Zhangadair6838

Mn0.5 Co0.5 PS3 (100) surface exhibits an ultralow overpotential of 0.39 V vs RHE switching ORR pathway from associative to dissociative. Spontaneous dissociation of H2 O2 on Mn0.5 Co0.5 PS3 proves 4e reduction pathway excluding 2e one. Electronic structure analysis reveals that pristine MnPS3 (100) surface is a narrow band gap semiconductor which upon Co substitution transforms into a conducting metallic surface enhancing ORR activity. Besides, Mn0.5 Co0.5 PS3 (100) surface obtains the apex of the volcano plot due to its optimal position of the d-band center which further justifies the improved ORR activity. With Pt-like onset potential, facile H2 O desorption ability, and robust dynamic and thermal stability, this CO tolerant Mn0.5 Co0.5 PS3 catalyst can be a potential alternative to Pt with encouraging practical viability.

This study was undertaken to describe clinical manifestations in patients with Th/To antibody-positive systemic sclerosis (SSc) during long-term follow-up.

We performed a case-control study involving anti-Th/To antibody-positive patients with SSc who were newly referred to the University of Pittsburgh Medical Center and the Pittsburgh Scleroderma Center from 1980 to 2015. For every case, 2 anti-Th/To antibody-negative SSc patients (the first 2 consecutively seen after a case) were used as controls. Long-term disease manifestations and survival were then compared between cases and controls.

A total of 204 anti-Th/To antibody-positive SSc patients and 408 controls were identified. see more The cohort had a mean ± SD age of 52 ± 12.9 years, and 76% of individuals were women. Anti-Th/To antibody-positive patients more often presented without skin thickening (P < 0.0001) and had a higher rate of pulmonary hypertension (PH) (P < 0.0001) and interstitial lung disease (P=0.05) compared to anti-Th/To antibody-negatt risk of anti-Th/To antibody-positive patients developing PH in follow-up, particularly in WHO Group 1 PAH patients, is striking. Patients presenting with limited skin involvement should be tested for Th/To antibodies, and if present, careful monitoring for PH is warranted.

This is the largest cohort of patients with anti-Th/To antibody-positive SSc with long-term follow-up data. The very high rate (38%) and associated independent risk of anti-Th/To antibody-positive patients developing PH in follow-up, particularly in WHO Group 1 PAH patients, is striking. Patients presenting with limited skin involvement should be tested for Th/To antibodies, and if present, careful monitoring for PH is warranted.

The aim of this study was to estimate the 1-year costs associated with treating diabetic macular oedema (DME) patients using current intravitreal anti-vascular endothelial growth factor (anti-VEGF) biologics compared with the dexamethasone implant.

We conducted a descriptive cost-evaluation analysis using data from Oslo University Hospital and literature to compare three different intravitreal drugs for DME bevacizumab, aflibercept and dexamethasone. Stratification of patients into 'Naive' or 'Switch' group was based on treatment history. We estimated the costs from healthcare and 'extended' healthcare perspectives. Sensitivity analysis evaluated the impact of various parameters.

The average injections per patient per year for the Naive group (bevacizumab), Switch group (aflibercept) and dexamethasone were 9.5, 9.1 and 3.0 respectively. From a healthcare perspective, the 1-year costs for the Naive group were 15% lower (bevacizumab, €3619), and for the Switch group, 23% higher (aflibercept, €5226) compared with dexamethasone (€4252). The 'extended' healthcare perspective showed the cost per patient per year for bevacizumab remained nominally lower in the Naive group, while dexamethasone remained lower for the Switch group (€5116 for dexamethasone, compared to €4987 for bevacizumab and €6537 for aflibercept).

From a primary healthcare perspective, the dexamethasone as a first-line DME treatment may increase economic costs in settings where bevacizumab is used off-label. Treating resistant DMEwith dexamethasone may reduce the costs and treatment burden compared with switching to aflibercept.

From a primary healthcare perspective, the dexamethasone as a first-line DME treatment may increase economic costs in settings where bevacizumab is used off-label. Treating resistant DMEwith dexamethasone may reduce the costs and treatment burden compared with switching to aflibercept.Palladium(II)-catalyzed C(alkenyl)-H alkenylation enabled by a transient directing group (TDG) strategy is described. The dual catalytic process takes advantage of reversible condensation between an alkenyl aldehyde substrate and an amino acid TDG to facilitate coordination of the metal catalyst and subsequent C(alkenyl)-H activation by a tailored carboxylate base. The resulting palladacycle then engages an acceptor alkene, furnishing a 1,3-diene with high regio- and E/Z-selectivity. The reaction enables the synthesis of enantioenriched atropoisomeric 2-aryl-substituted 1,3-dienes, which have seldom been examined in previous literature. Catalytically relevant alkenyl palladacycles were synthesized and characterized by X-ray crystallography, and the energy profiles of the C(alkenyl)-H activation step and the stereoinduction model were elucidated by density functional theory (DFT) calculations.The life-threatening adverse effects of doxorubicin (Dox) caused by its cardiotoxic properties limit its clinical application. DDX3X has been shown to participate in a variety of physiological processes, and it acts as a regulator of Wnt/β-catenin signaling. However, the role of DDX3X in Dox-induced cardiotoxicity (DIC) remains unclear. In this study, we found that DDX3X expression was significantly decreased in H9c2 cardiomyocytes treated with Dox. Ddx3x knockdown and RK-33 (DDX3X ATPase activity inhibitor) pretreatment exacerbated cardiomyocyte apoptosis and mitochondrial dysfunction induced by Dox treatment. In contrast, Ddx3x overexpression ameliorated the DIC response. Moreover, Wnt/β-catenin signaling in cardiomyocytes treated with Dox was suppressed, but this suppression was reversed by Ddx3x overexpression. Overall, this study demonstrated that DDX3X plays a protective role in DIC by activating Wnt/β-catenin signaling.The switch from the normal quiescent vasculature to angiogenesis in tumors is induced by a variety of growth factors, released from cancer and stromal cells upon oxygen and nutrients deprivation. Vascular endothelial growth factor A (VEGF-A) is a potent-secreted mitogen and the only growth factor specific to endothelial cells that is observed almost ubiquitously at sites of angiogenesis. Expression of VEGF-A in cancer cells is controlled through transcriptional and post-transcriptional mechanisms. Post-transcriptional regulation of VEGF-A occurs at multiple levels, through the control of splicing, mRNA stability and translation rate, enabling a fine-tuned expression and release of VEGF-A. Mounting evidence is highlighting the important role played by microRNAs (miRNAs) in the control of VEGF-A mRNA stability and translation in cancer. Moreover, non-coding RNAs, as long non-coding RNAs and circular RNAs, are emerging as crucial modulators of VEGF-A-targeting miRNAs, with consequent ability to modulate VEGF-A expression. This review discusses the recent progress on the ncRNA-related networks controlling VEGF-A expression in cancer cells and provides insights into the complexity of VEGF-A post-transcriptional regulation.We present a case report of a 74-year-old male patient with an implantable cardioverter defibrillator who suffered an inappropriate defibrillation shock while bathing in the tub. Insight in the ICD stored electrogram episodes revealed electromagnetic interferences, with a typical 50 Hz electrical artifact mimicking fast ventricular tachycardia as a device misinterpreted. After this event, the maintenance workers investigated the electrical installation in the bathroom and revealed that there was voltage leaking between electrical installation and metal pipes. After the repair was completed without any additional programming, the patient has had no subsequent shocks.

This study aimed to evaluate whether the 2017 European Alliance of Associations for Rheumatology (EULAR)/American College of Rheumatology (ACR) classification criteria for adult and juvenile idiopathic inflammatory myopathies (IIMs) could appropriately classify the diagnosis in adult patients with anti-melanoma differentiation-associated protein 5 (anti-MDA-5)-positive IIM. In addition, this study sought to determine whether a status of anti-MDA-5 positivity could be incorporated into the EULAR/ACR IIM classification criteria set and whether the recently modified criteria based on the presence of myositis-specific autoantibodies (MSAs) could be used to appropriately classify the diagnosis in patients with anti-MDA-5-positive IIM.

Consecutive adult patients clinically diagnosed as having anti-MDA-5-positive IIM from 10 hospitals in Hong Kong were retrospectively recruited; patient characteristics were obtained from electronic medical records. We used a commercial line blot immunoassay to detect MSAs. We althe EULAR/ACR criteria in almost 30% of patients. We suggest incorporating anti-MDA-5 antibody positivity as a criterion into existing criteria sets or developing specific criteria for patients with anti-MDA-5-positive IIM.

In this cohort of patients with anti-MDA-5-positive IIM, the diagnosis could not be classified by the EULAR/ACR criteria in almost 30% of patients. We suggest incorporating anti-MDA-5 antibody positivity as a criterion into existing criteria sets or developing specific criteria for patients with anti-MDA-5-positive IIM.

Platelets shed platelet microparticles (PMP) when activated or stored. As the removal of sialic acid (desialylation) promotes platelet uptake and clearance from the circulation, similar mechanisms for PMP uptake were hypothesized. The aim of the study was to investigate the role of surface glycans in the in vitro uptake of PMP from stored platelet components.

Apheresis platelet components were stored in 40% plasma/60% SSP+ and sampled on day 1, 5, and 7 post-collection. PMP were characterized by staining with annexin-V (AnV) for phosphatidylserine (PS)-exposure, CD41 antibody, and fluorescently labeled glycan-binding lectins using flow cytometry. The procoagulant function of PMP following desialylation by neuraminidase treatment was assessed by AnV binding and a procoagulant phospholipid assay. PMP were isolated and stained with Deep Red, and phagocytosis by HepG2 cells was measured. Isolated PMP were deglycosylated with neuraminidase and galactosidase to assess the involvement of glycans in mediating phagocytosis.

While the overall platelet surface glycan profile was unchanged during storage, PS

platelets were sialylated, indicating different glycoproteins were changed. In contrast, sialic acid was removed from PS

and CD41

PMP, which specifically lost α-2,3-linked sialic acid during platelet storage. PMP were phagocytized by HepG2 cells, and PMP from platelets stored for 7 days were phagocytized to a lesser extent than on day 1. Desialylation by neuraminidase induced PS-exposure on PMP, decreased PPL clotting time, and increased PMP phagocytosis.

PMP glycans change during platelet storage. Desialylation influences the procoagulant function of PMP and phagocytosis by HepG2 cells.

PMP glycans change during platelet storage. Desialylation influences the procoagulant function of PMP and phagocytosis by HepG2 cells.