Comparison of standardized clinical evaluation of wounds using ruler length by width and Scout length by width measure and Scout perimeter trace.

The study objective was to examine precision in wound measurement using a recently Food and Drug Administration-approved Scout (WoundVision, LLC, Indianapolis, Indiana) device to measure wound length (L) and width (W). Wound perimeter and a ruler measurement of L and W were also made. Images of 40 actual patient wounds were measured using the Scout device.

Assessment of pre-gastroscopy fasting period using ultrasonography.

Discomfort is frequent in patients undergoing esophagogastroduodenoscopy who are routinely recommended to abstain at least for 6 h from liquid or solid food prior to the procedure. We investigated the minimal period of time required for the stomach to clear fluids in order to define a safe minimal pre-endoscopy fasting period. Gastric emptying was sonographically assessed in 54 patients by measurement of the antrum surface area prior to, immediately after, and 30, 60, and 90 min after ingestion of 300 ml water and water containing 75 g glucose or apple juice.

The absence of cutaneous lymph nodes results in a Th2 response and increased susceptibility to Leishmania major infection in mice.

Lymph nodes (LNs) are important sentinel organs where antigen-presenting cells interact with T cells to induce adaptive immune responses. In cutaneous infection of mice with Leishmania major, resistance depends on the induction of a T-helper-cell-1 (Th1)-mediated cellular immune response in draining, peripheral LNs. We investigated whether draining, peripheral LNs are absolutely required for resistance against L.

Endoscopic visualization of angiotensin-converting enzyme inhibitor-induced small bowel angioedema as a cause of relapsing abdominal pain using double-balloon enteroscopy.

A 40-year-old woman presented with 3 episodes of abdominal pain. Abdominal ultrasound demonstrated edema of the small bowel. Double-balloon enteroscopy (DBE) showed diffuse swelling of the small intestine, petechial bleeding in the jejunum, and focal inflammation of the ileum.

Resistance of chemokine receptor 6-deficient mice to Yersinia enterocolitica infection: evidence of defective M-cell formation in vivo.

M cells, specialized cells within Peyer's patches (PPs), are reduced in number in chemokine receptor 6 (CCR6)-deficient mice. The pathogenic microorganism Yersinia enterocolitica exploits M cells for the purpose of mucosal tissue invasion exclusively through PPs. The aim of this study was to evaluate the course of yersiniosis in CCR6-deficient mice and to investigate whether these mice might be used as an in vivo model to determine M-cell function.

Role of lymphotoxins in the development of Peyer's patches and mesenteric lymph nodes: relevance to intestinal inflammation and treatment.

Hallmarks of the adaptive immune system are antigen-specific cellular and humoral immune responses. Secondary lymphoid organs serve as sites of contact between antigen-presenting cells (APCs) and immune effector T and B lymphocytes. The gut-associated lymphatic system (GALT) as the intestinal branch of the immune system provides different mechanisms to protect organisms against pathogens.

Chromoendoscopy is a valuable tool for screening of high-risk patients with head and neck cancer for early detection of esophageal cancer.

Background: The incidence of esophageal cancer is markedly increased in patients with head and neck cancer, and the presence of esophageal cancer is associated with reduced survival rates.

Aims: We investigated whether the results of screening for esophageal cancer in patients with head and neck cancer using chromoendoscopy would change the treatment of such patients.

Patients: 87 patients with head and neck cancer and known alcohol or nicotine abuse were screened for esophageal cancer.

Expression of vascular cell adhesion molecule-1 (CD 106) in normal and neoplastic human esophageal squamous epithelium.

Vascular cell adhesion molecule-1 (VCAM-1), a key receptor for the leukocyte-associated integrin (VLA4), is a crucial mediator of leukocyte adhesion and has co-stimulatory functions in inflammation at various organ sites. Specifically, VCAM-1/VLA4 interactions have been shown to play important roles in the setting of cutaneous immune responses, such as psoriatic lesions in humans and acute Graft-versus-Host-Disease in mice. VCAM-1 is generally expressed on activated endothelial cells in inflamed tissues, mediating endothelium-leukocyte interactions, leading to leukocyte diapedesis to the site of inflammation.

Absence of CCR6 inhibits CD4+ regulatory T-cell development and M-cell formation inside Peyer's patches.

The chemokine Mip3alpha is specifically expressed by the follicle-associated epithelia (FAE) covering intestinal Peyer's patches (PPs) and is the only known chemokine ligand for the chemokine receptor CCR6. Although CCR6-deficient mice are known to have a perturbed intestinal immune system, little is known about the specific impact of this interaction for Peyer's patch formation. To elucidate the effect of Mip3alpha on PP lymphocyte development, we used a CCR6/enhanced green fluorescent protein (EGFP) knock-in mouse model and analyzed lymphocyte development by immunohistochemistry and flow cytometry.

The lymphotoxin-beta receptor is critical for control of murine Citrobacter rodentium-induced colitis.

Background And Aims: Lymphotoxin is a tumor necrosis factor-family cytokine. Blocking of lymphotoxin alpha 1 beta 2 /lymphotoxin-beta receptor interactions prevents experimental colitis in mice, and this suggests a potential treatment principle of human inflammatory bowel disease. Infection of mice with Citrobacter rodentium serves as an animal model for human infectious colitis induced by enteropathogenic Escherichia coli .

Human intestinal microvascular endothelial cells express Toll-like receptor 5: a binding partner for bacterial flagellin.

Bacterial flagellin has recently been identified as a ligand for Toll-like receptor 5 (TLR5). Human sites known to specifically express TLR5 include macrophages and gastric and intestinal epithelium. Because infection of intestinal epithelial cells with Salmonella leads to an active transport of flagellin to the subepithelial compartment in proximity to microvessels, we hypothesized that human intestinal endothelial cells functionally express TLR5, thus enabling an active inflammatory response upon binding of translocated flagellin.

Oral tolerance induced by continuous feeding: enhanced up-regulation of transforming growth factor-beta/interleukin-10 and suppression of experimental autoimmune encephalomyelitis.

Oral administration of antigen leads to specific immune hyporesponsiveness termed as oral tolerance. Different doses and feeding regimens have been demonstrated to induce different types of tolerance and degrees of immune suppression. Herein, we compare distinct different regimens of feeding using equivalent final doses of antigen in order to investigate the role of frequency of antigen uptake in the induction of oral tolerance.

Induction of colitis in mice deficient of Peyer's patches and mesenteric lymph nodes is associated with increased disease severity and formation of colonic lymphoid patches.

Inflammatory bowel disease is associated with immune activation in Peyer's patches and mucosal lymph nodes. The role of these organs in dextran sodium sulfate (DSS)-induced colitis was investigated. We used mice lacking Peyer's patches and/or lymph nodes because of lymphotoxin-alpha gene deficiency or treatment in utero with lymphotoxin-beta-receptor IgG and tumor necrosis factor-receptor-I (55)-IgG fusion proteins.

Mesenteric lymph nodes are critical for the induction of high-dose oral tolerance in the absence of Peyer's patches.

We have previously demonstrated the loss of oral tolerance (OT) in lymphotoxinalpha-/- (LTalpha-/-) and TNFalpha / lymphotoxinalpha deficient (TNFalpha / LTalpha-/-) mice which have defective Peyer's patches (PP) and lymph node (LN) development. We have now studied OT in BALB / c mice with differential defects of the gut-associated lymphoid tissue (GALT) caused by inhibition of LTbetaR signaling during fetal development. Treatment of pregnant mice with LTbetaR-IgG (LTbetaRIgG) and TNFR I55-IgG (TNFR55IgG) abrogates the formation of PP (LTbetaRIgG) or of PP and mesenteric LN (MLN) (LTbetaRIgG / TNFRIgG) without genetically deleting the respective cytokine pathways.