Training, Drills Pivotal in Mounting Response to Orlando Shooting.

Emergency providers at Orlando Regional Medical Center in Orlando. FL, faced multiple challenges in responding to the worst mass shooting in U.S.

Patients with inflammatory bowel disease exhibit dysregulated responses to microbial DNA.

Background: A critical role for the gut epithelium lies in its ability to discriminate between pathogens and commensals and respond appropriately. Dysfunctional interactions between microbes and epithelia are believed to have a role in inflammatory bowel disease (IBD). In this study, we analyzed microbiota and gene expression in IBD patients and examined responses of mucosal biopsies to bacterial DNA.

Intravenous injection of endogenous microbial components abrogates DSS-induced colitis.

Background: The etiology of inflammatory bowel diseases (IBD) is largely unknown, but appears to be perpetuated by uncontrolled responses to antigenic components of the endogenous flora. Tolerance to antigenic stimulation can be achieved by exposure to a given antigen in high amounts (high dose tolerance). Colitis induced by feeding of Dextran Sodium Sulfate (DSS) is an often-used animal model mimicking clinical and histological features of human IBD.

Estrogen receptor-β signaling modulates epithelial barrier function.

Impaired epithelial barrier function and estrogens are recognized as factors influencing inflammatory bowel disease (IBD) pathology and disease course. Estrogen receptor-β (ERβ) is the most abundant estrogen receptor in the colon and a complete absence of ERβ expression is associated with disrupted tight-junction formation and abnormal colonic architecture. The aim of this study was to determine whether ERβ signaling has a role in the maintenance of epithelial permeability in the colon.

Tissue eosinophilia in a mouse model of colitis is highly dependent on TLR2 and independent of mast cells.

The mechanisms initiating eosinophil influx into sites of inflammation have been well studied in allergic disease but are poorly understood in other settings. This study examined the roles of TLR2 and mast cells in eosinophil accumulation during a nonallergic model of eosinophilia-associated colitis. TLR2-deficient mice (TLR2(-/-)) developed a more severe colitis than wild-type mice in the dextran sodium sulfate (DSS) model.

cis-Urocanic acid attenuates acute dextran sodium sulphate-induced intestinal inflammation.

On exposure to sunlight, urocanic acid (UCA) in the skin is converted from trans to the cis form and distributed systemically where it confers systemic immunosuppression. The aim of this study was to determine if administration of cis-UCA would be effective in attenuating colitis and the possible role of IL-10. Colitis was induced in 129/SvEv mice by administering 5% dextran sodium sulfate (DSS) for 7 days in drinking water.

[Factorial validation of the French scale for perceived stress in the workplace].

This article aims to validate the factorial structure of the perceived stress scale (PSS10) within the French working population. The analyses conducted confirmed the presence of two distinct factors, interpreted in terms of perceived work overload and perceived personal efficacy. Both factors presented good internal consistency and adequate validity of construct.

The gut microbiota of toll-like receptor 2-deficient mice exhibits lineage-specific modifications.

Mutations in toll-like receptors that mediate bacterial recognition by the mammalian innate immune system have the potential to substantially alter the composition of an individual's microbiota. Here we tested this hypothesis by comparing the intestinal microbiota of toll-like receptor 2-deficient mice, both young and middle aged, with that of wild-type mice of the same genetic background, housed together under specific pathogen-free conditions. Bacterial DNA was extracted from mouse caecal tissue samples, amplified using universal bacterial 16S ribosomal RNA gene primers, and cloned into a plasmid vector.

Aging in the absence of TLR2 is associated with reduced IFN-gamma responses in the large intestine and increased severity of induced colitis.

Age-associated changes in immune function and their implications for intestinal inflammation are poorly understood. Defects in innate immunity have been shown to enhance intestinal inflammation and have been demonstrated upon aging. This study aimed to determine the consequences of aging in the presence and absence of TLR2 on intestinal inflammation.

IgE-mediated mast cell activation induces Langerhans cell migration in vivo.

Langerhans cells and mast cells are both resident in large numbers in the skin and act as sentinel cells in host defense. The ability of mast cells to induce Langerhans cell migration from the skin to the draining lymph node in vivo was examined. Genetically mast cell-deficient (W/Wv) mice and control mice were sensitized with IgE Ab in the ear pinna.