1,721,426 research outputs found
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No full textPPARγ est un récepteur nucléaire ligand-activé qui contrôle, dans différents organes, de nombreuses fonctions cellulaires, impliquées notamment dans le contrôle de l'inflammation, de la carcinogenèse ou du métabolisme. Au niveau de la cellule épithéliale intestinale, certaines fonctions de PPARγ, comme son rôle métabolique, reste méconnu. Les effets génomiques des ligands de PPARγ sont eux aussi très mal connus dans cette cellule. L'objectif de ce travail était de comparer l'expression génomique induite par différents agonistes de PPARγ dans la cellule épithéliale intestinale par la technique de microarrays, et ainsi identifier de nouveaux gènes cibles de PPARγ et les différentes fonctions cellulaires contrôlées par ce récepteur nucléaire. Nous avons pu identifier le gène lactase, dont le déficit d'expression est responsable de l'intolérance au lactose, comme un gène cible de PPARγ. Nous avons ensuite pu montrer que les agonistes de PPARγ étaient capables d'augmenter l'expression et l'activité de la lactase in vitro et in vivo, ainsi que d'améliorer les symptômes d'intolérance au lactose dans un modèle animal ; identifiant les agonistes de PPARγ comme potentiellement le premier traitement pharmacologique de l'intolérance au lactose. Nous avons pu ensuite confirmer l'effet antinéoplasique du 5ASA au niveau de la cellule épithéliale intestinale, in vivo et in vitro, et confirmer que cette action était dépendante de PPARγ. Comme dans d'utres organes, PPARγ régule dans la cellule épithéliale intestinale les voies de l'inflammation, la différenciation et la maturation cellulaire mais aussi des fonctions métaboliques, confirmant le rôle clé de PPARγ dans le contrôle de l'homéostasie intestinale, et le potentiel thérapeutique des agonistes de PPARγPPARγ is a ligand-activated nuclear receptor that controls, in various organs, numerous cellular functions, involved in the control of inflammation, carcinogenesis or metabolism. In intestinal epithelial cell, some functions of PPARγ, as its metabolic role, remain unknown. The genomic effects of PPARγ ligands are also poorly known in this cell. Our objective was to compare the genomic expression induced by different PPARγ agonists in the intestinal epithelial cells by a microarrays technique, and thus to identify new PPARγ target genes and the different cellular functions controlled by this nuclear receptor. We have identified the lactase gene, whose lack of expression is responsible for lactose intolerance, as a target gene of PPARγ. We then showed that PPARγ agonists were able to increase lactase expression and activity in vitro and in vivo, identifying PPARγ agonists as potentially the first pharmacological treatment of lactose intolerance. We then confirmed the antineoplastic effect of 5ASA in intestinal epithelial cell, both in vivo and in vitro, and confirmed that this action was PPARγ-dependent. As in other organs, PPARγ regulates in intestinal epithelial cell inflammation, cell differentiation and maturation as well as metabolic functions, confirming the key role of PPARγ in the control of intestinal homeostasis, and the potential therapeutic effect of PPARγ agonist
MICI : tous concernés !
No full textInternational audienceInflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), had become a major public health challenge due to their increasing incidence, projected to affect 0.6% of the French population by 2025. While the number of environmental factors involved may be significant, this justifies the implementation of ambitious preventive measures. The management of IBD is complex and multidisciplinary, involving gastroenterologists, general practitioners, and various specialists, particularly for monitoring treatments, managing extra-intestinal manifestations, or addressing complications. Recent therapeutic advances aim for increasingly ambitious goals, such as deep remission. This special issue aims to disseminate practical knowledge to better support patients facing these diseases.Les maladies inflammatoires chroniques de l'intestin (MICI), incluant la maladie de Crohn (MC) et la rectocolite hémorragique (RCH), sont devenues un enjeu majeur de santé publique en raison de leur incidence croissante, qui touchera 0,6 % de la population française d'ici 2025. Alors que lenombre de facteurs environnementaux pourrait être important, des mesures préventives ambitieuses semblent justifiées. La prise en charge, complexe et multidisciplinaire, implique gastroentérologues, médecins généralistes et spécialistes divers, notamment pour gérer la surveillancedes traitements, les manifestations extra-digestives ou les complications. Les avancées thérapeutiques récentes visent des objectifs de plus en plus ambitieux comme la rémission profonde. Ce numéro spécial a pour but de diffuser des connaissances pratiques pour mieux accompagner lespatients face à ces pathologies
PPARγ et homéostasie intestinale
No full textPPARγ is a ligand-activated nuclear receptor that controls, in various organs, numerous cellular functions, involved in the control of inflammation, carcinogenesis or metabolism. In intestinal epithelial cell, some functions of PPARγ, as its metabolic role, remain unknown. The genomic effects of PPARγ ligands are also poorly known in this cell. Our objective was to compare the genomic expression induced by different PPARγ agonists in the intestinal epithelial cells by a microarrays technique, and thus to identify new PPARγ target genes and the different cellular functions controlled by this nuclear receptor. We have identified the lactase gene, whose lack of expression is responsible for lactose intolerance, as a target gene of PPARγ. We then showed that PPARγ agonists were able to increase lactase expression and activity in vitro and in vivo, identifying PPARγ agonists as potentially the first pharmacological treatment of lactose intolerance. We then confirmed the antineoplastic effect of 5ASA in intestinal epithelial cell, both in vivo and in vitro, and confirmed that this action was PPARγ-dependent. As in other organs, PPARγ regulates in intestinal epithelial cell inflammation, cell differentiation and maturation as well as metabolic functions, confirming the key role of PPARγ in the control of intestinal homeostasis, and the potential therapeutic effect of PPARγ agonistsPPARγ est un récepteur nucléaire ligand-activé qui contrôle, dans différents organes, de nombreuses fonctions cellulaires, impliquées notamment dans le contrôle de l'inflammation, de la carcinogenèse ou du métabolisme. Au niveau de la cellule épithéliale intestinale, certaines fonctions de PPARγ, comme son rôle métabolique, reste méconnu. Les effets génomiques des ligands de PPARγ sont eux aussi très mal connus dans cette cellule. L'objectif de ce travail était de comparer l'expression génomique induite par différents agonistes de PPARγ dans la cellule épithéliale intestinale par la technique de microarrays, et ainsi identifier de nouveaux gènes cibles de PPARγ et les différentes fonctions cellulaires contrôlées par ce récepteur nucléaire. Nous avons pu identifier le gène lactase, dont le déficit d'expression est responsable de l'intolérance au lactose, comme un gène cible de PPARγ. Nous avons ensuite pu montrer que les agonistes de PPARγ étaient capables d'augmenter l'expression et l'activité de la lactase in vitro et in vivo, ainsi que d'améliorer les symptômes d'intolérance au lactose dans un modèle animal ; identifiant les agonistes de PPARγ comme potentiellement le premier traitement pharmacologique de l'intolérance au lactose. Nous avons pu ensuite confirmer l'effet antinéoplasique du 5ASA au niveau de la cellule épithéliale intestinale, in vivo et in vitro, et confirmer que cette action était dépendante de PPARγ. Comme dans d'utres organes, PPARγ régule dans la cellule épithéliale intestinale les voies de l'inflammation, la différenciation et la maturation cellulaire mais aussi des fonctions métaboliques, confirmant le rôle clé de PPARγ dans le contrôle de l'homéostasie intestinale, et le potentiel thérapeutique des agonistes de PPAR
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Unanswered Questions About the Future Development of Gastroenterology Hospitalists Reply
No full textInternational audienc
Histological Scores in Inflammatory Bowel Disease: A New Kid in the Block
No full textInternational audienc
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Modifying Our Environment to Improve Outcomes in Inflammatory Bowel Diseases?
No full textInternational audienceOver the past decades, inflammatory bowel disease (IBD) has emerged as a significant public health challenge worldwide. In Europe alone, it is estimated that around 1.3 million people suffer from IBD, representing at least 0.2% of the population [1, 2]. Numerous environmental factors—such as smoking, urban living, consumption of ultra-processed food, and exposure to antibiotics—have been linked to an increased risk of developing IBD, with varying levels of evidence [3]. Developing a robust understanding of how modifiable environmental exposures impact IBD risk is essential for informing effective prevention strategies. Similarly, identifying modifiable environmental factors that influence the disease course could guide interventions to mitigate risks and slow disease progression among IBD patients. While smoking and ultra-processed foods have been associated with active disease or worse outcomes, there is a paucity of data on the broader impact of environmental factors on IBD activity, severity, and phenotype [4, 5].In the current issue of the journal, Attauabi et al. present the first prospective population-based study examining the impact of various environmental factors—collected at the time of diagnosis—on the clinical presentation and short-term disease course of early IBD [6]. The study utilized data from the well-established prospective Copenhagen IBD Inception Cohort, which included 208 and 128 incident UC and CD patients, respectively, diagnosed between 2021 and 2023. This cohort was meticulously monitored using clinical activity indices (Simple Clinical Colitis Activity Index, Harvey-Bradshaw Index), biomarkers (CRP, calprotectin), and endoscopic assessments (Mayo Endoscopic Score, Simple Endoscopic Score-CD), enabling the evaluation of disease activity and complication. Data on environmental factors were captured through International Organization for the Study of IBD (IOIBD) and HeartDiet questionnaires, which encompass 87 questions covering 25 key areas of environmental risk. These included early-life factors (e.g., breastfeeding, exposure to pets), dietary and physical activity habits prior to diagnosis, smoking status, sanitary conditions, and the use of specific medications such as contraceptives. Early disease course (3 months) was assessed, with severe disease course defined as the need for oral steroids, immunomodulators, biologics, or colectomy.Despite the relatively small cohort, the authors made several notable observations. The adverse impact of smoking use was reaffirmed in CD, with smokers experiencing higher rates of hospitalizations and a greater likelihood of developing a stricturing phenotype. Conversely, certain healthy dietary behaviors—such as daily consumption of fruits and vegetables and a high fiber intake—were associated with a reduced occurrence of stricturing or penetrating CD phenotypes.Of course, the limitations of this study must be acknowledged. These include the small sample size, short follow-up period, and the absence of data on certain critical environmental risk factors. Future environmental studies will have to also consider the role of pollutants such as heavy metals, air pollutants, per- and polyfluoroalkyl substances (PFAS), and pesticides, which have been linked to an increased risk of IBD [7]. Their influence on disease activity and progression remains an important question for further research. Additionally, while the study highlighted that exposure to multiple environmental factors was associated with a younger age at diagnosis, the potential interaction effects between these factors require exploration in larger, well-characterized cohorts. Future research should also account for the influence of genetic background and other modifiers. Moreover, analyses on the duration and timing of environmental exposures in relation to IBD outcomes are needed to propose relevant environmental and nutritional interventions for newly diagnosed IBD patients.In conclusion, while awaiting high-level evidence from further studies and interventional trials, the findings of Attauabi et al. underscore the importance of providing personalized guidance to newly diagnosed IBD patients. This includes smoking cessation and the promotion of healthy dietary habits, which could offer benefits far beyond intestinal health
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