Objective To evaluate the early diagnostic value of Heart-type fatty acid-binding protein(H-FABP) for myocardial infarction in patients post off-pump coronary artery bypass (OPCAB).Methods Between March 2009 and July 2009,59 patients had been undergone OPCAB for the first time.They were divided into 3 groups (normal group,myocardial injury group and myocardial infarction group) by myocardial-bound creatiue kinase (CK-MB) 、cardiac troponio Ⅰ (cTnI) 、electrocardiogram (ECG) and echocardiogram.Serial blood samples were taken during perioperation to quantify blood levels of H-FABP,CK-MB,cTnI.Results The average H-FABP value for the patients in the myocardial infarction group is higher than the others ( P ＜ 0.01 ).H-FABP reached the peak valve at 2 hours and decreased at 4 hours after the patients arrived at ICU.H-FABP got back to the baseline one day postoperation.Receiver operating characteristic curves( ROC curve) demonstrated that H-FABP had greater diagnostic ability of myocardial infarction postoperation with area under the curve at the time of arriving at ICU ( 0.900,95％ CI 0.818 -0.981 )and 2 hours later (0.832,95％ CI 0.718 -0.946).At the time of arriving at ICU,sensitivity of H-FABP for diagnosis was 90.9％ and specificity was 77.1％.At the point of 2 hours later,sensitivity was 72.7％ and specificity was 75.0％.Conclusion The H-FABP seems to be an excellent early biomarker of cardiac necrosis after OPCAB.

Objective To evaluate the relationship between the change of Heart-fatty acid-binding protein and myocardial injury/infarction in postoperative of off-pump coronary artery bypass grafting (OPCAB).Methods 59 patients (male 37 and female 22,from 46 to 83 years old) who were the first time to undergoing OPCAB were included in this study.Serial venous blood samples were taken at after induction of anesthesia,the OPCAB finished (after the last anastomosis),entered ICU,2,4 and 8 hours after the patient entered ICU,and at 1 and 2 day postoperative to test H-FABP.The cTnI and CK-MB were tested at 4 and 8 hours,after entering ICU,and at 1 and 2 days postoperative.Patients were divided into 3 groups by the changes of ECG and the level of cTnl at 8 hours after they entered ICU:normal group (group I,cTnI ＜0.1 ng/ml),myocardial injury group(group Ⅱ,cTnI 0.l-1.0 ng/ml) and.myocardial infarction group(group Ⅲ,cTnI ＞ 1.0 ng/ml).Results The level of H-FABP released was significantly higher in the myocardial infarction group than normal group and myocardial injury group (P ＜ 0.01).There is good correlation between the H-FABP and cTnI or CK-MB.But the peak level of H-FABP is earlier (finished OPCAB) (P ＜ 0.05),and it peaked early at 2h after entered ICU (P ＜ 0.01),it began to decrease at 4 hours after entered ICU and returned to baseline at 1 day postoperative,while the cTnI and CK-MB peaked at postoperative day 1 and 8h after entered ICU respectively,and maintained in higher level at postoperative 2 days.Conclusion There is good correlation between the H-FABP and perioperative myocardial infarction in OPCAB,and it has superiority compared with cTnI,which is as gold standard for perioperative myocardial infarction,on a certain degree.It can benefit from early detection of H-FABP for myocardial infarction in perioperative of OPCAB.

Objective To investigate the phenotype and function of CD8+T cells cultured with SK-OV-3. Methods Transwell coculture experiments were conducted in 24-well plates with inner wells to separate CD8+ T cells and SK-OV-3. After 5 days of culture, CD8+ T cells were washed, and 1 × 106 cells were collected for Foxp3, CD25, CD28, CTLA-4 and GITR mRNA analysis and 2 × 106 cells were collected to detect expression of Foxp3, CD25, CD28, CTLA-4 and GITR in CD8+ T cells by flow cytometry. CD8+T cells that cultured alone or with SK-OV-3 were added at ratios of 1∶0 , 1∶1 , 1∶5 , 1∶10 , and 0∶1 to na?ve CD4+ T cells in 96-well plates. All wells were cultured with the presence of irradiated PBMCs and anti-CD3 antibody. After 72 h, [3H]-thymidine was added for 16 h prior to the determination of proliferation by scintillation counting. Results Compared with CD8+ T cells cultured without SK-OV-3 , the expression of Foxp3 and CTLA-4 was increased and CD28 expression was decreased in CD8+ T cells cultured with SK-OV-3 (both P < 0.001). We found that CD8+T cells cultured with SK-OV-3 significantly suppressed the na?ve CD4+ T cell proliferation induced by the anti-CD3 stimulation in a dose-dependent manner. In contrast, CD8+ T cells cultured without SK-OV-3 did not suppress na?ve CD4+ T cell proliferation. Conclusion Ovarian cancer cell can induce the suppressive CD8+Treg, which is an important link of the immunosuppressive microenvironment in ovarian cancer.

Previous studies have suggested that various kinds of inflammatory factors can influence the formation and development of tumor cells.Researche has shown that gallbladder cancer is closely linked with local inflammation,which is a risk factor for the development of gallbladder cancer.It is widely known that cholecystitis is closely correlated with gallstones,and that bile obtained from patients with gallbladder cancer contains a large variety of bacteria,such as Salmonella typhi,Helicobacter,and Escherichia coli.It is proposed that the gallbladder may be the result of the joint action of inflammation with the bacterial flora.Similarly,the inflammatory “tumor infiltrating lymphocyte” (TIL)can be observed in the tumor and its surrounding tissues,and may also play a role in tumor growth and metastasis.However,detailed mechanisms about the relationship between inflammation and gallbladder cancer is still not clear.No specific anti-inflammatory drugs for gallbladder cancer have been developed. In the near future,anti inflammatory drugs may play a more important role in gallbladder cancer prevention and treatment.

Objective: To investigate the peak time and peak area of elements in cadmium telluride quantum dots (CdTe QDs) using size exclusion chromatography-high-performance liquid chromatography-inductively coupled plasma mass spectrometry, as well as the biological stability of CdTe QDs in vivo and in vitro. Methods: Transmission electron microscope and ultraviolet fluorescence were used for characterization and synthesis of water-soluble CdTe QDs, and CdTe QDs were added to double-distilled water, mobile phase, or bovine serum medium to observe the change in stability after different periods of time. CdTe QDs were injected into the vein of mice, and the changes in the morphology of CdTe QDs in serum and the liver were measured at 1, 24, and 72 hours after exposure. Size exclusion chromatography-high-performance liquid chromatography was used for the elution of the compounds in the solution based on their volume, and then inductively coupled plasma mass spectrometry was performed for the eluent. The flow time of ¹¹⁴Cd and ¹³⁰Te and molar ratio were used for qualitative analysis of CdTe QDs, and the peak area was used to judge whether CdTe QDs were degraded. Results: CdTe QDs were diluted to a concentration of 0.5 mmol/L with double-distilled water and then placed in a dark place at room temperature; CdTe QDs were completely degraded after 60 minutes. CdTe QDs were diluted to a concentration of 0.005 mmol/L with a mobile phase, and the peak of CdTe QDs was not detected. After CdTe QDs were placed in a dark place at room temperature for 48 hours at a concentration of 0.005 mmol/L in bovine serum mediumin vitro, the peak area of ¹¹⁴Cd was 6179841-7346084, and the peak area of ¹³⁰Te was 1077913-1191066. CdTe QDs had the highest peak area at 1 hour after exposure, and the peak areas of ¹¹⁴Cd and ¹³⁰Te were 18183894 and 25187987, respectively. CdTe QDs were quickly degraded in the liver; at 1 hour after exposure, the degradation products of CdTe QDs containing Cd were observed in liver tissue homogenate, and CdTe QDs were largely degradedat 24 hours. Conclusion This method can be used to investigate the biological stability of CdTe QDs. CdTe QDs are degraded in the liver and produce Cd²⁺, which may cause toxic reaction.

Objective To explore the pathogen characteristics and related factors of nosocomial infection in adult ICU pa-tients after cardiac surgery, and provide a basis for the rational and standardized use of antibiotics and the control of nosocomial infection.Methods Patients in ICU after adult cardiac surgery from January 2015 to December 2017 were studied.Through the nosocomial infection monitoring and reporting system(HIS and LIS system), data of infected sites, specimens, pathogen and drug-sensitivity results were recorded, and the clinical data were collected and the related factors of nosocomial infection af-ter cardiac surgery were analyzed.Results 213 patients with nosocomial infections were diagnosed , and the nosocomial infec-tion rate was 3.59％.There were 261 cases of nosocomial infection, with a total infection cases rate of 4.39％.232 strains of pathogen were detected.Gram-negative bacteria173 strains(74.57％), klebsiella pneumoniae and acinetobacterbaumannii ac-count for 65(28.07％) and 37(15.95％)strains respectively.35 strains of gram-positive bacteria account for 15.08％, 12 strains of staphylococcus aureus account for 5.17％.24 strains of fungi account for 10.34％, 12 strains of candida albicans(5. 17％) were the most.The resistance rates of klebsiella pneumoniae to amoxicillin/kclavitrate, piperasil/tazobatan, tigacy-cline, tobramycin, and impenan were all<10％.Acinetobacter baumannii show high resistance rate to commonly used antibi-otics other than tigacycline(2.70％).The resistance rates of staphylococcus aureus and staphylococcus epidermis to vancomy-cin and linazolamide were 0.Logistic regression analysis showed that preoperative and postoperative stroke, secondary endotra-cheal intubation, postoperative low cardiac output, postoperative stroke, mechanical ventilation time >48 h, and postoperative ICU stay>72 h were related factors of postoperative nosocomial infection .Conclusion The main pathogen of nosocomial in-fection in ICU after adult cardiac surgery is gram-negative bacteria.Klebsiella pneumoniae, the most common bacteria, has a low resistance rate to antibiotics, while the secondary acinetobacter baumannii has a high resistance rate .According to the fac-tors related to nosocomial infection after cardiac surgery , prevention measures should be formulated .According to the results of pathogen and drug sensitivity, antimicrobial drugs should be selected reasonably so as to postoperative nosocomial infection and the occurrence of drug-resistant strains could be controlled effectively .

Objective To explore the effect of knocking down Rho-associated coiled-coil kinase (ROCK2) gene on the cognitive function of amyloid precursor protein/presenilin-1 (APP/PS1) double transgenic mice and its mechanism. Methods APP/PS1 double transgenic mice were randomly divided into AD model group (AD group), ROCK2 gene knock-down group (shROCK2 group), ROCK2 gene knock-down control group (shNCgroup), and wild-type C57BL/6 mice of the same age served as the wild-type control (WT group). Morris water maze and Y maze were employed to test the cognitive function of mice. Neuron morphology was detected by Nissl staining. Immunofluorescence histochemical staining was used to detect the expression of phosphorylated dynamin-related protein 1 (p-Drp1) and mitochondrial fusion 1 (Mfn1). Western blot analysis was used to detect the expression ROCK2, cleaved-caspase-3 (c-caspase-3), B-cell lymphoma 2 (Bcl2), Bcl2-related protein X (BAX), p-Drp1, mitochondrial fission 1 (Fis1), optic atrophy 1 (OPA1), Mfn1 and Mfn2. Results Compared with AD group mice, the expression of ROCK2 in shROCK2 group mice was significantly reduced; the cognitive function was significantly improved with the number of neurons in the hippocampal CA3 and DG areas increasing, and nissl bodies were deeply stained; the expression of c-caspase-3 and BAX was decreased, while the expression of Bcl2 was increased; the expression of mitochondrial division related proteins p-Drp1 and Fis1 were decreased, while the expression of mitochondrial fusion-related proteins OPA1, Mfn1 and Mfn2 were increased. Conclusion Knock-down of ROCK2 gene can significantly improve the cognitive function and inhibit the apoptosis of nerve cells of APP/PS1 mice. The mechanism may be related to promoting mitochondrial fusion and inhibiting its division.
Animals ; Mice ; Alzheimer Disease/pathology* ; Amyloid beta-Peptides/metabolism* ; Amyloid beta-Protein Precursor ; Apoptosis/genetics* ; bcl-2-Associated X Protein ; Caspase 3 ; Cognition ; Disease Models, Animal ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondrial Dynamics/genetics*