16 research outputs found

    Skeletal muscle in MuRF1 null mice is not spared in low-gravity conditions, indicating atrophy proceeds by unique mechanisms in space

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    Microgravity exposure is associated with loss of muscle mass and strength. The E3 ubiquitin ligase MuRF1 plays an integral role in degrading the contractile apparatus of skeletal muscle; MuRF1 null (KO) mice have shown protection in ground-based models of muscle atrophy. In contrast, MuRF1 KO mice subjected to 21 days of microgravity on the International Space Station (ISS) were not protected from muscle atrophy. In a time course experiment microgravity-induced muscle loss on the ISS showed MuRF1 gene expression was not upregulated. A comparison of the soleus transcriptome profiles between spaceflight and a publicly available data set for hindlimb suspension, a claimed surrogate model of microgravity, showed only marginal commonalities between the models. These findings demonstrate spaceflight induced atrophy is unique, and that understanding of effects of space requires study situated beyond the Earth's mesosphere

    Comparison of a Barcode-Based Smartphone Application to a Questionnaire to Assess the Use of Cleaning Products at Home and Their Association with Asthma Symptoms

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    International audienceHousehold disinfectant and cleaning products (HDCPs) assessment is challenging in epidemiological research. We hypothesized that a newly-developed smartphone application was more objective than questionnaires in assessing HDCPs. Therefore, we aimed to compare both methods, in terms of exposure assessments and respiratory health effects estimates. The women of the SEPAGES birth cohort completed repeated validated questionnaires on HDCPs and respiratory health and used an application to report HDCPs and scan products barcodes, subsequently linked with an ingredients database. Agreements between the two methods were assessed by Kappa coefficients. Logistic regression models estimated associations of HDCP with asthma symptom score. The 101 participants (18 with asthma symptom score ≥1) scanned 617 different products (580 with available ingredients list). Slight to fair agreements for sprays, bleach and scented HDCP were observed (Kappa: 0.35, 0.25, 0.11, respectively). Strength of the associations between HDCP and asthma symptom score varied between both methods but all odds ratios (OR) were greater than one. The number of scanned products used weekly was significantly associated with the asthma symptom score (adjusted-OR [CI 95%]: 1.15 [1.00-1.32]). This study shows the importance of using novel tools in epidemiological research to objectively assess HDCP and therefore reduce exposure measurement errors

    A single regulatory gene is sufficient to alter Vibrio aestuarianus pathogenicity in oysters

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    Oyster diseases caused by pathogenic vibrios pose a major challenge to the sustainability of oyster farming. In France since 2012 a disease affecting specifically adult oysters has been associated with the presence of Vibrio aestuarianus. Here, by combining genome comparison, phylogenetic analyses and high throughput infections of strains isolated before or during the recent outbreaks, we show that virulent strains cluster into two V. aestuarianus lineages independently of the sampling dates. The bacterial lethal dose was not different between strains isolated before or after 2012. Hence the emergence of a new highly virulent clonal strain is unlikely. Each lineage comprises nearly identical strains, the majority of them being virulent, suggesting that within these phylogenetically coherent virulent lineages a few strains has lost their pathogenicity. Comparative genomics allowed the identification of a single frameshift in a non-virulent strain. This mutation affects the varS gene that codes for a signal transduction histidine-protein kinase. Genetic analyses confirmed that varS is necessary for infection of oysters and for a secreted metalloprotease expression. For the first time in a Vibrio species we show here that VarS is a key factor of pathogenicit

    Antimicrobial Resistance of Listeria monocytogenes Isolates from Food and the Environment in France over a 10-Year Period▿†

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    In order to assess antimicrobial resistance in Listeria monocytogenes, 202 food and environmental isolates from 1996 to 2006 were tested. Only four strains displayed acquired resistance. Resistance to erythromycin, tetracycline-minocycline, and trimethoprim was evidenced, and the genes erm(B), tet(M), and dfrD, already found in L. monocytogenes, were detected

    Genetic association of SNPs in the leukotriene pathway genes with chronic rhinosinusitis

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    Each subfigure presents the result of one gene. The top line indicates the gene name and symbol. The upper part of each subfigure shows the exon-intron structure of the gene and the localization of the genotyped SNPs. The coding exons are shown in black and the untranslated regions are shown in grey. The lower part of each subfigure illustrated the association results for chronic rhinosinusitis. The x-axis shows the localization of the gene and SNPs on build 36. The y-axis shows the p values on a log scale. The lower and upper dash lines represent p value thresholds of 0.05 and 0.0012, respectively. The gene structure for CYSLTR2 was taken from Fukai et al. [38]. The upper and lower parts of each subfigure are shown on the same scale.<p><b>Copyright information:</b></p><p>Taken from "Influence of leukotriene gene polymorphisms on chronic rhinosinusitis"</p><p>http://www.biomedcentral.com/1471-2350/9/21</p><p>BMC Medical Genetics 2008;9():21-21.</p><p>Published online 26 Mar 2008</p><p>PMCID:PMC2292155.</p><p></p

    Modulation of Microglia by Voluntary Exercise or CSF1R Inhibition Prevents Age-Related Loss of Functional Motor Units

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    Age-related loss of skeletal muscle innervation by motor neurons leads to impaired neuromuscular function and is a well-established clinical phenomenon. However, the underlying pathogenesis remains unclear. Studying mice, we find that the number of motor units (MUs) can be maintained by counteracting neurotoxic microglia in the aged spinal cord. We observe that marked innervation changes, detected by motor unit number estimation (MUNE), occur prior to loss of muscle function in aged mice. This coincides with gene expression changes indicative of neuronal remodeling and microglial activation in aged spinal cord. Voluntary exercise prevents loss of MUs and reverses microglia activation. Depleting microglia by CSF1R inhibition also prevents the age-related decline in MUNE and neuromuscular junction disruption, implying a causal link. Our results suggest that age-related changes in spinal cord microglia contribute to neuromuscular decline in aged mice and demonstrate that removal of aged neurotoxic microglia can prevent or reverse MU loss
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