time of the method was 7～10 d. It was 18～21 d shorter than that of the L-J method (28 days).Conclusion The method shortened significantly the report time of culture、drug susceptibility testing and identification of group in mycobacterium. The rate of positive was raised.This method was economic, practical and suitable to expansion and application in the substrata units.

Objective To investigate the conception implicit memory (CIM) and perception implicit memory (PIM) impairment in patients with frontal and occipital lobe stroke patients.Method Patients with frontal lobe stroke (n =23) and occipital lobe stroke (n =21) and healthy controls (n =26) were administered with a neuropsychological battery of tests including conception and perception implicit memory (CIM and PIM) tasks,as well as explicit memory tasks including immediately recall,delay recall,delay recognition.Results Compared with healthy controls,patients with frontal lobe stroke performed poor CIM test (1.96 ± 1.00 and 3.52 ±0.52,t =6.987,P ＜0.01),as well as its performance in explicit memory tasks including immediate recall(3.91 ± 1.53 and 5.42 ± 1.06),delay recall (6.04 ± 3.05 and 8.19 ±1.60),delay recognition (22.61 ± 4.71 and 25.38 ± 3.24 ; t =2.428,3.990,3.138 ; all P ＜ 0.05).PIM was impaired in the patients with occipital lobe stroke (5.56 ± 8.19 and 22.12 ± 4.68,t =0.011,P ＜0.01),while there was no significant difference between occipital lobe stroke and healthy group in CIM task.Conclusion Frontal lobe stroke present CIM damage and PIM relative retention,while occipital lobe stroke patients perform PIM damage and CIM relative retention,confirm the dual separation in implicit memory neural mechanism.

Objective To establish a mouse model of acute graft-versus-host disease (aGVHD) after allogeneic bone marrow transplantation,and using exogenous interleukin-7 receptor alpha (IL-7Rα) intervene mice aGVHD and analyse its possible mechanism.Methods The BALB/C (H-2d) female mice as recipients were grouped by rat: the irradiation group (group A),irradiation transplantation group (group B) and IL-7Rα in the intervention group (group C),each 10.ALL mice were accepted 9 Gy60Co total body irradiation.1×107 bone marrow cells and 2×107 spleen cells of donor C57BL/6 (H-2b) via the tail vein were infused to recipient mice.The signs of the recipient mice,hematopoietic functional recovery and survival time of change,and pathology,chimerism and cytokine levels in checkwere observed.Results Mice in A group after irradiation were gradually death,in group B and group C mice after transplantation had typical aGVHD symptoms,but lighter signs and a longer survival time of Group C than in group B.WBC count in Group C was +14 d (4.53± 0.21) ×109/L,+21 d (3.63±0.06) ×109/L,+28 d (4.31±0.04) ×109/L,was hematopoietic recovery compared with Group B [+14 d (1.81±0.05) ×109/L,+21 d (1.32±0.04) ×109/L,+28 d (1.76±0.04) ×109/L],the difference was statistically significant (t =0.237,0.108,0.359,P ＜ 0.05).The pathological results of liver,spleen,skin histopathology in group C were better than group B.Chimera implants,plasma IL-7 levels after transplant +7 d,concentration was significantly increased.IL-7 concentration in group C was +14 d (194.32±1.02) pg/ml,+21 d (131.63±1.54) pg/ml and in group B was +14 d (330.24±8.08) pg/ml,+21 d (184.09±2.05) pg/ml,the difference was statistically significant (t =1.590,1.285,P ＜0.05).Conclusion The stable aGVHD mouse model was established.In aGVHD early,plasma IL-7 levels were significantly increased.Exogenous IL-7Rαcan reduce the plasma IL-7 levels,thereby reducing the incidence of aGVHD after allogeneic bone marrow transplantation.

Background and purpose:Ethanol has been reported to stimulate progression of breast cancer, yet the underlying mechanism is not fully understood. This study aimed to investigate effects of ethyl alcohol (EtOH) on the calcium-activated neutral protease (CANP)-cyclin E/focal adhesion kinase (FAK) signaling and cell migration in breast cancer cells, as well as the role of epidermal growth factor receptor (EGFR) in the EtOH-stimulated effects, in order to assess the signaling mechanism(s) underlying how EtOH enhances cancer progression.Methods:Human breast cancer cell line MCF-7 was employed as a model system, with MCF-10A mammary epithelial cells as control. In vitro wound healing assay was carried out to evaluate EtOH-induced cell migration. The effects of EtOH or epidermal growth factor on the proteolysis of cyclin E/FAK were detected by Western blot. EGFR inhibitor (EGFR-I) and a speciifc inhibitor for CANP, Calpeptin, were applied to pretreat cultured cells to explore their inlfuences on the cell migration and cyclin E/FAK proteolysis triggered by EtOH.Results:Treatment of model cells with EtOH (0.3%) stimulated significant proteolysis of cyclin E/FAK in a dose-/time-dependent manner and increased migration (+47.30%,P<0.05) in MCF-7 breast cancer cells, but had no signiifcant effect on migration in MCF-10A cells. Pretreatment with Calpeptin (10 μmol/L) signiifcantly reduced EtOH (0.3%)- or EGFR (10 ng/mL)-induced cyclin E/FAK truncation. EGFR-I (3 μmol/L) pro-foundly reduced EtOH-indcued CANP dependent proteolysis of CANP1 and cyclin E/FAK as well as cell migration (-53.00%,P<0.01).Conclusion:EtOH signiifcantly stimulates activation of CANP via EGFR pathway, resulting in proteolysis of cyclin E/FAK and migration in MCF-7 breast cancer cells, suggesting EGFR-CANP signaling to be a potential target for suppression of metastasis in breast cancer.

Objective:To determine risk factors for postoperative esophageal refractory stenosis after endoscopic submucosal dissection (ESD) of large-scale early esophageal carcinomas and precancerous lesions.Methods:Two hundred and twelve early esophageal carcinomas or precancerous lesions in 186 patients who underwent ESD larger than 3/4 the total esophageal circumference in Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, between July 2013 and December 2017 were divided into two groups according to session number of endoscopic balloon dilatation (EBD), the refractory stenosis group ( n=69, ≥6 EBD sessions) and non-refractory stenosis group ( n=117, ≤5 EBD sessions). Student′s t-test or Mann-Whitney U test was used for univariate analysis and χ2 test and Fisher exact test were used for comparison of categorical variables. Logistic regression was used for multivariate analysis. Results:Compared with the non-refractory stenosis group, the refractory stenosis group had statistically significant differences in the longitudinal diameter of lesions, the longitudinal diameter of artificial ulcer, lesion location, the circumferential range of lesions and the composition of the muscular layer injury (all P<0.05). After eliminating the factor of the vertical diameter of artificial ulcer (because there was significant correlation between the vertical diameter of artificial ulcer and the longitudinal diameter of lesion in clinical practice), multivariate logistic regression analysis showed that the longitudinal diameter of lesion>5 cm (VS ≤5 cm: P=0.003, OR=3.531, 95% CI:1.547-8.060), the location of lesion in the upper thoracic segment (VS lower thoracic segment: P=0.001, OR=36.720, 95% CI:4.233-318.551), in the cervical segment (VS lower thoracic segment: P=0.003, OR=24.959, 95% CI:2.927-212.795), the whole circumferential lesion (VS ≥3/4 but not the whole circumference: P<0.001, OR=10.082, 95% CI:4.196-24.226) and the presence of muscular layer injury ( P<0.001, OR=7.128, 95% CI:2.748-18.486) were more likely to lead to esophageal refractory stenosis after ESD. Conclusion:The longitudinal lesion diameter of more than 5 cm, the circumferential extent of esophageal ESD, cervical or upper-thoracic esophageal lesions, and muscular layer damage are independent risk factors for postoperative esophageal refractory stenosis after ESD for large-scale esophageal cancer and precancerous lesions.

Aim To study the effect of estrogen on the migration of breast cancer cells and the possible underlying mechanisms.Methods Human breast cancer cell lines MCF-7(estrogen receptor, ER+) and MDA-MB-468(ER-) were employed as a model system.Cells were treated with E2 and pretreated with CANP inhibitor(calpeptin)where needed.Wound-healing assay was applied to evaluate cell migration, Western blot assay was performed to observe protein level, and fibronectin expression was silenced by specific siRNA transfection.Results ① Treatmentof MCF-7 and MDA-MB-468 cellswith E2(50 nmol·L-1) increased cell migration by(51.55±5.50) ％(P<0.01)and (40.78±4.78)％(P<0.05), respectively;② E2 significantly up-regulated the expression of FN protein in MCF-7 and MDA-MB-468 breast cancer cells, which was 2.11 times(P<0.05)and 1.86 times(P<0.01), respectively;③ Pretreatment with calpeptin(10 μmol·L-1) decreased E2-induced cell migration by (49.55±6.44)％(P<0.05) in MCF-7 and(36.85±4.40)％ (P<0.01)in MDA-MB-468 cells;④ Calpeptin pretreatment inhibited E2-induced fibronectin up-regulation by(80.12±4.55)％ and(78.84±5.70) ％(P<0.01), respectively;⑤ Knockdown of FN with siRNA suppressed cell E2-induced migration by(40.65±5.80)％(P<0.01)in MCF-7 and(40.88±6.02)％(P<0.05)in MDA-MB-468 cells.Conclusion E2 stimulates the migration of breast cancer cells with or without ER expression and a calpain-FN signaling pathway may be involved in the E2 action.

Objective To observe the symptom and characteristics of liver injury induced by different dosage of long-term administration of rifampicin(RIF) in mice.Methods Twenty-four healthy female ICR mice were randomly divided into 4 groups(6 mice in each group):control group,low dosage group,medium dosage group and high dosage group.The four groups were treated with 0,100,200,400 mg·kg-1·d-1 RIF respectively for 2 weeks.Mice blood and liver tissue samples were collected at 6 hours after the last administration for serological test and liver histological observation.Results No mice died before execution.The TBA,DBIL and TBIL of high dosage group all increased compared with the control group, but the ALT,AST and ALP showed no obvious change.The TBA and DBIL of medium dosage group increased compared with the control group, while the TBIL,ALT,AST and ALP showed no obvious change.In the low dosage group,there was no obvious change in terms of TBA,DBIL,TBIL,ALT,AST,and ALP compared with the control group.Obvious pathological change occured in the liver of mice in all the experimental groups.HE staining showed edema and feather steatosis in liver cells, accompanied by a large number of inflammatory cells infiltration and a few sporadic cholestasis.With the increasing of RIF dosage,the liver pathological change became more obviously.In the experimental group,electron microscope showed that there were a lot of fat droplets in the liver cells wrapped slurry,and part of the capillary bile duct were slightly expanded with different electron density and irregular shape of bile sample material inside.The pathologic changes get more obvious with the increase of the concentration of rifampicin as well.Conclusion RIF could induce liver injury after 2 weeks' treatment at different dosages,mainly pathological changes included liver cell steatosis,inflammatory cell infiltration,and cholestasis.Rifampicin induced liver injury in a concentration-dependent manner.However,the mechanism of rifampicin-induced liver injury in mice needs further study.