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Biotinidase was identified in secretome analysis of thyroid cancer cell lines using proteomics. The goal of the current study was to analyze the expression of biotinidase in thyroid cancer tissues and fine needle aspiration (FNA) samples to evaluate its diagnostic and prognostic potential in thyroid cancer. Immunohistochemical analysis of biotinidase was carried out in 129 papillary thyroid cancer (PTC, 34 benign thyroid tissues and 43 FNA samples and correlated with patients’ prognosis. Overall biotinidase expression was decreased in PTC compared to benign nodules (p = 0.001). Comparison of aggressive and non-aggressive PTC showed decrease in overall biotinidase expression in the former (p = 0.001). Loss of overall biotinidase expression was associated with poor disease free survival (p = 0.019, Hazards ratio (HR) = 3.1). We examined the effect of subcellular compartmentalization of nuclear and cytoplasmic biotinidase on patient survival. Decreased nuclear expression of biotinidase was observed in PTC as compared to benign tissues (p<0.001). Upon stratification within PTC, nuclear expression was reduced in aggressive as compared to non-aggressive tumors (p<0.001). Kaplan-Meier survival analysis showed significant association of loss of nuclear biotinidase expression with reduced disease free survival (p = 0.014, HR = 5.4). Cytoplasmic biotinidase expression was reduced in aggressive thyroid cancers in comparison with non-aggressive tumors (p = 0.002, Odds ratio (OR) = 0.29) which was evident by its significant association with advanced T stage (p = 0.003, OR = 0.28), nodal metastasis (p<0.001, OR = 0.16), advanced TNM stage (p<0.001, OR = 0.21) and extrathyroidal extension (p = 0.001, OR = 0.23). However, in multivariate analysis extrathyroidal extension emerged as the most significant prognostic marker for aggressive thyroid carcinomas (p = 0.015, HR = 12.8). In conclusion, loss of overall biotinidase expression is a novel marker for thyroid cancer aggressiveness. 相似文献
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Denise Cazzato Emma Assi Claudia Moscheni Silvia Brunelli Clara De Palma Davide Cervia Cristiana Perrotta Emilio Clementi 《Experimental cell research》2014
The muscle-specific variant of neuronal nitric oxide (NO) synthase (NOS-I), is developmentally regulated in mouse suggesting a role of NO during myogenesis. In chick embryo, a good model of development, we found that the expression of NOS-I is up-regulated, but only in the early phase of development. Through a pharmacological intervention in ovo we found that NO signalling plays a relevant role during embryonic development. The inhibition of NOS-I decreased the growth of embryo, in particular of muscle tissue, while the restoring of physiological NO levels, via administration of a NO donor, reversed this effect. We found a selective action of NO, produced by NOS-I, on regulatory factors involved in myogenic differentiation in the early phase of chick embryo development: inhibition of NO generation leads to a decreased expression of the Myocyte enhancer factor 2a (Mef2a), Mef2c, Myogenin and Myosin, which was reversed by the administration of a NO donor. NO had no effects on Myf5 and MyoD, the myogenic regulatory factors necessary for myogenic determination. The action of NO on the myogenic regulatory factors was mediated via generation of cyclic GMP (cGMP) and activation of the cGMP-dependent protein kinase G (PKG). Finally we found in myoblasts in vitro that the activation of Mef2c was the key event mediating the NO-induced modulation of myogenesis. 相似文献
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P. Gourlay A. Decors M. Moinet O. Lambert B. Lawson F. Beaudeau S. Assié 《European Journal of Wildlife Research》2014,60(6):865-873
Multiple schemes for wildlife disease surveillance have been in operation in France for decades and data on wild bird carcasses presented to the national SAGIR network have been recorded since the 1980s. Over the same period, wildlife rescue centres (WRCs) have admitted thousands of birds each year. However, the reasons for casualty submission have been poorly explored to date. To assess the potential capacity of WRCs to monitor infectious and non-infectious diseases of wild birds in addition to SAGIR, we used Fringillidae and Passeridae data from January 2004 to April 2013 from SAGIR and the WRC of Nantes (CVFSE/Oniris) which is in operation in North-West France. Firstly, the Centre Vétérinaire de la Faune Sauvage et des Ecosystèmes des Pays de la Loire (CVFSE) contributed more than 30 % of all the birds submitted and was complementary to the SAGIR network in terms of species, age of the birds collected, location and date found. Secondly, the CVFSE was able to detect the emergent finch trichomonosis, in addition to the SAGIR network. Some causes of passerine submission were detected by one or other of the two schemes leading to their complementarity in overviewing Fringillidae and Passeridae infectious and non-infectious diseases in France. In order to improve the efficiency of its wild bird disease monitoring and to participate in an effective national and/or European surveillance network, the CVFSE, as for other WRCs, must enhance its diagnostic capabilities, in particular post-mortem examinations and laboratory testing. 相似文献
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Terraced landscapes of the Shouf Biosphere Reserve (Lebanon): analysis of geomorphological variables
Corrieri Federica Piras Francesco Abou Assi Marwa Focacci Marco Conti Leonardo 《Biodiversity and Conservation》2022,31(10):2421-2433
Biodiversity and Conservation - This work aims to characterize the agricultural heritage system surrounding the Shouf Biosphere Reserve (SBR) in Lebanon, through a landscape analysis based on... 相似文献
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The clayed filling of an holocene paleolagoon, from ?25 to ?11 m and dating from 8630 B.P. to 4300 B.P., is rich in fossil leaves of trees of swamp forest. It also contains some molluscan shells of a brackish environment. An attempt of palaeoecological reconstitution is made. 相似文献
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Fan Zhang Jessica L. Weckhorst Adrien Assié Ciara Hosea Christopher A. Ayoub Anastasia S. Khodakova Mario Loeza Cabrera Daniela Vidal Vilchis Marie-Anne Félix Buck S. Samuel 《Current biology : CB》2021,31(12):2603-2618.e9
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