We then demonstrated that the increase in VSMC migratory capacity caused by C. pneumoniae infection was inhibited by either TLR2 or CXCR4 depletion, and down-regulating both TLR2 and CXCR4 further decreased C. pneumoniae infection-induced VSMC migration by suppressing the infection-stimulated F-actin reorganization through the inhibition of the phosphorylation of focal adhesion kinase. Taken together, our data indicate that TLR2/CXCR4 co-association facilitates C. 4μ8C price pneumoniae infection-induced acceleration of atherosclerosis by inducing VSMC migration via focal adhesion kinase-mediated F-actin reorganization.Macrophages play a pivotal role in tissue repair following myocardial infarction (MI). In response to injury, they exist along a spectrum of activation states tightly regulated by their microenvironment. Cardiosphere-derived cells (CDCs) have been shown to mediate cardioprotection via modulation of the macrophage response. Our study was designed to gain mechanistic insight into the role of CDC-derived extracellular vesicles (EVs) in modulating macrophage phenotypes and operant signaling pathways to better understand their potential contribution to immunomodulatory cardioprotection. We found that CDC-derived EVs alter the functional phenotype of macrophages, modifying levels of phagocytosis and efferocytosis without changing viability or proliferation. Interestingly, extracellular vesicles differentially regulate several M1/M2 genes dependent on macrophage activation prior to EV treatment, but consistently upregulate Arginase 1 regardless of macrophage origin or polarization state. CDC-derived EVs polarize M1 macrophages to a pro-angiogenic phenotype dependent on Arginase 1 upregulation and independent of VEGF-A. In addition, EV-dependent Arginase 1 upregulation downregulates NO secretion in activated macrophages. These data suggest a novel urea-cycle dependent mechanism in macrophages that promotes angiogenesis and provides additional mechanistic insight into the potential contribution of CDC-derived extracellular vesicles in immunomodulatory cardioprotection.Venous thromboembolism (VTE), which includes deep venous thrombosis and pulmonary embolism, is a significant cause of morbidity and mortality. In recent decades, US, CT, and MRI have surpassed catheter-based angiography as the imaging examinations of choice for evaluation of vascular structures and identification of thrombus owing to their ready availability, noninvasive nature, and, in the cases of US and MRI, lack of exposure to ionizing radiation. As a result, VTE and associated complications are commonly identified in day-to-day radiologic practice across a variety of clinical settings. A wide range of hereditary and acquired conditions can increase the risk for development of venous thrombosis, and many patients with these conditions may undergo imaging for unrelated reasons, leading to the incidental detection of VTE or one of the associated complications. Although the development of VTE may be an isolated occurrence, the imaging findings, in conjunction with the clinical history and vascular risk factors, may indicate a predisposing condition or underlying diagnosis. Furthermore, awareness of the many clinical conditions that result in an increased risk of venous thrombosis may aid in detection of thrombus and any concomitant complications. For these reasons, it is important that practicing radiologists be familiar with the multimodality imaging findings of thrombosis, understand the spectrum of diseases that contribute to the development of thrombosis, and recognize the potential complications of hypercoagulable states and venous thrombosis. Online DICOM image stacks and supplemental material are available for this article. ©RSNA, 2020.Abdominal wall masses, masslike lesions, and diffuse processes are common and often incidental findings at cross-sectional imaging. Distinguishing among these types of masses on the basis of imaging features alone can be challenging. The authors present a diagnostic algorithm that may help in distinguishing different types of abdominal wall masses accurately. Hernias may mimic discrete masses at clinical examination, and imaging is often ordered for evaluation of a possible abdominal wall mass. Once a discrete mass is confirmed to be present, the next step is to determine if it is a fat-containing, cystic, or solid mass. The most common fat-containing masses are lipomas. Fluid or cystic masses include postoperative abscesses, seromas, and rectus sheath hematomas. Solid masses are the most common abdominal wall masses and include desmoid tumors, sarcomas, endometriomas, and metastases. Multiple masses and other diffuse abdominal wall processes are often manifestations of an underlying condition or insult. The most frequently found diffuse processes are multiple injection granulomas from administration of subcutaneous medication. This article offers an algorithmic approach to characterizing abdominal wall masses on the basis of their composition and reviews abdominal wall diffuse processes. Online supplemental material is available for this article. ©RSNA, 2020.This study investigated the effect of chemical substances, such as Mg2+ (as magnesium sulphate), Zn2+ (as zinc sulphate), Fe2+ (as iron sulphate), ascorbic acid, and citric acid, on the formation of 4-methylimidazole (4-MI) and colour stability of caramel colour. The 4-MI concentration in the caramel colour without chemical substances was 963.10 μg/g, and this decreased the most (67.7%) with the addition of 0.1 molar ratio of citric acid. Colour stability was evaluated by measuring the total colour change (ΔE) after storage, and heating in pH 2, 4, and 7 solutions and 50% solution in ethyl alcohol. Among the chemical substances added to reduce 4-MI in the caramel colour, Mg2+ (0.1 molar ratio) and ascorbic acid improved the colour stability more than the others.This editorial announces this journal’s policy on transparency, openness and replication. From 1 July 2020, authors of manuscripts submitted to Journal of Health Psychology (JHP) are required to make the raw data fully accessible to all readers. JHP will only consider manuscripts which follow an open publication model defined as follows M = Mandatory, I = Inclusion (of), R = Raw, D = Data (MIRD). All data and analytical procedures must be sufficiently well described to enable a third party with the appropriate expertise to replicate the data analyses. It is expected that findings and analyses in the JHP will be fully capable of being accurately reproduced.