Carrilloperkins3790

The resulting pEGFRvIII-CAR@SNPG1/800 was used for Jurkat cell transient transfection, and the EGFRvIII-CAR expressed in transfected cells was measured by flow cytometry and Western blot. Finally, the response of EGFRvIII CAR-positive Jurkat T cell to target tumor cell was evaluated. Results The pDNA@SNPG1/800 showed the highest efficacy in Jurkat cell gene transfection and exhibited low cytotoxicity. pEGFRvIII-CAR@SNPG1/800 can efficiently deliver pEGFRvIII-CAR into Jurkat T cells, thereby resulting in transient EGFRvIII-CAR expression in transfected cells. EGFRvIII-CAR that is present on the cell membrane enabled Jurkat T cells to recognize and bind specifically with EGFRvIII-positive tumor cells. Conclusion These results indicated that pEGFRvIII-CAR@SNPG1/800 can effectively achieve T-cell transient CAR modification, thereby demonstrating considerable potential in CAR-T cancer therapy. © 2020 Yu et al.Backgrounds and Aims It is well known that angiogenesis contributes to the progression of chronic obstructive pulmonary disease (COPD) by initiating the remodeling of bronchial vasculature. However, the specific molecular mechanisms are incompletely understood. This research aimed to explore whether endostatin, a member of endogenous antiangiogenic proteins, is a biomarker in COPD and plays a role in the angiogenesis of COPD. Methods 100 stable COPD patients, 130 patients with acute exacerbation (AECOPD) and 68 healthy volunteers were recruited in this research. Lung function test was conducted in the healthy people and stable COPD patients. Serum endostatin, C-reactive protein (CRP) and vascular endothelial growth factor (VEGF) of all the subjects were measured by Human Magnetic Luminex Screening Assay. Results Serum endostatin level was significantly higher in stable COPD compared with healthy control and even more in AECOPD patients (P less then 0.001). Besides, stable COPD patients with frequent exacerbation (≥2 exacerbations per year) in the last 1 year had a higher concentration of endostatin in the circulation compared to the patients with less exacerbation (P=0.037). Furthermore, circulatory endostatin was negatively associated with forced expiratory volume in 1 s % predicted (FEV1%pre), an index of lung function in the stable COPD group (P=0.009). Finally, endostatin was positively correlated to serum CRP in COPD group (including stable and AECOPD) (P=0.005) and all the subjects (P less then 0.001), but only associated with VEGF in the total participants (P=0.002), not in the COPD group. Conclusion These results suggested that endostatin is a biomarker for COPD and associated with lower lung function, exacerbation, and systemic inflammation. CID-1067700 purchase Endostatin potentially contributes to the pathogenesis of COPD. © 2020 Wu et al.Background Cardiovascular events are, after cancer, the most common cause of death in COPD patients. Arterial stiffness is an independent predictor of all-cause mortality and cardiovascular events. Several cross-sectional studies have confirmed increased arterial stiffness in patients with COPD. Various mechanisms in the development of arterial stiffness in COPD such as reduced lung function or systemic inflammation have been proposed. However, clinical predictors of arterial stiffness that had been reported in cross-sectional studies have not yet been confirmed in a longitudinal setting. We have assessed the course of augmentation index (AIx) - a measure of systemic arterial stiffness - and possible predictors in a cohort of COPD patients over a period of up to 7 years. Methods COPD patients underwent annual AIx measurement by applanation tonometry for a maximum duration of 7 years. Additionally, we performed annual assessments of lung function, blood gases, systemic inflammation, serum lipids and blood pressure. Associations between the course of AIx and potential predictors were investigated through a mixed effect model. Results Seventy-six patients (mean (SD) age 62.4 (7.1), male 67%) were included. The AIx showed a significant annual increase of 0.91% (95% CI 0.21/1.60) adjusted for baseline. The change in diffusion capacity (DLco), low-density lipoprotein (LDL), and high-sensitivity c-reactive protein (hsCRP) was independently associated with the increasing evolution of AIx (Coef. - 0.10, p less then 0.001, Coef. 1.37, p=0.003, and Coef. 0.07, p=0.033, respectively). Conclusion This study demonstrated a meaningful increase in arterial stiffness in COPD over time. A greater annual increase in arterial stiffness was associated with the severity of emphysema (measured by DLco), systemic inflammation, and dyslipidaemia. Clinical Trial Registration www.ClinicalTrials.gov, NCT01527773. © 2020 Roeder et al.Purpose Chronic obstructive pulmonary disease (COPD) is a progressive lung disease characterized by poor airflow. The purpose of this study was to explore the mechanisms involved in the development of COPD. Patients and Methods The mRNA expression profile GSE100281, consisting of 79 COPD and 16 healthy samples, was acquired from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) between COPD samples and healthy samples were analyzed using the limma package. Functional enrichment analysis for the DEGs was carried out using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) tool. Furthermore, DEG-compound pairs were predicted using the Comparative Toxicogenomics Database. The KEGG metabolite IDs corresponding to the compounds were also obtained through the MetaboAnalyst pipeline. Based on the diffusion algorithm, the metabolite network was constructed. Finally, the expression levels of key genes were determined using quantitative PCR (qPCR). Results There were 594 DEGs identified between the COPD and healthy samples, including 242 upregulated and 352 downregulated genes. A total of 696 DEG-compound pairs, such as BCL2-C00469 (ethanol) and BCL2-C00389 (quercetin) pairs, were predicted. CYP1B1, VEGFA, BCL2, and CDKN1A were included in the top 10 DEG-compound pairs. Additionally, 57 metabolites were obtained. In particular, hsa04750 (inflammatory mediator regulation of TRP channels)-C00469 (ethanol) and hsa04152 (AMPK signaling pathway)-C00389 (quercetin) pairs were found in the metabolite network. The results of qPCR showed that the expression of CYP1B1, VEGFA, BCL2, and CDKN1A was consistent with that predicted using bioinformatic analysis. Conclusion CYP1B1, VEGFA, BCL2, and CDKN1A may play important functions in the development and progression of COPD. © 2020 Yang et al.Purpose Bradykinesia and muscle weaknesses are common symptoms of Parkinson's Disease (PD) and are associated with impaired functional performance, increased risk of falls, and reduced quality of life. Recent studies have pointed to progressive resistance training (PRT) as an effective method to control and reduce these symptoms, increasing possibilities to treat the disease. However, few studies have focused on assessing the PRT effects in the short-term. Therefore, the present study aimed to assess the short-term PRT effects on people with PD, in order to offer new parameters for a better understanding of its effects, so as an adequation and PRT use as a complementary therapy. Patients and Methods Forty individuals diagnosed with PD from stage 1 to 3 on the Hoehn and Yahr scale took part on the study and were allocated into 2 groups; Training Group (TG) performed a 9-week RT program twice a week, and the Control Group (CG) attended disease lectures. Bradykinesia UPDRS subscale (BSS), knee extensors isokinetic strength, Ten Meters Walk Test (TMW), Timed Up&Go Test (TUG) and 30-Second Chair Stand (T30) were measured before and after the intervention period. Statistical significance was set at p ≤ 0.05. Results Significant time was noted by the group interaction for all functional tests (TUG, T30, and TWM; all p 0.05). Moreover, TUG, T30, TWM, and BSS were significantly different between TG and CG in the post-training assessments (all p less then 0.01). Isokinetic muscle strength was slightly increased in the TG (2.4%) and decreased in the CG (-2.2%), but statistical analyses did not reach significance for interaction but only a trend (p = 0.12). Conclusion The results indicate that 9 weeks of PRT reduces bradykinesia and improves functional performance in patients with mild to moderate PD. These findings reinforce this mode of exercise as an important component of public health promotion programs for PD. © 2020 Vieira de Moraes Filho et al.Purpose This study tried to establish a metric framework of patient adherence to doctor's advice based on the expected utility and prospect theories, and it explained why the key to patient adherence to doctor's advice is patients' perceptions. Methods Our framework is primarily based on two mature theories expected utility theory and prospect theory. We started with a basic assumption the doctor is rational and cares for patient's health utility. We analyzed the expected utility of therapy with a definite diagnosis. Then, we considered the impacts of the accuracy of diagnostic techniques. After that, we explored the patient's response to the doctors' advices based on behavioral economics. In addition, we launched a discrete choice experiment to test our main point perception is the key to patients' adherence. A total of 200 undergraduate students participated in the discrete choice experiment. Results Three main factors might impact a rational clinical decision the therapeutic and side effects of the treatment, patient's true disease risk, and diagnostic accuracy. However, another factor, patient's individual percepion, was crucial for patient's adherence since it may bias the patient's estimations regarding the above three factors. As a result, doctors and patients would have a cognitive gap in the estimation of the disease and the treatment. Conclusion The results indicate that without the necessary information, better clinical techniques may not help to improve patient adherence, which support our theoretical reasoning forcefully. Therefore, improving patient adherence should be more of a process of empathy and communication rather than a promotion of medical technology. © 2020 Lin et al.Objective Poor patient adherence to anti-TNF treatment has proven to be a major roadblock to effective management. Therapeutic patient education (TPE) is now recognized as a crucial tool in managing conditions like chronic inflammatory rheumatism and in improving treatment adherence. This study aimed to assess whether different TPE programs might improve adherence to subcutaneous anti-tumor necrosis factor (anti-TNF) treatment in patients with rheumatoid arthritis (RA), ankylosing spondyloarthritis (AS), and psoriatic arthritis (PsA). Methods This was a retrospective, observational, monocentric study of current care practices. We included 193 patients (124 women; mean age 53.3 ± 14.8 years). All patients received subcutaneous anti-TNF treatment and one of three TPE models, delivered by a nurse, from 2009 to 2013. The cohort was grouped according to different educational models M1 information (N=92); M2 individual TPE (N=80); and M3 individual and group TPE sessions (N=21). Adherence was assessed with the Morisky Medication Adherence Scale (MMAS-4™).