Topografía Infraclavicular De Los Fascículos Del Plexo Braquial En Diferentes Posiciones Del Miembro Superior

Brachial plexus neuropathies are common complaints among patients seen at orthopedic clinics. The causes range from traumatic to occupational factors and symptoms include paresthesia, paresis, and functional disability of the upper limb. Treatment can be surgical or conservative, but detailed knowledge of the brachial plexus is required in both cases to avoid iatrogenic injuries and to facilitate anesthetic block, preventing possible vascular punctures. Therefore, the objective of this study was to evaluate the topography of the infraclavicular brachial plexus fascicles in different upper limb positions adopted during some clinical procedures. A formalin-preserved, adult, male cadaver was used. The infraclavicular and axillary regions were dissected and the distance of the brachial plexus fascicles from adjacent bone structures was measured. No anatomical variation in the formation of the brachial plexus was observed. The metric relationships between the brachial plexus and adjacent bone prominences differed depending on the degree of shoulder abduction. Detailed knowledge of the infraclavicular topography of neurovascular structures helps with the diagnosis and especially with the choice of conservative or surgical treatment of brachial plexus neuropathies. © 2016, Universidad de la Frontera. All rights reserved.3431063106

Plasma-Based Longitudinal Evaluation of ESR1 Epigenetic Status in Hormone Receptor-Positive HER2-Negative Metastatic Breast Cancer

Background: Endocrine therapy (ET) is the mainstay of treatment for hormone receptor-positive human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer; however, adaptive mechanisms emerge in about 25\u201330% of cases through alterations in the estrogen receptor ligand-binding domain, with a consequent ligand-independent estrogen receptor activity. Epigenetic-mediated events are less known and potentially involved in alternative mechanisms of resistance. The aim of this study was to test the feasibility of estrogen receptor 1 (ESR1) epigenetic characterization through liquid biopsy and to show its potential longitudinal application for an early ET sensitivity assessment. Methods: A cohort of 49 women with hormone receptor-positive HER2-negative MBC was prospectively enrolled and characterized through circulating tumor DNA using methylation-specific droplet digital PCR (MS-ddPCR) before treatment start (BL) and after 3 months concomitantly with computed tomography (CT) scan restaging (EV1). ESR1 epigenetic status was defined by assessing the methylation of its main promoters (promA and promB). The most established cell-free tumor DNA (ctDNA) factors associated with ET resistance [ESR1 and phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (PIK3CA) mutations] were assessed through next-generation sequencing. Associations were tested through Mann\u2013Whitney U test, matched pairs variations through Wilcoxon signed rank test, and survival was analyzed by log-rank test. Results: The ET backbone was mainly based on aromatase inhibitors (AIs) (70.83%) in association with CDK4/6 inhibitors (93.75%). Significantly lower promA levels at baseline were observed in patients with liver metastases (P = 0.0212) and in patients with ESR1 mutations (P = 0.0091). No significant impact on PFS was observed for promA (P = 0.3777) and promB (P = 0.7455) dichotomized at the median while a 652-fold increase in promB or in either promA or promB at EV1 resulted in a significantly worse prognosis (respectively P = 0.0189, P = 0.0294). A significant increase at EV1 was observed for promB among patients with PIK3CA mutation (P = 0.0173). A trend was observed for promB in ESR1 wild-type patients and for promA in the ESR1 mutant subgroup. Conclusion: The study proofed the concept of an epigenetic characterization strategy based on ctDNA and is capable of being integrated in the current clinical workflow to give useful insights on treatment sensitivity

On the origin and processes controlling the elemental and isotopic composition of carbonates in hypersaline Andean lakes

H.J. and J.W.B. Rae acknowledge funding from the European Research Council under the European Union’s Horizon 2020 research and innovation program (grant agreement 805246).The Altiplano-Puna Plateau of the Central Andes hosts numerous lakes, playa-lakes, and salars with a great diversity and abundance of carbonates forming under extreme climatic, hydrologic, and environmental conditions. To unravel the underlying processes controlling the formation of carbonates and their geochemical signatures in hypersaline systems, we investigated coupled brine-carbonate samples in a high-altitude Andean lake using a wide suite of petrographic (SEM, XRD) and geochemical tools (δ2H, δ18O, δ13C, δ11B, major and minor ion composition, aqueous modelling). Our findings show that the inflow of hydrothermal springs in combination with strong CO2 degassing and evaporation plays an important role in creating a spatial diversity of hydro-chemical sub-environments allowing different types of microbialites (microbial mounds and mats), travertines, and fine-grained calcite minerals to form. Carbonate precipitation occurs in hot springs triggered by a shift in carbonate equilibrium by hydrothermal CO2 degassing and microbially-driven elevation of local pH at crystallisation. In lakes, carbonate precipitation is induced by evaporative supersaturation, with contributions from CO2 degassing and microbiological processes. Lake carbonates largely record the evaporitic enrichment (hence salinity) of the parent water which can be traced by Na, Li, B, and δ18O, although other factors (such as e.g., high precipitation rates, mixing with thermal waters, groundwater, or precipitation) also affect their signatures. This study is of significance to those dealing with the fractionation of oxygen, carbon, and boron isotopes and partitioning of elements in natural brine-carbonate environments. Furthermore, these findings contribute to the advancement in proxy development for these depositional environments.Peer reviewe

Data processing on simulated data for SHARK-NIR

A robust post processing technique is mandatory to analyse the coronagraphic high contrast imaging data. Angular Differential Imaging (ADI) and Principal Component Analysis (PCA) are the most used approaches to suppress the quasi-static structure in the Point Spread Function (PSF) in order to revealing planets at different separations from the host star. The focus of this work is to apply these two data reduction techniques to obtain the best limit detection for each coronagraphic setting that has been simulated for the SHARK-NIR, a coronagraphic camera that will be implemented at the Large Binocular Telescope (LBT). We investigated different seeing conditions ($0.4"-1"$) for stellar magnitude ranging from R=6 to R=14, with particular care in finding the best compromise between quasi-static speckle subtraction and planet detection.Comment: 9 pages, 8 figures, proceeding for the fifth Adaptive Optics for Extremely Large Telescopes (AO4ELT5) meeting in 201

Activity theory, complexity and sports coaching: An epistemology for a discipline

The aim of this article is two-fold. Firstly, it is to advance the case for Activity Theory (AT) as a credible and alternative lens to view and research sports coaching. Secondly, it is to position this assertion within the wider debate about the epistemology of coaching. Following a framing introduction, a more comprehensive review of the development and current conceptualisation of AT is given. Here, AT’s evolution through three distinct phases and related theorists, namely Vygotsky, Leont’ev and Engeström, is initially traced. This gives way to a more detailed explanation of AT’s principal conceptual components, including ‘object’, ‘subject’, ‘tools’ (mediating artefacts), ‘rules’, a ‘community’ and a ‘division of labour’. An example is then presented from empirical work illustrating how AT can be used as a means to research sports coaching. The penultimate section locates such thinking within coaching’s current ‘epistemological debate; arguing that the coaching ‘self’ is not an autonomous individual, but a relative part of social and cultural arrangements. Finally, a conclusion summarises the main points made, particularly in terms in presenting the grounding constructivist epistemology of AT as a potential way forward for sports coaching

CDKN1B mutation and copy number variation are associated with tumor aggressiveness in luminal breast cancer

The CDKN1B gene, encoding for the CDK inhibitor p27kip1, is mutated in defined human cancer subtypes, including breast, prostate carcinomas and small intestine neuroendocrine tumors. Lessons learned from small intestine neuroendocrine tumors suggest that CDKN1B mutations could be subclonal, raising the question of whether a deeper sequencing approach could lead to the identification of higher numbers of patients with mutations. Here, we addressed this question and analyzed human cancer biopsies from breast (n = 396), ovarian (n = 110) and head and neck squamous carcinoma (n = 202) patients, using an ultra-deep sequencing approach. Notwithstanding this effort, the mutation rate of CDKN1B remained substantially aligned with values from the literature, showing that essentially only hormone receptor-positive breast cancer displayed CDKN1B mutations in a relevant number of cases (3%). However, the analysis of copy number variation showed that another fraction of luminal breast cancer displayed loss (8%) or gain (6%) of the CDKN1B gene, further reinforcing the idea that the function of p27kip1 is important in this type of tumor. Intriguingly, an enrichment for CDKN1B alterations was found in samples from premenopausal luminal breast cancer patients (n = 227, 4%) and in circulating cell-free DNA from metastatic luminal breast cancer patients (n = 59, 8.5%), suggesting that CDKN1B alterations could correlate with tumor aggressiveness and/or occur later during disease progression. Notably, many of the identified somatic mutations resulted in p27kip1 protein truncation, leading to loss of most of the protein or of its C-terminal domain. Using a gene-editing approach in a luminal breast cancer cell line, MCF-7, we observed that the expression of p27kip1 truncating mutants that lose the C-terminal domains failed to rescue most of the phenotypes induced by CDKN1B gene knockout, indicating that the functions retained by the C-terminal portion are critical for its role as an oncosuppressor, at least in luminal breast cancer. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland