bluuebunny/crossref_metadata_2025_split huggingface dataset:
Médiatisation de l' économie et fabrication de la popularité du président français (2007-2010)
Authors: Gerstlé Jacques , François Abel 
Published: May 2011

Résumé La popularité présidentielle dépend-elle davantage de l’état de l’économie que de l’état médiatisé de l’économie ? Après l’examen des facteurs de la popularité de l’exécutif est spécifié un modèle d’influence de l’économie sur la popularité avec des indicateurs sondagiers, des mesures de bruit médiatique et des résultats de l’économie réelle. L’information économique n’affecte que de manière indirecte la popularité à travers les variables de l’économie « subjective » (perception de l’économie, préoccupations). Par ailleurs, la préférence partisane conditionne largement le soutien à la politique économique très liée à la popularité présidentielle. Le déclenchement de la crise économique ponctue l’évolution de la popularité de N. Sarkozy. Au total, les vicissitudes de la popularité présidentielle semblent bien liées à l’« influence impersonnelle » de l’économie médiatisée.
Aim2 Deficiency in Mice Suppresses the Expression of the Inhibitory Fcγ Receptor (FcγRIIB) through the Induction of the IFN-Inducible p202, a Lupus Susceptibility Protein
Authors: Panchanathan Ravichandran , Shen Hui , Duan Xin , Rathinam Vijay A. K. , Erickson Loren D. , Fitzgerald Katherine A. , Choubey Divaker 
Published: May 2011

Abstract
Murine Aim2 and Ifi202 genes (encoding for the Aim2 and p202 proteins) are members of the IFN-inducible Ifi200 gene family. The Aim2 deficiency in mice activates IFN signaling and stimulates the expression of the lupus susceptibility gene, the Ifi202, located within the NZB autoimmunity 2 (Nba2) interval. Given that the deficiency in the expression of the Fcgr2b gene (encoding for the inhibitory FcγRIIB receptor) is associated with increased lupus susceptibility in mice, we investigated whether the Aim2 protein could regulate the expression of Fcgr2b gene. In this article, we report that Aim2 deficiency in mice suppresses the expression of the FcγRIIB receptor. Interestingly, the Fcgr2b-deficient cells expressed increased levels of the IFN-β, activated IFN signaling, and expressed reduced levels of the Aim2 protein. Treatment of splenic cells with IFN-α or -γ reduced levels of the FcγRIIB mRNA and protein and also decreased the activity of the FcγRIIB p(−729/+585) Luc reporter. Moreover, levels of the FcγRIIB receptor were significantly higher in the Stat1-deficient splenic cells than in the wild-type cells. Accordingly, increased expression of IFN-β in lupus-prone B6.Nba2-ABC mice, as compared with non–lupus-prone C57BL/6 (B6) or B6.Nba2-C mice, was associated with reduced expression of the FcγRIIB receptor. Notably, overexpression of the p202 protein in cells decreased the expression of the Aim2 gene, activated the IFN response, and suppressed the expression of the Fcgr2b gene. These observations demonstrate that the expression of Aim2 protein is required to maintain the expression of the Fcgr2b gene and also predict epistatic interactions between the Ifi200 genes and the Fcgr2b gene within the Nba2 interval.
Novel TGF-β Antagonist Inhibits Tumor Growth and Angiogenesis by Inducing IL-2 Receptor-Driven STAT1 Activation
Authors: Penafuerte Claudia , Bautista-Lopez Norma , Bouchentouf Manaf , Birman Elena , Forner Kathy , Galipeau Jacques 
Published: May 2011

Abstract
Carcinoma derived TGF-β acts as a potent pro-oncogenic factor and suppresses antitumor immunity. To antagonize TGF-β–mediated effects in tandem with a proinflammatory immune stimulus, we generated a chimeric protein borne of the fusion of IL-2 and the soluble extracellular domain of TGF-βR II (FIST). FIST acts as a decoy receptor trapping active TGF-β in solution and interacts with IL-2–responsive lymphoid cells, inducing a distinctive hyperactivation of STAT1 downstream of IL-2R, which in turn promotes SMAD7 overexpression. Consequently, FIST-stimulated lymphoid cells are resistant to TGF-β–mediated suppression and produce significant amounts of proinflammatory cytokines. STAT1 hyperactivation further induces significant secretion of angiostatic CXCL10. Moreover, FIST upregulates T-bet expression in NK cells promoting a potent Th1-mediated antitumor response. As a result, FIST stimulation completely inhibits pancreatic cancer (PANC02) and melanoma (B16) tumor growth in immunocompetent C57BL/6 mice. In addition, melanoma cells expressing FIST fail to form tumors in CD8−/−, CD4−/−, B cell-deficient (μMT), and beige mice, but not in NOD-SCID and Rag2/γc knockout mice, consistent with the pivotal role of FIST-responsive, cancer-killing NK cells in vivo. In summary, FIST constitutes a novel strategy of treating cancer that targets both the host’s angiogenic and innate immune response to malignant cells.
CD44 Reciprocally Regulates the Differentiation of Encephalitogenic Th1/Th17 and Th2/Regulatory T Cells through Epigenetic Modulation Involving DNA Methylation of Cytokine Gene Promoters, Thereby Controlling the Development of Experimental Autoimmune Encephalomyelitis
Authors: Guan Hongbing , Nagarkatti Prakash S. , Nagarkatti Mitzi 
Published: May 2011

Abstract
CD44 is expressed by a variety of cells, including glial and T cells. Furthermore, in the demyelinating lesions of multiple sclerosis, CD44 expression is chronically elevated. In this study, we demonstrate that targeted deletion of CD44 attenuated myelin oligodendrocyte glycoprotein peptide-induced experimental autoimmune encephalitomyelitis (EAE) through novel regulatory mechanisms affecting Th differentiation. Specifically, by developing chimeras and using adoptive transfer experiments, we noted that CD44 deficiency on CD4+ T cells, but not other cells, conferred protection against EAE induction. CD44 expression played a crucial role in Th differentiation, inasmuch as deletion of CD44 inhibited Th1/Th17 differentiation while simultaneously enhancing Th2/regulatory T cell differentiation. In contrast, expression of CD44 promoted Th1/Th17 differentiation. When osteopontin and hyaluronic acid, the two major ligands of CD44, were tested for their role in Th differentiation, osteopontin, but not hyaluronic acid, promoted Th1/Th17 differentiation. Furthermore, activation of CD44+ encephalitogenic T cells with myelin oligodendrocyte glycoprotein peptide led to demethylation at the ifnγ/il17a promoter region while displaying hypermethylation at the il4/foxp3 gene promoter. Interestingly, similar activation of CD44-deficient encephalitogenic T cells led to increased hypermethylation of ifnγ/il17a gene and marked demethylation of il4/foxp3 gene promoter. Together, these data suggested that signaling through CD44, in encephalitogenic T cells, plays a crucial role in the differentiation of Th cells through epigenetic regulation, specifically DNA methylation of Th1/Th17 and Th2 cytokine genes. The current study also suggests that molecular targeting of CD44 receptor to promote a switch from Th1/Th17 to Th2/regulatory T cell differentiation may provide a novel treatment modality against EAE.
IL-17A–Dependent CD4+CD25+ Regulatory T Cells Promote Immune Privilege of Corneal Allografts
Authors: Cunnusamy Khrishen , Chen Peter W. , Niederkorn Jerry Y. 
Published: May 2011

Abstract
IL-17A is a proinflammatory cytokine that has received attention for its role in the pathogenesis of several autoimmune diseases. IL-17A has also been implicated in cardiac and renal allograft rejection. Accordingly, we hypothesized that depletion of IL-17A would enhance corneal allograft survival. Instead, our results demonstrate that blocking IL-17A in a mouse model of keratoplasty accelerated the tempo and increased the incidence of allograft rejection from 50 to 90%. We describe a novel mechanism by which CD4+CD25+ regulatory T cells (Tregs) respond to IL-17A and enhance corneal allograft survival. Our findings suggest the following: 1) IL-17A is necessary for ocular immune privilege; 2) IL-17A is not required for the induction of anterior chamber-associated immune deviation; 3) Tregs require IL-17A to mediate a contact-dependent suppression; 4) corneal allograft Tregs suppress the efferent arm of the immune response and are Ag specific; 5) Tregs are not required for corneal allograft survival beyond day 30; and 6) corneal allograft-induced Treg-mediated suppression is transient. Our findings identify IL-17A as a cytokine essential for the maintenance of corneal immune privilege and establish a new paradigm whereby interplay between IL-17A and CD4+CD25+ Tregs is necessary for survival of corneal allografts.
Recruitment of Dendritic Cells Is Responsible for Intestinal Epithelial Damage in the Pathogenesis of Necrotizing Enterocolitis by Cronobacter sakazakii
Authors: Emami Claudia N. , Mittal Rahul , Wang Larry , Ford Henri R. , Prasadarao Nemani V. 
Published: May 2011

Abstract
Cronobacter sakazakii is a Gram-negative pathogen associated with the cases of necrotizing enterocolitis (NEC) that result from formula contamination. In a mouse model of NEC, we demonstrate that C. sakazakii infection results in epithelial damage by recruiting greater numbers of dendritic cells (DCs) than macrophages and neutrophils in the gut and suppresses DC maturation, which requires outer membrane protein A (OmpA) expression in C. sakazakii. Pretreatment of intestinal epithelial cell monolayers with supernatant from OmpA+ C. sakazakii/DC culture markedly enhanced membrane permeability and enterocyte apoptosis, whereas OmpA− C. sakazakii/DC culture supernatant had no effect. Analysis of OmpA+ C. sakazakii/DC coculture supernatant revealed significantly greater TGF-β production compared with the levels produced by OmpA− C. sakazakii infection. TGF-β levels were elevated in the intestinal tissue of mice infected with OmpA+ C. sakazakii. Cocultures of CaCo-2 cells and DCs in a “double-layer” model followed by infection with OmpA+ C. sakazakii significantly enhanced monolayer leakage by increasing TGF-β production. Elevated levels of inducible NO synthase (iNOS) were also observed in the double-layer infection model, and abrogation of iNOS expression prevented the C. sakazakii-induced CaCo-2 cell monolayer permeability despite the presence of DCs or OmpA+ C. sakazakii/DC supernatant. Blocking TGF-β activity using a neutralizing Ab suppressed iNOS production and prevented apoptosis and monolayer leakage. Depletion of DCs in newborn mice protected against C. sakazakii-induced NEC, whereas adoptive transfer of DCs rendered the animals susceptible to infection. Therefore, C. sakazakii interaction with DCs in intestine enhances the destruction of the intestinal epithelium and the onset of NEC due to increased TGF-β production.
HIV-1 Reduces Aβ-Degrading Enzymatic Activities in Primary Human Mononuclear Phagocytes
Authors: Lan Xiqian , Xu Jiqing , Kiyota Tomomi , Peng Hui , Zheng Jialin C. , Ikezu Tsuneya 
Published: May 2011

Abstract
The advent and wide introduction of antiretroviral therapy has greatly improved the survival and longevity of HIV-infected patients. Unfortunately, despite antiretroviral therapy treatment, these patients are still afflicted with many complications including cognitive dysfunction. There is a growing body of reports indicating accelerated deposition of amyloid plaques, which are composed of amyloid-β peptide (Aβ), in HIV-infected brains, though how HIV viral infection precipitates Aβ accumulation is poorly understood. It is suggested that viral infection leads to increased production and impaired degradation of Aβ. Mononuclear phagocytes (macrophages and microglia) that are productively infected by HIV in brains play a pivotal role in Aβ degradation through the expression and execution of two endopeptidases, neprilysin (NEP) and insulin-degrading enzyme. In this study, we report that NEP has the dominant endopeptidase activity toward Aβ in macrophages. Further, we demonstrate that monomeric Aβ degradation by primary cultured macrophages and microglia was significantly impaired by HIV infection. This was accompanied with great reduction of NEP endopeptidase activity, which might be due to the diminished transport of NEP to the cell surface and intracellular accumulation at the endoplasmic reticulum and lysosomes. Therefore, these data suggest that malfunction of NEP in infected macrophages may contribute to acceleration of β amyloidosis in HIV-inflicted brains, and modulation of macrophages may be a potential preventative target of Aβ-related cognitive disorders in HIV-affected patients.
Tumor-Infiltrating Programmed Death Receptor-1+ Dendritic Cells Mediate Immune Suppression in Ovarian Cancer
Authors: Krempski James , Karyampudi Lavakumar , Behrens Marshall D. , Erskine Courtney L. , Hartmann Lynn , Dong Haidong , Goode Ellen L. , Kalli Kimberly R. , Knutson Keith L. 
Published: May 2011

Abstract
Within the ovarian cancer microenvironment, there are several mechanisms that suppress the actions of antitumor immune effectors. Delineating the complex immune microenvironment is an important goal toward developing effective immune-based therapies. A dominant pathway of immune suppression in ovarian cancer involves tumor-associated and dendritic cell (DC)-associated B7-H1. The interaction of B7-H1 with PD-1 on tumor-infiltrating T cells is a widely cited theory of immune suppression involving B7-H1 in ovarian cancer. Recent studies suggest that the B7-H1 ligand, programmed death receptor-1 (PD-1), is also expressed on myeloid cells, complicating interpretations of how B7-H1 regulates DC function in the tumor. In this study, we found that ovarian cancer-infiltrating DCs progressively expressed increased levels of PD-1 over time in addition to B7-H1. These dual-positive PD-1+ B7-H1+ DCs have a classical DC phenotype (i.e., CD11c+CD11b+CD8−), but are immature, suppressive, and respond poorly to danger signals. Accumulation of PD-1+B7-H1+ DCs in the tumor was associated with suppression of T cell activity and decreased infiltrating T cells in advancing tumors. T cell suppressor function of these DCs appeared to be mediated by T cell-associated PD-1. In contrast, ligation of PD-1 expressed on the tumor-associated DCs suppressed NF-κB activation, release of immune regulatory cytokines, and upregulation of costimulatory molecules. PD-1 blockade in mice bearing ovarian cancer substantially reduced tumor burden and increased effector Ag-specific T cell responses. Our results reveal a novel role of tumor infiltrating PD-1+B7-H1+ DCs in mediating immune suppression in ovarian cancer.
Fluorescence Correlation Spectroscopy: Detecting and Interpreting the Mobility of Transmembrane Proteins In Vivo
Authors: Malchus Nina 
Published: May 2011

AbstractMobility of proteins is crucial for their functionality. Fluorescence correlation spectroscopy (FCS) is a sensitive tool for assessing dynamics in vivo. It can reveal properties of diffusing proteins, as well as of the surrounding medium. Hence, subtle changes in the dynamics after treatment with toxic substances can be visualized. On biological membranes, the high concentration of transmembrane and peripheral membrane proteins leads to molecular crowding, and thus to a change in the diffusion behavior, i.e., to anomalous diffusion of membrane proteins. Presented here is a protocol for conducting and evaluating FCS measurements of membrane proteins before and after treatment. Curr. Protoc. Toxicol. 48:2.19.1‐2.19.16. © 2011 by John Wiley & Sons, Inc.
Cellular fura‐2 Manganese Extraction Assay (CFMEA)
Authors: Kwakye Gunnar F. , Li Daphne , Kabobel Olympia A. , Bowman Aaron B. 
Published: May 2011

AbstractCellular manganese (Mn) uptake and transport dynamics can be measured using a cellular fura‐2 manganese extraction assay (CFMEA). The assay described here uses immortalized murine striatal cell line and primary cortical astrocytes, but the method is equally adaptable to other cultured mammalian cells. An ultrasensitive fluorescent nucleic acid stain for quantification of double‐stranded DNA (dsDNA) in solution, Quant‐iT PicoGreen, has been utilized for normalization of Mn concentration in the cultured cells, following Mn (II) chloride (MnCl2) exposure. Depending on the cell type and density, other methods, e.g., protein determination assays or cell counts, may also be used for normalization. Methods are described for rapidly stopping Mn uptake and transport processes at specified times, extraction, and quantification of cellular Mn content, and normalization of Mn levels to dsDNA concentration. Curr. Protoc. Toxicol. 48:12.18.1‐12.18.20. © 2011 by John Wiley & Sons, Inc.
Novel‐Type Inorganic Foams from Preceramic Polymers with Embedded Titania Nanoparticles for Photo‐Catalytic Applications
Authors: Bhattacharjee Sarama , Das Pratik Ranjan , Ohl Christiane , Wilker Viola , Kappa Mathias , Scheffler Franziska , Scheffler Michael 
Published: May 2011

AbstractPhotocatalytic active silica‐based foams were prepared by embedding nanotitania (anatase) into a self‐foaming glass particle‐loaded preceramic polymer and then thermally converting it in air into a silica‐based material. The foaming behavior of the mixture was found to be influenced by the volume fraction of the filler materials, resulting in open‐cellular or fused composite materials. Transformation from the anatase modification into the rutile modification is prevented even at 800 °C by the formation of SiOTi bonds. The composite foam structure with embedded nanotitania was tested in methylene blue decomposition under UV irradiation and it was found to have higher photocatalytic activity compared to unsupported nanotitania.
An innovative approach to interdisciplinary occupational safety and health education
Authors: Rosen Mitchel A. , Caravanos Jack , Milek Debra , Udasin Iris 
Published: May 2011

AbstractBackgroundThe New York and New Jersey Education and Research Center (ERC) provides a range of graduate continuing education for occupational safety and health (OSH) professionals in training. A key element of the education is to provide interdisciplinary training to industrial hygienists, ergonomists, occupational medicine physicians and other health and safety trainees to prepare them for the collaboration required to solve the complex occupational health and safety problems they will face in their careers.MethodsThis center has developed an innovative interdisciplinary training approach that provides an historical aspect, while allowing the graduate students to identify solutions to occupational issues from a multi‐disciplinary approach. The ERC developed a tour that brings students to sites of historical and/or contemporary significance in the occupational safety and health and environmental fields.ResultsThe ERC has conducted five tours, and has included 85 students and residents as participants. 80% of participants rated the tour as providing a high amount of OSH knowledge gained. 98% of the participants felt the goal of providing interdisciplinary education was achieved.ConclusionsThis tour has been successful in bridging the OSH fields to better understand how occupational and environmental exposures have occurred, in order to prevent future exposures so that workplace conditions and health can be improved. Am. J. Ind. Med. 54:515–520, 2011. © 2011 Wiley‐Liss, Inc.
Reproducibility of asbestos body counts in digestions of autopsy and surgical lung tissue
Authors: Velasco‐García María‐Isabel , Cruz María‐Jesus , Ruano Laura , Montero María‐Angeles , Freixa Asunción , Ferrer Jaume 
Published: May 2011

AbstractBackgroundAsbestos body (AB) counting by a single observer is the most commonly used objective technique to demonstrate asbestos deposition in the lung. In this study, the accuracy and reliability of this procedure is analyzed by evaluating the degree of agreement between two experienced readers.MethodsLung tissue specimens from 66 individuals, most of whom had not been exposed to asbestos, were studied: 35 were obtained in postmortem studies (upper, middle, and lower lung) and 31 were from patients who underwent surgery for lung cancer. Overall, 167 samples were analyzed. Lung tissue sections weighing 0.5 g were obtained prospectively and processed, and the inorganic residue was analyzed by light microscopy at 400× magnification by two experienced readers. Results were expressed as AB/g of dry lung tissue. Interobserver variability was analyzed using the Spearman correlation coefficient and agreement was evaluated by the Bland–Altman method and the kappa index.ResultsThe interobserver correlation was 0.8975: 0.8029 for autopsy samples and 0.9592 for biopsy samples. Bland–Altman plots showed that most values were grouped around the 95% limits of agreement. The kappa index was 0.87 for all samples, and 0.79, 0.65, and 0.54 for upper, middle, and lower lung specimens, respectively.ConclusionsAsbestos body counting by a single reader is a reliable method, especially at low concentrations of asbestos bodies in lung tissue. Double reading may be indicated in borderline cases with asbestos body levels close to levels of 1 000 AB/g. Am. J. Ind. Med. 54:597–602, 2011. © 2011 Wiley‐Liss, Inc.
Common genetic influences on depression, alcohol, and substance use disorders in Mexican‐American families
Authors: Olvera R.L. , Bearden C.E. , Velligan D.I. , Almasy L. , Carless M.A. , Curran J.E. , Williamson D.E. , Duggirala R. , Blangero J. , Glahn D.C. 
Published: May 2011

AbstractMultiple genetic and environmental factors influence the risk for both major depression and alcohol/substance use disorders. In addition, there is evidence that these illnesses share genetic factors. Although, the heritability of these illnesses is well established, relatively few studies have focused on ethnic minority populations. Here, we document the prevalence, heritability, and genetic correlations between major depression and alcohol and drug disorders in a large, community‐ascertained sample of Mexican‐American families. A total of 1,122 Mexican‐American individuals from 71 extended pedigrees participated in the study. All subjects received in‐person psychiatric interviews. Heritability, genetic, and environmental correlations were estimated using SOLAR. Thirty‐five percent of the sample met criteria for DSM‐IV lifetime major depression, 34% met lifetime criteria for alcohol use disorders, and 8% met criteria for lifetime drug use disorders. The heritability for major depression was estimated to be h2 = 0.393 (P = 3.7 × 10−6). Heritability estimates were higher for recurrent depression (h2 = 0.463, P = 4.0 × 10−6) and early onset depression (h2 = 0.485, P = 8.5 × 10−5). While the genetic correlation between major depression and alcohol use disorders was significant (ρg = 0.58, P = 7 × 10−3), the environmental correlation between these traits was not significant. Although, there is evidence for increased rates of depression and substance use in US‐born individuals of Mexican ancestry, our findings indicate that genetic control over major depression and alcohol/substance use disorders in the Mexican‐American population is similar to that reported in other populations. © 2011 Wiley‐Liss, Inc.
Influence of the pH on the formation of pyrazine compounds by the Maillard reaction of L‐ascorbic acid with acidic, basic and neutral amino acids
Authors: Yu Ai‐Nong , Tan Zhi‐Wei , Shi Bo‐An 
Published: May 2011

ABSTRACTThe influence of different pHs, ranging from 5.0 to 9.0, on the formation of pyrazines in the Maillard reaction of L‐ascorbic acid with acidic, basic and neutral amino acids was studied. The results clearly showed that pyrazine formation was favored at higher pH. These findings suggest that the formation of pyrazines is catalyzed by base. However, pH affects the formation of pyrazines at different degrees for neutral, acidic and basic amino acids. The pH has the greatest impact on acidic amino acids and the least impact on basic amino acids and the impact of pH on neutral amino acids is in between. L‐Cysteine behaves similar to acidic amino acids because of its weakly acidic mercapto group. Another finding is that the formation of some pyrazines is independent of the amino acid structure, and the amino acids are solely a nitrogen source and do not provide carbon skeletons. © 2011 Curtin University of Technology and John Wiley & Sons, Ltd.