Objective:To prepare and evaluate the effectiveness of chitosan-carboxymethylcellulose membrane in preventing postoperative intestinal adhesion.Methods: Chitosan-carboxymethylcellulose membrane was prepared with 11 ratio of chitosan and carboxymethylcellulose.Glutaraldehyde and ammonium aluminium sulfate were used for cross-linkage,glycerin for enhancing plasticity;and then the product was dried.The membrane was observed with scanning electron microscopy(SEM) and its tensile strength and breaking elongation were measured.Forty-eight SD rats with ileum injury were randomly divided into A,B and C groups(n=16).During operation,the injury in group A was treated with chitosan-carboxymethylcellulose membrane,in group B with chitosan membrane,and in group C without treatment(control group).The adhesion was observed on the 14~(th) postoperative day.Results: The tensile strength of chitosan-carboxymethylcellulose membrane was 20 MPa and the breaking elongation was 65%.SEM showed that the morphology of the membrane had crossed fibroid structures and irregular pores. The severity of adhesion in group A and B was significantly lower than that in group C(P

Objective:To investigate the effect of carboxymethylchitosan on autocrine growth factor and morphology of fibroblasts cultured in vitro,so as to discuss the possible mechanism by which carboxymethylchitosan alleviates overhealing and prevents adhesion in wound healing.Methods: Fibroblasts were cultured in vitro.Fibroblasts of passage 4-6 were treated with different concentrations of carboxymethylchitosan(0.01,0.1,1.0 and 10 mg/ml) for 4 days or with 0.1 mg/ml carboxymethylchitosan for 1,2,3, 4,5,and 6 days.The levels of autocrine transforming growth factor-?_(1 )(TGF-?_(1)) and epidermal growth factor(EGF) of fibroblasts were determined by ELISA and radioimmunoassay.The fibroblastic morphology was detected by transmission electron microscopy(TEM) and microscope after fibroblasts were treated with different strategies.Results: Carboxymethylchitosan(≥0.1 mg/ml)inhibited autocrine TGF-?_(1) of fibroblast in a time-and concentration dependent manner(P0.05).Carboxymethylchitosan ((≥0.1 mg/ml))also inhibited the proliferation of fibroblasts and caused their ultrastructural changes.Conclusion: Carboxymethylchitosan (≥0.1 mg/ml)can inhibit fibroblasts proliferation and reduce tissue adhesion, possibly through altering fibroblast ultrastructure and selectively inhibiting secretion of TGF-?_(1).

AIM: To observe the curative effect of titanium wiring in treatment of the fractures of Neer Ⅱ type distal clavicle and dislocation of Tossy Ⅲ type acromioclavicular joint. METHODS: From March 2004 to December 2006, 37 cases with Neer Ⅱ type distal clavicle fractures or Tossy Ⅲ type acromioclavicular joint dislocation were treated with titanium wiring in Changzheng Hospital, Second Military Medical University of Chinese PLA. Titanium wiring (produced by Sofamor-Danek Company in USA) had good histocompatibility, intensity of tension and flexibility. The broken coracoclavicular ligament was repaired directly by titanium wiring in all cases. The outcomes were evaluated according to Herscovici's criteria. RESULTS: All the cases were followed up for 6 to 24 months. All the dislocated acromioclavicular joints returned to normal 2 weeks after operation. Excellent and good rate of shoulder function was 100% according to Herscovici standard. X-ray imaging showed all clavicle fractures united, acromioclavicular joint had no redislocation or titanium wiring breaking. The incisions of all cases had no obvious swelling and exudation. CONCLUSION: When Neer Ⅱ type distal clavicular fracture and Tossy Ⅲ type acromioclavicular joint dislocation are treated with titanium wiring, the acromioclavicular joint can exercise earlier and recover quickly.

Objective To evaluate the effect of gamma irradiation on the proliferation,differentiation,and mineralization of murine osteoblastic cells,and to investigate the related molecular mechanism.Methods Osteoblastic cells were irradiated by different doses (0,0.5,1.0,2.0,5.0 Gy)of 137Cs γ-rays.Cell morphology was observed with a microscopy,cell viability was analyzed by MTT assay,and ALP activity was analyzed by the methods of enzyme histochemistry and PNPP.Meanwhile,gene expressions of ALP,osteocalcin (OC),collagen Ⅰ,osteoprotegerin (OPG) and receptor activator of nuclear factor-kB ligand (RANKL) were measured by semi-quantified RT-PCR.Results Cell viability decreased with the radiation doses over 1.0 Gy ( t =6.197 - 18.677,P ＜ 0.05 ).After radiation with a dose over 2.0 Gy,the cell number and the junctions of cell protrusions decreased,the cells had low refractivity and the activity and mineralization ability of ALP were also inhibited ( t =2.790 -2l.374,P ＜0.05).In addition,the expressions of ALP and OC mRNA were down-regulated significantly (t =3.563 -16.508,P ＜ 0.05) when the radiation dose was higher than 0.5 Gy,and the expressions of OPG,OPG/RANKL mRNA were down-regulated ( t =12.942,4.954,P ＜ 0.05 ) at 5 Gy.But the expressions of collagen Ⅰ and RANKL mRNA were not affected by irradiation.Conclusions The osteoblastic cells were significantly influenced by γ-irradiation,including morphological changes,inhibition of cell proliferation,differentiation and mineralization ability. Meanwhile,mRNA expressions of ALP and OC were downregulated.OPG/RANKL may be a main pathway of osteoblastic cell damage under high dose radiation.

Objective Saxagliptin regulates the level of blood glucose by selectively inhibiting high-performance dipeptidyl peptidase 4, but its action mechanism is not yet clear .This study was to investigate the effect of the novel hypoglycemic agent Saxaglip -tin on the expression of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and its target gene products transforming growth factor-β1 ( TGF-β1 ) in human umbilical vein endothelial cells ( HUVECs) stimulated by high glucose. Methods HUVECs were cultured in with D-glucose (D-GS) at the concentrations of 5.5, 10, 20, and 30 mmol/L and Saxagliptin at 0, 0.01, 0.1, 1, and 10μmol/L.The best concentrations of D-GS and Saxagliptin were determined as 30 mmol/L and 1 μmol/L, respectively.The HUVECs were divided into four groups:control (5.5 mmol/L D-GS), Saxagliptin (5.5 mmol/L D-GS+1 μmol/L Saxagliptin ) , high glucose ( 30 mmol/L D-GS ) , and high glucose +Saxagliptin (30 mmol/L D-GS +1μmol/L Saxaglip-tin), all cultured for 24 hours.Then the expressions of MALAT1 and TGF-β1 mRNA in the cells were detected by qRT-PCR, that of the TGF-β1 protein determined by Western blot , and the level of TGF-β1 in the supernatant measured by ELISA . Results The expressions of LncRNA-MALAT1 and TGF-β1 were significantly increased in the high glucose group as compared with the control ( 8.65 ±0.70 vs1.00 ±0.00 and 1.36 ±0.07 vs 1.00 ±0.00, P<0.01) but markedly inhibited in the high glucose +Saxagliptin group in compari-son with the high glucose group (2.17 ±0.24 vs 8.65 ±0.70 and 1.15 ±0.02 vs 1.36 ±0.07, P<0.05). Conclusion High glu-cose can induce the overexpression of LncRNA-MALAT1 and its target gene products TGF-β1 in HUVECs and cause damage to the cells, while Saxagliptin can significantly suppress this effect .

ObjectiveTo explore the role of BTBD10 overexpression in the proliferation of insulinoma cell line INS-1and its mechanism. MethodsThe recombined expression plasmid of pcDNA4.0-BTBD10 was constructed by gene cloning technique and was transfected into INS-1 cell by lipofectamine 2000. The stable overexpression BTBD10 of INS-1cell was selected at 48th hour after transfection.INS-1 cell proliferation activity was measured by MTT method.The expression of BTBD10,protein kinase B(Akt),phospho-Akt(p-Akt),mammal target of rapamycin (mTOR) and phospho-mTOR (p-mTOR) were determined by Western blot.ResultsThe stable overexpression BTBD10 of INS-1 cell wassuccessfullyconstructed.OverproductionofBTBD10promotedbetacellproliferation.The phosphorylation of Akt and mTOR was increased and the ratio of p-Akt/Akt and p-mTOR/mTOR was enhanced in the INS-1 overexpressed by BTBD10.But the expression of total Akt and mTOR presented no obvious changes. Conclusion The overexpression BTBD10 of INS-1 cell could activate of Akt/mTOR signalling pathway via stimulating phospho-mTOR and Akt,and enhance overall cell protein translation,so as to promote proliferation of INS-1 cell.

Objective To investigate the results of defect reconstruction using anterolateral thigh free flap in medial and lateral approaches.Methods We reviewed the soft tissue defect reconstruction in 200 patients from February 2010 to June 2014 with anterolateral thigh flap in medial or lateral approach,to compare the operative time and donor site morbidity.Results The mean time of flap raising in medial group was (45 ± 4.5) minutes,while in lateral group was (65 ± 3.5) minutes.In medial group,fascial lata was closed directly in 39 cases (39％),while fascial lata was closed directly in all the cases (100％) in lateral group.All the 200 flaps survived uneventfully.All the donor sites healed smoothly.No infection occurred.An 8 to 32 months follow-up revealed a high satisfactory rate from the patients.No sensory deficit or functional impairment was noted in the donor sites.Conclusions Both in medial and lateral approach can achieve safely harvesting free anterolateral thigh flap.

Objective:To discuss the etiology, clinical manifestations and renal pathological features of acute interstitial nephritis (AIN) in children.Methods:The etiology, clinical manifestations, pathological characteristics, clinical effects and outcome of the children with AIN diagnosed by renal biopsy from January 2010 to December 2019 in Nanjing Jinling Hospital were analyzed retrospectively. The Kaplan-Meier method was used to evaluate the kidney survival rate. Cox regression model was built to analyze the risk factors for developing end-stage renal disease (ESRD) at baseline in AIN children.Results:A total of 51 children with AIN were diagnosed by renal biopsy, including 36 males and 15 females. The age was (12.94±2.55) years old (2-17 years old). The clinical manifestations of AIN in children were various and lack of specificity. Only 2 cases (3.92%) had triad. All of the 51 children with AIN showed acute renal injury (AKI), accompanied by increased serum creatinine and decreased estimated glomerular filtration rate. The stage of AKI was mainly stageⅢ(33 cases, 64.71%). Infection was the main cause (38 cases, 74.51%) and drug factor was the second cause (27 cases, 52.94%) in children with AIN. Nonsteroidal antiinflammatory drugs (NSAIDs) were the main inducers of drug-induced AIN (18 cases, 35.29%). The interstitial inflammatory cell infiltration or interstitial edema was found in 51 children. The infiltration of inflammatory cells was mainly mononuclear cells (46 cases, 90.20%). After 4 weeks of treatment, 32 cases (62.75%), 11 cases (21.57%) and 8 cases (15.69%) showed complete, partial and no recovery of renal function, respectively. After 12 weeks of treatment, 49 cases (96.08%), 0 cases (0) and 2 cases (3.92%) showed complete, partial and no recovery of renal function, respectively. After an average follow-up of 4.0(2.0-15.0) months, 2 case (3.92%) patients developed ESRD. The cumulative survival rates of ESRD at 1 year and 2 years after renal biopsy both were 100%, and renal survival rates at 5 years and 10 years were 96.55% and 72.41%, respectively. Multivariate Cox regression analysis results showed that N-acetyl-β-D-glucosidase (NAG) enzyme level>17.6 U/g·cr ( HR=15.729, 95% CI 1.045-15.977, P=0.042) and IgM deposition in renal tissue ( HR=7.523, 95% CI 1.142-9.541, P=0.033) were independent risk factors for developing ESRD in AIN children. Conclusions:AKI is the main clinical manifestation of AIN in children. The characteritic of renal pathology in AIN is tubulointerstitial lesions. After active treatment, most of the patients have a good prognosis. Prevention of infection and rational use of drugs are the key to reduce the incidence rate of AIN in children. The N-acetyl-β-D-glucosidase enzyme level>17.6 U/g·cr and IgM deposition in renal tissue are independent risk factors for developing ESRD in AIN children.

Objective To investigate the effect of atorvastatin on the expressions of long non-coding RNA (LncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)and inflammation factors in human umbilical vein endothelial cells (HUVECs) stimulated by high glucose. Methods The expression of MALAT1 in HUVECs incubated with high glucose(30 mmol/L) for different time periods were detected by real-time PCR. Under high glucose condition, the expressions of MALAT1, interleukin-6(IL-6), and interleukin-8 (IL-8) in HUVECs were detected after MALAT1 was silenced by siRNA or atorvastatin was added. Results (1) After HUVECs were incubated with high glucose for different time periods, the expressions of MALAT1 were increased to some extent(P<0.05), with the peak at 12h (P<0.01). The levels of IL-6 and IL-8 expression and secretion were increased after HUVECs were stimulated by high glucose for 12h (P<0.05). (2)The silence of MALAT1 markedly suppressed high glucose-stimulated expression and secretion of IL-6 and IL-8 (P<0.05). (3) Atorvastatin significantly inhibited high glucose-stimulated expressions of MALAT1, IL-6, and IL-8(all P<0.05). Conclusions High glucose induces the secretion of inflammatory factors by stimulating MALAT1 expression in endothelial cells. Atorvastatin significantly inhibits high glucose-stimulated MALAT1 expression and decreases inflammatory reaction.

Objective To investigate the role of NF-?B in high glucose (HG) and cytokines (TNF-? and IL-1?)-induced impairment of ECV-304 cells (vascular endothelial cell line). Methods Recombinant adenovirus containing NF-?B supper-repressor I?B?M with mutant I?B? was constructed. Western blot, electrophoretic mobility shift assay (EMSA) and thiazolyl blue viability assay were applied in this study. Results TNF-?-induced I?B? degradation and NF-?B activation (P