Application of protective cultures against Listeria monocytogenes and Campylobacter jejuni in chicken products packaged under modified atmosphere

To control the growth, or reduce the numbers, of food pathogens such as Listeria monocytogenes and Campylobacter jejuni in chicken products packaged under modified atmosphere (MAP), the effectiveness of protective cultures was evaluated in this study. Leuconostoc pseudomesenteroides PCK18 reduced the counts of L. monocytogenes by 1.22 log cfu/g in chicken burgers under MAP after 24 d. Furthermore, a reduction of 1.16 log cfu/g in C. jejuni together with a delay in the growth of lactic acid bacteria was obtained in chicken legs inoculated with Bifidobacterium longum ssp. longum PCB133 and packaged under MAP after 9 d. The combination and concentration of gases in the MAP doubled the products’ shelf-life in comparison with air-packaged samples in both experiments. In conclusion, this study has shown the effectiveness of 2 protective culture strains against 2 foodborne pathogens, resulting in safer products with a longer shelf-life.This study forms part of the projects FOOD-CT-2005-007081 (PathogenCombat), supported by the European Commission through the Sixth Framework Programme for Research and Development (Brussels. Belgium), and BU264A11-2, supported by the Consejería de Educación, Junta de Castilla y León (Valladolid. Spain

Attenuation of AMPK signaling by ROQUIN promotes T follicular helper cell formation

T follicular helper cells (Tfh) are critical for the longevity and quality of antibody-mediated protection against infection. Yet few signaling pathways have been identified to be unique solely to Tfh development. ROQUIN is a post-transcriptional repressor of T cells, acting through its ROQ domain to destabilize mRNA targets important for Th1, Th17, and Tfh biology. Here, we report that ROQUIN has a paradoxical function on Tfh differentiation mediated by its RING domain: mice with a T cell-specific deletion of the ROQUIN RING domain have unchanged Th1, Th2, Th17, and Tregs during a T-dependent response but show a profoundly defective antigen-specific Tfh compartment. ROQUIN RING signaling directly antagonized the catalytic α1 subunit of adenosine monophosphate-activated protein kinase (AMPK), a central stress-responsive regulator of cellular metabolism and mTOR signaling, which is known to facilitate T-dependent humoral immunity. We therefore unexpectedly uncover a ROQUIN–AMPK metabolic signaling nexus essential for selectively promoting Tfh responses

Diseño e implementación de un controlador de ratón gestual para Microsoft Windows con Kinect - Touchless Gesture User Interface

El dispositivo Microsoft Kinect for Windows y similares, han introducido en el mundo del PC una nueva forma de interacción denominada “Touchless Gesture User Interface” o TGUI (Interfaz de Usuario por Gestos sin Contacto) [Gentile et al. 2011]. Se trata de una tecnología novedosa en proceso de evolución. La tecnología de Kinect detecta la presencia de un usuario y monitoriza la posición en el espacio de sus articulaciones principales. Esta información permite desarrollar aplicaciones que posibiliten interactuar al usuario con una computadora mediante gestos y sin la necesidad de estar en contacto con periférico alguno. Desde la invención del periférico ratón en los años 60, resulta curioso que con la frenética evolución que ha experimentado el mundo de la informática en todos estos años, este dispositivo no haya sufrido cambios significativos o no haya sido incluso sustituido por otro periférico. En este proyecto se ha abordado el reto de desarrollar un controlador de ratón gestual para Windows utilizando Microsoft Kinect, de tal forma que se sustituya el uso del típico ratón y sea el propio usuario el que actúe como controlador mediante gestos y movimientos de sus manos. El resultado es llamativo y aporta numerosas mejoras y novedades frente a aplicaciones similares, aunque deja en evidencia algunas de las limitaciones de la tecnología implementada por Kinect a día de hoy. Es de esperar que cuando evolucione su tecnología, su uso se convierta en cotidiano

Diseño e implementación de un controlador de ratón gestual para Microsoft Windows con Kinect - Touchless Gesture User Interface

El dispositivo Microsoft Kinect for Windows y similares, han introducido en el mundo del PC una nueva forma de interacción denominada “Touchless Gesture User Interface” o TGUI (Interfaz de Usuario por Gestos sin Contacto) [Gentile et al. 2011]. Se trata de una tecnología novedosa en proceso de evolución. La tecnología de Kinect detecta la presencia de un usuario y monitoriza la posición en el espacio de sus articulaciones principales. Esta información permite desarrollar aplicaciones que posibiliten interactuar al usuario con una computadora mediante gestos y sin la necesidad de estar en contacto con periférico alguno. Desde la invención del periférico ratón en los años 60, resulta curioso que con la frenética evolución que ha experimentado el mundo de la informática en todos estos años, este dispositivo no haya sufrido cambios significativos o no haya sido incluso sustituido por otro periférico. En este proyecto se ha abordado el reto de desarrollar un controlador de ratón gestual para Windows utilizando Microsoft Kinect, de tal forma que se sustituya el uso del típico ratón y sea el propio usuario el que actúe como controlador mediante gestos y movimientos de sus manos. El resultado es llamativo y aporta numerosas mejoras y novedades frente a aplicaciones similares, aunque deja en evidencia algunas de las limitaciones de la tecnología implementada por Kinect a día de hoy. Es de esperar que cuando evolucione su tecnología, su uso se convierta en cotidiano

Orthogonal Polynomials and their Applications

The Segovia meeting set out to stimulate an intensive exchange of ideas between experts in the area of orthogonal polynomials and its applications, to present recent research results and to reinforce the scientific and human relations among the increasingly international community working in orthogonal polynomials. This volume contains original research papers as well as survey papers about fundamental questions in the field (Nevai, Rakhmanov & López) and its relationship with other fields such as group theory (Koornwinder), Padé approximation (Brezinski), differential equations (Krall, Littlejohn) and numerical methods (Rivlin)

Interferon-y excess leads to pathogenic accumulation of follicular helper T cells and germinal centers

Free to read at publisher's site. Overactivity of the germinal center (GC) pathway resulting from accumulation of follicular helper T (Tfh) cells causes autoimmunity, underscoring the need to understand the factors that control Tfh cell homeostasis. Here we have identifed posttranscriptional repression of interferon-gamma (Ifng) mRNA as a mechanism to limit Tfh cell formation. By using the sanroque lupus model, we have shown that decreased Ifng mRNA decay caused excessive IFN-gamma signaling in T cells and led to accumulation of Tfh cells, spontaneous GC, autoantibody formation, and nephritis. Unlike ICOS and T-bet deficiency that failed to rescue several autoimmune manifestations, interferon-gamma receptor (IFN-gammaR) deficiency prevented lupus development. IFN-gamma blockade reduced Tfh cells and autoantibodies, demonstrating that IFN-gamma overproduction was required to sustain lupus-associated pathology. Increased IFN-gammaR signaling caused Bcl-6 overexpression in Tfh cells and their precursors. This link between IFN-gamma and aberrant Tfh cell formation provides a rationale for IFN-gamma blockade in lupus patients with an overactive Tfh cell-associated pathway

Interferon-y excess leads to pathogenic accumulation of follicular helper T cells and germinal centers

Overactivity of the germinal center (GC) pathway resulting from accumulation of follicular helper T (Tfh) cells causes autoimmunity, underscoring the need to understand the factors that control Tfh cell homeostasis. Here we have identifed posttranscriptional repression of interferon-y (Ifng) mRNA as a mechanism to limit Tfh cell formation. By using the sanroque lupus model, we have shown that decreased Ifng mRNA decay caused excessive IFN-g signaling in T cells and led to accumulation of Tfh cells, spontaneous GC, autoantibody formation, and nephritis. Unlike ICOS and T-bet deficiency that failed to rescue several autoimmune manifestations, interferon-y receptor (IFN-gR) deficiency prevented lupus development. IFN-y blockade reduced Tfh cells and autoantibodies, demonstrating that IFN-y overproduction was required to sustain lupus-associated pathology. Increased IFN-yR signaling caused Bcl-6 overexpression in Tfh cells and their precursors. This link between IFN-y and aberrant Tfh cell formation provides a rationale for IFN-y blockade in lupus patients with an overactive Tfh cell-associated pathway.We thank C. Gillespie for help in the preparation of electron microscopy slides, C.G.V. is supported by an Elizabeth Blackburn NHMRC fellowship. This work was funded by NHMRC program and project grants to C.G.V

Heterozygosity for Roquinsan leads to angioimmunoblastic T-cell lymphoma-like tumors in mice

Angioimmunoblastic T-cell lymphoma (AITL) is the second most common peripheral T-cell lymphoma with unusual clinical and pathologic features and a poor prognosis despite intensive chemotherapy. Recent studies have suggested AITL derives from follicular helper T (TFH) cells, but the causative molecular pathways remain largely unknown. Here we show that approximately 50% of mice heterozygous for the “san” allele of Roquin develop tumors accompanied by hypergammaglobulinemia by 6 months of age. Affected lymph nodes displayed the histologic features diagnostic of AITL, except for the presence of expanded FDC networks. Accumulation of TFH cells preceded tumor development, and clonal rearrangements in the TCR-B genes were present in most tumors. Furthermore, TFH cells exhibited increased clonality compared with non-TFH cells from the same lymph nodes, even in the absence of tumors. Genetic manipulations that prevent TFH development, such as deletion of ICOS, CD28, and SAP, partially or completely abrogated tumor development, confirming a TFH-derived origin. Roquinsan/+ mice emerge as a useful model to investigate the molecular pathogenesis of AITL and for preclinical testing of therapies aimed at targeting dysregulated TFH cells or their consequences.This work was supported by a Viertel Senior Medical Research Fellowship and National Health and Medical Research Council program and project grants (C.G.V.) and a National Health and Medical Research Council Overseas Biomedical Fellowship (J.I.E.)