Objective To investigate the expressions of Stat3, CyclinD1 and proliferating cell nuclear antigen (PCNA) in non-small cell lung cancer (NSCLC), and analyze their relationships with carcinogenesis and progression of NSCLC. Methods SP immunohistochemistry was used to detect the expressions of Stat3, CyclinD1 and PCNA in 45 cases of NSCLC. Results The positive rate of Stat3 was 71. 1 % in NSCLC. The expression intensities of Stat3 was not associated with different tumor sizes and histological type, but it was associated with the expression intensities of CyclinDi and PCNA (r= 0.531, P

Objective By studying the different blood volume blood donors machine adopt platelet product aggregation,platelet content,the machine adopt circulating volume,etc,analysis of different blood volume machine adopt donors on appropriate conditions.Methods The base material of randomly selected 307 blood donors,through blood related index in the study of circulating volume,blood volume,gender,platelets,Hct,Pct count before collection,machine adopt of platelet aggregation and the relationship between the acquisition time;different blood volume,blood platelet count grouping machine adopt the different of platelet aggregation rate,different amount of platelets collect blood volume group,the comparison of blood circulation.The use of statistical software SPSS 17.0,data analysis,analysis including multiple regression analysis,chi-square test,t test,etc.Results 1)The lower count of platelets,Hct,Pct count before collection,the longer the acquisition time,and gender and Pct has nothing to do with the acquisition time the longer the acquisition time,the higher the machine adopt the possibility of platelet aggregation.2)Low blood volume and low platelet count group,machine mining platelet aggregation rate is higher.3)Machine adopt donors of blood volume is higher,the machine adopt the platelet collection amount,the more and the less blood circulation.Conclusion According to the different blood volume blood donors check-up indicators,further carries on the reasonable analysis,optimized machine mining scheme,especially to reasonable arrangement of low blood volume blood donors,so as to improve the quality of platelet collection.

Objective : o evaluate the association between Crohn's disease (CD) and frailty using a Mendelian randomization (MR) approach, so as to provide the evidence for prevention and control strategies. Methods: Genetic association data for CD were collected through the International Inflammatory Bowel Disease Genetics Consortium, with 20 883 samples and 12 276 506 single nucleotide polymorphism (SNP), and genetic association data for frailty were collected through a meta-analysis including 175 226 samples and 7 589 717 SNPs. A forward MR analysis was performed using the inverse-variance weighted (IVW) method with 37 CD-associated SNPs as instrumental variables, and frailty as the study outcome, and a reverse MR analysis was performed with 13 frailty-associated SNPs as instrumental variables and CD as the study outcome. The heterogeneity was assessed using the Cochran's Q test, and the horizontal pleiotropy was assessed using the MR-PRESSO global test and MR-Egger regression. In addition, the robustness of the results was verified with the leave-one-out. Results: Forward MR analysis results showed that patients with genetically predicted CD had an increased risk of frailty index relative to those without CD (β=0.018, 95%CI: 0.011-0.026, P<0.05). Cochran's Q test detected no heterogeneity (P>0.05), and neither the MR-PRESSO test nor the MR-Egger regression revealed horizontal pleiotropy of instrumental variables (both P>0.05). Leave-one-out analysis showed robustness of the MR analysis results. Reverse MR analysis showed no association between frailty index and the risk of CD (OR=0.740, 95%CI: 0.206-2.661, P>0.05). Conclusions Genetically predicted CD is associated with an increased risk of frailty. It is suggested that screening and prevention of frailty should be reinforced among CD patients.

Objective : To examine the causal relationship between ulcerative colitis (UC) and pancreatitis, to provide basis for early screening of pancreatitis among UC patients. Methods: Genomic data of UC were obtained from 47 745 European individuals pooled by the International Inflammatory Bowel Disease Genetics Consortium, including 156 116 single nucleotide polymorphism (SNP), and genomic data of pancreatitis were obtained from 198 166 European individuals pooled from FinnGen, including 16 380 428 SNPs. Mendelian randomization (MR) analysis was performed using the inverse variance weighted (IVW) method with 72 UC-associated SNPs as instrumental variables and pancreatitis as the study outcome. The heterogeneity was assessed using Cochran Q test, the horizontal pleiotropy was assessed using MR-Egger regression, MR-PRESSO was performed with the exclusion of outliers, and effect of individual SNP on the results was tested with the leave-one-out method. Results: MR analysis results showed that patients with genetically predicted UC had an increased risk of pancreatitis relative to those without UC (OR=1.076, 95%CI: 1.019-1.136, P<0.05). Cochran Q test showed no heterogeneity (P>0.05), and MR-Egger regression did not reveal horizontal pleiotropy of instrumental variables (P>0.05). The MR analysis results were robust after removing SNP one by one. Conclusions Genetically predicted UC is associated with an increased risk of pancreatitis. The screening for pancreatitis risk should be enhanced in patients with UC.

Adolescent ; Adult ; Age Factors ; Child ; Child, Preschool ; Electroencephalography ; Epilepsy, Temporal Lobe ; diagnosis ; etiology ; Humans ; Infant ; Male ; Middle Aged

Objective To observe the change of JAK-STAT-SOCS signal molecules after interferons alpha acting on the cancerous oral cells in 3 different degrees,namely NOK,DOK and KB cells,and to provide research foundation for the deep understanding of OSCC (oral squamous cell cancer) tumor ceils immune escape mechanism.Methods NOK,DOK,and KB cells were all cultured respectively,and then the third passage cells in the logarithmic growth phase were inoculated in cell culture plate.Blank control group of each hole was added 2 ml complete medium containing 10 ％ FPS.DMSO control group of each hole was added 2 ml complete medium containing 0.1％ DMSO.And in experimental groups containing 10 U/ml,100 U/ml,and 500 U/ml interferons,complete culture medium were added to each hole containing different concentrations of interferons alpha.CP-690550 (100 μmol/L) was added before interferons alpha was added 1 h.All were detected by RT-PCR test and Western blot test after conventional cultured for 24 h.Results RT-PCR detection showed that JAK1 and JAK2 in NOK cells had a small amount of expression,interferons alpha and CP-690550 cells could not influence the expression of JAK1 and JAK2 of NOK group,and there was no statistically significant difference (P ＞ 0.05).Interferons alpha in 100 and 500 U/ml could stimulate the increase of JAK1 and JAK2 expression in DOK and KB cells,and the differences were statistically significant (P ＜ 0.05).CP-690550 could effectively reduce the JAK1 expression of DOK and KB cells,while had no effect on the expression of JAK2,and the differences were statistically significant (P ＜ 0.05).Western blot showed that STAT1,STAT3 and pSTAT3 (Tyr705) all expressed in the control group,while pSTAT1 (Tyr701) didn't express in the control group.Interferons alpha and CP-690550 cells had no effect on STAT1,STAT3 and pSTAT3 (Tyr705) expression of NOK group,and there was no statistically significant difference (P ＞ 0.05).100 U/ml and 500 U/ml of interferons alpha could stimulate the increases of pSTAT3 (Tyr705) expression of DOK and KB cells,and the differences were statistically significant (P ＜ 0.05).While they had no effect on pSTAT1 (Tyr701) expression.CP-690550 could effectively reduce the pSTAT3 DOK and KB cells (Tyr705) expression,and the differences were statistically significant (P ＜ 0.05).Western blot showed that there were expression of SOCS1 and SOCS3 in control group.Interferons alpha and CP-690550 had no effect on SOCS1 and SOCS3 expression of NOK cell group,and there was no statistically significant difference (P ＞ 0.05).100 U/ml and 500 U/ml of interferons alpha could stimulate the increase of SOCS 1 expression of DOK and KB cells,and differences were statistically significant (P ＜ 0.05).For the expression of SOCS3,no influence.CP-690550 could effectively reduce the expression of SOCS1 of DOK and KB cells,and the differences were statistically significant (P ＜ 0.05).Conclusions Interferons alpha activate DOK JAK1 and KB cells and the expression of JAK2,mainly JAK1 activation.Interferons alpha,by activating DOK JAK1 and KB cells and the expression of JAK2,promote STAT3 phosphorylation in Tyr705 locus.Interferons alpha,by promoting STAT3 phosphorylation,further promote the expression of SOCS1,which plays the role in inhibiting interferons alpha and reducing the apoptosis.

Objective:To investigate the risk factors for anterior circulation and posterior circulation symptomatic intracranial atherosclerotic stenosis (sICAS).Methods:The clinical data of patients admitted to Hebei General Hospital for ischemic stroke or transient ischemic attack (TIA) and diagnosed with sICAS by digital subtraction angiography from May 2019 to May 2020 were retrospectively included. The patients were divided into anterior circulation group and posterior circulation group according to the stenosis sites, and the distribution of sICAS and its risk factors were analyzed.Results:A total of 134 patients with sICAS were enrolled, including 82 males (61.2%) and 52 females (38.8%). Their age was 60.28±11.46 years; 115 (85.8%) had ischemic stroke and 19 (14.2%) had TIA. There were 92 patients (68.7%) in the anterior circulation group and 42 (31.3%) in the posterior circulation group. Body mass index (BMI), systolic and diastolic blood pressure levels, as well as the proportion of patients with hypertension, diabetes, smoking and drinking in the posterior circulation group were significantly higher than those in the anterior circulation group (all P<0.05). Multivariate logistic regression analysis showed that higher BMI (odds ratio [ OR] 1.191, 95% confidence interval [ CI] 1.029-1.379; P=0.019), hypertension ( OR 4.073, 95% CI 1.135-14.616; P=0.031) and diabetes ( OR 2.783, 95% CI 1.149-6.738; P=0.023) were independently correlated with the posterior circulation sICAS. Conclusions:Compared with anterior circulation, high BMI, hypertension and diabetes are the independent risk factors for posterior circulation sICAS.

Objective:To investigate the difference of metabolomics between acute heart failure (AHF) patients and control. To find and validate new metabolic biomarkers.Methods:This was a single-center case-control study which included 89 acute heart failure patients admitted to the emergency department of Henan Provincial People's Hospital from January 2018 to June 2019. Eighty people without heart failure and diastolic dysfunction were enrolled as control group whose age and sex were matched to the study group. The fasting blood samples were collected from femoral arterial. Qualitative and quantitative analyses of plasma metabolites were performed in 2 groups by high performance liquid chromatography tandem mass spectrometry (UHPLC-MS), Orthogonal partial least squares-discriminant analysis (OPLS-DA) model and ROC curve method were applied.Results:Compared with the control group, we found that AHF group had higher likelihood to groups with coronary heart disease (37% vs. 7%, P<0.001), hypertension (58% vs. 28%, P<0.001), diabetes (33% vs. 18%, P=0.033), atrial fibrillation (24% vs. 4%, P<0.001), smoking history (42% vs. 18%, P=0.001), and that AHF group had higher creatinine level [(121.6 ± 78.4) vs. (69.0 ± 21.0), P<0.001], higher urea level [(11.5 ± 7.6) vs. (6.2 ± 2.0), P<0.001], higher heart rate [(92 ± 23) vs. (78 ± 14), P<0.001], hypoproteinemia [(32.4 ± 5 .2) vs. (40.4 ± 2.2), P<0.001], and significantly increased BNP level [(4 200 ± 5 229) vs. (100 ± 68), P<0.001], lower left ventricular ejection fraction[(45 ± 8) vs. (57 ± 6), P<0.001], low serum sodium level ( P<0.001). The metabolites of AHF group were significantly different from those of the control group. The metabolites involved amino acids, fatty acids, lipids, nucleosides and their derivatives. Adenine, N-acetyl-L-glutamic, pseudouridine and Gamma-Glutamylcysteine had certain diagnostic value for AHF comparing to control. The AUC were 0.995, 0.932, 0.920 and 0.900. And the AUC value for BNP diagnosis of AHF is 0.978. Conclusions:There were significant differences in metabolism between AHF group and control group including multiple substances. Adenine, N-acetyl-L-glutamic, pseudouridine and Gamma-Glutamylcysteine has similar diagnostic value compared with BNP for diagnosing AHF.

Objective To explore the association of ATP-binding cassette (ABC) efflux pump gene Rv1217c-Rv1218c and the drug resistance of Mycobacterium tuberculosis.Methods A total of 34 Mycobacterium tuberculosis clinical isolates including 24 drug-resistance isolates which were resistant to riffampicin,isoniazid,streptomycin or ethambutol and resistant to at least one second-line antituberculosis drug,and 10 drug-sensitive isolates were involved in this study.The RNA of isolated strains was extracted and then reverse transcribed. Gene expression was performed by real-time polymerase chain reaction (PCR) and data was analyzed by t test and Logistic regression analysis.Results The expressions of Rv1217c in rifampicin-resistant group (2.13 ± 1.89,t =3.44,P＜0.01),isoniazid-resistant group ( 1.84 ± 1.86,t =3.16,P＜ 0.05),streptomycin-resistant group ( 1.86 ±1.96,t=2.78,P＜0.05) and ethambutol-resistant groups (3.36±2.35,t=3.04,P＜0.05) were all higher than sensitive isolates (0.42 ± 0.31).The expressions of Rv1218c in rifampicin-resistant group (2.54±1.84,t=3.82,P＜0.01),isoniazid-resistant group (2.34± 1.84,t=3.72,P＜0.01),streptomycin-resistant group (2.15±1.86,t=3.01,P＜0.01) and ethambutol-resistant groups (3.78± 1.78,t=4.22,P＜0.01 ) were all higher than sensitive isolates (0.65 ± 0.42).The expressions of Rv1217c and Rv1218c in multidrug resistant group were 2.74±2.07 and 3.33± 1.77,respectively,which were both higher than polydrug resistant group (0.79 ± 0.47 and 1.03 ± 0.79,respectively; t =2.91,P＜0.05 ; t =3.84,P＜0.01,respectively).Logistic regression analysis found that high Rv1217c expression was positively correlated with rifampicin resistance and negatively correlated with isoniazid resistance (both P＜ 0.01 ),while high Rv1218c expression was negatively correlated with rifampicin resistance and positively correlated with isoniazid resistance (both P＜0.01 ).High expressions of two genes were both positively correlated with ethambutol resistance and multidrug resistance (both P＜0.01 ) and not statistically correlated with streptomycin resistance (P＞0.05).Conclusions The expressions of ABC efflux pump gene,Rv1217c-Rv1218c,are correlated with multiple drug resistance.The overexpression may contribute to the multidrug resistance of Mycobacterium tuberculosis.

Objective To investigate whether conventional protein kinase C (cPKC ) βⅡ-interacting collapsin response mediator protein-2 (CRMP-2) provides neuroprotection against cerebral ischemic (I) injuries. Methods Male BALB/c mice were randomly divided into normoxic control (Nor) , HPC, Nor + Sham, HPC + Sham, Nor + I and HPC + I groups (n = 6 per group). Using our HPC and MCAO mouse models, we applied immunoprecipita-tion, two-dimensional electrophoresis and mass spectrometry to characterize cPKCβⅡ-interacting proteins and combined with SDS-PAGE and Western blot to quantitatively analyze CRMP-2 phosphorylation and degradation levels in the brain of mice after HPC and MCAO. Results The expression level of 10 cPKCβⅡ-interacting proteins changed obviously in cerebral cortex of HPC mice when compared with Nor group. One of these proteins, CRMP-2 protein level increased in particulate fraction and decreased in cytosolic fraction of cerebral cortex of HPC mice. CRMP-2 phosphorylation level in ischemic core (Ic) of cerebral cortex decreased significantly ( P < 0. 05 , n = 6) as compared with that of Nor + sham group, but CRMP-2 phosphorylation level in HPC +I group increased significantly as compared with that of Nor +I group ( P < 0. 05, n = 6). In ischemic cortex, CRMP-2 degradation (proteolysis) was observed as the appearance of 55 ku breakdown products (BDP). However, the CRMP-2 degradation level, BDPs products decreased significantly in penumbra ( P) of ischemic cortex from HPC +I group when we compared with that of Nor +I group (P < 0. 05, n = 6 ). Conclusion CRMP-2 is involved in attenuating the decrease of CRMP-2 phosphorylation in ischemic core and in inhibiting its degradation in penumbra of cerebral cortex of mice thereby to lessen the ischemic injuries.