Objective:Evaluate the application of Fourier transform infrared spectroscopy in the identification of homology of carbapenem-resistant Escherichia coli(CREC). Methods:A total of 26 carbapenem-resistant Escherichia coli strains were isolated from 9 provinces in China in 2018. The 900-1 200 cm -1 was selected as a spectral region for the Euclidean distance calculating and average linkage clustering between all isolates.The single nucleotide polymorphism (SNP) was analyzed by whole genome sequencing (WGS). Results:Twenty-six CREC strains were divided into 14 infrared spectros copy(IR) types by FTIR. The same IR type belonged to the same sequence type type.Compared with cluster analysis based on WGS, the consistency of FTIR cluster analysis was 92.3% (24/26).Conclusions:FTIR presented excellent performance in identification of homology of CREC.Besides, with the advantages of simple operation and rapid acquisition of results, FTIR may be a useful tool in clinical labs.

Objective:To establish a disease risk prediction model for the newborn screening system of inherited metabolic diseases by artificial intelligence technology.Methods:This was a retrospectively study. Newborn screening data ( n=5 907 547) from February 2010 to May 2019 from 31 hospitals in China and verified data ( n=3 028) from 34 hospitals of the same period were collected to establish the artificial intelligence model for the prediction of inherited metabolic diseases in neonates. The validity of the artificial intelligence disease risk prediction model was verified by 360 814 newborns ' screening data from January 2018 to September 2018 through a single-blind experiment. The effectiveness of the artificial intelligence disease risk prediction model was verified by comparing the detection rate of clinically confirmed cases, the positive rate of initial screening and the positive predictive value between the clinicians and the artificial intelligence prediction model of inherited metabolic diseases. Results:A total of 3 665 697 newborns ' screening data were collected including 3 019 cases ' positive data to establish the 16 artificial intelligence models for 32 inherited metabolic diseases. The single-blind experiment ( n=360 814) showed that 45 clinically diagnosed infants were detected by both artificial intelligence model and clinicians. A total of 2 684 cases were positive in tandem mass spectrometry screening and 1 694 cases were with high risk in artificial intelligence prediction model of inherited metabolic diseases, with the positive rates of tandem 0.74% (2 684/360 814)and 0.46% (1 694/360 814), respectively. Compared to clinicians, the positive rate of newborns was reduced by 36.89% (990/2 684) after the application of the artificial intelligence model, and the positive predictive values of clinicians and artificial intelligence prediction model of inherited metabolic diseases were 1.68% (45/2 684) and 2.66% (45/1 694) respectively. Conclusion:An accurate, fast, and the lower false positive rate auxiliary diagnosis system for neonatal inherited metabolic diseases by artificial intelligence technology has been established, which may have an important clinical value.

Objective To evaluate the role of phosphatidylinositol 3?kinase(PI3K)∕serine?threo?nine kinase(Akt)signaling pathway in propofol?induced invasion of human liver cancer cell line HepG2. Methods HepG2 cells were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum in a 5% CO2incubator at 37℃. HepG2 cells at the logarithmic growth phase were divided into 6 groups(n=18 each)using a random number table: control group(group C), propofol group(group P), PI3K∕Akt signaling pathway agonist IGF?1 group(group IGF), PI3K∕Akt signaling pathway inhibitor LY294002 group(group LY), IGF?1 plus propofol group(group IGF+P)and LY294002 plus propofol group (group LY + P). Propofol 120 μg∕ml was added in group P. IGF?1 10 nmol∕L was added in group IGF. LY294002 10 μmol was added in group LY. In group IGF+P, 10 nmol∕L IGF?1 was added, cells were in?cubated for 24 h, and then 120 μg∕ml propofol was added. In group LY+P, 10 μmol LY294002 was add?ed, cells were incubated for 24 h, and then 120 μg∕ml propofol was added. The invasion of cells was measured by Transwell invasion assay at 24 h of incubation. The expression of PI3K and Akt mRNA in cells was determined by real?time polymerase chain reaction. The expression of Akt, PI3K and phosphorylated Akt(p?Akt)was detected by using Western blot. Results Compared with group C, the invasive cell count was significantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was decreased, and the expression of Akt mRNA was down?regulated in P, P+IGF, LY and P+LY groups, and the invasive cell count was significantly increased, the expression of PI3K protein and mRNA was up?regulated, p?Akt∕Akt ratio was increased, and the expression of Akt mRNA was up?regulated in group IGF(P<0.05). Compared with group P, the invasive cell count was significantly increased, the expression of PI3K protein and mRNA was up?regulated, p?Akt∕Akt ratio was increased, and the expres?sion of Akt mRNA was up?regulated in group P+IGF, and the invasive cell count was significantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was decreased, and the ex?pression of Akt mRNA was down?regulated in group P+LY(P<0.05). The invasive cell count was signifi?cantly reduced, the expression of PI3K protein and mRNA was down?regulated, p?Akt∕Akt ratio was de?creased, and the expression of Akt mRNA was down?regulated in group P+IGF as compared with group IGF (P<0.05)and in group P+LY as compared with group LY(P<0.05). Conclusion The mechanism by which propofol inhibits invasion of HepG2 cells is related to inhibiting activation of PI3K∕Akt signaling path?ways.

Objective To investigate the current status of job satisfaction,stressful events and self-efficacy among nurses in cancer hospital,and explore correlation among job satisfaction,stressful events and self-efficacy.Methods Totally 260 nurses from Zhejiang Cancer Hospital were inquired by Minnesota satisfaction questionnaire,inventory of stressful events,and general self-efficacy scale.Descriptive analysis and Pearson correlation analysis were adopted to analyze the data.Results A total of 260 questionnaires were given out,while 246 valid questionnaires returned,and the effective rate was 94.6％.The total average scores of job satisfaction,stressful events and self-efficacy were (3.41 ± 0.45),(117.72 ± 18.92) and (2.50 ± 0.44).There was a significant negative correlation between overall satisfaction and stressful event (r =-0.458,P＜0.001).However,satisfaction were positively correlated with self-efficacy (r =0.257,P =0.020).Conclusions Job satisfaction among nurses of cancer hospital is higher than data of previous studies,but the overall self-efficacy is still low,and most of them is in the middle-high stressful events.Managers can improve nurses' job satisfaction by reducing occupational stress and increasing self-efficacy.That might reduce dimission rate,and maintain the stability of care team.

Objective To investigate the expressions of metastasis suppressor 1 (MTSS1 )and calcium activated protein 43 (Cap43)in esophageal squamous cell carcinoma (ESCC)tissue,and to clarify the relationship between the expressions of MTSS1,Cap43 and the clinicopathological features of ESCC.Methods 80 cases of ESCC tissue and 30 cases of normal adjacent-cancer tissue were collected,and the protein and mRNA expressions of MTSS1 and Cap43 in ESCC tissue and normal tissue were detected by streptavidin-perosidase (SP)immunohistochemistry and RT-PCR;their relationships with the clinicopathological features of ESCC were analyzed.Results The positive expression rate of MTSS1 in normal esophagus tissue was significantly higher than that in ESCC tissue detected by SP (83.3%vs 21.3%,P<0.01)and RT-PCR (0.703±0.085 vs 0.295±0.065,P<0.01),However,the positive expression rate of Cap43 in normal esophagus tissue was significantly lower than that in ESCC tissue by SP method (16.7%vs 76.3%,P<0.01)and by RT-PCR (0.236±0.052 vs 0.693±0.078,P<0.01).The mRNA expression levels of MTSS1 and Cap43 in ESCC tissue were significantly related with the invasive extent, histological differentiation,TNM stage,and lymphatic metastases (P<0.05)of ESCC,but not related with the age,sex,tumor size and pathological type (P>0.05). The mRNA expression of MTSS1 was negatively correlated with the expression of Cap43 (r=-0.457,P<0.05).Conclusion The low-expression of MTSS1 and over-expression of Cap43 in ESCC tissue may contribute to tumor invasion and metastasis;the imbalance of MTSS1 and Cap43 may be one of the mechanisms of tumor invasion and metastases.

Objective To investigate the effect of type 2 diabetes mellitus (DM) on the attenuation of myocardial ischemia-reperfusion (I/R) injury by sufentanil postconditioning in rats.Methods Male pathogen-free Sprague-Dawley rats,weighing 160-180 g,were used in the study.A model for type 2 DM was established by the feeding of high-fat diet-induced insulin resistance and intraperitoneal streptozocin 35 mg/kg.DM was confirmed by blood glucose level ≥ 16.7 mmol/L one week after injection.Eighteen type 2 diabetic rats were randomly divided into 3 groups (n =6 each):DM sham operation group (DM-S group) ; DM-I/R group; DM sufentanil postconditioning group (DM-SP group).Another 18 healthy nondiabetic rats were chosen and randomly divided into 3 groups (n =6 each):nondiabetes mellitus sham operation group (NDM-S group) ; nondiabetes mellitus I/R group (NDM-I/R group) ; nondiabetes mellitus sufentanil postconditioning group (NDM-SP group).Myocardial I/R was induced by 30 min occlusion of the left anterior descending branch of coronary artery (after 30 min of equilibration) followed by 120 min of reperfusion.Sufentanil 1.0 μg/kg was injected via the right jugular vein 5 min before reperfusion in NDM-SP and DM-SP groups.MAP,SP and HR were recorded immediately before ischemia,at 30 min of ischemia and at 120 min of reperfusion and rate-pressure product (RPP) was calculated.Arterial blood samples were collected at 120 min of reperfusion for measurement of plasma cardiac troponin Ⅰ (cTnⅠ) concentration.The rats were then sacrificed for determination of the myocardial infract size.Results MAP and RPP were decreased,while the plasma cTnl concentration was increased during reperfusion in diabetic and nondiabetic rats.Sufentanil postconditioning decreased the myocardial infract size and plasma concentrations of cTnⅠ,and increased MAP and RPP during reperfusion in nondiabetic rats,but had no effect on the parameters in diabetic rats.Conclusion Type 2 DM interferes with sufentanil postconditioning-induced myocardial protection in rats.

Objective To evaluate the role of different opioid receptors in sufentanil postconditioning-induced attenuation of myocardial ischemia-reperfusion (I/R) injury in rats.Methods Fifty adult male Sprague-Dawley rats,aged 4-6 months,weighing 200-330 g,were randomly divided into 9 groups:I/R group (n =7),ischemic postconditioning (IPC) group (n =7),sufentanil postconditiong (SP) group (n =6),κ-opioid receptor antagonist nor-binaltorphimine (nor-BNI) + SP group (group BNI + SP,n =5),δ-opioid receptor antagonist naltrindole + SP group (group NTD + SP,n =5) and μ-opioid receptor antagonist CTOP + SP group (group CTOP +SP,n =5).Myocardial I/R was produced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion.IPC was induced by 3 episodes of 10 s reperfusion followed by 10 s ischemia at the end of 30 min myocardial ischemia.Sufentanil 1 μg/kg was injected intravenously at 5 min before reperfusion in SP group.In groups BNI + SP,NTD + SP and CTOP + SP,nor-BNI 5 mg/kg,naltrindole 5 mg/kg and CTOP 1 mg/kg were injected intravenously,respectively,before SP and the corresponding doses of nor-BNI,naltrindole and CTOP were injected intravenously,respectively,at 5 min before reperfusion.Arterial blood samples were collected at 120 min of reperfusion for measurement of the plasma cardiac tropnin I (cTnI) concentration.The rats were then sacrificed and hearts removed for determination of myocardial infarct size (IS) and area at risk (AAR).IS/AAR was calculated.Results Compared with I/R group,the plasma cTnI concentration and IS/AAR were significantly decreased in groups IPC,SP,BNI + SP and NTD + SP (P ＜ 0.05),and no significant change was found in the plasma cTnI concentration and IS/AAR in groups CTOP + SP,NTD,BNI and CTOP (P ＞ 0.05).Compared with SP group,IS/AAR was increased in NTD + SP and BNI + SP groups and the plasma cTnI concentration and IS/AAR were significantly increased in CTOP + SP group (P ＜ 0.05).Conclusion The μ-,κ-and δ-opioid receptors mediate sufentanil postconditioning-induced attenuation of myocardial I/R injury in rats.

Objective To evaluate the role of mitochondrial permeability transition pore (mPTP) in attenuation of myocardial ischemia-reperfusion (I/R) injury by sufentanil postconditioning in rats.Methods Sixty male Sprague-Dawley rats,aged 14-15 weeks,weighing 350-420 g,were randomly divided into 4 groups (n =15 each):sham operation group (group S),group I/R,cyclosporin A group (group CP) and sufentanil postconditioning group (group SP).Myocardial I/R was produced by occlusion of left anterior descending branch of coronary artcry for 30 min followed by reperfusion.In groups CP and SP,cyclosporin A 5 mg/kg and sufentanil 1 μg/kg were injected via the jugular vein at 5 min before reperfusion respectively,while the equal volume of normal saline was injected in group I/R.At 10 min of reperfusion,hearts were excised,the myocardial mitochondria were immediately isolated and the activity of mPTP was measured by spectrophotometry.MAP and HR were recorded at 30 min of equilibration,at 30 min of ischemia and at 120 min of reperfusion and rate-pressure product (RPP) was calculated.Arterial blood samples were obtained at 120 min of reperfusion for determination of the plasma cardiac troponin Ⅰ (cTnⅠ) concentration.The animals were then sacrificed for determination of infarct size (IS) and area at risk (AAR),and IS/AAR was calculated.The mitochondrial ultra-structure was examined with electron microscope.Results Compared with group S,the mPTP activity and plasma cTnI concentration were significantly increased,and MAP and RPP were significantly decreased in the other three groups (P ＜ 0.05).Compared with group I/R,the mPTP activity,plasma cTnI concentration and IS/ARR were significantly decreased in groups CP and SP,and MAP was significantly increased in group CP (P ＜ 0.05).Compared with group CP,MAP was significantly decreased (P ＜ 0.05),while no significant change was found in the other indexes in group SP (P ＞0.05).Significant mitochondrial swelling,and disruption and disappearance of cristae were showed in I/R group.The mitochondrial structure was more complete in CP and SP groups than that in group I/R,and the disrupted cristae were found in a small number of mitochondria in CP and SP groups.Conclusion The mechanism by which sufentanil postconditioning reduces myocardial I/R injury is related to inhibition of mPTP opening in rats.

Objective To evaluate the effect of propofol on proliferation of human liver cancer cell line HepG2.Methods HepG2 cells were seeded in 96-well plates (100μl/hole) with a density of 1 × 105/ml and randomly divided into 5 groups (n =33 each)∶ control group (group C),group intralipid (group Ⅰ),and propofol 30,60 and 120μg/ml groups (groups P1-3).In groups P1-3,propofol 30,60 and 120 μg/ml were added to the culture medium and then the cells were cultured for 72 h.In group Ⅰ,10％ intralipid was added to the culture medium and then the cells were cultured for 72 h.The morphology of cells was observed with the light microscope after 24 h of incubation with propofol.The proliferation of the cells was determined at 0,24,48 and 72 h of incubation with propofol.The expression of Fas was determined at 48 h of incubation with propofol.Results The number of the cells was gradually smaller in groups P1-3.The proliferation of the cells was significantly higher in group Ⅰ,while lower in groups P1-3 than in group C (P ＜ 0.05).There was no significant difference in the expression of Fas between group Ⅰ and group C (P ＞ 0.05).The expression of Fas was significantly higher in groups P1-3 than in group C (P ＜ 0.05).The proliferation of the cells was significantly lower,and the expression of Fas was significantly higher in group P3 than in group P1 or group P2 (P ＜ 0.05).Conclusion Propofol can inhibit the proliferation of human liver cancer cell line HepG2 in a concentration-dependent manner and up-regulation of the expression of Fas is involved in the mechanism.

Objective To investigate the effect of propofol on the invasion of human liver cancer cell line HepG2.Methods HepG2 cell were seeded in 96-well plates (100μl/hole) with a density of 1 × 105/ml and randomly divided into 5 groups (n =9 each):control group (group C),intralipid group (group Ⅰ),and propofol 30,60 and 120 μg/ml groups (groups P1-3).Propofol 30,60 and 120 μg/ml were added to the culture medium in groups P1-3,respectively,and then the cells were cultured for 48 h.In group Ⅰ,10％ intralipid was added to the culture medium and then the cells were cultured for 48 h.The invasion of cells was measured by Transwell invasion assay at 48 h of incubation.The expression of matrix metalloproteinases-2 (MMP-2) and mRNA and matrix metalloproteinases-9 (MMP-9) and mRNA was determined at 48 h of incubation.Results Compared with group C,the invasion of HepG2 cells was significantly decreased and the expression of MMP-2,MMP-9 and MMP-2 mRNA and MMP-9 mRNA was down-regulated in groups P1-3 (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group Ⅰ (P ＞ 0.05).The invasion of HepG2 cells was gradually decreased and the expression of MMP-2,MMP-9 and MMP-2 mRNA and MMP-9 mRNA was gradually down-regulated in groups P1-3 (P ＜0.05).Conclusion Propofol can inhibit the invasion of HepG2 cells in a concentration-dependent manner and down-regulation of the expression of MMP-2 and MMP-9 may be involved in the mechanism.