ObjectiveTo establish rat model of traumatic brain injury combined with hemorrhagic shock.Methods Rat models of traumatic brain injury (produced by free fall impact method) combined with hemorrhagic shock (produced by venous injury method) were established and the related physiological parameters were recorded.The neurological impairment score,cerebral edema degree and blood brain barrier (BBB) were determined by using neurofunction scales,dry-wet method and Evans blue (EB) respectively.HE staining and immunohistochemical staining were applied to evaluate the pathological changes in brain sections.ResultsBlood pressure dropped from 95 mm Hg to 25 mm Hg within three minutes after modeling and maintained around 60 mm Hg one hour later.Neurological impairment score was increased dramatically.The ratio of water content in the brain tissue was elevated nearly from 77％ to 81％.The concentration of EB residual in the brain tissue was increased more than one fold.Neuronal pathological abnormalities,including neuron shrinking,dark eosinophilic staining,perineuronal vacuole in HE staining,and positive staining of β-amyloid precursor protein (β-APP) in immunohistochemical staining were also observed. ConclusionsRat models of traumatic brain injury combined with hemorrhagic shock are successfully established.In addition,the main pathological changes,such as cerebral edema,disruption of BBB,neuron damage,and expression of β-APP are replicated.

Aged ; Arthroplasty, Replacement, Knee ; adverse effects ; methods ; Bone Malalignment ; diagnosis ; etiology ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Quadriceps Muscle ; surgery ; Retrospective Studies

Objective To investigate the effect of mangiferin on the apoptosis of rat primary cardiomyocytes induced by hypoxia. Methods Rat primary cardiomyocytes were separated and cultured under aseptic condition. Cardiomyocytes were treated with hypoxia of 2, 4, 8 and 12 h, and then the time of hypoxia of cardiomyocyte apoptosis model was determined according to the apoptosis outcome.The cardiomyocytes were divided into normal group, hypoxia group and mangiferin intervention group, each group was subjected to 3 batches in parallel, and 3 holes were done in parallel with each batch. After the experiment, cardiomyocytes apoptosis was deteced by flow cytometry;apoptosis protease caspase-3 and caspase-9 activity in cell lysates was detected by spectrophotometry;the protein expression of Bax and Bcl-2 was detected by Western blot. Results After treated with hypoxia for 12 h, the cardio-myocytes apoptosis rate was significantly increased (P < 0.05), the apoptosis protease caspase-3 and caspase-9 activity was increased markedly (P＜0.05), the protein expression of proapoptotic protease Bax was increased notablely (P＜ 0.05 ) , and the protein expression of anti apoptotic protease Bcl-2 was decrease memorably (P＜0.05) in hypoxia group as compared with those in the control group. After mangiferin intervention, above indexes in mangiferin group can be significantly relieved as compared with those in the hypoxia group. Conclusions Mangiferin can significantly inhibit the apoptosis of rat primary cardiomyocytes induced by hypoxia.

Objective To develop a method of isolation and identification of exosomes of bone marrow mesenchymal stem cells.Methods The mesenchymal stem cells were cultured by whole bone marrow adherence method.A new reagent -exosomes extraction kit was used to isolate and collecte exosomes.The exosomes were identified by elec-tron microscopy,particle size detection,flow cytometry and Western blot.Results The expression of CD45 on the surface of the third generation bone marrow mesenchymal stem cells was negative,and CD73 and CD105 were posi-tive;exosomes derived from bone marrow mesenchymal stem cells were round or oval,the size is non-uniform,the diameter is 30~100 nm,have a complete membrane structure,and containing low-density substances;Particle size detection particle diameter of the main peak was 61.25 nm, in which the diameter of particles was about 20-200 nm accounted for 72.4%;exosome expressed CD63 and CD81;The expression of CD9 and CD63 from cell cul-ture supernatants was positive.Conclusions The exosomes can be collected in the medium of mesenchymal stem cells.The exosomes derived from bone marrow mesenchymal stem cells can be identified by electron microscopy, particle size detection,flow cytometry and Western blot.

Objective To explore the strategies of using psychological crisis intervention in public emergencies.Methods In the early stage,psychological crisis intervention concepts and behavioral responses were formed through literature research and qualitative research methods.Use three rounds of Delphi for expert advice.Three indexes including positive coefficient,authority and coordination were used to test the reliability of expert consultation.Results Overall,it passed 239 out of 269 entries.The first round passed item 210,modified item 18,no consensus item 41;In the second round,8 new entries were added,and 22 entries were deleted through 24 entries.In the third round,there were 5 entries and 16 entries were deleted.The authority coefficient was 0.859,indicating that the experts were very familiar with the items.The coordination coefficient of three rounds of consultations were 0.464,0.696,and 0.407 (P＜0.001)respectively,showing that the coordination degree of experts was excellent,the credibility of feedback was high,and results were highly reliable.Conclusions The strategies of field psychological crisis intervention for public emergencies developed in this study received the consensus by domestic psychological crisis intervention experts,it is will provide a basis for systematic,comprehensive and effective guidance for this work.

Objective:To investigate the expression of kinase-like gene CT10 regulatory fac-tor(CRKL)in intrahepatic cholangiocarcinoma(ICC)and its effect on the proliferation and invasion of intrahepatic cholangiocarcinoma cells.Methods:qRT-PCR detected CRKL transcription in ICC pa-tient tissues and adjacent tissues.Immunohistochemistry assessed CRKL expression in ICC tissues and adjacent tissues,and analyzed its relationship with clinicopathological features.For the inhibition of CRKL expression in QBC939 cells by siRNA technology,the effect of CRKL silencing on AKT and ERK signaling pathway was measured by Western blot.CRKL's influence on QBC939 cell prolifera-tion and invasion was analyzed by MTT,clonogenesis,and Transwell assays.Results:The expres-sion of CRKL in ICC tissues was up-regulated,and there were statistically significant differences in CRKL expression in ICC with different clinicopathological features such as tumor size,lymph node metastasis and TNM stage.Cellular experiments showed a significant decrease in the phosphoryla-tion of AKT and ERK upon inhibition of CRKL,and the proliferation and invasion ability of ICC cells was significantly diminished(P＜0.05).Conclusion:CRKL promotes ICC cell proliferation and invasion through AKT and ERK pathways,offering new molecular targets and directions for targeted therapy.

Objective: This cross-sectional study aimed to address the relationship between the volume of epicardial adipose tissue (EAT) with cardiovascular risk factors and coronary artery calcification(CAC) in the community residents. Methods: Individuals were recruited from the Jidong Community (Tangshan City, Northern China) which mainly comprised employees of the Jidong Co. Ltd. and their family members. From July 2013 to August 2014, 2 647 participants aged ≥40 years were included in this study. The volume of EAT and coronary artery calcification score (CAC score) were determined by a 64-slice CT. Carotid intima-media thickness (CIMT) was measured by a trained sonographer using a high-resolution B-mode topographic ultrasound system. Venous blood samples were analyzed by automated analyzers in the central laboratory. A validated questionnaire specifically designed for this study was used to collect demographic data from all participants by trained doctors. Characteristics of study cohort were compared according to quartiles of EAT volume (n=660, 663, 662, 662, repectively). Results: (1) The mean age of participants was (55.31±7.76) years and 49.94% (n=1 322) were men. The median EAT volume (interquartile) was 129.42 (95.66, 176.51)cm³. (2) Age, BMI, waist circumference and hip circumference, systolic blood pressure, LDL-C, triglycerides, and fasting blood glucose were significantly higher, while HDL-C level was significantly lower in participants with higher EAT volume than participants with lower EAT volume (all P<0.05). Carotid intima-media thicken (CIMT) and higher CAC score were also significantly higher in participants with higher volume of EAT. Furthermore, percentage of diabetes mellitus, hypertension, hyperlipidemia increased in proportion with increasing EAT volume (P<0.05). (3) In the linear regression, significant positive relations were found for age (β=0.019 3, 95%CI 0.017-0.021, P<0.001), waist circumference (β=0.012 7, 95%CI 0.009-0.016, P<0.001), BMI (β=0.022 4, 95%CI 0.013-0.032, P<0.001), LDL-C (β=0.048 4, 95%CI 0.021-0.076, P<0.001), and HDL-C (β=-0.098 1, 95%CI-0.164--0.032, P<0.001) was inversely related to the EAT volume. (4) Logistic regression analysis indicated that EAT volume was an independent risk factor for CAC score>0 (OR=1.233, 95%CI 1.205-1.262, P<0.001) . Conclusions Our findings indicate that EAT volume is strongly correlated to cardiovascular risk factors and coronary calcification and is an independent risk factor of increased coronary calcification in community residents.

Objective: To determine the value of N-terminal pro-B-type natriuretic peptide (NT-proBNP) on predicting the long-term outcome of patients with hypertrophic cardiomyopathy (HCM) . Methods: NT-proBNP was measured in 831 consecutive patients with HCM at Fuwai Hospital from October 2009 to December 2013 and patients were followed up clinically for (53.3±15.4) months. Patients were divided into 3 groups according to NT-proBNP values: NT-proBNP<860 pmol/L (n=276) , 860 pmol/L≤NT-proBNP≤1 905 pmol/L (n=278) , NT-proBNP>1 905 pmol/L (n=277) . The related baseline data, laboratory examination and echocardiographic results were compared among groups. The primary endpoints of this study were all-cause mortality and cardiac transplantation. Cox proportional hazards model was used to estimate hazard ratio (HR) . Kaplan-Meier analysis was used to evaluate the survival status of patients among the 3 groups. Results: During a median follow-up of (53.3±15.4) months, all-cause mortality or cardiac transplantation occurred in 37 patients (4.5%) , event rate was 1.4% (4/276) , 4.0% (11/278) and 7.9% (22/277) in patients with NT-proBNP<860 pmol/L, 860 pmol/L≤NT-proBNP≤1 905 pmol/L and NT-proBNP>1 905 pmol/L, respectively. Multivariable Cox regression analysis identified that age (HR 1.066, 95%CI 1.027-1.107) and NT-proBNP (HR 1.026, 95% CI 1.010-1.042) were independent predictors of all-cause mortality or cardiac transplantation. Among the 3 groups, the survival rate of the NT-proBNP<860 pmol/L group was the highest,and that of the NT-proBNP>1 905 pmol/L group was the lowest (P<0.01) . Conclusions The level of NT-proBNP provides clinically relevant information for long-term adverse events risk stratification in patients with HCM.

Background: and Purpose To explore the causal relationships of elements of the exposome with ischemic stroke and its subtypes at the omics level and to provide evidence for stroke prevention. Methods We conducted a Mendelian randomization study between exposure and any ischemic stroke (AIS) and its subtypes (large-artery atherosclerotic disease [LAD], cardioembolic stroke [CE], and small vessel disease [SVD]). The exposure dataset was the UK Biobank involving 361,194 subjects, and the outcome dataset was the MEGASTROKE consortium including 52,000 participants. Results: We found that higher blood pressure (BP) (systolic BP: odds ratio [OR], 1.02; 95% confidence interval [CI], 1.01 to 1.04; diastolic BP: OR, 1.03; 95% CI, 1.01 to 1.05; pulse pressure: OR, 1.03; 95% CI, 1.00 to 1.06), atrial fibrillation (OR, 1.18; 95% CI, 1.13 to 1.25), and diabetes (OR, 1.13; 95% CI, 1.07 to 1.18) were significantly associated with ischemic stroke. Importantly, higher education (OR, 0.69; 95% CI, 0.60 to 0.79) decreased the risk of ischemic stroke. Higher systolic BP (OR, 1.06; 95% CI, 1.02 to 1.10), pulse pressure (OR, 1.08; 95% CI, 1.02 to 1.14), diabetes (OR, 1.28; 95% CI, 1.13 to 1.45), and coronary artery disease (OR, 1.58; 95% CI, 1.25 to 2.00) could cause LAD. Atrial fibrillation could cause CE (OR, 1.90; 95% CI, 1.71 to 2.11). For SVD, higher systolic BP (OR, 1.04; 95% CI, 1.00 to 1.07), diastolic BP (OR, 1.06; 95% CI, 1.01 to 1.12), and diabetes (OR, 1.22; 95% CI, 1.10 to 1.36) were causal factors. Conclusions The study revealed elements of the exposome causally linked to ischemic stroke and its subtypes, including conventional causal risk factors and novel protective factors such as higher education.

Objective To determine whether thyroid hormone (TH) level could also be an independent and incremental predictor of adverse events in patients with hypertrophic cardiomyopathy (HCM).Methods A total of 982 consecutive patients with HCM at the National Center for Cardiovascular Diseases (China) from October 2009 to December 2013 were included in the present study,and followed up till the end of December 2016.The patients were divided into three groups according to the levels of free triiodothyronine (FT3):the group 1 (FT3≤4.28 pmol/L,n=335),the group 2 (FT3＞4.28-＜4.79 pmol/L,n=310),and the group 3 (FT34.79-6.30 pmol/L,n=337).Results After a follow-up period of (53.8 ± 14.1) months,39 patients (4.0％) either suffered death with all causes or received a cardiac transplantation (7.8％,2.9％ and 1.2％ of the patients in the group 1,group 2 and group 3,respectively).A multivariable Cox regression analysis revealed that FT3≤4.28 pmol/L was associated with a significantly higher risk of all-cause mortality or cardiac transplantation (HR 8.83,95％ CI 1.115-69.905,P=0.039) in HCM patients.Conclusions Low levels of FT3 is a risk factor of adverse events for patients with HCM,indicting a role of FT3 as a marker for assessing the risk of long-term adverse events in these patients.