Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
ISSN: 0003-4975

hal-01563338
http://hal.univ-brest.fr/hal-01563338
DOI : 10.1016/j.athoracsur.2016.03.093
PUBMED : 27262916

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Aims: The aims of this study were to compare short-and long-term outcomes for clinical T2N0 oesophageal cancer with analysis of (i) primary surgery (S) versus neoadjuvant therapy plus surgery (NS), (ii) squamous cell carcinoma and adenocarcinoma subsets; and (iii) neoadjuvant chemoradiotherapy versus neoadjuvant chemotherapy.Methods: Data were collected from 30 European centres from 2000 to 2010. Among 2944 included patients, 355 patients (12.1%) had cT2N0 disease; 285 (S) and 70 (NS), were compared in terms of short-and long-term outcomes. Propensity score matching analyses were used to compensate for differences in baseline characteristics.Results: No significant differences between the groups were shown in terms of in hospital morbidity and mortality. Nodal disease was observed in 50% of S-group at the time of surgery, with 20% pN2/N3. Utilisation of neoadjuvant therapy was associated with significant tumour downstaging as reflected by increases in pT0, pN0 and pTNM stage 0 disease, this effect was further enhanced with neoadjuvant chemoradiotherapy. After adjustment on propensity score and confounding factors, for all patients and subset analysis of squamous cell and adenocarcinoma, neoadjuvant therapy had no significant effect upon survival or recurrence (overall, loco-regional, distant or mixed) compared to surgery alone. There were no significant differences between neoadjuvant chemotherapy and chemoradiotherapy in short-or long-term outcomes.Conclusion: The results of this study suggest that a surgery alone treatment approach should be recommended as the primary treatment approach for cT2N0 oesophageal cancer despite 50% of patients having nodal disease at the time of surgery.
ISSN: 0959-8049

hal-01666517
https://hal.univ-lorraine.fr/hal-01666517
DOI : 10.1016/j.ejca.2015.11.024

Éditeur(s) : HAL CCSD Oldendorf/Luhe
Résumé : International audience
Non-calcifying photosynthetic anthozoans have emerged as a group that may thrive under high carbon dioxide partial pressure (pCO(2)) conditions via increased productivity. However, the physiological mechanisms underlying this potential success are unclear. Here we investigated the impact of high pCO(2) on the dissolved inorganic carbon (DIC) use in the temperate sea anemone Anemonia viridis. We assessed the impacts of long-term exposure to high pCO(2), i.e. sampling in situ natural CO2 vents (Vulcano, Italy), and short-term exposure, i.e. during a 3 wk controlled laboratory experiment. We focused on photo-physiological parameters (net photosynthesis rates, chlorophyll a content and Symbiodinium density) and on carbonic anhydrase (CA) activity, an enzyme involved in the energy-demanding process of DIC absorption. Long-term exposure to high pCO(2) had no impact on Symbiodinium density and chlorophyll a content. In contrst, short-term exposure to high pCO(2) induced a significant reduction in Symbiodinium density, which together with unchanged net photosynthesis resulted in the increase of Symbiodinium productivity per cell. Finally, in both in situ long-term and laboratory short-term exposure to high pCO(2), we observed a significant decrease in the CA activity of sea anemones, suggesting a change in DIC use (i.e. from an HCO3- to a CO2 user). This change could enable a shift in the energy budget that may increase the ability of non-calcifying photosynthetic anthozoans to cope with ocean acidification.
ISSN: 0171-8630

hal-01546163
https://hal.archives-ouvertes.fr/hal-01546163
DOI : 10.3354/meps11916

Éditeur(s) : HAL CCSD Landes Bioscience
Résumé : International audience
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
Autophagy

hal-00735751
https://hal.archives-ouvertes.fr/hal-00735751
PUBMED : 22966490

Éditeur(s) : HAL CCSD Inter-Research
Résumé : International audience
The effects of global change are particularly serious in areas where range shiftsof species are physically constrained such as the Ligurian Sea, which is one ofthe coldest sectors of the Mediterranean. In this basin, historical informationon water temperature (from the sea surface down to 75 m depth) dates backto the 1950s. Early studies also recorded warm-water species occurrence.Thanks to these data we provide the first detailed characterization of watertemperature variation from 1958 up to 2010 in the layer 0–75 m depth. Wecoupled this analysis with the available information on rocky reef epibenthiccommunities (literature review from 1955 to 1964 and field data from 1980 to2010). The analysis of water temperature revealed several patterns of variation:a cooling phase from 1958 to 1980, a phase of rapid warming from 1980 to1990 and a phase of slower warming from 1990 to 2010. Inter-annual variationin temperature increased over the entire period for the water layer down to20 m. Warm-water native and alien species richness increased during thewarming phases. Literature estimates suggest a decrease in warm-water nativespecies richness during the cooling phase. The analysis of quantitative data collectedin the early 1990s and late 2000s indicated a decrease in the cover ofwarm-water native species on shallow rocky reefs and an increase in deeperwaters. We argue that increased inter-annual variation in water temperaturemay disadvantage native warm-water species in shallow waters. Our resultsindicate that the effect of temperature rises in cold, constrained basins may bemore complex than the simple prediction of species changing their geographicalrange according to their thermal limits.
Marine Ecology Progress Series

hal-01239259
https://hal-univ-perp.archives-ouvertes.fr/hal-01239259
DOI : 10.1111/maec.12277

Éditeur(s) : HAL CCSD European Centre for Disease Prevention and Control
Résumé : International audience
In 2002, the French Food Safety Agency drew attention to the lack of information on the prevalence of human cryptosporidiosis in the country. Two years later, the ANOFEL Cryptosporidium National Network (ACNN) was set up to provide public health authorities with data on the incidence and epidemiology of human cryptosporidiosis in France. Constituted on a voluntary basis, ACNN includes 38 hospital parasitology laboratories (mainly in university hospitals). Each laboratory is engaged to notify new cases of confirmed human cryptosporidiosis, store specimens (e.g. stools, duodenal aspirates or biopsies) and related clinical and epidemiological data, using data sheet forms. From January 2006 to December 2009, 407 cryptosporidiosis cases were notified in France and 364 specimens were collected. Of the notified cases, 74 were children under four years of age, accounting for 18.2%. HIV-infected and immunocompetent patients represented 38.6% (n=157) and 28% (n=114) of cases, respectively. A marked seasonal pattern was observed each year, with increased number of cases in mid to late summer and the beginning of autumn. Genotyping of 345 isolates from 310 patients identified C. parvumin 168 (54.2%) cases, C. hominis in 113 (36.4%) and other species in 29 (9.4%), including C. felis (n=15), C. meleagridis (n=4), C. canis (n=4), Cryptosporidium chipmunk genotype (n=1), Cryptosporidium rabbit genotype (n=1) and new Cryptosporidium genotypes (n=4). These data represent the first multisite report of laboratory-confirmed cases of cryptosporidiosis in France.
ISSN: 1560-7917

hal-00926813
https://hal-unilim.archives-ouvertes.fr/hal-00926813
PUBMED : 20739000

Éditeur(s) : HAL CCSD
Résumé : International audience
Up-to-date estimates of the health outcomes of preterm children are needed for assessing perinatal care, informing parents, making decisions about care, and providing evidence for clinical guidelines. To determine survival and neonatal morbidity of infants born from 22 through 34 completed weeks' gestation in France in 2011 and compare these outcomes with a comparable cohort in 1997. The EPIPAGE-2 study is a national, prospective, population-based cohort study conducted in all maternity and neonatal units in France in 2011. A total of 2205 births (stillbirths and live births) and terminations of pregnancy at 22 through 26 weeks' gestation, 3257 at 27 through 31 weeks, and 1234 at 32 through 34 weeks were studied. Cohort data were collected from January 1 through December 31, 1997, and from March 28 through December 31, 2011. Analyses for 1997 were run for the entire year and then separately for April to December; the rates for survival and morbidities did not differ. Data are therefore presented for the whole year in 1997 and the 8-month and 6-month periods in 2011. Survival to discharge and survival without any of the following adverse outcomes: grade III or IV intraventricular hemorrhage, cystic periventricular leukomalacia, severe bronchopulmonary dysplasia, retinopathy of prematurity (stage 3 or higher), or necrotizing enterocolitis (stages 2-3). A total of 0.7% of infants born before 24 weeks' gestation survived to discharge: 31.2% of those born at 24 weeks, 59.1% at 25 weeks, and 75.3% at 26 weeks. Survival rates were 93.6% at 27 through 31 weeks and 98.9% at 32 through 34 weeks. Infants discharged home without severe neonatal morbidity represented 0% at 23 weeks, 11.6% at 24 weeks, 30.0% at 25 weeks, 47.5% at 26 weeks, 81.3% at 27 through 31 weeks, and 96.8% at 32 through 34 weeks. Compared with 1997, the proportion of infants surviving without severe morbidity in 2011 increased by 14.4% (P < .001) at 25 through 29 weeks and 6% (P < .001) at 30 through 31 weeks but did not change appreciably for those born at less than 25 weeks. The rates of antenatal corticosteroid use, induced preterm deliveries, cesarean deliveries, and surfactant use increased significantly in all gestational-age groups, except at 22 through 23 weeks. The substantial improvement in survival in France for newborns born at 25 through 31 weeks' gestation was accompanied by an important reduction in severe morbidity, but survival remained rare before 25 weeks. Although improvement in survival at extremely low gestational age may be possible, its effect on long-term outcomes requires further studies. The long-term results of the EPIPAGE-2 study will be informative in this regard.
ISSN: 2168-6211

hal-01258705
http://hal.univ-brest.fr/hal-01258705
PUBMED : 25621457
DOI : 10.1001/jamapediatrics.2014.3351

Éditeur(s) : HAL CCSD Nature Publishing Group
Résumé : While Amazonian forests are extraordinarily diverse, the abundance of trees is skewed strongly towards relatively few 'hyperdominant' species. In addition to their diversity, Amazonian trees are a key component of the global carbon cycle, assimilating and storing more carbon than any other ecosystem on Earth. Here we ask, using a unique data set of 530 forest plots, if the functions of storing and producing woody carbon are concentrated in a small number of tree species, whether the most abundant species also dominate carbon cycling, and whether dominant species are characterized by specific functional traits. We find that dominance of forest function is even more concentrated in a few species than is dominance of tree abundance, with only ≈1% of Amazon tree species responsible for 50% of carbon storage and productivity. Although those species that contribute most to biomass and productivity are often abundant, species maximum size is also influential, while the identity and ranking of dominant species varies by function and by region.
ISSN: 2041-1723

hal-01204225
https://hal.archives-ouvertes.fr/hal-01204225
DOI : 10.1038/ncomms7857
PRODINRA : 305614
PUBMED : 25919449

Éditeur(s) : HAL CCSD Nature Publishing Group
Résumé : International audience
Treacher Collins/Franceschetti syndrome (TCS; OMIM 154500) is a disorder of craniofacial development belonging to the heterogeneous group of mandibulofacial dysostoses. TCS is classically characterized by bilateral mandibular and malar hypoplasia, downward-slanting palpebral fissures, and microtia. To date, three genes have been identified in TCS:,TCOF1, POLR1D, and POLR1C. We report a clinical and extensive molecular study, including TCOF1, POLR1D, POLR1C, and EFTUD2 genes, in a series of 146 patients with TCS. Phenotype-genotype correlations were investigated for 19 clinical features, between TCOF1 and POLR1D, and the type of mutation or its localization in the TCOF1 gene. We identified 92/146 patients (63%) with a molecular anomaly within TCOF1, 9/146 (6%) within POLR1D, and none within POLR1C. Among the atypical negative patients (with intellectual disability and/or microcephaly), we identified four patients carrying a mutation in EFTUD2 and two patients with 5q32 deletion encompassing TCOF1 and CAMK2A in particular. Congenital cardiac defects occurred more frequently among patients with TCOF1 mutation (7/92, 8%) than reported in the literature. Even though TCOF1 and POLR1D were associated with extreme clinical variability, we found no phenotype-genotype correlation. In cases with a typical phenotype of TCS, 6/146 (4%) remained with an unidentified molecular defect.
ISSN: 1098-3600

hal-01134364
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01134364
DOI : 10.1038/gim.2015.29
PUBMED : 25790162

Éditeur(s) : HAL CCSD BMJ Publishing Group
Résumé : International audience
BACKGROUND: Chronic HCV infection is associated with the development of hepatic fibrosis. The direct role of HCV in the fibrogenic process is unknown. Specifically, whether HCV is able to infect hepatic stellate cells (HSCs) is debated. OBJECTIVE: To assess whether human HSCs are susceptible to HCV infection. DESIGN: We combined a set of original HCV models, including the infectious genotype 2a JFH1 model (HCVcc), retroviral pseudoparticles expressing the folded HCV genotype 1b envelope glycoproteins (HCVpp) and a subgenomic genotype 1b HCV replicon, and two relevant cellular models, primary human HSCs from different patients and the LX-2 cell line, to assess whether HCV can infect/replicate in HSCs. RESULTS: In contrast with the hepatocyte cell line Huh-7, neither infectious HCVcc nor HCVpp infected primary human HSCs or LX-2 cells. The cellular expression of host cellular factors required for HCV entry was high in Huh-7 cells but low in HSCs and LX-2 cells, with the exception of CD81. Finally, replication of a genotype 2a full-length RNA genome and a genotype 1b subgenomic replicon was impaired in primary human HSCs and LX-2 cells, which expressed low levels of cellular factors known to play a key role in the HCV life-cycle, suggesting that human HSCs are not permissive for HCV replication. CONCLUSIONS: Human HSCs are refractory to HCV infection. Both HCV entry and replication are deficient in these cells, regardless of the HCV genotype and origin of the cells. Thus, HCV infection of HSCs does not play a role in liver fibrosis. These results do not rule out a direct role of HCV infection of hepatocytes in the fibrogenic process.
ISSN: 0017-5749

hal-01063909
https://hal.archives-ouvertes.fr/hal-01063909
DOI : 10.1136/gutjnl-2013-305634
PUBMED : 25063678

Éditeur(s) : HAL CCSD Nature Publishing Group
Résumé : International audience
The etiology of congenital heart defect (CHD) combines environmental and genetic factors. So far, there were studies reporting on the screening of a single gene on unselected CHD or on familial cases selected for specific CHD types. Our goal was to systematically screen a proband of familial cases of CHD on a set of genetic tests to evaluate the prevalence of disease-causing variant identification. A systematic screening of GATA4, NKX2-5, ZIC3 and Multiplex ligation-dependent probe amplification (MLPA) P311 Kit was setup on the proband of 154 families with at least two cases of non-syndromic CHD. Additionally, ELN screening was performed on families with supravalvular arterial stenosis. Twenty-two variants were found, but segregation analysis confirmed unambiguously the causality of 16 variants: GATA4 (1 x), NKX2-5 (6 x), ZIC3 (3 x), MLPA (2 x) and ELN (4 x). Therefore, this approach was able to identify the causal variant in 10.4% of familial CHD cases. This study demonstrated the existence of a de novo variant even in familial CHD cases and the impact of CHD variants on adult cardiac condition even in the absence of CHD. This study showed that the systematic screening of genetic factors is useful in familial CHD cases with up to 10.4% elucidated cases. When successful, it drastically improved genetic counseling by discovering unaffected variant carriers who are at risk of transmitting their variant and are also exposed to develop cardiac complications during adulthood thus prompting long-term cardiac follow-up. This study provides an important baseline at dawning of the next-generation sequencing era.
ISSN: 1018-4813

hal-01404211
https://hal-univ-bourgogne.archives-ouvertes.fr/hal-01404211
DOI : 10.1038/ejhg.2015.105
PUBMED : 26014430

Éditeur(s) : HAL CCSD American Society for Microbiology
Résumé : International audience
The bivalve Codakia orbicularis, hosting sulfur-oxidizing gill endosymbionts, was starved (in artificial seawater filtered through a 0.22- m-pore-size membrane) for a long-term experiment (4 months). The effects of starvation were observed using transmission electron microscopy, fluorescence in situ hybridization and catalyzed reporter deposition (CARD-FISH), and flow cytometry to monitor the anatomical and physiological modifications in the gill organization of the host and in the symbiotic population housed in bacteriocytes. The abundance of the symbiotic population decreased through starvation, with a loss of one-third of the bacterial population each month, as shown by CARD-FISH. At the same time, flow cytometry revealed significant changes in the physiology of symbiotic cells, with a decrease in cell size and modifications to the nucleic acid content, while most of the symbionts maintained a high respiratory activity (measured using the 5-cyano-2,3-ditolyl tetrazolium chloride method). Progressively, the number of symbiont subpopulations was reduced, and the subsequent multigenomic state, characteristic of this symbiont in freshly collected clams, turned into one and five equivalent genome copies for the two remaining subpopulations after 3 months. Concomitant structural modifications appeared in the gill organization. Lysosymes became visible in the bacteriocytes, while large symbionts disappeared, and bacteriocytes were gradually replaced by granule cells throughout the entire lateral zone. Those data suggested that host survival under these starvation conditions was linked to symbiont digestion as the main nutritional source.
ISSN: 0099-2240

hal-00750419
https://hal.univ-antilles.fr/hal-00750419
DOI : 10.1128/AEM.02659-08

Éditeur(s) : HAL CCSD
Résumé : This paper develops a two-way director-firm fixed effect model to study the relationship between independent directors’ individual heterogeneity and firm operating performance, using French data. This strategy allows considering and differentiating in a unified empirical framework mechanisms related to board functioning and mechanisms related to director selection. We first show that the independence status, netted out unobservable individual heterogeneity, is negatively related to performance. This result suggests that independent board members experience a strong informational gap that outweighs other monitoring benefits. However, we show that industry-specific expertise as well as informal connections inside the boardroom may help to bridge this gap. Second, we provide evidence that independent directors have higher intrinsic ability as compared to affiliated board members, consistent with a reputation-based selection process.
https://hal.archives-ouvertes.fr/hal-01060211

hal-01060211
https://hal.archives-ouvertes.fr/hal-01060211
https://hal.archives-ouvertes.fr/hal-01060211v2/document
https://hal.archives-ouvertes.fr/hal-01060211/file/cahier%202014-29.pdf

Éditeur(s) : HAL CCSD Station Biologique
Résumé : International audience
This study deals with temporal variations in eel diet Anguilla anguilla sampled at each of the four seasons in the Languedocian Prévost lagoon (Gulf of Lion) from Autumn 1998 to Summer 1999. The following feeding indices were calculated based on observations of 12 categories of prey found in the contents of full stomachs: coefficient of vacuity CV, degree of fullness DR, occurrence frequency PP, relative abundance N (in %) and relative weight P (in %). The interpretation of results is also based on the Costello's method (1990) which combines PP and N. Anguilla anguilla mainly feeds on benthic organisms, primarily Gammarus gr. locusta, Polychaeta, insect larvae, small fish. Based on variations in eel diet, seasonal influence is illustrated by a decrease in feeding activity in summer which gradually increases during the following seasons. The good trophic quality available to eels in the Prévost lagoon depends on its hydrodynamics which is directly related to the movement of water entering and leaving lagoon by a short communication with the sea. This water movement accelerates the enrichment and production processes of this ecosystem. Changes observed during the four seasons illustrate an opportunistic type of feeding behaviour. Eels consume the most available benthic prey. They favour the importance of the prey at a given moment without using a particular feeding strategy like specialisation or generalisation. Thus, eel adapts its diet in adjusting available energy resources in the ecosystem. Because of this, the lagoon-resident species Anguilla anguilla is an obvious indirect bioindicator of the trophic capacity and present level of confinement in the brackish water lagoon ecosystem of Prévost.
ISSN: 0007-9723

hal-00753021
https://hal.univ-antilles.fr/hal-00753021

Éditeur(s) : HAL CCSD
Résumé : International audience
Objective The objective of the study was to investigate the joint effect of occupational exposure to asbestos, and tobacco and alcohol consumption, on the risk of laryngeal cancer among men. Methods We used data from a large population-based case–control study conducted in France. We estimated two-way and three-way interactions between asbestos exposure (never vs ever exposed), tobacco consumption ( extless20 vs ≥20 pack-years) and alcohol consumption ( extless5 vs ≥5 drinks per day). The interaction on an additive scale was assessed by estimating the relative excess risk due to interaction (RERI) and the attributable proportion due to interaction, and the interaction on a multiplicative scale was assessed by estimating the multiplicative interaction parameter (ψ). Multiplicative interactions were also assessed using fractional polynomials for alcohol drinking, tobacco smoking and asbestos exposure. Results When compared with light-to-moderate smokers and drinkers never exposed to asbestos, the increase in laryngeal cancer risk was smallest among light-to-moderate drinkers and smokers exposed to asbestos (OR=2.23 (1.08 to 4.60)), and highest among heavy smokers and drinkers ever exposed to asbestos (OR=69.39 (35.54 to 135.5)). We found an additive joint effect between asbestos exposure and alcohol consumption (RERI=4.75 (−4.29 to 11.12)), whereas we observed a more than additive joint effect between asbestos exposure and tobacco consumption (RERI=8.50 (0.71 to 23.81)), as well as between asbestos exposure, and tobacco and alcohol consumption (RERI=26.57 (11.52 to 67.88)). However, our results did not suggest any interaction on a multiplicative scale. Conclusions Our results suggest that asbestos exposure, in combination with tobacco and alcohol exposure, accounted for a substantial number of laryngeal cancer cases. Our findings therefore highlight the need for prevention in activities, such as construction work, where exposure to asbestos-containing materials remains
Occupational and Environmental Medicine

hal-01269904
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01269904
DOI : 10.1136/oemed-2015-102954
PUBMED : 26403532

Éditeur(s) : HAL CCSD Publisher : Baltimore : Williams & Wilkins, c1950-. Latest Publisher : Bethesda, MD : American Association of Immunologists
Résumé : International audience
Hepatic periportal fibrosis, which affects 5–10% of subjects infected by Schistosoma mansoni, is caused by the T cell-dependent granuloma that develop around schistosome eggs. Experimental models of infection have shown that granuloma and fibrosis are tightly regulated by cytokines. However, it is unknown why advanced periportal fibrosis occurs only in certain subjects. The goal of the present study was to evaluate the cytokine response of S. mansoni-infected subjects with advanced liver disease in an attempt to relate susceptibility to periportal fibrosis with an abnormal production of cytokines that regulate granuloma and fibrosis. Fibrosis was evaluated by ultrasound on 795 inhabitants of a Sudanese village in which S. mansoni is endemic: advanced periportal fibrosis was observed in 12% of the population; 35% of the affected subjects exhibited signs of portal hypertension. Age (odds ratio (OR), 11.5), gender (OR, 4.2), and infection levels (OR, 2.2) were significantly (p < 0.01) associated with hepatic fibrosis. Cytokines produced by egg-stimulated blood mononuclear cells from 99 subjects were measured (75 with no or mild fibrosis; 24 subjects with advanced fibrosis). Multivariate analysis of cytokine levels showed that high IFN-γ levels were associated with a marked reduction of the risk of fibrosis (p = ‫OR, 0.1); in contrast, high TNF-α levels were associated with an increased risk (p = 0.05; OR, 4.6) of periportal fibrosis. Moreover, infection levels were negatively associated with IFN-γ production. These results with observations in experimental models strongly suggest that IFN-γ plays a key role in the protection of S. mansoni-infected patients against periportal fibrosis, whereas TNF-α may aggravate the disease.
ISSN: 0022-1767

Droits : http://creativecommons.org/licenses/by-nc-nd/
hal-01211587
https://hal.archives-ouvertes.fr/hal-01211587
https://hal.archives-ouvertes.fr/hal-01211587/document
https://hal.archives-ouvertes.fr/hal-01211587/file/929.full.pdf
DOI : 10.4049/jimmunol.169.2.929

Éditeur(s) : HAL CCSD
Résumé : While often criticized, independence remains the ultimate criterion for evaluating board composition, whether for regulators or shareholder activists. In this study, we examine the relationship between board independence and firm operating performance in a panel of French listed companies, paying particular attention to heterogeneity and endogeneity concerns. We take advantage of an original database, with a time-series dimension that can be used to mitigate heterogeneity and dynamic endogeneity issues through GMM estimators. In addition, this database can be disaggregated at the individual (director) level. This design enables us to introduce firm fixed effects and individual fixed effects in (firm) performance equations, thereby controlling for heterogeneity at the firm and individual levels. To our knowledge, this is the first paper so far to provide a systematic account on this issue for France. Our main result is to document a significant negative relationship between accounting performance and the independence status (irrespective of the person). This result supports the argument of an information gap suffered by independent board members, as developed by Adams and Ferreira (2007).
https://hal.archives-ouvertes.fr/hal-00919408

hal-00919408
https://hal.archives-ouvertes.fr/hal-00919408
https://hal.archives-ouvertes.fr/hal-00919408v2/document
https://hal.archives-ouvertes.fr/hal-00919408/file/cahier_de_recherche_2014-01.pdf

Éditeur(s) : HAL CCSD Nature Publishing Group
Résumé : International audience
Mantle cell lymphoma (MCL) is a hematologic neoplasm characterised by the t(11;14)(q13;q32) translocation leading to aberrant cyclin D1 expression. The cell functions of cyclin D1 depend on its partners and/or subcellular distribution, resulting in different oncogenic properties. We observed the accumulation of cyclin D1 in the cytoplasm of a subset of MCL cell lines and primary cells. In primary cells, this cytoplasmic distribution was correlated with a more frequent blastoid phenotype. We performed immunoprecipitation assays and mass spectrometry on enriched cytosolic fractions from two cell lines. The cyclin D1 interactome was found to include several factors involved in adhesion, migration and invasion. We found that the accumulation of cyclin D1 in the cytoplasm was associated with higher levels of migration and invasiveness. We also showed that MCL cells with high cytoplasmic levels of cyclin D1 engrafted more rapidly into the bone marrow, spleen, and brain in immunodeficient mice. Both migration and invasion processes, both in vivo and in vitro, were counteracted by the exportin 1 inhibitor KPT-330, which retains cyclin D1 in the nucleus. Our data reveal a role of cytoplasmic cyclin D1 in the control of MCL cell migration and invasion, and as a true operator of MCL pathogenesis.
ISSN: 2045-2322

hal-01635754
https://hal.archives-ouvertes.fr/hal-01635754
DOI : 10.1038/s41598-017-14222-1
PUBMED : 29066743

Éditeur(s) : HAL CCSD Springer Verlag
Résumé : International audience
ISSN: 0944-1344

hal-01587582
https://hal.archives-ouvertes.fr/hal-01587582
DOI : 10.1007/s11356-016-6993-6

Éditeur(s) : HAL CCSD Oxford University Press (OUP): Policy A1 - Oxford Open Option C
Résumé : International audience
BACKGROUND: Infections of renal grafts with Candida species can induce life-threatening complications in the recipient. METHODS: A 9-year retrospective study involving all of the transplant centers in France was designed to determine the incidence, origin, characteristics, and outcome of graft-site candidiasis that occurred after kidney transplantation. Yeasts cultured from preservation or drainage solutions and graft specimens were recorded. RESULTS: Among 18,617 kidney grafts, 18 recipients corresponding to 12 donors developed culture-confirmed graft-site candidiasis (incidence, 1 case per 1000 grafts) a median of 25 days after the graft procedure. Clinical presentations included 14 cases of renal arteritis (13 were complicated by aneurysm), 1 urinoma, 2 graft site abscesses, and 1 surgical site infection. Candida albicans was involved in 13 cases. A unique C. albicans genotype or a single rare Candida species was involved in each episode. Together with the clinical history, these findings demonstrate that organ contamination followed by transmission to the recipient occurred during recovery. Therapeutic management varied from simple monitoring in 1 case to a combination of surgery (nephrectomy in 9 cases and arterial bypass in 9 cases) and antifungal therapy (14 cases). Overall, 3 of 18 kidney transplant recipients died, and 9 had their graft surgically removed. CONCLUSION: Graft-transmitted candidiasis that ends most often in fungal arteritis is associated with high morbidity and mortality after kidney transplantation and is related to organ contamination during recovery in the donor.
Clinical Infectious Diseases

hal-00676313
https://hal.archives-ouvertes.fr/hal-00676313
DOI : 10.1086/595688
PUBMED : 19090753