Pricebell6548
of pneumoconiosis.Objective To analyze the levels of T lymphocyte subsets (CD3, CD4, CD8 and CD4/CD8) in patients with paraquat poisoning, and to explore the relationship between the changes of T lymphocyte subsets and the prognosis of pulmonary fibrosis. Methods In October 2019, a total of 47 patients with oral 20% paraquat low water solvent poisoning in Guangzhou 12th people's Hospital from June 2018 to June 2019 were selected as the research objects. Patients were divided into early death group (16 cases died within 2 weeks) and non early death group (31 cases survived more than 2 weeks) . The non early death group was divided into pulmonary fibrosis group (23 cases) and normal lung group (8 cases) . 20 healthy people in the same period were randomly selected as the control group. The neutrophils (N) , C reaction protein (CRP) , alanine aminotransferase (ALT) , creatinine (Cr) , amylase (aAMY) , creatine kinase isoenzyme (CKMB) , pH, HCO(3)(-), blood oxygen saturation (SO(2)) and lactic acid (Lac) of patients poisoned withifibrosis.Objective To investigate the effect of heat shock protein 60 (HSP60) overexpression on the ability of bone marrow mesenchymal stem cells (MSCs) and its therapeutic effect on rats with phosgene induced acute lung injury. Methods HSP60 was transfected into MSCs by adenovirus. Western blot was used to measure the expressions of HSP60 before and after transfection. CCK-8 assay was used to detect the activity of MSCs, flow cytometry was used to detect the apoptotic ability of MSCs, and Transwell assay was used to observe the migration ability of MSCs. Sixty SPF grade male SD rats were randomly divided into control group, phosgene exposure group (inhalation of phosgene for 5 min) , MSCs group (phosgene exposure, MSCs treatment group) and transfected MSCs group (phosgene exposure, overexpression of HSP60 MSCs treatment group) . The pathological changes of lung were observed by lung pathological section, lung wet dry ratio, the degree of pulmonary edema, the total cell count and total protein content of alveolar lavaration, anti apoptosis, migration and the curative effect in rats with phosgene induced acute lung injury.Objective To study the cytotoxicity and malignant transformation ability of chrysotile on MeT-5A cells. Methods In June 2016, lactate dehydrogenase (LDH) method was used to detect the cytotoxicity of chrysotile to MeT-5A cells. MeT-5A cells were treated with 5 μg/cm(2) chrysotile intermittently for 24 h a time, once a week and a total of 28 times. After the cells showed anchorage independent growth, the cell features of malignant transformation were identified by colony forming frequency in soft agar, and the soft agar colony formation rates were calculated. The activities of key speed limiting enzymes of glycolysis metabolism including hexokinase (HK) , phosphofructokinase (PFK) and pyruvate kinase (PK) were determined by UV colorimetry. Results Chrysotile was cytotoxic to MeT-5A cells in a concentration-dependent decline. Nanvuranlat mouse Compared with the control group, the relative survival rates of MeT-5A cells were significantly decreased after exposed to chrysotile at 10, 20, 40 and 80 μg/cm(2) (P less then 0.05) . link2 After 28 times of exposure, the growth rate of the cells in chrysotile transformed MeT-5A cells was accelerated, the arrangement was disordered, the contact inhibition was lost, and the double layer growth appeared, which could grow on soft agar. The colony forming rate of the chrysotile transformed MeT-5A cells was 18.33‰±2.49‰. Compared with the control group (0) , the difference was statistically significant (P less then 0.01) . The activities of glycolysis related kinase including PK [ (19.51±1.52) U/L], PFK[ (0.12±0.02) U/10(4) cell] and HK[ (0.26±0.01) U/10(4) cell] were increased in the chrysotile transformed MeT-5A cells compared with control group [ (25.00±1.04) U/L、(0.15±0.01) U/10(4) cell and (0.33±0.01) U/10(4) cell] (P less then 0.01) . Conclusion Chrysotile can induce malignant transformation of MeT-5A cells and increase the activities of glycolysis related kinases including PK, PFK and HK.Objective To investigate the inhibitory effect and molecular mechanism of microRNA-30d (miR-30d) in the process of proliferation, migration and invasion of malignant mesothelioma cell line MSTO-211H. Methods In April 2017, the human MSTO-211H cells was used to establish miR-30d overexpressed MSTO-211H cell model by transfection of miR-30d mimics. The qRT-PCR was performed to detect the expression level of miR-30d in the cells transfected miR-30d mimics. The effects of miR-30d on the proliferation, apoptosis, migration and invasion of MSTO-211H cells were analyzed by CCK-8 experiment, flow cytometry, cell scratch experiment and Transwell method. Results After transfection of miR-30d, the expression level of miR-30d in the MSTO-211H+miR-30d cells group was significantly higher than MSTO-211H+miR NC cells group (P less then 0.01) . The cell activity of MSTO-211H+miR-30d group (105.13%±2.35%) was significantly lower than MSTO-211H+miR NC cells group (115.40%±1.35%) , and the level of apoptosis (3.97%±0.36%) was significantly higher than MSTO-211H+miR NC cells group (1.47%±0.10%) (P less then 0.01) . The relative migration areas at 12 and 24 h of MSTO-211H+miR-30d cells group (9.35±3.16 μm(2) and 58.19±1.82 μm(2)) were significantly lower than MSTO-211H+miR NC cells group (54.42±5.26 μm(2) and 88.32±1.96 μm(2)) (P less then 0.01) . Compared with the MSTO-211H+miR NC cells group, the numbers of cell migration and cell invasion were reduced in the MSTO-211H+miR-30d cells group (P less then 0.01) . Conclusion miR-30d can regulate the progression of malignant pleural mesothelioma by inhibiting the proliferation, apoptosis, migration and invasion of MSTO-211H cells.Objective To analyze the gene mutation profile in malignant pleural mesothelioma (MPM) and investigate the expression of high-frequency mutant genes and its relationship with clinicopathological parameters. To screen out key genes and clinicopathologic factors related to the prognosis of MPM patients. Methods The second generation sequencing data, somatic mutation data and clinical pathological data of 86 MPM cases and gene chip expression data of 89 MPM cases were downloaded from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) in March 2020. Summarize the gene mutation profile of tissue samples in the TCGA database and analyze the relationship between the expression level of high-frequency mutation genes and the clinicopathological characteristics, asbestos exposure history and prognosis of MPM patients. The genes significantly related to MPM prognosis were screened out for gene set enrichment analysis (GSEA) . Survival analysis and GSEA were performed for the selected key genes and clinicopnse and uv response. Conclusion MPM is accompanied with higher frequency of gene mutations represented by BAP1, NF2, TP53, TTN, SETD2, LATS2 and so on. SETD2 expression level and epithelia type of MPM may be influential factors for MPM prognosis.Objective To investigate the survival and death risk factors of mesothelioma cases stratified by the expression levels of CD8 and cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) , providing new clue to evaluate disease progression and clinical outcome. Methods This was a retrospective case report, which included 47 clinically and pathologically confirmed mesothelioma cases on November 2016. Their clinical and pathological information, asbestos exposure history and survival data were collected. link3 Infiltrated lymphocyte, 5-methylcytosine (5-mC) , CTLA-4, CD8 and Ki-67 antigen were detected using hematoxylin-eosin staining and immunohistochemistry. Survival time and death risk factors of mesothelioma patients with different CD8 and CTLA-4 protein expression characteristics were analyzed. And analyze the influence of Ki-67 expression on the survival of patients with different CD8 and CTLA-4 protein and gene expression characteristics. Results Among the 47 cases, 63.8% (30/47) had low/medium level of infiltrate the median survival times of those with high and low Ki-67 mRNA expression were 1.20±0.36 years and 3.38±0.43 years, respectively (P=0.018) . Conclusion Mesothelioma case with high CD8 but low CTLA-4 content might coexist DNA hypomethylation. In the presence of high Ki-67 expression, their survival time appears to be shortened with increased death risk.
Fractional exhaled nitric oxide (FeNO) is a recognized marker for eosinophilic airway inflammation and treatment decisions for corticosteroid response. Our study aimed to compare two FeNO analyzers and derive a conversion equation for adults.
We included 99 participants with chronic cough and difficulty in breathing who attended outpatient clinics. They underwent concurrent FeNO measurement randomly using NIOX VERO® (Circassia AB, Solna, Sweden) and NObreath® (Bedfont, Kent, UK). We compared the two devices according to values, correlation and agreement. We then formulated an equation to convert FeNO values measured by NObreath® into those obtained by NIOX VERO®.
The mean age was 51.2 ± 17.1 years, with female predominance (58.6%). Approximately 60% of the participants had asthma. The median (interquartile range) FeNO level measured by NIOX VERO® (27, 15-45) was significantly lower than that by NObreath® (38, 22-58, p < 0.001). FeNO level measurement had a strong positive correlation between the devices (r = 0.779, p < 0.001). Additionally, Bland-Altman plots and intraclass correlation coefficient demonstrated a good strength of agreement. Using linear regression, we derived the following conversion equation natural log (Ln) (NObreath®) = 0.728 × Ln (NIOX VERO®) + 1.244.
The values of these two FeNO analyzers were in good agreement and had positive correlations. Our proposed conversion equation could help assess the data obtained by these two analyzers.
The values of these two FeNO analyzers were in good agreement and had positive correlations. Our proposed conversion equation could help assess the data obtained by these two analyzers.
New onset atrial fibrillation (AF) is associated with poor outcomes in several different patient populations.
To assess the effect of developing AF on cardiovascular events such as myocardial infarction (MI) and cerebrovascular accident (CVA) during the acute index hospitalization for trauma patients.
The Healthcare Cost and Utilization Project State Inpatient Databases for California and Florida were used to identify adult trauma patients (18 years of age or older) who were admitted between 2007 and 2010. After excluding patients with a history of AF and prior history ofcardiovascular events, patients were evaluated for MI,CVA, and death during the index hospitalization. Asecondary analysis was performed using matched propensity scoring based on age, race, and preexisting comorbidities.
During the study period, 1,224,828 trauma patients were admitted. A total of 195,715 patients were excluded for a prior history of AF, MI, or CVA. Of theremaining patients, 15,424 (1.5%) met inclusion criteria and had new onset AF after trauma. There was an associated increase in incidence of MI (2.9 vs. 0.7%; p<0.001), CVA (2.6 vs. 0.4%; p<0.001), and inpatient mortality (8.5vs. 2.1%; p<0.001) during the index hospitalization in patients who developed new onset AF compared with those who did not. Cox proportional hazards regression demonstrated an increased risk of MI (odds ratio [OR], 2.35 [2.13-2.60]), CVA (OR, 3.90 [3.49-4.35]), and inpatient mortality (OR, 2.83 [2.66-3.00]) for patients with new onset AF after controlling for all other potential risk factors.
New onset AF in trauma patients was associated with increased incidence of myocardial infarction (MI), cerebral vascular accident (CVA), and mortality during index hospitalization in this study.
New onset AF in trauma patients was associated with increased incidence of myocardial infarction (MI), cerebral vascular accident (CVA), and mortality during index hospitalization in this study.
