Background and Purpose: The reintroduction of colistin as a last resort treatment against multi-resistant Gram-negative bacilli, is currently challenged by the emergence of colistin-resistant bacteria. The aim of this...Background and Purpose: The reintroduction of colistin as a last resort treatment against multi-resistant Gram-negative bacilli, is currently challenged by the emergence of colistin-resistant bacteria. The aim of this study was to assess the susceptibility of Pseudomonas and Acinetobacter strains to colistin, to identify carbapenemase production, and to investigate the plasmid genes involved in colistin resistance and carbapenemase production. Methodology: In order to establish the susceptibility profiles of 17 strains of Pseudomonas and Acinetobacter to colistin, their Minimum Inhibitory Concentrations (MICs) were determined using the liquid microdilution method. The possible production of carbapenemases was investigated with the modified Carbapenem Inactivation Method (mCIM). The search for genes encoding carbapenemases (bla<sub>OXA</sub>, bla<sub>IMP</sub>, bla<sub>Carba</sub>) and those responsible for plasmid resistance to colistin (mcr-1 and mcr-2) was performed by conventional PCR. Results and Conclusion: Ninety-four percent (94%) (16/17) of the strains were resistant to colistin. Intraspecies distribution was 50% (8/16), 31% (5/16), 13% (2/16) and 6% (1/16) for Acinetobacter baumannii, Pseudomonas aeruginosa, Pseudomonas luteola, and Pseudomonas fluorescens, respectively. Twenty-nine percent (29%) (6/17) of the strains produced carbapenemases. No mcr-1 and mcr-2 plasmid genes were detected. On the other hand, 17.6% (3/17) of the strains possessed the carbapenemase genes distributed as follows: Carba type (60%), OXA type (40%) and IMP type (0%). The results of this study highlight a high resistance to colistin in strains belonging to the genera Acinetobacter and Pseudomonas, and some of these strains produce carbapenemases.展开更多
Purpose: The incidence of hyperplastic thyroid nodular disease has been consistently rising over the last decades. In addition, unsuspected papillary thyroid carcinoma (PTC) can be found in up to 34% of patients opera...Purpose: The incidence of hyperplastic thyroid nodular disease has been consistently rising over the last decades. In addition, unsuspected papillary thyroid carcinoma (PTC) can be found in up to 34% of patients operated for benign thyroid lesions. PTC tends to occur multi-focally and is commonly of polyclonal origin. We set out to test the hypothesis that in benign thyroid disease, a unique genetic signature can already be identified in the benign pathology, which is associated with a susceptibility of the thyroid tissue to neoplastic transformation in the context of additional growth promoting stimuli. Patients and Methods: We obtained a set of 23 samples from patients with multinodular goiter (MNG), 12 of whom also harbored an unsuspected PTC. We used global gene expression analysis to evaluate for dissimilarities in the gene expression patterns between these two groups. We also compared these patterns to the profiles of 3 normal thyroid and 7 PTC samples. Results: We were able to accurately distinguish between hyperplastic nodules of patients with multinodular goiter and those that were associated with a PTC. One of the strongest differentially expressed genes, CDC42, has been implicated to respond to environmental factors such as UVB radiation and might point to novel factors contributing to PTC genesis in the setting of pre-existing benign proliferative disease. Conclusion: While the comparison between histologically identical samples cannot distinguish the two groups of goiters, unsupervised or supervised approaches allowed us to identify a molecular signature associated with PTC susceptibility in multinodular goiter.展开更多
文摘Background and Purpose: The reintroduction of colistin as a last resort treatment against multi-resistant Gram-negative bacilli, is currently challenged by the emergence of colistin-resistant bacteria. The aim of this study was to assess the susceptibility of Pseudomonas and Acinetobacter strains to colistin, to identify carbapenemase production, and to investigate the plasmid genes involved in colistin resistance and carbapenemase production. Methodology: In order to establish the susceptibility profiles of 17 strains of Pseudomonas and Acinetobacter to colistin, their Minimum Inhibitory Concentrations (MICs) were determined using the liquid microdilution method. The possible production of carbapenemases was investigated with the modified Carbapenem Inactivation Method (mCIM). The search for genes encoding carbapenemases (bla<sub>OXA</sub>, bla<sub>IMP</sub>, bla<sub>Carba</sub>) and those responsible for plasmid resistance to colistin (mcr-1 and mcr-2) was performed by conventional PCR. Results and Conclusion: Ninety-four percent (94%) (16/17) of the strains were resistant to colistin. Intraspecies distribution was 50% (8/16), 31% (5/16), 13% (2/16) and 6% (1/16) for Acinetobacter baumannii, Pseudomonas aeruginosa, Pseudomonas luteola, and Pseudomonas fluorescens, respectively. Twenty-nine percent (29%) (6/17) of the strains produced carbapenemases. No mcr-1 and mcr-2 plasmid genes were detected. On the other hand, 17.6% (3/17) of the strains possessed the carbapenemase genes distributed as follows: Carba type (60%), OXA type (40%) and IMP type (0%). The results of this study highlight a high resistance to colistin in strains belonging to the genera Acinetobacter and Pseudomonas, and some of these strains produce carbapenemases.
文摘Purpose: The incidence of hyperplastic thyroid nodular disease has been consistently rising over the last decades. In addition, unsuspected papillary thyroid carcinoma (PTC) can be found in up to 34% of patients operated for benign thyroid lesions. PTC tends to occur multi-focally and is commonly of polyclonal origin. We set out to test the hypothesis that in benign thyroid disease, a unique genetic signature can already be identified in the benign pathology, which is associated with a susceptibility of the thyroid tissue to neoplastic transformation in the context of additional growth promoting stimuli. Patients and Methods: We obtained a set of 23 samples from patients with multinodular goiter (MNG), 12 of whom also harbored an unsuspected PTC. We used global gene expression analysis to evaluate for dissimilarities in the gene expression patterns between these two groups. We also compared these patterns to the profiles of 3 normal thyroid and 7 PTC samples. Results: We were able to accurately distinguish between hyperplastic nodules of patients with multinodular goiter and those that were associated with a PTC. One of the strongest differentially expressed genes, CDC42, has been implicated to respond to environmental factors such as UVB radiation and might point to novel factors contributing to PTC genesis in the setting of pre-existing benign proliferative disease. Conclusion: While the comparison between histologically identical samples cannot distinguish the two groups of goiters, unsupervised or supervised approaches allowed us to identify a molecular signature associated with PTC susceptibility in multinodular goiter.
