Initial impact of COVID-19's stay-at-home order on motor vehicle traffic and crash patterns in Connecticut: an interrupted time series analysis.

Introduction: Understanding how the COVID-19 pandemic has impacted our health and safety is imperative. This study sought to examine the impact of COVID-19's stay-at-home order on daily vehicle miles travelled (VMT) and MVCs in Connecticut.

Methods: Using an interrupted time series design, we analysed daily VMT and MVCs stratified by crash severity and number of vehicles involved from 1 January to 30 April 2017, 2018, 2019 and 2020.

CD13 deficiency leads to increased oxidative stress and larger atherosclerotic lesions.

Background And Aims: Atherosclerosis is an inflammatory cardiovascular disorder characterized by accumulation of lipid-loaded macrophages in the intima. Prolonged accumulation leads to apoptosis of macrophages and eventually to progression of lesion development. Prevention of macrophage accumulation within the intima has been shown to reduce lesion formation.

Metabolic syndrome's risk factors and its association with nutritional status in schoolchildren.

The metabolic risk factors (RF) to the diagnosis of metabolic syndrome (MetS) have been evidenced at early ages, including children. The aim of the present study was to identify the prevalence of RF to the diagnosis of MetS and its association with nutritional status of schoolchildren from 6 to 10 years old. A cross-sectional study was carried out in 505 students of municipal schools in Macae, Brazil, conducted from 2013 to 2014.

Molecular mechanisms regulating CD13-mediated adhesion.

CD13/Aminopeptidase N is a transmembrane metalloproteinase that is expressed in many tissues where it regulates various cellular functions. In inflammation, CD13 is expressed on myeloid cells, is up-regulated on endothelial cells at sites of inflammation and mediates monocyte/endothelial adhesion by homotypic interactions. In animal models the lack of CD13 alters the profiles of infiltrating inflammatory cells at sites of ischaemic injury.

CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice.

Aims: To determine the role of CD13 as an adhesion molecule in trafficking of inflammatory cells to the site of injury in vivo and its function in wound healing following myocardial infarction induced by permanent coronary artery occlusion.

Methods And Results: Seven days post-permanent ligation, hearts from CD13 knockout (CD13(KO)) mice showed significant reductions in cardiac function, suggesting impaired healing in the absence of CD13. Mechanistically, CD13(KO) infarcts showed an increase in small, endothelial-lined luminal structures, but no increase in perfusion, arguing against an angiogenic defect in the absence of CD13.

CD13 is dispensable for normal hematopoiesis and myeloid cell functions in the mouse.

The robust and consistent expression of the CD13 cell surface marker on very early as well as differentiated myeloid hematopoietic cells has prompted numerous investigations seeking to define roles for CD13 in myeloid cells. To address the function of myeloid CD13 directly, we created a CD13 null mouse and assessed the responses of purified primary macrophages or DCs from WT and CD13 null animals in cell assays and inflammatory disease models, where CD13 has been implicated previously. We find that mice lacking CD13 develop normally with normal hematopoietic profiles except for an increase in thymic but not peripheral T cell numbers.

Pre-clinical antitumour evaluation of Biphosphinic Palladacycle Complex in human leukaemia cells.

Previous studies reported by our group have introduced a new antitumoural drug called Biphosphinic Palladacycle Complex (BPC). In this paper we show that BPC causes apoptosis in leukaemia cells (HL60 and Jurkat), but not in normal human lymphocytes. IC(50) values obtained for both cell lines using the MTT and trypan blue exclusion assays 5h after BPC treatment were lower than 8.

Activation of protein kinase C and disruption of endothelial monolayer integrity by sodium arsenite--Potential mechanism in the development of atherosclerosis.

Arsenic exposure has been shown to exacerbate atherosclerosis, beginning with activation of the endothelium that lines the vessel wall. Endothelial barrier integrity is maintained by proteins of the adherens junction (AJ) such as vascular endothelial cadherin (VE-cadherin) and beta-catenin and their association with the actin cytoskeleton. In the present study, human aortic endothelial cells (HAECs) were exposed to 1, 5 and 10 microM sodium arsenite [As(III)] for 1, 6, 12 and 24 h, and the effects on endothelial barrier integrity were determined.