Molecular identification of Nocardia species using the sodA gene Identificación molecular de especies de Nocardia utilizando el gen sodA.

Currently for bacterial identification and classification the rrs gene encoding 16S rRNA is used as a reference method for the analysis of strains of the genus Nocardia. However, it does not have enough polymorphism to differentiate them at the species level. This fact makes it necessary to search for molecular targets that can provide better identification. The sodA gene (encoding the enzyme superoxide dismutase) has had good results in identifying species of other Actinomycetes. In this study the sodA gene is proposed for the identification and differentiation at the species level of the genus Nocardia. We used 41 type species of various collections; a 386 bp fragment of the sodA gene was amplified and sequenced, and a phylogenetic analysis was performed comparing the genes rrs (1171 bp), hsp65 (401 bp), secA1 (494 bp), gyrB (1195 bp) and rpoB (401 bp). The sequences were aligned using the Clustal X program. Evolutionary trees according to the neighbour-joining method were created with the programs Phylo_win and MEGA 6. The specific variability of the sodA genus of the genus Nocardia was analysed. A high phylogenetic resolution, significant genetic variability, and specificity and reliability were observed for the differentiation of the isolates at the species level. The polymorphism observed in the sodA gene sequence contains variable regions that allow the discrimination of closely related Nocardia species. The clear specificity, despite its small size, proves to be of great advantage for use in taxonomic studies and clinical diagnosis of the genus Nocardia

Spectroscopy of horizontal branch stars in NGC6752 - Anomalous results on atmospheric parameters and masses

We used the ESO VLT-FORS2 facility to collect low-resolution spectra of 51 targets distributed along the Horizontal Branch. We determined atmospheric parameters by comparison with theoretical models through standard fitting routines, and masses by basic equations. Results are in general in good agreement with previous works, although not always with theoretical expectations for cooler stars (Teff<15000 K). The calculated color excess is systematically lower than literature values, pointing towards a possible underestimation of effective temperatures. Moreover, we find two groups of stars at Teff=14000 K and at Teff=27000$ K that present anomalies with respect to the general trend and expectations. We suppose that the three peculiar bright stars at Teff=14000 K are probably affected by an enhanced stellar wind. For the eight Extreme Horizontal Branch stars at Teff=27000 K which show unusually high masses we find no plausible explanation. While most of our results agree well with the predictions of standard horizontal branch evolution, we still have problems with the low masses we derive in certain temperature ranges. We believe that Kurucz ATLAS9 LTE model atmospheres with solar-scaled abundances are probably inadequate for these temperature ranges. Concerning the group of anomalous stars at Teff=27000 K, a Kolmogorov-Smirnov test indicates that there is only an 8.4% probability that these stars are randomly drawn from the general distribution in the color-magnitude diagram. This is not conclusive but points out that these stars could be both (and independently) spectroscopically and photometrically peculiar with respect to the general Extreme Horizontal Branch population.Comment: 12 pages, 10 figures, accepted for pubblication in A&A. Replaced for typos and better LaTeX outpu

Development of a nursing intervention to facilitate optimal antiretroviral-treatment taking among people living with HIV

<p>Abstract</p> <p>Background</p> <p>Failure by a large portion of PLHIV to take optimally ARV treatment can have serious repercussions on their health. The absence of a systematic treatment-taking promotion program in Quebec prompted stakeholders to develop jointly a theory- and evidence-based nursing intervention to this end. This article describes the results of a collective effort by researchers, clinicians and PLHIV to share their knowledge and create an appropriate intervention.</p> <p>Methods</p> <p>Intervention mapping was used as the framework for developing the intervention. First, the target population and environmental conditions were analyzed and a literature review conducted to identify predictors of optimal treatment taking. The predictors to emerge were self-efficacy and attitudes. Performance objectives were subsequently defined and crossed-referenced with the predictors to develop a matrix of change objectives. Then, theories of self-efficacy and persuasion (the predictors to emerge from step 1), together with practical strategies derived from these theories, were used to design the intervention. Finally, the sequence and content of the intervention activities were defined and organized, and the documentary material designed.</p> <p>Results</p> <p>The intervention involves an intensive, personalized follow-up over four direct-contact sessions, each lasting 45–75 minutes. Individuals are engaged in a learning process that leads to the development of skills to motivate themselves to follow the therapeutic plan properly, to overcome situations that make taking the antiretroviral medication difficult, to cope with side-effects, to relate to people in their social circle, and to deal with health professionals.</p> <p>Conclusion</p> <p>The intervention was validated by various health professionals and pre-tested with four PLHIV. Preliminary results support the suitability and viability of the intervention. A randomized trial is currently underway to verify the effectiveness of the intervention in promoting optimal antiretroviral treatment taking.</p

Neural Reuse and the Nature of Evolutionary Constraints

In humans, the reuse of neural structure is particularly pronounced at short, task-relevant timescales. Here, an argument is developed for the claim that facts about neural reuse at task-relevant timescales conflict with at least one characterization of neural reuse at an evolutionary timescale. It is then argued that, in order to resolve the conflict, we must conceptualize evolutionary-scale reuse more abstractly than has been generally recognized. The final section of the paper explores the relationship between neural reuse and human nature. It is argued that neural reuse is not well-described as a process that constrains our present cognitive capacities. Instead, it liberates those capacities from the ancestral tethers that might otherwise have constrained them

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin