Evaluating the impact of international airline suspensions on the early global spread of COVID-19.

Global airline networks play a key role in the global importation of emerging infectious diseases. Detailed information on air traffic between international airports has been demonstrated to be useful in retrospectively validating and prospectively predicting case emergence in other countries. In this paper, we use a well-established metric known as effective distance on the global air traffic data from IATA to quantify risk of emergence for different countries as a consequence of direct importation from China, and compare it against arrival times for the first 24 countries.

Draft genome sequences of two Campylobacter jejuni clinical isolates, NW and D2600.

The Campylobacter jejuni human clinical isolates NW and D2600 colonized C57BL/6 interleukin-10-deficient (IL-10(-/-)) mice without inducing a robust inflammatory response (J. A. Bell et al.

HIF-2alpha regulates glyceraldehyde-3-phosphate dehydrogenase expression in endothelial cells.

Endothelial cells (EC) express both hypoxia inducible factor-1alpha (HIF-1alpha) and -2alpha (HIF-2alpha), yet their roles in the EC hypoxic response are unclear. Hypoxia upregulates the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in EC through a 5' hypoxic regulatory element (HRE). We compared the upregulation of GAPDH in human lung microvascular EC to that in hep3B cells, another cell type known to express both HIF-1alpha and HIF-2alpha.

Identification of protein disulfide isomerase as an endothelial hypoxic stress protein.

Endothelial cells (EC) exposed to hypoxia upregulate a unique set of five stress proteins. These proteins are upregulated in human and bovine aortic and pulmonary artery EC and are distinct from heat shock or glucose-regulated proteins. We previously identified two of these proteins as the glycolytic enzymes glyceraldehyde-3-phosphate dehydrogenase and enolase and postulated that the remaining proteins were also glycolytic enzymes.