Gene expression in gastric biopsies from patients infected with Helicobacter pylori.

Background: Helicobacter pylori infection has protean effects on gene expression in the host gastric mucosa, which have been investigated by gene chip analysis in vitro. In this study the effects of H. pylori infection on host gene expression in the gastric antral mucosa in patients were examined.

Altered phenotype of dextran sulfate sodium colitis in interferon regulatory factor-1 knock-out mice.

Background And Aims: Interferon regulatory factor-1 (IRF-1) is a transcription factor with antiviral, proinflammatory and tumor suppressor properties. We examined the role of IRF-1 in dextran sulfate sodium colitis, a murine model of inflammatory bowel disease, to determine if absence of the gene would protect against colitis.

Methods: C57BL/6J mice with a targeted disruption of IRF-1 and wild-type C57BL/6J controls received five 7-day cycles of 2% dextran sulfate sodium alternating with five 7-day cycles of water.

Gene expression in mononuclear cells from patients with inflammatory bowel disease.

Objectives: Discovery of Nod2 as the inflammatory bowel disease 1 (IBD1) susceptibility gene has brought to light the significance of mononuclear cells in inflammatory bowel disease pathogenesis. The purpose of this study was to examine changes in gene expression in peripheral blood mononuclear cells in patients with untreated Crohn's disease (CD) and ulcerative colitis (UC) as compared to patients with other inflammatory gastrointestinal disorders and to healthy controls.

Methods: We used a 2400 gene cDNA glass slide array (MICROMAX) to examine gene expression in peripheral blood mononuclear cells from seven patients with Crohn's disease, five patients with ulcerative colitis, 10 patients with other inflammatory gastrointestinal disorders, and 22 age- and sex-matched controls.

Association of the T allele of an intronic single nucleotide polymorphism in the colony stimulating factor 1 receptor with Crohn's disease: a case-control study.

BACKGROUND: Polymorphisms in several genes (NOD2, MDR1, SLC22A4) have been associated with susceptibility to Crohn's disease. Identification of the remaining Crohn's susceptibility genes is essential for the development of disease-specific targets for immunotherapy. Using gene expression analysis, we identified a differentially expressed gene on 5q33, the colony stimulating factor 1 receptor (CSF1R) gene, and hypothesized that it is a Crohn's susceptibility gene.

Use of infliximab in pediatric patients with inflammatory bowel disease.

Background: The concentration of tumor necrosis factor, a proinflammatory cytokine, is increased in the gastrointestinal mucosa of patents with active Crohn's disease (CD) and ulcerative colitis (UC). Neutralization of tumor necrosis factor decreases the mucosal inflammatory response of adults with CD. Little information is available on the use of monoclonal antibody to tumor necrosis factor (infliximab) in children and adolescents with CD or UC.

Syndrome of hypokalemic metabolic alkalosis and hypomagnesemia associated with gentamicin therapy: case reports.

Nephrotoxicity, as evidenced by renal insufficiency is a well-known consequence of gentamicin therapy. We report two patients with gentamicin-induced syndrome of hypokalemic metabolic alkalosis and hypomagnesemia. Both had complete recovery of renal tubular function after cessation of antibiotic therapy.

Detection of interferon regulatory factor-1 in lamina propria mononuclear cells in Crohn's disease.

Background: The transcription factor, interferon regulatory factor (IRF)-1, is stimulated by interferon-gamma and regulates the expression of several genes implicated in the pathogenesis of inflammatory bowel disease, including interleukin-6, major histocompatibility complex class II molecules, and inducible nitric oxide synthase. Interferon regulatory factor-1 also stimulates naive CD4+ T-cells to differentiate into T-helper-1 cells, the T-cell subset that appears to be upregulated in Crohn's disease. The purpose of this study was to examine the expression of IRF-1 in the nuclei of lamina propria mononuclear cells in situ in colonoscopic biopsy specimens from pediatric patients with Crohn's disease, in patients with ulcerative colitis, and in control patients with no histopathologic abnormalities.

Antiinflammatory actions of cat's claw: the role of NF-kappaB.

Background: Uncaria tomentosa is a vine commonly known as cat's claw or 'uña de gato' (UG) and is used in traditional Peruvian medicine for the treatment of a wide range of health problems, particularly digestive complaints and arthritis.

Purpose: The aim of this study was to determine the proposed anti-inflammatory properties of cat's claw. Specifically: (i) does a bark extract of cat's claw protect against oxidant-induced stress in vitro, and (ii) to determine if UG modifies transcriptionally regulated events.

Localization of inducible nitric oxide synthase mRNA in inflamed gastrointestinal mucosa by in situ reverse transcriptase-polymerase chain reaction.

Immunohistochemistry has been critical in determining the tissue localization of inducible nitric oxide synthase (iNOS). However, this technique suffers from nonspecific staining which may lead to false-positive results and the failure of antisera to recognize iNOS from different species. We developed a technique to determine the localization of iNOS mRNA, as opposed to protein, in tissue sections using an in situ RT-PCR (IS RT-PCR) technique.

Gastroesophageal reflux and Nissen fundoplication following percutaneous endoscopic gastrostomy in children.

Background: Abnormal gastroesophageal reflux after percutaneous endoscopic gastrostomy is a serious problem in neurologically impaired children. Protective fundoplication has been advocated. Whether esophageal pH monitoring before percutaneous endoscopic gastrostomy will predict later problems with gastroesophageal reflux is unclear.

Genistein and gut inflammation: role of nitric oxide.

Genistein, a principal soy isoflavone, has been identified as a protein kinase inhibitor that possesses immunosuppressive and anti-inflammatory properties. The aim of the study was to determine if genistein modified chronic ileitis in guinea pigs induced by the hapten trinitrobenzene sulfonic acid (TNBS), and the activity index of cultured macrophages (RAW 264.7 cells) stimulated with lipopolysaccharide (LPS).

Peroxynitrite-induced apoptosis in human intestinal epithelial cells is attenuated by mesalamine.

Background & Aims: Peroxynitrite (PN), a potent oxidant, has been implicated in the pathogenesis of gut inflammation and epithelial cell apoptosis. The aim of this study was to investigate mesalamine, a standard therapy for inflammatory bowel disease, to see if it attenuates PN-induced cytotoxicity in human intestinal epithelial cells and if mesalamine directly interacts with PN or its precursor, nitric oxide.

Methods: T84 and HT29 cells were divided in several protocols: mesalamine was administered 2 hours before, simultaneously, or 30 minutes after PN.

Inhibitors of nuclear factor kappa B cause apoptosis in cultured macrophages.

The precise role of the transcription factor nuclear factor kappa B (NF- kappaB) in the regulation of cell survival and cell death is still unresolved and may depend on cell type and position in the cell cycle. The aim of this study was to determine if three pharmacologic inhibitors of NF-kappaB, pyrrolidine dithiocarbamate, N-tosyl-L-lysl chloromethyl ketone and calpain I inhibitor, induce apoptosis in a murine macrophage cell line (RAW 264.7) at doses similar to those required for NF-kappaB inhibition.

Peroxynitrite-induced apoptosis in T84 and RAW 264.7 cells: attenuation by L-ascorbic acid.

The free radicals nitric oxide and superoxide react to form peroxynitrite (ONOO-), a potent cytotoxic oxidant. This study was designed to evaluate whether addition of L-Ascorbic acid (AsC) into the culture medium decreases peroxynitrite-induced apoptosis in human intestinal epithelial (T84) and murine macrophage (RAW 264.7) cell lines.

Nutrition and HIV infection in children.

HIV infection has profound effects on a patient's nutritional status because it can modulate appetite, nutrient absorption and basal metabolic rate. In addition, HIV infection can lead to the depletion of a variety of vitamins and micronutrients including vitamins A, D, B2, B6, B12, L-carnitine, iron, zinc and selenium. This review article summarizes existing data regarding nutritional defects in HIV-infected patients and the results of clinical studies addressing the effects of nutritional supplementation in infected patients.

Inducible nitric oxide synthase, nitrotyrosine, and apoptosis in Helicobacter pylori gastritis: effect of antibiotics and antioxidants.

Helicobacter pylori infection is a known risk factor for gastric cancer. We hypothesized that H. pylori infection would lead to the sustained production of the reactive nitrogen species nitric oxide and peroxynitrite as part of the host immune response.

Neonatal gastrointestinal mucosal immunity.

The gastrointestinal mucosal immune system is a complex system with multiple interacting cells, which express different markers and elaborate a variety of mediators in response to noxious stimuli and pathogens. At birth this system is quite immature, putting the newborn mammal at risk for a variety of infectious and noninfectious diseases. With age and antigenic stimulation, maturation occurs and intestinal host defense then functions quite effectively to protect the host from ingested noxious substances and microorganisms.

Epidemiology of congenital heart disease in Louisiana: an association between race and sex and the prevalence of specific cardiac malformations.

We hypothesized that susceptibility to the genetic and environmental factors that disrupt cardiac development is associated with race and sex. To evaluate this hypothesis, we asked whether the prevalence of specific cardiac malformations differs by race and sex. We attempted to include all infants born alive in the State of Louisiana from January 1, 1988, through December 31, 1989, and diagnosed by echocardiography, catheterization and/or autopsy within a year of birth as having one of ten specific cardiac malformations.