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The article offers information on Latino Outdoors, a nonprofit organization working to inspire Latinos to protect nature, and its founder José González. Topics discussed include the González's rural life in Mexico; the work of Alicia Cruz, who worked for the Boy Scouts, with Latino Outdoors; and the popularity of the organization with immigrant families in the U.S.

In this work the reason of the cracks found in SAE 1018 carbon steel pipelines used for potable water supply is determined. In order to accomplish it, some techniques of microanalysis using X-rays (SEM: Scanning Electron Microscopy) over some samples of faulty and normal pipes as well as the Digital Image Processing (DIP) of its microphotographs captured by means of SEM, were used. The obtained results prove that the low quality of the raw material and the steel manufacturing process were the reason of the cracks observed in the SAE 1018 carbon steel pipelines.

ABSTRACTGastric epithelial cells (GECs) express the class II major histocompatibility complex (MHC) and costimulatory molecules, enabling them to act as antigen-presenting cells (APCs) and affect local T cell responses. During Helicobacter pyloriinfection, GECs respond by releasing proinflammatory cytokines and by increasing the surface expression of immunologically relevant receptors, including class II MHC. The CD4+T cell response during H. pyloriinfection is skewed toward a Th1 response, but these cells remain hyporesponsive. Activated T cells show decreased proliferation during H. pyloriinfection, and CD4+CD25+FoxP3+regulatory T cells (Tregs) are present at the site of infection. In this study, we examined the mechanisms surrounding the CD4+T cell responses during H. pyloriinfection and found that transforming growth factor β (TGF-β) plays a major role in these responses. GECs produced TGF-β1 and TGF-β2 in response to infection. Activated CD4+T cells in culture with H. pylori-treated GECs were decreased in proliferation but increased upon neutralization of TGF-β. Naïve CD4+T cell development into Tregs was also enhanced in the presence of GEC-derived TGF-β. Herein, we demonstrate a role for GEC-produced TGF-β in the inhibition of CD4+T cell responses seen during H. pyloriinfection.

ABSTRACTWhile a link between Helicobacter pyloriexposure and gastric cancer has been established, the underlying mechanisms remain unclear. H. pyloriinduces a chronic inflammatory response in infected individuals. A link between chronic inflammation and carcinogenesis has long been suggested but never elucidated. Epidermal growth factor receptor (EGFR) signaling plays an important role in both proinflammatory and procarcinogenic mechanisms and is upregulated on gastric epithelial cells (GECs) during H. pyloriexposure. The aim of this study was to examine the effects of two important proinflammatory cytokines released during H. pyloriinfection, macrophage migration inhibitory factor (MIF) and interleukin-8 (IL-8), on the expression and transactivation of EGFR and on the proliferation of GECs during H. pyloriexposure. The expression of EGFR by GECs was increased by exposure to either H. pylori, recombinant MIF, or recombinant IL-8. However, cagpathogenicity island knockout strains of H. pylorihad very little effect on expression. MIF and IL-8 also induced phosphorylation of EGFR, signaling events, and proliferation during H. pyloriexposure, all of which were decreased when they were neutralized by these cytokines or were blocked from their receptors. The overall role of EGFR in these responses to H. pyloriexposure was assessed by knocking down EGFR expression by small interfering RNA.

During Helicobacter pylori infection, T cells are recruited to the gastric mucosa, but the host T-cell response is not sufficient to clear the infection. Some of the recruited T cells respond in a polarized manner to a Th1 response, while others become anergic. We have previously shown that T-cell anergy may be induced during infection by the interaction of T cells with B7-H1, which is up-regulated on the gastric epithelium during H. pylori infection. Recently, regulatory T (Treg) cells with a CD4+CD25highFoxP3+phenotype were found at an increased frequency in the gastric mucosa of biopsy specimens from H. pylori-infected patients. While Treg cells are important in maintaining tolerance, they can also suppress immune responses during infection. In this study, we examined the induction of the Treg phenotype when naïve T cells were incubated with gastric epithelial cells exposed to H. pylori. The frequency of this phenotype was markedly decreased when B7-H1 was blocked with monoclonal antibodies or its expression was blocked with small interfering RNA. The functional role of these Treg cells was assessed in proliferation assays when the cells were cocultured with activated T cells, which effectively decreased proliferation of the cells.

ABSTRACTDuring Helicobacter pyloriinfection, T cells are recruited to the gastric mucosa, but the host T-cell response is not sufficient to clear the infection. Some of the recruited T cells respond in a polarized manner to a Th1 response, while others become anergic. We have previously shown that T-cell anergy may be induced during infection by the interaction of T cells with B7-H1, which is up-regulated on the gastric epithelium during H. pyloriinfection. Recently, regulatory T (Treg) cells with a CD4+CD25highFoxP3+phenotype were found at an increased frequency in the gastric mucosa of biopsy specimens from H. pylori-infected patients. While Treg cells are important in maintaining tolerance, they can also suppress immune responses during infection. In this study, we examined the induction of the Treg phenotype when naïve T cells were incubated with gastric epithelial cells exposed to H. pylori. The frequency of this phenotype was markedly decreased when B7-H1 was blocked with monoclonal antibodies or its expression was blocked with small interfering RNA. The functional role of these Treg cells was assessed in proliferation assays when the cells were cocultured with activated T cells, which effectively decreased proliferation of the cells.

ABSTRACTHelicobacter pyloriinfection is associated with altered gastric epithelial cell turnover. To evaluate the role of oxidative stress in cell death, gastric epithelial cells were exposed to various strains of H. pylori, inflammatory cytokines, and hydrogen peroxide in the absence or presence of antioxidant agents. Increased intracellular reactive oxygen species (ROS) were detected using a redox-sensitive fluorescent dye, a cytochrome creduction assay, and measurements of glutathione. Apoptosis was evaluated by detecting DNA fragmentation and caspase activation. Infection with H. pylorior exposure of epithelial cells to hydrogen peroxide resulted in apoptosis and a dose-dependent increase in ROS generation that was enhanced by pretreatment with inflammatory cytokines. Basal levels of ROS were greater in epithelial cells isolated from gastric mucosal biopsy specimens from H. pylori-infected subjects than in cells from uninfected individuals. H. pyloristrains bearing the cagpathogenicity island (PAI) induced higher levels of intracellular oxygen metabolites than isogenic cagPAI-deficient mutants. H. pyloriinfection and hydrogen peroxide exposure resulted in similar patterns of caspase 3 and 8 activation. Antioxidants inhibited both ROS generation and DNA fragmentation by H. pylori. These results indicate that bacterial factors and the host inflammatory response confer oxidative stress to the gastric epithelium during H. pyloriinfection that may lead to apoptosis.

ABSTRACTThe pathogenesis associated with Helicobacter pyloriinfection is the result of both bacterial factors and the host response. We have previously shown that H. pyloribinds to CD74 on gastric epithelial cells. In this study, we sought to identify the bacterial protein responsible for this interaction. H. pyloriurease from a pool of bacterial surface proteins was found to coprecipitate with CD74. To determine how urease binds to CD74, we used recombinant urease A and B subunits. Recombinant urease B was found to bind directly to CD74 in immunoprecipitation and flow cytometry studies. By utilizing both recombinant urease subunits and urease B knockout bacteria, the urease B-CD74 interaction was shown to induce NF-κB activation and interleukin-8 (IL-8) production. This response was decreased by blocking CD74 with monoclonal antibodies. Further confirmation of the interaction of urease B with CD74 was obtained using a fibroblast cell line transfected with CD74 that also responded with NF-κB activation and IL-8 production. The binding of the H. pyloriurease B subunit to CD74 expressed on gastric epithelial cells presents a novel insight into a previously unrecognized H. pyloriinteraction that may contribute to the proinflammatory immune response seen during infection.

Abstract: In this paper the development of a smart imaging core following a SystemC-based design flow is presented. The smart imaging core integrates an ARM processor and two specific hardware blocks for image processing: a smart imaging coprocessor and a motion estimation coprocessor. A SystemC-based design flow is applied, comprising the design, synthesis and verification and synthesis of the two coprocessors, as well as the development and integration of the embedded software on the smart imaging core. The two coprocessors are successfully modeled and refined from C/C++-based algorithmic descriptions down to architecture reference models using SystemC and TLM concepts. For the RTL implementation of the coprocessor hardware high-level synthesis tools are used. The applied SystemC-based design flow enabled the iterative refinement of the architecture towards an optimal RTL implementation. Furthermore, the use of SystemC TLM supports the integration of fast functional models of the coprocessors on a virtual prototype platform of the target architecture. This virtual prototype is beneficially used during the embedded software development phase.

ABSTRACTThe pathogenesis associated with Helicobacter pyloriinfection requires consistent contact with the gastric epithelium. Although several cell surface receptors have been suggested to play a role in adhesion, the bacterium-host interactions that elicit host responses are not well defined. This study investigated the interaction of H. pyloriwith the class II major histocompatibility complex (MHC)-associated invariant chain (Ii; CD74), which was found to be highly expressed by gastric epithelial cells. Bacterial binding was increased when CD74 surface expression was increased by gamma interferon (IFN-γ) treatment or by fibroblast cells transfected with CD74, while binding was decreased by CD74 blocking antibodies, enzyme cleavage of CD74, and CD74-coated bacteria. H. pyloriwas also shown to bind directly to affinity-purified CD74 in the absence of class II MHC. Cross-linking of CD74 and the engagement of CD74 were verified to stimulate IL-8 production by unrelated cell lines expressing CD74 in the absence of class II MHC. Increased CD74 expression by cells increased IL-8 production in response to H. pylori, and agents that block CD74 decreased these responses. The binding of H. pylorito CD74 presents a novel insight into an initial interaction of H. pyloriwith the gastric epithelium that leads to upregulation of inflammatory responses.

The synthesis and characterisation of novel bis salen complexes, M(salenH2), N,N′-bis-[5(1,1,3,3-tetramethyl- butyl)salicylidene]-1,2-diaminoethane complexes, (M = Ni or Cu), and the corresponding less studied, bis-tetrahydrosalen complexes, M[H2(salenH2)], N,N′-bis-[2-hydroxy-5(1,1,3,3-tetramethylbutyl)benzyl]-1,2-diaminoethane complexes, (M = Ni or Cu), with a highly branched substitution pattern at C-5 of the benzene ring is described. The Schiff bases behave as dibasic tetradentate ligands. The tetrahydrosalen complexes show structural properties, chemical and thermal behaviour which is different from those of the corresponding salen complexes. The melting points and decomposition temperatures of these complexes were determined by d.s.c. and t.g.a.

The role for Helicobacter pyloriin the pathogenesis of disease provides the conundrum that only a subset of subjects infected with H. pyloriwill ever develop peptic ulcer or gastric cancer. Thus, variation in strain as well as environmental or host factors converge in the gastroduodenal milieu and control the final outcome of infection. The host immune and inflammatory response is emerging as an important element in the pathogenesis of these gastric diseases. The ideal host response provides protection to clear an infection without causing excessive amounts of inflammation that could compromise the integrity and function of host cells. This review will cover four main questions: (1) What are the mucosal immune/inflammatory responses that confer protection without damaging the host? (2) How do the gastric immune responses during infection with H. pyloridiffer from this ideal scenario? (3) Do these responses contribute to autoimmune-mediated damage to gastric tissue? (4) Can immunomodulation through vaccination enhance protective, nondestructive responses that prevent or treat infection or, at least, attenuate inflammation?

Helicobacter pylori infection is associated with gastric epithelial damage, including apoptosis, ulceration, and cancer. Although bacterial factors and the host response are believed to contribute to gastric disease, no receptor has been identified that explains how the bacteria attach and signal the host cell to undergo apoptosis. Using H. pylori as “bait” to capture receptor proteins in solubilized membranes of gastric epithelial cells, class II major histocompatibility complex (MHC) molecules were identified as a possible receptor. Signaling through class II MHC molecules leading to the induction of apoptosis was confirmed using cross-linking IgM antibodies to surface class II MHC molecules. Moreover, binding of H. pylori and the induction of apoptosis were inhibited by antibodies recognizing class II MHC. Since type 1 T helper cells are present during infection and produce interferon (IFN)-γ, which increases class II MHC expression, gastric epithelial cell lines were exposed to H. pylori in the presence or absence of IFN-γ. IFN-γ increased the attachment of the bacteria as well as the induction of apoptosis in gastric epithelial cells. In contrast to MHC II–negative cell lines, H. pylori induced apoptosis in cells expressing class II MHC molecules constitutively or after gene transfection. These data describe a novel receptor for H. pylori and provide a mechanism by which bacteria and the host response interact in the pathogenesis of gastric epithelial cell damage.

Graft-versus-host disease (GVHD) is a major obstacle to successful bone marrow transplantation. The role of interferon (IFN) in GVHD is currently unclear. We have previously shown that interferon (IFN) is produced in vitro by alloantigen-stimulated murine bone marrow cells. This study was initiated to examine whether IFN production occurs in vivo during GVHD. Lethally irradiated mice were given bone marrow (107) and/or spleen cells (2×107) from either allogeneic or syngeneic mice. Mice given allogeneic spleen cells or bone marrow and spleen cells showed signs of GVHD within 10 days and usually died within 20 days of transplantation. Mice undergoing GVHD were found to have significant levels of IFN activity in their sera. Serum IFN was detected early (day 3) after transplantation with optimal IFN activity (∼80 units) occurring at 5–6 days. The IFN activity present in the sera obtained from mice with GVHD was identified as IFN α/β by using specific antisera against IFN α/β and IFNγ. In contrast, irradiated mice given T-cell-depleted allogeneic bone marrow and spleen cells failed to develop GVHD and had no detectable serum IFN activity. Irradiated mice given syngeneic bone marrow and spleen cells or only allogeneic bone marrow cells did not develop GVHD and did not produce detectable IFN activity in their sera. These results show that serum IFN activity correlates well with GVHD and opens for speculation the possibility that IFN may be involved in the pathogenesis associated with GVHD.