IntroductionUnderstanding 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.MethodsUsing 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. MVC data were collected from the Connecticut Crash Data Repository; daily VMT estimates were obtained from StreetLight Insight’s database. We used segmented Poisson regression models, controlling for daily temperature and daily precipitation.ResultsThe mean daily VMT significantly decreased 43% in the post stay-at-home period in 2020. While the mean daily counts of crashes decreased in 2020 after the stay-at-home order was enacted, several types of crash rates increased after accounting for the VMT reductions. Single vehicle crash rates significantly increased 2.29 times, and specifically single vehicle fatal crash rates significantly increased 4.10 times when comparing the pre-stay-at-home and post-stay-at-home periods.DiscussionDespite a decrease in the number of MVCs and VMT, the crash rate of single vehicles increased post stay-at-home order enactment in Connecticut after accounting for reductions in VMT.

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. Moreover, in in vitro assays, CD13 appears to be largely dispensable for the aspects of phagocytosis, proliferation, and antigen presentation that we tested, although we observed a slight decrease in actin-independent erythrocyte uptake. However, in agreement with our published studies, we show that lack of monocytic CD13 completely ablates anti-CD13-dependent monocyte adhesion to WT endothelial cells. In vivo assessment of four inflammatory disease models showed that lack of CD13 has little effect on disease onset or progression. Nominal alterations in gene expression levels between CD13 WT and null macrophages argue against compensatory mechanisms. Therefore, although CD13 is highly expressed on myeloid cells and is a reliable marker of the myeloid lineage of normal and leukemic cells, it is not a critical regulator of hematopoietic development, hemostasis, or myeloid cell function.

In the ischaemic heart, while compensatory mechanisms apparently relieve potential angiogenic defects, CD13 is essential for proper trafficking of the inflammatory cells necessary to prime and sustain the reparative response, thus promoting optimal post-infarction healing.

SummaryCD13/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. Here, we found that CD13 expression is enriched specifically on the pro-inflammatory subset of monocytes, suggesting that CD13 may regulate trafficking and function of specific subsets of immune cells. To further dissect the mechanisms regulating CD13-dependent trafficking we used the murine model of thioglycollate-induced sterile peritonitis.

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