Scientific innovation teams are key weight indicators and promoters in science and technology of a hospital.The First Affiliated Hospital of Anhui Medical University(the Hospital)draws funding support from the Natural Science Foundation,to empower its innovative teams with programs and funding.These efforts have effectively propelled its innovations spearheaded by the dermatology team to give rise to outstanding outcomes and power teams.The application for talents support from NSF,the project approval for the hospital funding is affected to some extent.With the help from NSF and the innovative teams,scientific teams of the hospital have harvested a general upgrading and accelerated development of disciplines,elevating the scientific level of hospital in general.

Objective To construct a Polyphosphate kinase 1 ( ppk1) gene deletion mutant of uro-pathogenic Escherichia coli (E.coli) CFT073, and to explore the biological properties of the mutant strain . Methods The ppk1 gene deletion strain (△pk1) was constructed based on CFT073 E.coli strain by usingλRed homologous recombination technology .A comparison analysis was conducted on adhesive and invasive abilities between CFT073 wild type strain and △pk1 strain in in vitro model of human bladder cancer epithe-lial cell 5637 .Crystal violet staining method was used to evaluate the influences of ppk1 gene deletion on biofilm formation.Results The CFT073 ppk1 deletion mutant strain was successfully constructed .Com-pared with the wild type strain ,△pk1 strain showed impaired adhesive and invasive abilities to 5637 cells. Moreover , the absorbance values of crystal violet at 570 nm at each time point of the mutant strain group were also lower than those of the wild-type strain group .Conclusion The ppk1 gene deletion mutant of uro-pathogenic E.coli CFT073 could be successfully constructed by Red homologous recombination technology and its biological properties indicates that ppk1 gene plays an important role in the pathogenesis of uropatho-genic E.coli infection through regulating the abilities of adhesion , invasion and biofilm formation .

Objective To study the inhibition of AP-1 transcription factor activity by Hint1 gene over expression in HepG2 cell lines. Methods The Hintl gene was amplified, and then was inserted into the pcDNA3/HA eukaryotic expression plasmid. The constructed pHA-Hint1 plasmid was confirmed by DNA sequencing. The pHA-Hint1 was transfected into the HepG2 human hepatoma cells. Semi-quantitative RT-PCR and Western-blot were used to detecte the expression of HA-Hint1. The HepG2 cells were co-transfected with pHA-Hint1 and pAP-1/Luc luciferase reporter. At 36 h after transfection, luciferase assay system was used to detect the AP-1 transcription factor activity. Results The constructed pHA-Hint1 was confirmed by DNA sequencing, pHA-Hint1 gene transduction through lipofectine induced over-expression in HA-Hint1 mRNA (t =3.89, P<0.05) and HA-Hintl protein (t=3. 12, P<0.05). Co-transfection of Hint1 gene inhibits AP-1 luciferase activity. Cotransfection with increased concentration of a pHA-Hint1 plasmid (0 μg/ml, 0. 5 μg/ml, 1.0 μg/ml, 1.5 μg/ml, 2. 0 μg/ml) produced a concentration-dependent inhibition of AP-1 transcription factor activity. At the concentration of 1.5 μg/ml, and 2.0 μg/ml, the activity inhibition reaches significant difference ( F = 72. 009, P < 0. 05 ). Conclusion Over-expression of Hintl can, at least in part, inhibit the AP-1 transcription factor activity in HepG2 cells.

Objective To explore the role of ppk1 gene in E.coli CFT073 strain during urinary tract infection (UTI). Methods C57BL/6 mouse models of acute UTI with the wild-type(CFT073) and ppk1 mutant (△pk1) infected, were used to compare the bacteria colonization and inflammation induction abilities of bladder tissues. Results In the mouse models, the △pk1 strain showed a significantly lower infection rate (73.3% vs 93.3%) and lower adhesion frequency of bladder (0.01%vs 0.5%) than those of the CFT073 strain. The expression of IL-6 and TNF-αwere reduced in the bladder of △pk1 infected group (P<0.05). Hematoxylin-Eosin tissue staining showed that the damage degree of bladders in △pk1 infected mice were less serious than the CFT073 infected mice. Conclusion ppk1 gene plays an important role in E.coli colonization to bladder and the inflammation induction ability.

OBJECTIVE:To explore the feasibility of question-and-answer practice teaching in the pharmacy department of our hospital. METHODS:The practice teaching of pharmacy department was taken as a pilot,and the question-and-answer practice teaching was used in emergency and outpatient pharmacies,inpatient pharmacy,PIVAS,drug warehouse,clinical pharmaceutics room,preparation room and drug testing laboratory. The effects of the practice teaching on internships,teachers,pharmacy depart-ments and patients were excavated. RESULTS & CONCLUSIONS:Satisfaction of teachers,pharmacy,patients and clinics for the question-and-answer practice teaching was 100%,and satisfaction of internships was 94.5%. The question-and-answer practice teaching has improved their professional knowledge and competence,resolved difficulty of patients about drug counseling and helped the improvement of overall business level in department.

Objective To evaluate the short-term prediction of high-sensitivity cardiac troponin T (hs-cTnT) and other cardiovascular risk biomarkers in patients undergoing maintenance hemodialysis (MHD).Methods We conducted a cohort survey in 296 consecutive MHD patients whose clinical data were retrospectively analyzed.Before MHD,hs-cTnT and other relative cardiovascular biomarkers were detected.The end point (all-cause death) and time of occurring were recorded in the next 13 months.The differences between survival and all-cause death were analyzed by t-test,Mann-Whitney test and x2 test.The best two percentile cutoff point was calculated by X-tile and the survival rate was calculated by Kaplan-Meier Logistic regression analysis was applied to analyze the odd ratio between high risk and non-high risk hs-cTnT group.Non-high risk group was divided into intermediate risk and low risk group based on the 99th percentile of hs-cTnT in healthy population,to further evaluate its short-term prediction value for MHD patients.The short-term significance of hs-cTnT was proved to be independently associated with all-cause death by Logistic regression analysis.Results The mean value of serum hs-cTnT in survival group was 0.05 (0.03～0.07) ng/mL,while in the death group it was 0.07 (0.04～0.14) ng/mL,which had statistical significance (P =0.027).The best two percentile cutoff of hs-cTnT in MHD patients was 0.1 ng/mL.The survival rate in high risk group (hs-cTnT＞0.1 ng/mL) is lower than it in non-high risk group (hs-cTnT≤0.1 ng/mL) (76.67％ vs.96.62％,P ＜0.05).The odd ratios for high risk group and non-high risk group was 7.288 (P＜ 0.001).Moreover,further grouping the non-high risk group by hs-cTnT =0.014 ng/mL,intermediate risk group (hs-cTnT＞0.014 ng/mL) group has lower survival rate than low risk group (hs-cTnT≤0.014ng/mL),while there wasn't any death case occurred in the low risk group.Conclusions Hs-cTnT is an independent risk factor to all-cause death.Thus hs-cTnT can be a strong indicator of short-term prediction and prognostic evaluation.

Objective To investigate the role and the mechanism of ppk1 gene (coding for polyphosphate kinase 1) in oxidative stress resistance in uropathogenic Escherichia coli (UPEC).MethodsMutant strains with ppk1-deletion (△pk1) and complemented strains (△pk1-C) were constructed based on the UPEC strain CFT073.A comparative analysis was conducted to analyze survival rates of CFT073, △pk1 and △pk1-C strains at different time points while they were under oxidative stress.Differences in protein expression between CFT073 and △pk1 strains were analyzed using mass spectrometric analysis.Differences between CFT073 and △pk1 strains in expression of katG and katE genes were analyzed using real-time quantitative RT-PCR.Results The survival rate of △pk1 strains was lower than that of CFT073 strains at every time point, while the survival rate of △pk1-C strains was basically the same as that of CFT073 strains.Gel image analysis and mass spectrometric analysis revealed that six proteins were down-regulated and one was up-regulated in △pk1 strains as compared with those in CFT073 strains.Expression of the catalase-coding genes katG and katE in △pk1 strains were respectively (20.5±8.2)% and (20.9±6.9)% of those in CFT073 strains (P<0.05).Conclusion The ppk1 gene plays an important role in oxidative stress resistance in UPEC by modulating the expression of catalase-coding genes katG and katE.

Objective To evaluate the value of T-cell spot of tuberculosis test (T-spot.TB) in differential diagnosis of Crohn's disease and intestinal tuberculosis.Methods From May 2010 to October 2010,in Xijing hospital,Fourth Military Medical University,the peripheral blood samples of 126 patients were collected and peripheral blood mononuclear cells were isolated with density gradient centrifugation.T-spot.TB was conducted according to the kit instructions.The clinical diagnosis of Crohn's disease and intestinal tuberculosis was according to clinical manifestations, imaging,endoscopy,pathology,laboratory tests and on empirical anti-TB treatment response.The sensitivity and specificity of T-spot.TB in diagnosis of Crohn's disease and intestinal tuberculosis was analyzed.Results Fifteen patients were diagnosed as Crohn's disease (11.9％,15/126),14 patients were intestinal tuberculosis (11.1％,14/126) and 40 patients were extraintestinal tuberculosis (31.7％,40/126).The positive rate of T- spot.TB in Crohn's disease,intestinal tuberculosis,extra-intestinal tuberculosis and other diseases was 1/15,12/14,70％ (28/40) and 0％ (0/57),respectively.Thedifference between the groups was statistically significant (P =0.00).There was statistically significant difference of T-spot.TB positive rate between Crohn's disease and intestinal tuberculosis (x2 =70.58,P=0.00).The sensitivity and specificity of T- spot.TB in Crohn's disease detection was 93.3％(14/15) and 87.5％(14/16),in intestinal tuberculosis was 85.7％(12/14) and 93.3％ (14/15).The negatively predictive value of Crohn's disease was higher [87.5％ (14/16)] than that of intestinal tuberculosis [12.5％ (2/16)].Conclusion T-spot.TB is helpful for differential diagnosis of Crohn's disease and intestinal tuberculosis.

OBJECTIVETo introduce the application of "tennis racket" flap with fascial pedicle on the healthy chest for radiation ulcer after surgical treatment of breast cancer.

METHODSThe " tennis racket" flap was designed on the healthy chest along the cartilage with fascia pedicle near the sternum. 9 cases were treated. The flaps size ranged from 5.0 cm x 3.5 cm to 13 cm x 11 cm with pedicle size of 2-8 cm in length and 2.0-3.0 cm in width.

RESULTSAll the 9 flaps survived completely with satisfactory appearance. The patients were followed up for 2 months to 3 years without ulcer reoccurrence.

CONCLUSIONSThe "tennis racket" flap has a slender fascial pedicle without major blood vessel. It has the advantages of good flexibility for rotation and large flap size for the reconstruction of the radiation ulcer after surgical treatment of breast cancer.

Breast Neoplasms ; radiotherapy ; Fascia ; Female ; Humans ; Radiodermatitis ; surgery ; Skin Ulcer ; etiology ; surgery ; Sternum ; Surgical Flaps ; Tennis

Objective To explore the beneficial effects and mechanisms of neutrophil elastase (NE) and myeloperoxidase (MPO) on lead-induced hepatic inflammation in mice. Methods The specific pathogen free male C57BL/6 mice were randomly divided into four groups： control group, lead-exposed group, NE inhibitor group, and MPO inhibitor group, with three mice in each group. The mice in lead-exposed group, NE inhibitor group, and MPO inhibitor group were intraperitoneally injected with a dose of 10 mg/kg body mass of lead acetate solution, while the mice of control group received an equal volume of 0.9% saline three times per week for four weeks. In the last seven days, mice in both inhibitor groups were intraperitoneally injected with a dose of 40 mg/kg NE inhibitor sivelestat sodium or MPO inhibitor 4-aminobenzoic acid hydrazide (4-ABAH) once per day. Mouse body weight and liver histopathological changes were observed. The mRNA expression of genes associated with inflammation, such as tumor necrosis factor-α (Tnfa), interleukin-1β (Il1b), interleukin-6 (Il6), and nucleotide-binding oligomerization domain-like receptor protein 3(Nlrp3), apoptosis-associated speck-like protein (Asc) and cysteinyl aspartate specific proteinase (Caspase1) in the mouse liver tissues was detected by real-time quantitative polymerase chain reaction. The protein expression of NLRP3, ASC, and CASPASE-1 was detected using Western blotting. Results The activities of mice in all four groups were generally normal, and there was no significant difference in body weight (P>0.05). The results of hematoxylin-eosin staining showed that the cell size of hepatocytes varied in the lead-exposed mice, with indistinct cell boundaries, indicating early inflammatory responses in liver tissues. After intervention with NE or MPO inhibitors, the early inflammatory responses improved in the liver tissues of the mice in both inhibitor groups, with a better improvement observed in MPO inhibitor group compared with the NE inhibitor group. The mRNA expression of Tnfa, Il1b, Il6, Nlrp3, Asc, and Caspase1, as well as the protein expression of ASC, and CASPASE-1 in the livers of mice in the lead-exposed group was higher compared with those in the control group (all P<0.05). Compared with the lead-exposed group, the relative mRNA expression of Tnfa, Il1b, Il6, Nlrp3 and Asc was decreased in the liver tissues of mice in the NE inhibitor group (all P<0.05), while the relative expression of mRNA of Tnfa, Il1b, Il6, Caspase1 and the protein expression of ASC and CASPASE-1 were decreased in the liver tissues of mice in the MPO inhibitor group (all P<0.05). Conclusion Lead induce hepatic inflammation in mice by activating NLRP3 inflammasome. The inhibition of NE or MPO improve the lead-induced hepatic inflammatory responses in mice by alleviating NLRP3 inflammasome activation.