The Modern Research Data Portal: a design pattern for networked, data-intensive science.

We describe best practices for providing convenient, high-speed, secure access to large data via research data portals. We capture these best practices in a new design pattern, the Modern Research Data Portal, that disaggregates the traditional monolithic web-based data portal to achieve orders-of-magnitude increases in data transfer performance, support new deployment architectures that decouple control logic from data storage, and reduce development and operations costs. We introduce the design pattern; explain how it leverages high-performance data enclaves and cloud-based data management services; review representative examples at research laboratories and universities, including both experimental facilities and supercomputer sites; describe how to leverage Python APIs for authentication, authorization, data transfer, and data sharing; and use coding examples to demonstrate how these APIs can be used to implement a range of research data portal capabilities.

Absence of bacterially induced RELMbeta reduces injury in the dextran sodium sulfate model of colitis.

Although inflammatory bowel disease (IBD) is the result of a dysregulated immune response to commensal gut bacteria in genetically predisposed individuals, the mechanism(s) by which bacteria lead to the development of IBD are unknown. Interestingly, deletion of intestinal goblet cells protects against intestinal injury, suggesting that this epithelial cell lineage may produce molecules that exacerbate IBD. We previously reported that resistin-like molecule beta (RELMbeta; also known as FIZZ2) is an intestinal goblet cell-specific protein that is induced upon bacterial colonization whereupon it is expressed in the ileum and colon, regions of the gut most often involved in IBD.

Enteropathogenic E. coli disrupts tight junction barrier function and structure in vivo.

Enteropathogenic Escherichia coli (EPEC) infection disrupts tight junctions (TJs) and perturbs intestinal barrier function in vitro. E. coli secreted protein F (EspF) is, in large part, responsible for these physiological and morphological alterations.

ClC-2 chloride secretion mediates prostaglandin-induced recovery of barrier function in ischemia-injured porcine ileum.

Background & Aims: Ischemia results in the breakdown of the intestinal barrier, predisposing patients to sepsis and multiple organ failure. Prostaglandins play a critical role in mediating recovery of barrier function in ischemia-injured intestine through a mechanism involving stimulation of Cl - secretion. In the present study, we investigated the contributory role of individual Cl - channels in the recovery of barrier function in ischemia-injured porcine ileum.

Physiological concentrations of bile salts inhibit recovery of ischemic-injured porcine ileum.

We have previously shown rapid in vitro recovery of barrier function in porcine ischemic-injured ileal mucosa, attributable principally to reductions in paracellular permeability. However, these experiments did not take into account the effects of luminal contents, such as bile salts. Therefore, the objective of this study was to evaluate the role of physiological concentrations of deoxycholic acid in recovery of mucosal barrier function.

Neutrophils augment recovery of porcine ischemia-injured ileal mucosa by an IL-1beta- and COX-2-dependent mechanism.

Polymorphonuclear neutrophils (PMNs) play a critical role in intestinal mucosal injury and repair. To study effects of PMNs on acutely injured mucosa, we applied PMNs isolated from circulation or peritoneal fluid from animals with chemically induced peritonitis to ischemia-injured porcine ileal mucosa. In preliminary experiments, PMNs enhanced recovery of transepithelial electrical resistance (TER), and this action was inhibited by pretreatment with the nonselective cyclooxygenase (COX) inhibitor indomethacin.

Mitogen-activated protein kinases regulate COX-2 and mucosal recovery in ischemic-injured porcine ileum.

Mitogen-activated protein kinase (MAPK) pathways transduce signals from a diverse array of extracellular stimuli. The three primary MAPK-signaling pathways are the extracellular regulated kinases (ERK1/2), p38 MAPK, and c-Jun NH(2)-terminal kinase (JNK). Previous research in our laboratory has shown that COX-2-elaborated prostanoids participate in recovery of mucosal barrier function in ischemic-injured porcine ileum.