Non-dysbaric arterial gas embolism associated with chronic necrotizing pneumonia, bullae and coughing: a case report.

Arterial gas embolism (AGE) can be clinically devastating, and is most often associated with exposure to changes in ambient pressure, medical procedure or congenital malformation. Here we report a case of AGE in a 78-year-old male without these traditional risk factors. Rather, the patient's history included chronic obstructive pulmonary disease, necrotizing pneumonia, bullous disease and coughing.

Successful treatment of pneumatosis intestinalis with associated pneumoperitoneum and ileus with hyperbaric oxygen therapy.

Pneumatosis intestinalis (PI), or the presence of air in the bowel wall, is a rare disorder that is associated with a variety of underlying diseases, including connective tissue disorders. PI presents on a spectrum from asymptomatic to bowel obstruction and acute abdomen. In general, treatment of PI consists of treating the underlying disease.

A randomized pilot validation of educational measures in teaching shoulder arthroscopy to surgical residents.

Background: Injuries to the shoulder joint commonly require the attention of an orthopedic surgeon. Shoulder arthroscopy plays an increasingly important role in the diagnosis and repair of shoulder pathology; however, the most effective manner in which to teach orthopedic residents fundamental knowledge of diagnostic shoulder arthroscopy before entering the operating room is unclear. We aimed to compare the existing cadaver-based teaching of diagnostic shoulder arthroscopy knowledge with a method that combines model- and video-based teaching to orthopedic surgery residents in a randomized pilot trial.

Phosphatidylinositol 3'-kinase is a critical mediator of interferon-gamma-induced increases in enteric epithelial permeability.

The epithelial lining of mucosal surfaces acts as a barrier to regulate the entry of antigen and pathogens. Nowhere is this function of the contiguous epithelium more important than in the gut, which is continually exposed to a huge antigenic load and, in the colon, an immense commensal microbiota. We assessed the intracellular signaling events that underlie interferon (IFN) gamma-induced increases in epithelial permeability using monolayers of the human colonic T84 epithelial cell line.

Conditioned medium from enterohemorrhagic Escherichia coli-infected T84 cells inhibits signal transducer and activator of transcription 1 activation by gamma interferon.

Gamma interferon (IFN-gamma) is a cytokine important to host defense which can signal through signal transducer and activator of transcription 1 (Stat1). Enterohemorrhagic Escherichia coli (EHEC) modulates host cell signal transduction to establish infection, and EHEC serotypes O113:H21 and O157:H7 both inhibit IFN-gamma-induced Stat1 tyrosine phosphorylation in vitro. The aim of this study was to delineate both bacterial and host cell factors involved in the inhibition of Stat1 tyrosine phosphorylation.

Modulation of host cell signal transduction pathways by Helicobacter pylori infection.

Bacterial pathogens modulate host cell signal transduction responses to establish infection and cause disease. The purpose of the present summary, first presented at the Canadian Helicobacter Study Group meeting, is to discuss current knowledge of specific Helicobacter pylori factors, including the vacuolating cytotoxin, cytotoxin-associated gene A and the type four secretion system encoded by the cytotoxin-associated gene pathogenicity island and review the host cell signal transduction cascades that they modulate.

Canadian Helicobacter Study Group Consensus Conference: Update on the approach to Helicobacter pylori infection in children and adolescents--an evidence-based evaluation.

As an update to previously published recommendations for the management of Helicobacter pylori infection, an evidence-based appraisal of 14 topics was undertaken in a consensus conference sponsored by the Canadian Helicobacter Study Group. The goal was to update guidelines based on the best available evidence using an established and uniform methodology to address and formulate recommendations for each topic. The degree of consensus for each recommendation is also presented.

Epithelial cell signaling responses to enterohemorrhagic Escherichia coli infection.

Enterohemorrhagic Escherichia coli, including the serotype O157:H7 that is most commonly identified with human disease, cause both sporadic cases and outbreaks of non-bloody diarrhea and hemorrhagic colitis. In about 10% of infected subjects, the hemolytic uremic syndrome (hemolytic anemic, thrombocytopenia, and acute renal failure) develops, likely as a consequence of systemic spread of bacterial-derived toxins variously referred to as Shiga-like toxin, Shiga toxin, and Verotoxin. Increasing evidence points to a complex interplay between bacterial products--for example, adhesins and toxins--and host signal transduction pathways in mediating responses to infection.

Helicobacter pylori infection induces interleukin-18 production in gastric epithelial (AGS) cells.

Helicobacter pylori colonization of the stomach results in a chronic-active gastritis characterized by mucosal infiltration of both neutrophils and lymphocytes. A T helper lymphocyte (Th1) profile predominates, which promotes the chronic and persistent inflammatory changes in the gastric mucosa in response to this bacterial pathogen. The cytokine interleukin-18 induces production of interferon-gamma by activated T lymphocytes and promotes a Th1 profile.

Interleukin-4- and -13-induced hypercontractility of human intestinal muscle cells-implication for motility changes in Crohn's disease.

Crohn's disease is an idiopathic inflammatory condition. However, little is known about the changes that occur in the muscularis externa, despite the fact that this tissue contributes to motility changes and stricture formation. We characterized immune activity in the muscularis externa from intestinal segments of Crohn's disease patients and evaluated the role of IL-4 and -13 as well as signal transducer and activator of transcription (STAT)6 in the contractility of the cultured human intestinal smooth muscle cells.

Helicobacter pylori induces apoptosis of macrophages in association with alterations in the mitochondrial pathway.

Helicobacter pylori is a gastric bacterial pathogen that evades host immune responses in vivo and is associated with the development of gastritis, peptic ulcer disease, and gastric cancers. Induction of macrophage apoptosis is a method employed by multiple pathogens to escape host immune responses. Therefore, we hypothesized that H.

Cytoskeletal rearrangements in gastric epithelial cells in response to Helicobacter pylori infection.

Helicobacter pylori causes host epithelial cell cytoskeletal rearrangements mediated by the translocation and tyrosine phosphorylation of an outer-membrane protein, CagA, and by the vacuolating cytotoxin, VacA. However, the mechanisms by which H. pylori mediates cytoskeletal rearrangements in infected host cells need to be more clearly defined.

Helicobacter pylori infection interferes with epithelial Stat6-mediated interleukin-4 signal transduction independent of cagA, cagE, or VacA.

Helicobacter pylori is a bacterial pathogen evolved to chronically colonize the gastric epithelium, evade immune clearance by the host, and cause gastritis, peptic ulcers, and even gastric malignancies in some infected humans. In view of the known ability of this bacterium to manipulate gastric epithelial cell signal transduction cascades, we determined the effects of H. pylori infection on epithelial IL-4-Stat6 signal transduction.

Helicobacter pylori activates Toll-like receptor 4 expression in gastrointestinal epithelial cells.

Helicobacter pylori activates the transcription factor NF-kappaB, leading to proinflammatory cytokine production by gastric epithelial cells. However, the receptors for the initial bacterial interaction with host cells which activate downstream signaling events have not been completely defined. Recently, it has been shown that microbial components activate Toll-like receptors (TLRs), thereby leading to AP-1- and NF-kappaB-dependent transcription and resulting in the production of proinflammatory cytokines.

Enterohemorrhagic Escherichia coli O157:H7 disrupts Stat1-mediated gamma interferon signal transduction in epithelial cells.

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is a clinically important bacterial enteropathogen that manipulates a variety of host cell signal transduction cascades to establish infection. However, the effect of EHEC O157:H7 on Jak/Stat signaling is unknown. To define the effect of EHEC infection on epithelial gamma interferon (IFN-gamma)-Stat1 signaling, human T84 and HEp-2 epithelial cells were infected with EHEC O157:H7 and then stimulated with recombinant human IFN-gamma.

Chronic stress induces mast cell-dependent bacterial adherence and initiates mucosal inflammation in rat intestine.

Background & Aims: Chronic psychological stress is an important factor in relapses of intestinal disorders, but it remains unclear if stress can induce primary gut inflammation in a previously healthy host.

Methods: Mast cell-deficient (Ws/Ws) rats and wild-type control (+/+) rats were submitted to water avoidance stress or sham stress (1 h/day) for 10 consecutive days, as a model of ongoing life stress.

Results: Both rat groups had similar systemic responses to stress, as assessed by changes in weight, corticosterone levels, and defecation.

Escherichia coli shiga-like toxins induce apoptosis and cleavage of poly(ADP-ribose) polymerase via in vitro activation of caspases.

Shiga-like toxin-producing Escherichia coli causes hemorrhagic colitis and hemolytic-uremic syndrome in association with the production of Shiga-like toxins, which induce cell death via either necrosis or apoptosis. However, the abilities of different Shiga-like toxins to trigger apoptosis and the sequence of intracellular signaling events mediating the death of epithelial cells have not been completely defined. Fluorescent dye staining with acridine orange and ethidium bromide showed that Shiga-like toxin 1 (Stx1) induced apoptosis of HEp-2 cells in a dose- and time-dependent manner.