Objective To evaluate the level situation of clinical doctors graduating from mil-itary medical university within a certain period, understand their career development, and explore and analyze the problems and deficiencies in doctoral education and training to provide reference for deep-ening the reform of clinical disciplines doctoral education. Methods Stratified random samples of 9 Hospitals were selected and the established evaluation index system of clinical discipline quality tracking and investigation questionnaire was used to evaluate doctoral quality. Evaluation was surveyed by self rating and other rating combination. Quality evaluation system contains 4 first level indicators such as the military and political quality, clinical, teaching and research level, the development po-tential as well as 15 second-level indexes. The scores of self-assessment and other evaluation were compared by Pearson rank correlation analysis. The corresponding indicator scores of different doctorate types were compared using the test of variance and the subject research and published papers were analyzed by χ2 inspection. Results The comprehensive score of graduated doctors is excellent, with self-evaluation score (92.72±7.06) and other evaluation score (93.61±8.05). Correlation coefficient is 0.33(P=0.04); The academic doctors have done better in publishing papers(χ2=5.97, P=0.01) and undertaking subject research(χ2=6.08, P=0.00), but poorer in clinical work compared with the doctors of professional degree. The assessed groups are inadequate in publishing high level papers and in un-dertaking research projects and doctors of different degree types have different cognition of the ele-ments of improving the quality. Conclusions Cultivating the doctors' clinical ability and innovation ability are the cores of deepening the reform of clinical doctoral education. We should focus on inno-vation ability , value the cultivation of the clinical professional doctoral degree and explore various joint evaluation systems to attain the goal of enhancing the education quality of doctors.

Pancreatic cancer is one of the most aggressive malignancies in the world.Little progress has been made on the treatment of advanced pancreatic cancer in the past 20 years.miRNAs perform a regulatory role in the determination of the final phenotype of cancer cells,including carcinogenesis,metastatic potential,and chemosensitivity.These features of miRNAs have turned them into one of the most popular and promising fields of scientific and clinical research.Issues such as miRNA toxicity to non-target tissues or cells and lack of proper delivery systems for human pancreatic cancer will be the challenges for the field to overcome.

Objective To explore the mechanism of the protection of acidic fibroblast growth factor (aFGF) for hippocampal astrocytes from injury induced by gentamicin. Methods Hippocampal astrocytes were isolated from newborn (24 hours) Sprague-Dawley rats, puri-fied, and identified with glial fibrillary acidic protein (GFAP) immunofluorescence. The third generations were cultured for 3 days and divid-ed into 3 groups:control group was cultured routinely, injury group was cultured with 2.0 g/L gentamicin for 24 hours, and protection group was cultured with 4.25μg/L aFGF for 24 hours and then cultured with 2.0 g/L gentamicin for 24 hours. Western blotting was adopted to de-tect the expressions of P38, extracellular signal-regulated kinase (ERK)1/2 and c-Jun N-terminal kinase (JNK)1/2. Results Hippocampal as-trocytes were culturated successfully with the purity above 95%. The ERK1 increased in the injury group compared with the control group (P<0.05). Compared with the injury group, the p38 increased (P<0.05) and the ERK1 decreased (P<0.05) in the protection group. There was no significant difference among others (P>0.05). Conclusion The mitogen-activated protein kinase signal pathway, especially P38 and ERK1, may associate with the protection of aFGF for hippocampal astrocytes from injury induced by gentamicin.

ObjectiveTo study the operative procedure and effect of anastomostic pseudoaneurysm(APA). Methods Eleven patients with APA were treated surgically. The diagnosis of APA in all the patients was comfirmed by angiography and ultras onic examination. A small rupture leading to APA was repaired by lateral arteri orrhaphy using autologous vein patch in 4 cases; the APA caused by a big rupture of anastomosis,resection of the pseudoaneurysm and interposition o f a PTFE or antologous vein were used in 7 cases.Results10cas es were followed -up for 5-38 months (mean19.6 months),and 1case loss of follow-up.9 cases recovered to be normal in activities and works, only 1 ca se had nerve paralysis of the affect extremity caused by popliteal artery APA compression . All the cases have good blood perfusion of the extremities wit hout recurrence. Conclusions APA should be treated by surgery. During operation control blood vessels effectively and remove the pathological changetissues completely are important,and reasonable application of antibi otics and antithrombotic agents are the guarantee of getting successful results .

Purpose To explore the correlation between normal pancreas and abdominal aorta in the peak enhancement (PE) and the shift time at the peak by applying the multislices spiral CT perfusion imaging.Materials and Methods Prospectively analyzed 62 patients who received enhancement CT examination for the superior or the middle abdomen,underwent optimum level CT perfusion imaging after plain scanning.These data were processed on a Vitreal 2.0 worker-station by using Toshiba body software package.The time-density curves (TDC) of the normal pancreas and the abdominal aorta were drawn,the PE and the shift time of PE were recorded and their correlation was analyzed.Results Compared with abdominal aorta,the mean value of PE of the normal pancreas was lower,and the difference was statistically significant [(111.94± 14.42)HU vs (351.83 ± 74.93)HU,P＜0.05],the mean difference was (246.10± 65.86)HU.Compared with abdominal aorta,the mean shift times of PE of the normal pancreas was latter,and the difference was statistically significant [(37.56±6.90) s vs (30.82±6.73) s,P＜0.05],the mean difference was (6.54±2.97)s.The PE and shift time of PE of the normal pancreas were positively and linearly correlated with that of abdominal aorta (r=0.438,r=0.379).Conclusion The PE of the normal pancreas is not synchronous with that of the abdominal aorta.The shift time of the former is usually 6～8 seconds slower than that of the latter.This provides a basis to find the PE of the normal pancreas in enhanced scan.

OBJECTIVETo study the expression of Toll-like receptor 4 (TLR-4) and caspase-3 in the intestine of neonatal rats with necrotizing enterocolitis (NEC), and explore the protective effects and possible regulatory mechanisms of glutamine (Gln) in NEC.

METHODSSixty premature rats were randomly divided into three groups (n=20 each): control, NEC model and Gln intervention group. NEC model was prepared by formula feeding, hypoxia and cold stress. The Gln intervention group was also subjected to hypoxia and cold stress but was fed with formula containing Gln (0.3 g/kg). Two days later, the rats were sacrificed and the intestine tissues were obtained. The histological changes of ileal tissues were observed by hemetoxylin and eosin staining. The expression of caspase-3 and TLR-4 protein in the jejunum, ileum and colon were detected by inmunohistochemistry. The expression of TLR-4 mRNA in the jejunum, ileum and colon were detected by RT-PCR.

RESULTSCompared with the control group, the histological score of ileal tissues, and the expression of caspase-3, TLR-4 protein and TLR-4 mRNA in the NEC model group increased significantly (P<0.01). Gln intervention decreased significantly the histological score of ileal tissues, and the expression of caspase-3, TLR-4 protein and TLR-4 mRNA compared with the NEC model group (P<0.05).

CONCLUSIONSTLR-4 might be involved in the pathogenesis of NEC. Gln may provide protective effects on intestine possibly through reducing the TLR-4 expression and then decreasing the apoptosis of intestinal epithelial cells.

Animals ; Animals, Newborn ; Caspase 3 ; analysis ; Enterocolitis, Necrotizing ; metabolism ; pathology ; Female ; Glutamine ; pharmacology ; Immunohistochemistry ; Pregnancy ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; Toll-Like Receptor 4 ; analysis ; genetics

Objective: To investigate the potential role of Bit1 in the pathogenesis of pancreatic ductal cancer cells(PDAC) and its potential clinical application value. Methods: Real-time PCR and Western blot were employed to detect the expression of Bit1 in six pancreatic cancer cells, then the tool cells were selected to further study the function of Bit1.PolyHEMA was used to monitor the suspended cell culture condition in vitro.The invasion and migration abilities of pancreatic cancer cells were detected through Transwell assay. Western blot and confocal assay were used to explore the potential mechanism of Bit1 in the process of metastasis.The expression of Bit1 was detected through tissue microarray, the potential relationship between Bit1 and other clinical factors were analyzed. Results: The results of real-time PCR and Western blot indicated that the expression of Bit1 was highest in the PANC1 cells and lowest in the Mia paca2 cells (gene: 3.13±0.40 vs. 1.00±0.35, protein: 1.77±1.00 vs. 0.23±0.45). The shBit1 PANC1 and Bit1-OE(over expression) Mia paca2 cells were successfully constructed.Bit1 over expression could promote the anoikis rate of Mia paca2 cells, and Bit knockdown could inhibit the anoikis incidence.Bit1 over expression suppressed the motility and invasion of Mia paca2 cells, but Bit1 knockdown could accelerate the migration and invasion ability of PANC1 cells.Bit1 could potentially affect pancreatic cancer cells′ malignant behaviors through epithelial-mesenchymal transition process.Bit1 expression was significantly associated with pancreatic cancer′s neural invasion (P<0.05). Conclusions Bit1 could affect the anoikis incidence of pancreatic cancer, Bit1 negatively affect the migration and invasion abilities of PDAC, the EMT process was potentially involved in the whole modulation process.Bit1 expression is associated with neural invasion in pancreatic cancer patients.

Objective:The effect of intermedin (IMD) on ATP-induced activation of inflammatory bodies and pyroptosis of cells and its mechanism were studied using lipopolysaccharide (LPS)-sensitized mouse macrophage line RAW 264.7.Methods:The cells were divided into the control groups, the LPS groups, LPS+IMD groups, and LPS+IMD+LY294002 groups. The expression of interleukin (IL)-1β and IL-18 and the activation of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammatory cells were detected by real-time PCR and western blotting, and the pyroptosis of cells was detected by propidium iodide (PI) staining. The measurement data was represented by MS± SD, and the inter-group difference was compared with ANOVA calculations, and P<0.05 represented the difference with statistical significance. Results:Compared with the control group [(0.83±0.09) vs (0.49±0.04)], the ratio of phosphorylated phosphatidylinositol-3-kinase, p-PI3K)/phosphatidylinositol-3-kinase (PI3K) (0.44±0.05) and p-Akt/Akt (0.27±0.06) in the LPS group was significantly decreased. The ratios of p-PI3K/PI3K (1.22±0.18) and pAkt/Akt (0.83±0.09) in LPS+IMD group was significantly increased ( F=31.40, P<0.001; F=50.88, P<0.001). Compared with the control group, the mRNA and protein expressions of IL-1β, IL-18 and NLRP3 inflammasome (NLRP3, caspase-1, ASC) in RAW264.7 cells were up-regulated in the LPS group (LPS and ATP). Compared with LPS group, IMD treatment inhibited the expression of inflammatory cytokines IL-1β, IL-18 and NLRP3 inflammasome, which was blocked by LY294002, a blocker of PI3K/Akt pathway. The results of real-time PCR showed that the relative expression of IL-1β mRNA was (1.00±0.11) in the control group, (8.32±0.61) in the LPS group, (8.32±0.55) in the LPS+IMD group, and (7.23±0.41) in the LPS+IMD+LY group ( F=15.42, P<0.001). The relative expression of IL-18 mRNA in the control group was (1.00±0.17), (1.82±0.21) in the LPS group, (1.14±0.15) in the LPS+IMD group, and (1.53±0.11) in the LPS+IMD+LY group respectively ( F=18.16, P<0.001). The relative expression of NLRP3 mRNA in the control group was (1.00±0.13), (2.58±0.18) in the LPS group, (1.07±0.17) in the LPS+IMD group, and (1.33±0.32) in the LPS+IMD+LY group respectively ( F=15.98, P< 0.001); The relative expression of caspase-1 mRNA in the control group was (1.00±0.09), (6.20±0.19) in the LPS group, (3.43±0.06) in the LPS+IMD group, and (5.50±0.45) in the LPS+IMD+LY group respectively ( F=18.39, P<0.001). The relative expression of ASC mRNA in the control group was (1.00±0.21), (4.58±0.48) in the LPS group, (2.07±0.51) in the LPS+IMD group, and (3.33±0.32) in the LPS+IMD+LY group respectively ( F=15.19, P<0.001). Western blotting results showed that the relative expression of IL-1β protein was as follows: (100%) in the control group, [(188±14)%] in the LPS group, [(112±11)%] in the LPS+IMD group, and [(171±27)%] in the LPS+IMD+LY group respectively ( F=21.25, P<0.001). The relative expression of IL-18 protein in the control group was 100%, [(183±16)%] in the LPS group, [(115±19)%] in the LPS+IMD group, and [(179±23)%] in the LPS+IMD+LY group respectively ( F=19.62, P<0.001). The relative expression of NLRP3 protein was 100% in the control group, [(149±15)%] in the LPS group, [(106±10)%] in the LPS+IMD group, and [(144±15)%] in LPS+IMD+LY group respectively ( F=14.35, P<0.001). The relative expression of ASC protein was 100% in the control group, [(188±12)%] in the LPS group, [(110±18)%] in the LPS+IMD group, and [(192±8)%] in the LPS+IMD+LY group ( F=15.79, P<0.001). Conclusion:IMD inhibits the activation of NLRP3 inflammasome and cell pyroptosis by regulating PI3K/Akt activity.