Brantleybarbour9817

Pharmacological blockade of this receptor for 4 weeks did not significantly alter cardiac function, but mimicked the effects of myeloid cell depletion Telmisartan (20 mg/kg/d, fed to C57BL/6J mice) diminished bone marrow myelopoesis and myeloid ROS production, attenuated endothelial leukocyte rolling and vascular accumulation of CD11b+Ly6G-Ly6Chigh monocytes and macrophages, resulting in improved vascular function with less abundance of Nox2+CD45+ cells. this website CONCLUSION Endothelial dysfunction in HF ensuing MI is mediated by inflammatory Nox2+ myeloid cells infiltrating the vessel wall that can be targeted by AT1R blockade. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions please email journals.permissions@oup.com.BACKGROUND Red and processed meat, recognized carcinogens, are risk factors for colorectal neoplasia, including polyps, the precursor for colorectal cancer. The mechanism is unclear. One possible explanation is the mutagenic activity of these foods, perhaps due to generation during cooking [e.g., heterocyclic amine (HCA) intake]. Few studies have evaluated meat intake and sessile serrated lesion (SSL) risk, a recently recognized precursor, and no study has evaluated meat cooking methods and meat-derived mutagens with SSL risk. OBJECTIVE We evaluated intakes of meat, meat cooking methods, and inferred meat mutagens with SSL risk and in comparison to risk of other polyps. METHODS Meat, well-done meat, and inferred meat mutagen intakes were evaluated. Polytomous logistic regression models were used to estimate ORs and 95% CIs among cases (556 hyperplastic polyp, 1753 adenoma, and 208 SSL) and controls (3804) in the large colonoscopy-based, case-control study, the Tennessee Colorectal Polyp Study. RESULTS The highest quartile intakes of red meat (OR 2.38; 95% CI 1.44, 3.93), processed meat (OR 2.03; 95% CI 1.30, 3.17), well-done red meat (OR 2.19; 95% CI 1.34, 3.60), and the HCA 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQX; OR 2.48; 95% CI 1.49, 4.16) were associated with increased risk of SSLs in comparison to the lowest quartile intake. CONCLUSIONS High intakes of red and processed meats are strongly and especially associated with SSL risk and part of the association may be due to HCA intake. Future studies should evaluate other mechanism(s) and the potential for primary prevention. Copyright © The Author(s) 2020.AIMS Diabetes is a known risk factor for coronary artery disease. There is accumulating evidence that coronary artery disease pathogenesis differs for individuals with type 1 diabetes. However, the genetic background has not been extensively studied. We aimed to discover genetic loci increasing coronary artery disease susceptibility especially in type 1 diabetes, to examine the function of these discoveries and to study the role of the known risk loci in type 1 diabetes. METHODS AND RESULTS We performed the largest genome-wide association study to date for coronary artery disease in type 1 diabetes, comprising 4869 individuals with type 1 diabetes (cases/controls 941/3928). Two loci reached genome-wide significance, rs1970112 in CDKN2B-AS1 (OR = 1.32, p=1.50 × 10-8), and rs6055069 on DEFB127 promoter (OR = 4.17, p=2.35 × 10-9), with consistent results in survival analysis. The CDKN2B-AS1 variant replicated (p=0.04) when adjusted for diabetic kidney disease in three additional type 1 diabetes cohorts (cases/colthough pending on future confirmation. TRANSLATIONAL PERSPECTIVE Genetic association studies enable the discovery of novel genes and genetic pathways associated with the disease. Thus, this study provides an insight into coronary artery disease mechanisms specific to type 1 diabetes. The DEFB127 discovery may lead to a therapeutic target and improve patient care, if replicated in the future. Furthermore, genetic studies on coronary artery disease in type 1 diabetes are required for accurate personalized treatment plans achieved through genetic data for those with type 1 diabetes. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions please email journals.permissions@oup.com.As nanotechnologies advance into clinical medicine, novel methods for applying nanomedicine to cardiovascular diseases are emerging. Extensive research has been undertaken to unlock the complex pathogenesis of atherosclerosis. However, this complexity presents challenges to develop effective imaging and therapeutic modalities for early diagnosis and acute intervention. The choice of ligand-receptor system vastly influences the effectiveness of nanomedicine. This review collates current ligand-receptor systems used in targeting functionalised nanoparticles for diagnosis and treatment of atherosclerosis. Our focus is on the binding affinity and selectivity of ligand-receptor systems, as well as the relative abundance of targets throughout the development and progression of atherosclerosis. Antibody-based targeting systems are currently the most commonly researched due to their high binding affinities when compared to other ligands, such as antibody fragments, peptides, and other small molecules. However, antibodies tend to be immunogenic due to their size. Engineering antibody fragments can address this issue but will compromise their binding affinity. Peptides are promising ligands due to their synthetic flexibility and low production costs. Alongside the aforementioned binding affinity of ligands, the choice of target and its abundance throughout distinct stages of atherosclerosis and thrombosis is relevant to the intended purpose of the nanomedicine. Further studies to investigate the components of atherosclerotic plaques are required as their cellular and molecular profile shifts over time. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions please email journals.permissions@oup.com.Importance Augmentation rhinoplasty requires adding cartilage to provide enhanced support to the structure of the nose. Autologous costal cartilage and irradiated homologous costal cartilage (IHCC) are well-accepted rhinoplasty options. Tutoplast is another alternative cartilage source. No studies, to our knowledge, have definitively demonstrated a higher rate of complications with IHCC grafts compared with autologous costal cartilage grafts. Objective To compare rates of outcomes in the published literature for patients undergoing septorhinoplasty with autologous costal cartilage vs IHCC grafts vs Tutoplast grafts. Data Sources For this systematic review and meta-analysis, the MEDLINE, Embase, Scopus, Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov databases were searched for articles published from database inception to February 2019 using the following keywords septorhinoplasty, rhinoplasty, autologous costal cartilage graft, cadaveric cartilage graft, and rib graft. Study Selection received IHCC grafts (regardless of type). When autologous cartilage (n = 748) vs IHCC (n = 153) vs Tutoplast cartilage (n = 140) grafts were compared, no difference in warping (5%; 95% CI, 3%-9%), resorption (2%; 95% CI, 0%-2%), contour irregularity (1%; 95% CI, 0%-3%), infection (2%; 95% CI, 0%-4%), or revision surgery (5%; 95% CI, 2%-9%) was found. Conclusions and Relevance No difference was found in outcomes between autologous and homologous costal cartilage grafts, including rates of warping, resorption, infection, contour irregularity, or revisions, in patients undergoing dorsal augmentation rhinoplasty. En bloc dorsal onlay grafts are commonly used in augmentation rhinoplasty to provide contour and structure to the nasal dorsum.OBJECTIVE To study the role of long non-coding RNA (lncRNA) LINC00978 in hepatocellular carcinoma (HCC) carcinogenesis. MATERIALS AND METHODS LINC00978 expression level was measured by reverse transcription quantitative real-time PCR (RT-qPCR) in HCC tissues and adjacent healthy liver tissues from 49 HCC patients. MTT assay, colony forming assay, and flow cytometry were performed to evaluate the effects of shRNA-mediated LINC00978 knockdown on HCC cell proliferation, cell cycle progression, and apoptosis in vitro. Xenograft tumor model was performed to determine the effects of LINC00978 knockdown on HCC tumor growth in vivo. Western blot was used to assess the activation of signaling molecules in the apoptosis and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway. RESULTS LINC00978 expression was significantly up-regulated in human HCC tissue relative to adjacent normal tissue, and LINC00978 high expression was correlated with poor HCC overall survival. LINC00978 was up-regulated in HCC cell lines. ShRNA-mediated LINC00978 knockdown significantly decreased HCC cell proliferation, and induced HCC cell cycle arrest and apoptosis in vitro. LINC00978 knockdown led to significant decrease in tumor xenograft size in vivo. Western blots revealed LINC00978 inhibition decreased ERK, p38, and c-Jun N-terminal kinase (JNK) phosphorylation in HCC cells. CONCLUSIONS LINC00978 is highly expressed in human HCC tissue and correlates with poor HCC prognosis. LINC00978 promotes HCC cell proliferation, cell cycle progression, and survival, partially by activating the MAPK/ERK pathway. Our findings partially elucidated the roles of LINC00978 in HCC carcinogenesis, and identified a therapeutic target for HCC. © 2020 The Author(s).The suitability, availability, and use of protective clothing are critical factors determining the actual dermal exposure (ADE) of operators and workers to pesticides. A realistic assessment of occupational exposure to pesticides requires information about the performance of protective clothing during everyday use. In this study, the performance of clothing or gloves has been investigated based on available dermal exposure data in order to provide recommendations for default protection factors that can be used in regulatory exposure assessments. Suitable dermal exposure data from available exposure databases were collated and analysed. The data that met the selection criteria for the analysis of the performance of protective clothing comprised studies in which protective clothing like cotton coveralls, cotton clothing, polyester-cotton coveralls, Sontara coveralls, Tyvek coveralls, butyl/neoprene gloves, latex/PE/vinyl/PVC gloves, or nitrile gloves were worn. Based on available potential and ADE levels, the miene Society.Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder mediated by complexes between platelet factor 4 (PF4) and heparin or other polyanions, but the risk of thrombosis extends beyond exposure to heparin implicating other PF4 partners. We recently reported that peri-thrombus endothelium is targeted by HIT antibodies, but the binding site(s) has not been identified. We now show that PF4 binds at multiple discrete sites along the surface of extended strings of von Willebrand Factor (VWF) released from the endothelium following photochemical injury in an endothelialized microfluidic system under flow. The HIT-like monoclonal antibody KKO and HIT patient antibodies recognize PF4-VWF complexes, promoting platelet adhesion and enlargement of thrombi within the microfluidic channels. Platelet adhesion to the PF4-VWF-HIT antibody complexes is inhibited by antibodies that block FcgRIIA or the glycoprotein Ib-IX complex on platelets. Disruption of PF4-VWF-HIT antibody complexes by drugs that prevent or block VWF oligomerization attenuate thrombus formation in a murine model of HIT.