Differential DARC/ACKR1 expression distinguishes venular from non-venular endothelial cells in murine tissues

This work was supported by the National Institutes of Health (NIH) grant AI112521 and the John and Virginia Kaneb Fellowship

Erosion and reorientation of the Sapodilla Cays, Mesoamerican Reef Belize from 1960 to 2012

The Sapodilla Cays Marine Reserve in southern Belize includes nine low-relief sand cays that were first surveyed in 1960. The purpose of this study is to reconstruct a 52-year history of the Sapodilla Cays (1960-2012) using a combination of historical topographic surveys, satellite imagery, and additional field data collection. Results suggest that the majority of islands are eroding with some islands having lost over 70% of their area, and many have become swash aligned, which suggests limited sediment availability. The proportion of area lost on each island is related to the width of the reef platform (to the 5 m isobaths) in the direction of the reef edge, while island area is dependent on the width of the reef platform in the direction of the resultant wind. This suggests that the width of the reef platform is a primary determinant of sediment supply between storms that tend to erode the eastern shoreline of the island through refraction along the reef edge. While storm erosion tends to be concentrated along the eastern shoreline through the loss of sediment offshore, alongshore transport to the lagoon shoreline, and the transfer of sediment to the interior of the island, net shoreline retreat is greatest along the lagoon, suggesting that the relatively small winter northers and a lack of sediment supply from the reef lagoon are responsible for the observed erosion. Extrapolations based on contemporary loss-rates suggest that the smallest cays will disappear by 2020, while the largest cays will begin to disappear by the end of century. © 2014 Taylor & Francis

A receptor for the malarial parasite Plasmodium vivax: the erythrocyte chemokine receptor

Plasmodium vivax and P. falciparum are the major causes of human malaria, except in sub-Saharan Africa where people lack the Duffy blood group antigen, the erythrocyte receptor for P. vivax. Duffy negative human erythrocytes are resistant to invasion by P. vivax and the related monkey malaria, P. knowlesi. Several lines of evidence in the present study indicate that the Duffy blood group antigen is the erythrocyte receptor for the chemokines interleukin-8 (IL-8) and melanoma growth stimulatory activity (MGSA). First, IL-8 binds minimally to Duffy negative erythrocytes. Second, a monoclonal antibody to the Duffy blood group antigen blocked binding of IL-8 and other chemokines to Duffy positive erythrocytes. Third, both MGSA and IL-8 blocked the binding of the parasite ligand and the invasion of human erythrocytes by P. knowlesi, suggesting the possibility of receptor blockade for anti-malarial therapy

Induction of Cell-Associated Chemokines after Endotoxin Administration to Healthy Humans

Erythrocytes express the Duffy antigen receptor for chemokines. Endotoxin injection into humans induced high levels of interleukin-8 (IL-8), growth-related oncogene α, and monocyte chemoattractant protein 1 in circulating erythrocytes. IL-8 was also recovered from mononuclear and polymorphonuclear cells. Cell-associated chemokines may more accurately reflect their production than plasma concentrations