0 05). 70 of 138 patients had serum PSA concentration remarkable elevation after prostate biopsy (P

Objective To try different concentrations of nicotine promotes the apoptosis of human umbilical vein en-dothelial cells and its mechanism .Methods Human umbilical vein endothelial cells were cultured .According to the concentration of nicotine , grouped as 10 -6 , 10 -7, 10 -8 mol/L, and control.After 24 h of nicotine treat-ment, proliferation/activity were tested by CCK-8 assay;Annexin V-FITC fluorescence staining detects the apoptot-ic cells.Western blot detects the expression of protein Bax , Bcl-2 and PARP-1, to study the mechanism of apopto-sis.Results Compared with control group , in 10 -6 ,10 -7 mol/L groups the proliferation/activity of HUVECs de-creased ( P<0.05 ) .And the number of apoptotic cells increased ( P<0.01 ) .The target proteins expression of 10 -6、10 -7 mol/L groups were changed as follow: Bax increased ( P <0.01 ) , Bcl-2 decreased ( P <0.01 ) and PARP-1 increased ( P<0.01 ) .Conclusions Nicotine may promote the apoptosis of vascular endothelial cells , which accelerates the development of atherosclerotic disease .

The paper analyzed the impact of the trial for "lump-sum prepayment practice of medical insurance" on tertiary hospitals in Shanghai initiated by Shanghai Medical Insurance Bureau since 2009. Based on the analysis, the authors recommended that the hospitals should adapt to the changes by raising quality of care, improving cost accounting, informationizing and refining medical insurance information management, as well as controlling expenses on a rational basis. These approaches will help them adapt to and promote the ongoing health reform in China.

Objective:To explore the lactate metabolism in brain tissue of the mice with early acute hypoxia-ischemia injury,and to provide data support for 9.4T 1 H-NMR spectroscopy in detecting the lactate level clinically.Methods:Eighty Kunming mice were randomly divided into sixteen groups (0 s,20 s,40 s,60 s,2 min,4 min, 6 min,8 min, 10 min, 12 min, 14 min, 16 min, 18 min,and 20 min)according to the duration of hypoxia-ischemia (n=5).The changes of lactate levels were detected by 9.4T 1 H-NMR spectroscopy. Results:After the initiation of hypoxia-ischemia injury,the lactate level began to increase rapidly to the highest value of (6.89 ± 0.34)μmol·g-1 at 20 s,then started to decline quickly from 40 s to 2 min,and eventually decreased to a stable level of (4.85±0.36)μmol·g-1 until 6 min.Compared with control group,the levels of lactate in brain tissue of the mice in hypoxic-ischemic groups were increased (P <0.01).Conclusion:40 s of acute hypoxia-ischemia may be the lactate cerebral neuron threshold during the anaerobic glycolysis. 9.4T1 H-MRS can provide the exact time window for detecting the lactate metabolism.

Objective:To screen the binding peptide against adenovirus type 7(Ad7) and evaluate the relevance with the ade-novirus receptor .Methods:Binding peptide against Ad 7 was screened by panning the phage display 12 peptides library .The antibody against the selected peptide was prepared and was used to study the binding to the membrane by immunofluorescence technique .Re-sults:Using Ad7 as the target protein , GTS09 peptide was selected from the phage display 12 peptides library by biopanning .GTS09-phage complex could significantly bind Ad 7, with the affinity constant up to 1.93 ×1010 L/mol;at the same time, immunofluorescence showed that antibody of GTS09 could specifically bind to membrane of 293 cell.Conclusion: Antibody against GTS09 peptide could specifically bind to membrane of 293 cell,which shows that the peptide may presumably have homology with the cell receptors of Ad 7.

BACKGROUND: Autophagy of osteocytes has been found to be implicated in the pathogenesis of steroid-induced necrosis of the femoral head and closely related to apoptosis.OBJECTIVE: To summarize the research progress of autophagy in the pathogenesis of steroid-induced necrosis of the femoral head by studying the interaction between cell autophagy and cell apoptosis as well as osteocytes.METHODS: A computer-based online retrieval of PubMed, Embase and CNKI databases was performed for relevant literatures published from October 1996 to October 2016 with the keywords of steroid, necrosis of the femoral head, cell apoptosis, cell autophagy, osteocyte in Chinese and English, respectively. The articles concerning steroid-induced necrosis of femoral head and cell autophagy were collected, and the redundant and old researches or Meta analysis were removed.RESULTS AND CONCLUSION: Mammalian target of rapamycin, Beclin-1, microtubule-associated protein 1 light chain 3, bone morphogenetic proteins, fork box protein and transcription gene family and transcription factor 4 are closely related to autophagy. The interaction between autophagy and osteocytes is correlated with steroid dose: the autophagy shows protective factor under the low dose corticosteroids; however, with the increase of the dosage, a large number of apoptotic cells, and the phenomenon of bone loss can been observed. Furthermore, the relationship of cell autophagy with apoptosis and bone mass maintenance is still controversial, which needs to be explored in depth via a series of rational experiments.

Objective To investigate prospectively effects of different drainage methods on preventing anastomotie leakage after Dixon operation in rectal carcinomas.Methods During the period of January 2002 to January 2007,450 patients with rectal carcinomas received Dixon operation.They were divided into three groups ( group A,B,and C) in order of admission.Presacral drainage was done in Group A,presaeral drainage + drainage through anus with one tubes in Group B,and presacral drainage + drainage through anus with two tubes in Group C.The postoperative complications of three groups were observed.Results There was 7.33% (11/150) ,8.00% (12/150) and 6.67% (10/150) wound infection in group A,B and C respectively.8.67% (13/150),6.67% (10/150) and 1.33% (2/150) anastomotic leakage occurred in group A,B and C respectively.Three groups had a similar wound infection ineidence(P ＞0.05).The occurrence of anastomotic leakage in group C was statistically lower than that in group A and B ( P ＜ 0.05 ).Conclusion Presacral drainage + drainage through anus with two tubes can effectively prevent anastomotic leakage after Dixon operation in rectal carcinomas.

Objective Intercellular adhesion molecule-1 (ICAM-1) plays an important role in mediating pulmonary infiltration of neutrophils .The aim of the study was to observe the expression of ICAM-1 and its potential regulators MK 2/HuR in pulmonary micro-vascular endothelial cells ( PMVEC ) in mice with acute respiratory distress syndrome ( ARDS) induced by lipopolysaccharide ( LPS) . Methods Ten 6-8 weeks old healthy C57BL/6 mice were randomly divided into an LPS and a control group of equal number , the former injected intraperitoneally with LPS diluted in 100 μL PBS while the latter with PBS only , both at 5 mg per kg of the body weight .At 24 hours after injection , all the mice were sacrificed .Real-time PCR was used to determine the mRNA expressions of HuR and ICAM-1 in the PMVECs, Western bolt employed to detect the protein expressions of MK2, HuR and ICAM-1, and flow cytometry adopted to measure the ICAM-1 expression on the surface of the PMVECs and pulmonary infiltration of neutrophils . Results The W/D ratio in the lung tissue of the mice was significantly lower in the LPS than in the control group (3.61 ±0.28 vs 6.16 ±0.40, P<0.05), while the rate of neutrophil infiltration markedly higher in the former than in the latter ([13.92 ±3.23]%vs [3.24 ±1.24]%, P<0.05).The mRNA and protein expressions of ICAM-1 in the PMVECs were significantly elevated in the LPS group as compared with that in the control (P<0.05), and so was the mRNA expression of HuR (P<0.05).No remarkable changes were observed in the expressions of total MK 2 and HuR proteins, but phosphorylated MK2 (p-MK2) and cytoplasmic HuR were increased in the LPS-stimulated mice. Conclusion Specific blockage or reduction of the HuR expression in PMVECs may lower the expression of ICAM-1, reduce neutrophil infiltration , and lessen pathophysiological changes in mice with ARDS .

Objective To investigate the pathophysiological features of rat hemorrhagic shock under high temperature conditions.Methods A total of 128 SD rats were assigned to high temperature group and normal temperature group according to the random number table,with 64 rats per group.Rats in high temperature group were pretreated at 342 for 12 h,and in normal temperature group were kept at 25℃.Hemorrhagic shock models in rats were produced by withdrawing 40％ of the total blood volume via the femoral artery.Parameters of the two groups were measured including blood electrolytes (Na +,K +),plasma osmotic pressure,liver function [aspartate aminotransferase (AST),alanine aminotransferase (ALT)],kidney function [creatinine (CREA)],arterial blood gases (pH,PO2 and PCO2) and cardiac function [heart rate (HR),cardiac output (CO),cardiac index (CI) and DO2].Animal survival time and survival rate were detected.Results Before shock,high temperature group versus normal temperature group showed higher detections of Na+ concentration [(142.3 ± 2.2) mmol/L:(139.1 ±1.5) mmol/L],plasma osmotic pressure [(304.8 ± 4.7) mmol/L:(300.0 ± 1.9) mmol/L],HR [(462 ±30) times/min:(402 ± 44) times/min],CO [(0.892 ± 0.190) L/min:(0.713 ± 0.090) L/min] and CI [(0.0030±0.0006)L·min-1 · cm-2:(0.0023 ±0.0002)L· min-1 · cm-2] (P＜0.05).After shock,normal temperature group showed further increased concentrations of Na + and K + and significantly enhanced AST,ALT and CREA compared to normal temperature group (P ＜ 0.05).After shock,CO,CI and DO2 in high temperature group were decreased by 63％,63％ and 69％ respectively compared to those before shock,but less decrease was observed in normal temperature group.Rat survival rate and survival time were significantly reduced in high temperature group compared to normal temperature group (P ＜ 0.05).Conclusion Pathophysiological changes of hemorrhagic shock in rats under high temperature are mainly manifested as impaired cardiac function,significantly increased concentrations of Na + and K + and significantly shortened survival time.

Objective PU.1 plays a key role in innate immune function in the alveolar macrophage.This study was to con-struct and identify recombinant adenovirus vectors carrying the human transcription factor PU.1 gene. Methods The recombinant shut-tle plasmid was obtained from the PU.1 gene ( SPI1) and eukaryotic expression vector that digested by restriction enzymes and connected by T4 DNA ligase.The target fragment SPI1-IRES-EGFP was amplified by PCR.The product was cloned into the intermediate pDONR221 and then recombined with the adenovirus backbone plasmid pAd/CMV/V5-DEST to form a recombinant adenovirus vector. The recombinant adenovirus vector was linearized by PacI and then transfected into human embryonic kidney (HEK293) cells to obtain the recombinant adenovirus pAD-SPI1-IRES-EGFP, which was then propagated in HEK293 cells, filtered and purified to obtain high-con-centration adenoviruses.The adenovirus titer was determined by TCID 50 assay.The PU.1 gene expression in the HEK293 cells was con-firmed by fluorescence microscopy and real-time qPCR. Results PCR amplification, restriction digestion and sequencing analysis showed the recombinant adenovirus carried the correct PU.1 gene.The final virus titer, calculated by TCID 50, was 8 ×1011 IU/mL. Green fluorescence was observed under the fluorescence microscope. Real-time qPCR confirmed that the expression of PU.1 mRNA was increased by 2189.93 folds. Conclusion The recombinant adenovirus vector carrying the PU.1 gene was constructed and obtained successfully, which could contribute to further studies of the influence of PU.1 overex-pression on the innate defense against Aspergillus fumigatus.