VARIABILIDADE NAS TAXAS FISIOLÓGICAS DO MEXILHÃO PERNA PERNA EM DOIS SÍTIOS DE CULTIVO DO LITORAL NORTE DE SANTA CATARINA

With the growing socioeconomic activity of mussel farming on Santa Catarina’s coast, the identification of new cultivation sites became necessary. Among a variety of methods used for the analysis of potential producing areas, studying of the mussel physiological rates may be considered as one of the most appropriated, specially when addressing the monitoring of sites already established and the negative effects of environmental pollution. This report presents a preliminary comparison between two areas of cultivation in the northern coast of the state (municipalities of Penha and Bombinhas). In both locations, environmental data (temperature, salinity and seston) and physiological parameters of the mussels (growth, and filtration, respiration and assimilation rates) were analysed. Our findings suggested a direct relationship between temperature and mussel growth rate and also between salinity and respiration rates for both areas. The seston concentration showed a high environmental variability as a response to the continental drainage. In addition, the filtration and assimilation rates seemed to be influenced by the stages of embryonic follicle maturation. In terms of production, the sites showed larger differences during the colder months as compared to the warmer ones, when the results were quite similar. More conclusive results are dependent of studies conducted along a complete annual cycle.Com a crescente atividade sócio-econômica da mitilicultura na costa do estado de Santa Catarina, problemas relacionados com a identificação de novos sítios de cultivo tornaram-se prioritários. Dentre os mais diferentes métodos utilizados para análise de potenciais regiões produtoras, o estudo das taxas fisiológicas dos mexilhões enquadram-se como uma das mais adequadas, incluindo neste caso, o monitoramento de sítios já estabelecidos e problemas relacionados com a poluição ambiental. Este relatório faz referência a uma preliminar comparação entre duas áreas de cultivo do mexilhão Perna perna no litoral norte do estado (municípios de Penha e Bombinhas). Dados ambientais de temperatura, salinidade, material em suspensão e fisiológicos do mexilhão como crescimento, filtração, respiração e assimilação foram comparados. Os principais resultados deste estudo podem ser resumidos em: relação direta entre a temperatura e a taxa de crescimento e relação entre a salinidade e a taxa de respiração para os dois ambientes. O material em suspensão apresentou uma maior variabilidade ambiental influenciada pelos aportes continentais mas que necessitam de maiores investigações. A importância das taxas de maturação dos folículos embrionários dos mexilhões foi sugerida na relação com as taxas de filtração e assimilação. Em termos de produção, os ambientes mostraram maiores diferenças nos meses frios e similar resultados nos meses quentes. Entretanto, resultados conclusivos estão dependentes de estudos ao longo de um ciclo anual

The N-P-K soil nutrient balance of portuguese cropland in the 1950s: the transition from organic to chemical fertilization

Agricultural nutrient balances have been receiving increasing attention in both historical and nutrient management research. The main objectives of this study were to further develop balance methodologies and to carry out a comprehensive assessment of the functioning and nutrient cycling of 1950s agroecosystems in Portugal. Additionally, the main implications for the history of agriculture in Portugal were discussed from the standpoint of soil fertility. We used a mass balance approach that comprises virtually all nitrogen (N), phosphorus (P) and potassium (K) inputs and outputs from cropland topsoil for average conditions in the period 1951–56. We found a consistent deficit in N, both for nationwide (−2.1 kg.ha−1.yr−1) and arable crops (−1.6 kg.ha−1.yr−1) estimates, that was rectified in the turn to the 1960 decade. P and K were, in contrast, accumulating in the soil (4.2–4.6 kg.ha−1.yr−1 and 1.0–3.0 kg.ha−1.yr−1, respectively). We observed that the 1950s is the very moment of inflection from an agriculture fertilized predominantly through reused N in biomass (livestock excretions plus marine, plant and human waste sources) to one where chemical fertilizers prevailed. It is suggested that N deficiency played an important role in this transitioninfo:eu-repo/semantics/publishedVersio

Activin A Induces Langerhans Cell Differentiation In Vitro and in Human Skin Explants

Langerhans cells (LC) represent a well characterized subset of dendritic cells located in the epidermis of skin and mucosae. In vivo, they originate from resident and blood-borne precursors in the presence of keratinocyte-derived TGFβ. Ιn vitro, LC can be generated from monocytes in the presence of GM-CSF, IL-4 and TGFβ. However, the signals that induce LC during an inflammatory reaction are not fully investigated. Here we report that Activin A, a TGFβ family member induced by pro-inflammatory cytokines and involved in skin morphogenesis and wound healing, induces the differentiation of human monocytes into LC in the absence of TGFβ. Activin A-induced LC are Langerin+, Birbeck granules+, E-cadherin+, CLA+ and CCR6+ and possess typical APC functions. In human skin explants, intradermal injection of Activin A increased the number of CD1a+ and Langerin+ cells in both the epidermis and dermis by promoting the differentiation of resident precursor cells. High levels of Activin A were present in the upper epidermal layers and in the dermis of Lichen Planus biopsies in association with a marked infiltration of CD1a+ and Langerin+ cells. This study reports that Activin A induces the differentiation of circulating CD14+ cells into LC. Since Activin A is abundantly produced during inflammatory conditions which are also characterized by increased numbers of LC, we propose that this cytokine represents a new pathway, alternative to TGFβ, responsible for LC differentiation during inflammatory/autoimmune conditions

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

Key mechanisms governing resolution of lung inflammation

Innate immunity normally provides excellent defence against invading microorganisms. Acute inflammation is a form of innate immune defence and represents one of the primary responses to injury, infection and irritation, largely mediated by granulocyte effector cells such as neutrophils and eosinophils. Failure to remove an inflammatory stimulus (often resulting in failed resolution of inflammation) can lead to chronic inflammation resulting in tissue injury caused by high numbers of infiltrating activated granulocytes. Successful resolution of inflammation is dependent upon the removal of these cells. Under normal physiological conditions, apoptosis (programmed cell death) precedes phagocytic recognition and clearance of these cells by, for example, macrophages, dendritic and epithelial cells (a process known as efferocytosis). Inflammation contributes to immune defence within the respiratory mucosa (responsible for gas exchange) because lung epithelia are continuously exposed to a multiplicity of airborne pathogens, allergens and foreign particles. Failure to resolve inflammation within the respiratory mucosa is a major contributor of numerous lung diseases. This review will summarise the major mechanisms regulating lung inflammation, including key cellular interplays such as apoptotic cell clearance by alveolar macrophages and macrophage/neutrophil/epithelial cell interactions. The different acute and chronic inflammatory disease states caused by dysregulated/impaired resolution of lung inflammation will be discussed. Furthermore, the resolution of lung inflammation during neutrophil/eosinophil-dominant lung injury or enhanced resolution driven via pharmacological manipulation will also be considered

Search for jet extinction in the inclusive jet-pT spectrum from proton-proton collisions at s=8 TeV

Published by the American Physical Society under the terms of the Creative Commons Attribution 3.0 License. Further distribution of this work must maintain attribution to the author(s) and the published articles title, journal citation, and DOI.The first search at the LHC for the extinction of QCD jet production is presented, using data collected with the CMS detector corresponding to an integrated luminosity of 10.7  fb−1 of proton-proton collisions at a center-of-mass energy of 8 TeV. The extinction model studied in this analysis is motivated by the search for signatures of strong gravity at the TeV scale (terascale gravity) and assumes the existence of string couplings in the strong-coupling limit. In this limit, the string model predicts the suppression of all high-transverse-momentum standard model processes, including jet production, beyond a certain energy scale. To test this prediction, the measured transverse-momentum spectrum is compared to the theoretical prediction of the standard model. No significant deficit of events is found at high transverse momentum. A 95% confidence level lower limit of 3.3 TeV is set on the extinction mass scale

Constraints on the Higgs boson width from off-shell production and decay to Z-boson pairs

Constraints are presented on the total width of the recently discovered Higgs boson, GH, using its relative on-shell and off-shell production and decay rates to a pair of Z bosons, where one Z boson decays to an electron or muon pair, and the other to an electron, muon, or neutrino pair. The analysis is based on the data collected by the CMS experiment at the LHC in 2011 and 2012, corresponding to integrated luminosities of 5.1fb-1 at a center-of-mass energy vs=7 TeV and 19.7fb-1at vs=8 TeV. A simultaneous maximum likelihood fit to the measured kinematic distributions near the resonance peak and above the Z-boson pair production threshold leads to an upper limit on the Higgs boson width of GH<22 MeV at a 95% confidence level, which is 5.4 times the expected value in the standard model at the measured mass of mH=125.6 GeV

The interstitium in cardiac repair: role of the immune-stromal cell interplay

Cardiac regeneration, that is, restoration of the original structure and function in a damaged heart, differs from tissue repair, in which collagen deposition and scar formation often lead to functional impairment. In both scenarios, the early-onset inflammatory response is essential to clear damaged cardiac cells and initiate organ repair, but the quality and extent of the immune response vary. Immune cells embedded in the damaged heart tissue sense and modulate inflammation through a dynamic interplay with stromal cells in the cardiac interstitium, which either leads to recapitulation of cardiac morphology by rebuilding functional scaffolds to support muscle regrowth in regenerative organisms or fails to resolve the inflammatory response and produces fibrotic scar tissue in adult mammals. Current investigation into the mechanistic basis of homeostasis and restoration of cardiac function has increasingly shifted focus away from stem cell-mediated cardiac repair towards a dynamic interplay of cells composing the less-studied interstitial compartment of the heart, offering unexpected insights into the immunoregulatory functions of cardiac interstitial components and the complex network of cell interactions that must be considered for clinical intervention in heart diseases