Monitoring wolves (Canis lupus italicus) by camera-traps in military camp (France-Var)

Un suivi de loups (Canis lupus) a été réalisé entre 2011 et 2015 dans le sud-est de la France au sein d’un Camp militaire de Canjuers (34 500 ha) situé sur des plateaux steppiques méditerranéens. Cette étude a permis de tester huit modèles différents de pièges-photographiques grâce à la pose de 16 pièges-photographiques en moyenne par an (min. 4 en 2011 et max. 26 en 2015). Plus de 1000 passages de loups et 3600 photos de loups ont été collectés durant ce suivi, ce qui a permis d’améliorer les connaissances sur la biologie et le comportement des loups en zone méditerranéenne française. Cette étude montre qu’un suivi individualisé (type CMR pour Capture-Marquage-Recapture) par enregistrement photographique n’est possible que si l’animal présente une marque distinctive (maladie, blessure ou organe sectionné). L'analyse de la taille des groupes de loups en déplacement a montré, sur les deux meutes étudiées, que les loups se déplacent principalement seuls ou par deux. Enfin, le très grand nombre de passages de loups enregistrés a permis de réaliser un graphique montrant le rythme d'activité de déplacement des loups, heure par heure, sur un cycle annuel complet, en fonction des heures de lever et de coucher du soleil.Les résultats suggèrent que l’utilisation de pièges-photographique est une technique fiable pour le suivi des populations de loups, au moins dans la zone prospectée, sans enneigement. Elle vient en complément des autres méthodes de suivis. Leur utilisation permet aux biologistes et gestionnaires d’obtenir rapidement un état de la population lupine (individus isolés ou en meutes) sur un territoire précis.A monitoring of wolves (Canis lupus) was carried out between 2011 and 2015 in south-eastern France in a 34,500 ha military estate localized in a Mediterranean steppic plateau. This study tested eight different camera trap models by setting an average of 16 camera traps per year (min. 4 in 2011 and a max. 26 in 2015). More than 1 000 wolf passages and 3 600 wolf photos were collected during this monitoring, which allowed improving the knowledge on the biology and behavior of wolves in this French Mediterranean area. This study shows that individualized monitoring (CMR) is only possible if the animal presents a distinctive mark (disease, injury or severed organ). The analysis of wolves group size on the move showed, on the two packs studied, that the wolves move mainly alone or in pairs. The large number of recorded wolf passages made it possible to produce a graph showing wolf movement rates, hour by hour, over a complete annual cycle, between sunrise and sunset times.Camera-trapping is a noninvasive method which has been used successfully to monitor wolf populations in the Mediterranean area without snow that complements other survey techniques. Their use allows biologists and managers to quickly obtain a status of wolf population (isolated individuals or packs) on a specific territory

Krüppel-like factor 5 is an important mediator for lipopolysaccharide-induced proinflammatory response in intestinal epithelial cells

Lipopolysaccharide (LPS) is a bacterially-derived endotoxin that elicits a strong proinflammatory response in intestinal epithelial cells. It is well established that LPS activates this response through NF-κB. In addition, LPS signals through the mitogen-activated protein kinase (MAPK) pathway. We previously demonstrated that the Krüppel-like factor 5 [KLF5; also known as intestine-enriched Krüppel-like factor (IKLF)] is activated by the MAPK. In the current study, we examined whether KLF5 mediates the signaling cascade elicited by LPS. Treatment of the intestinal epithelial cell line, IEC6, with LPS resulted in a dose- and time-dependent increase in KLF5 messenger RNA (mRNA) and protein levels. Concurrently, mRNA levels of the p50 and p65 subunits of NF-κB were increased by LPS treatment. Pretreatment with the MAPK inhibitor, U0126, or the LPS antagonist, polymyxin B, resulted in an attenuation of KLF5, p50 and p65 NF-κB subunit mRNA levels from LPS treatment. Importantly, suppression of KLF5 by small interfering RNA (siRNA) resulted in a reduction in p50 and p65 subunit mRNA levels and NF-κB DNA binding activity in response to LPS. LPS treatment also led to an increase in secretion of TNF-α and IL-6 from IEC6, both of which were reduced by siRNA inhibition of KLF5. In addition, intercellular adhesion molecule-1 (ICAM-1) levels were increased in LPS-treated IEC6 cells and this increase was associated with increased adhesion of Jurkat lymphocytes to IEC6. The induction of ICAM-1 expression and T cell adhesion to IEC6 by LPS were both abrogated by siRNA inhibition of KLF5. These results indicate that KLF5 is an important mediator for the proinflammatory response elicited by LPS in intestinal epithelial cells

Butyrate Transcriptionally Enhances Peptide Transporter PepT1 Expression and Activity

Background: PepT1, an intestinal epithelial apical di/tripeptide transporter, is normally expressed in the small intestine and induced in colon during chronic inflammation. This study aimed at investigating PepT1 regulation by butyrate, a short-chain fatty acid produced by commensal bacteria and accumulated inside inflamed colonocyte. Results: We found that butyrate treatment of human intestinal epithelial Caco2-BBE cells increased human PepT1 (hPepT1) promoter activity in a dose- and time-dependent manner, with maximal activity observed in cells treated with 5 mM butyrate for 24 h. Under this condition, hPepT1 promoter activity, mRNA and protein expression levels were increased as assessed by luciferase assay, real-time RT-PCR and Western blot, respectively. hPepT1 transport activity was accordingly increased by,2.5-fold. Butyrate did not alter hPepT1 mRNA half-life indicating that butyrate acts at the transcriptional level. Molecular analyses revealed that Cdx2 is the most important transcription factor for butyrate-induced increase of hPepT1 expression and activity in Caco2-BBE cells. Butyrate-activated Cdx2 binding to hPepT1 promoter was confirmed by gel shift and chromatin immunoprecipitation. Moreover, Caco2-BBE cells overexpressing Cdx2 exhibited greater hPepT1 expression level than wild-type cells. Finally, treatment of mice with 5 mM butyrate added to drinking water for 24 h increased colonic PepT1 mRNA and protein expression levels, as well as enhanced PepT1 transport activity in colonic apical membranes vesicles

p21WAF1/CIP1 Upregulation through the Stress Granule-Associated Protein CUGBP1 Confers Resistance to Bortezomib-Mediated Apoptosis

p21(WAF1/CIP1) is a well known cyclin-dependent kinase inhibitor induced by various stress stimuli. Depending on the stress applied, p21 upregulation can either promote apoptosis or prevent against apoptotic injury. The stress-mediated induction of p21 involves not only its transcriptional activation but also its posttranscriptional regulation, mainly through stabilization of p21 mRNA levels. We have previously reported that the proteasome inhibitor MG132 induces the stabilization of p21 mRNA, which correlates with the formation of cytoplasmic RNA stress granules. The mechanism underlying p21 mRNA stabilization, however, remains unknown.We identified the stress granules component CUGBP1 as a factor required for p21 mRNA stabilization following treatment with bortezomib ( =  PS-341/Velcade). This peptide boronate inhibitor of the 26S proteasome is very efficient for the treatment of myelomas and other hematological tumors. However, solid tumors are sometimes refractory to bortezomib treatment. We found that depleting CUGBP1 in cancer cells prevents bortezomib-mediated p21 upregulation. FISH experiments combined to mRNA stability assays show that this effect is largely due to a mistargeting of p21 mRNA in stress granules leading to its degradation. Altering the expression of p21 itself, either by depleting CUGBP1 or p21, promotes bortezomib-mediated apoptosis.We propose that one key mechanism by which apoptosis is inhibited upon treatment with chemotherapeutic drugs might involve upregulation of the p21 protein through CUGBP1

Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome associated with COVID-19: An Emulated Target Trial Analysis.

RATIONALE: Whether COVID patients may benefit from extracorporeal membrane oxygenation (ECMO) compared with conventional invasive mechanical ventilation (IMV) remains unknown. OBJECTIVES: To estimate the effect of ECMO on 90-Day mortality vs IMV only Methods: Among 4,244 critically ill adult patients with COVID-19 included in a multicenter cohort study, we emulated a target trial comparing the treatment strategies of initiating ECMO vs. no ECMO within 7 days of IMV in patients with severe acute respiratory distress syndrome (PaO2/FiO2 <80 or PaCO2 ≥60 mmHg). We controlled for confounding using a multivariable Cox model based on predefined variables. MAIN RESULTS: 1,235 patients met the full eligibility criteria for the emulated trial, among whom 164 patients initiated ECMO. The ECMO strategy had a higher survival probability at Day-7 from the onset of eligibility criteria (87% vs 83%, risk difference: 4%, 95% CI 0;9%) which decreased during follow-up (survival at Day-90: 63% vs 65%, risk difference: -2%, 95% CI -10;5%). However, ECMO was associated with higher survival when performed in high-volume ECMO centers or in regions where a specific ECMO network organization was set up to handle high demand, and when initiated within the first 4 days of MV and in profoundly hypoxemic patients. CONCLUSIONS: In an emulated trial based on a nationwide COVID-19 cohort, we found differential survival over time of an ECMO compared with a no-ECMO strategy. However, ECMO was consistently associated with better outcomes when performed in high-volume centers and in regions with ECMO capacities specifically organized to handle high demand. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/)

L'apoptose dans l'épithélium intestinal humain (hiérarchisation des étapes d'exécution - contrôle par le monoxyde d'azote (NO))

En physiologie intestinale, l'apoptose est une fonction qui, en assurant une mort cellulaire dite "propre", participe au maintien de l'homéostasie de la barrière épithéliale...L'objectif de cette thèse était double. D'une part, ce travail visait à déterminer 1) l'expression dans l'épithélium intestinal humain de la protéine DFF45, impliquée dans la dégradation internucléosomale de l'ADN dans le système murin, et 2) son éventuel rôle dans l'apoptose épithéliale. D'autre part, ce travail visait à explorer le rôle pro-apoptotique d'un médiateur physiologique, le monoxyde d'azote (NO), vis-à-vis de cellules épithéliales intestinales en culture, et à décrypter les voies de signalisation impliquées. Nos résultats montrent que 1) l'épithélium colique humain normal exprime DFF45 et 2) l'expression de DFF45 est dépendante de la phase de croissance, dans la lignée cancéreuse colique humaine HT29-Cl16E.....In intestinal physiology, apoptosis is a cellular function leading to a "clean" cell death that participates in epithelial barrier homeostasis. As any other physiological function, apoptosis comprises execution mechanisms which are coupled to intracellular signaling systems and cellular receptors, and are activated by extracellular mediators. In colonic cancer, a deficient expression of apoptosis-activating receptors (Fas) or receptor-proximal proteins could account for the resistance of various colonic cancer cell lines to apoptotic stimuli. The execution mechanisms of apoptosis in both human normal intestinal epithelium and colonic cancers have not been extensively elucidated yet. Finally, the capacity of some physiological mediators to regulate apoptosis in the human normal intestinal epithelium or in colonic cancers is not well known. The aims of this work were twofold. The first aim was to examine the expression by the human intestinal epithelium of DFF45, a protein known to be involved in internucleosomal DNA fragmentation in mice, and to determine its role in the apoptosis of the intestinal barrier.....NANTES-BU Médecine pharmacie (441092101) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF

Processing strategies to obtain clean interleaved ultrafast 2D NMR spectra

Ultrafast (UF) 2D NMR enables the acquisition of 2D spectra in a single-scan. In spite of its promising potential, the accessible spectral width is highly limited by the maximum gradient amplitude, which limits the general applicability of the method. A number of solutions have been recently described to deal with this limitation, among which stands the possibility to record several interleaved scans. However, this alternative acquisition scheme leads to numerous ghost peaks characteristic of interleaved acquisitions. These artefacts highly affect the readability of 2D spectra for structural elucidation, as well as their quantitative performance. Here, we propose several pre-FT or post-FT processing corrections to clean artefacts from interleaved ultrafast NMR spectra. Their performances are compared, and their potentialities are illustrated in a small organic molecule context. Post-FT processing corrections such as ArSub (Artefact Subtraction) or symmetrisation appear to be the most efficient ones in terms of artefact removal. While not purely single-scan, these strategies open new perspectives towards the routine use of UF 2D NMR for structural or quantitative analysis. (C) 2013 Elsevier Inc. All rights reserved