1,164 research outputs found

    Resisting austerity in the era of COVID-19.:Between nationwide mobilisation and decentralised organising in Ecuador

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    Since 2017, the return of a neoliberal government in Ecuador has been characterized by austerity measures designed to lower state debt, particularly through cuts to social and environmental programs and the privatisation of state institutions. These policies have worsened ongoing economic and environmental crises suffered by the country’s poor, leading to massive protests in October 2019, which temporarily blocked further austerity measures. Yet, in subsequent months, the COVID-19 emergency enabled the government to move forward with neoliberal reforms and with policies promoting the expansion of extractive frontiers and the corporate food system. In this chapter, we examine decentralised organising among anti-neoliberal movements during the pandemic, particularly anti-extractivist and peasant agro-ecological collectives. We confirm prior findings regarding austerity that qualify it as a strategy not only to reduce state expenditure, but also to privately appropriate the commons, actively redirecting wealth to capital. Our research highlights that, in a context where mass protests are hindered by the pandemic, anti-neoliberal resistance in Ecuador operates in flexible articulations or assemblages that respond to shifting contexts. In 2019, marginalized sectors converged on urban political centres, concentrating a popular mass to pressure the central government and later, during COVID-19, local organisations advanced forms of decentralised resistance across the country, constructing or expanding solidarity networks, using legal and digital systems, and mobilizing alliances with local governments. Thus, subaltern anti-neoliberal movements continued to advance a politics of solidarity across changing contexts by flexibly articulating organisationally and tactically

    HIPE: HMC Instruction Predication Extension Applied on Database Processing

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    The recent Hybrid Memory Cube (HMC) is a smart memory which includes functional units inside one logic layer of the 3D stacked memory design. In order to execute instructions inside the Hybrid Memory Cube (HMC), the processor needs to send instructions to be executed near data, keeping most of the pipeline complexity inside the processor. Thus, control-flow and data-flow dependencies are all managed inside the processor, in such way that only update instructions are supported by the HMC. In order to solve data-flow dependencies inside the memory, previous work proposed HMC Instruction Vector Extensions (HIVE), which embeds a high number of functional units with a interlock register bank. In this work we propose HMC Instruction Prediction Extensions (HIPE), that supports predicated execution inside the memory, in order to transform control-flow dependencies into data-flow dependencies. Our mechanism focus on removing the high latency iteration between the processor and the smart memory during the execution of branches that depends on data processed inside the memory. In this paper we evaluate a balanced design of HIVE comparing to x86 and HMC executions. After we show the HIPE mechanism results when executing a database workload, which is a strong candidate to use smart memories. We show interesting trade-offs of performance when comparing our mechanism to previous work

    Semiclassical approach to fidelity amplitude

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    The fidelity amplitude is a quantity of paramount importance in echo type experiments. We use semiclassical theory to study the average fidelity amplitude for quantum chaotic systems under external perturbation. We explain analytically two extreme cases: the random dynamics limit --attained approximately by strongly chaotic systems-- and the random perturbation limit, which shows a Lyapunov decay. Numerical simulations help us bridge the gap between both extreme cases.Comment: 10 pages, 9 figures. Version closest to published versio

    Transcriptome analysis of Loxosceles laeta (Araneae, Sicariidae) spider venomous gland using expressed sequence tags

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    <p>Abstract</p> <p>Background</p> <p>The bite of spiders belonging to the genus <it>Loxosceles </it>can induce a variety of clinical symptoms, including dermonecrosis, thrombosis, vascular leakage, haemolysis, and persistent inflammation. In order to examine the transcripts expressed in venom gland of <it>Loxosceles laeta </it>spider and to unveil the potential of its products on cellular structure and functional aspects, we generated 3,008 expressed sequence tags (ESTs) from a cDNA library.</p> <p>Results</p> <p>All ESTs were clustered into 1,357 clusters, of which 16.4% of the total ESTs belong to recognized toxin-coding sequences, being the Sphingomyelinases D the most abundant transcript; 14.5% include "possible toxins", whose transcripts correspond to metalloproteinases, serinoproteinases, hyaluronidases, lipases, C-lectins, cystein peptidases and inhibitors. Thirty three percent of the ESTs are similar to cellular transcripts, being the major part represented by molecules involved in gene and protein expression, reflecting the specialization of this tissue for protein synthesis. In addition, a considerable number of sequences, 25%, has no significant similarity to any known sequence.</p> <p>Conclusion</p> <p>This study provides a first global view of the gene expression scenario of the venom gland of <it>L. laeta </it>described so far, indicating the molecular bases of its venom composition.</p

    Influence of the Human Lipidome on Epicardial Fat Volume in Mexican American Individuals

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    Introduction: Cardiovascular disease (CVD) is the leading cause of mortality worldwide and is the leading cause of death in the US. Lipid dysregulation is a well-known precursor to metabolic diseases, including CVD. There is a growing body of literature that suggests MRI-derived epicardial fat volume, or epicardial adipose tissue (EAT) volume, is linked to the development of coronary artery disease. Interestingly, epicardial fat is also actively involved in lipid and energy homeostasis, with epicardial adipose tissue having a greater capacity for release and uptake of free fatty acids. However, there is a scarcity of knowledge on the influence of plasma lipids on EAT volume. Aim: The focus of this study is on the identification of novel lipidomic species associated with CMRI-derived measures of epicardial fat in Mexican American individuals. Methods: We performed lipidomic profiling on 200 Mexican American individuals. High-throughput mass spectrometry enabled rapid capture of precise lipidomic profiles, providing measures of 799 unique species from circulating plasma samples. Because of our extended pedigree design, we utilized a standard quantitative genetic linear mixed model analysis to determine whether lipids were correlated with EAT by formally testing for association between each lipid species and the CMRI epicardial fat phenotype. Results: After correction for multiple testing using the FDR approach, we identified 135 lipid species showing significant association with epicardial fat. Of those, 131 lipid species were positively correlated with EAT, where increased circulating lipid levels were correlated with increased epicardial fat. Interestingly, the top 10 lipid species associated with an increased epicardial fat volume were from the deoxyceramide (Cer(m)) and triacylglycerol (TG) families. Deoxyceramides are atypical and neurotoxic sphingolipids. Triacylglycerols are an abundant lipid class and comprise the bulk of storage fat in tissues. Pathologically elevated TG and Cer(m) levels are related to CVD risk and, in our study, to EAT volume. Conclusion: Our results indicate that specific lipid abnormalities such as enriched saturated triacylglycerols and the presence of toxic ceramides Cer(m) in plasma of our individuals could precede CVD with increased EAT volume

    The low affinity glucose transporter HxtB is also involved in glucose signalling and metabolism in Aspergillus nidulans

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    One of the drawbacks during second-generation biofuel production from plant lignocellulosic biomass is the accumulation of glucose, the preferred carbon source of microorganisms, which causes the repression of hydrolytic enzyme secretion by industrially relevant filamentous fungi. Glucose sensing, subsequent transport and cellular signalling pathways have been barely elucidated in these organisms. This study therefore characterized the transcriptional response of the filamentous fungus Aspergillus nidulans to the presence of high and low glucose concentrations under continuous chemostat cultivation with the aim to identify novel factors involved in glucose sensing and signalling. Several transcription factor- and transporter-encoding genes were identified as being differentially regulated, including the previously characterized glucose and xylose transporter HxtB. HxtB was confirmed to be a low affinity glucose transporter, localizing to the plasma membrane under low- and high-glucose conditions. Furthermore, HxtB was shown to be involved in conidiation-related processes and may play a role in downstream glucose signalling. A gene predicted to encode the protein kinase PskA was also identified as being important for glucose metabolism. This study identified several proteins with predicted roles in glucose metabolic processes and provides a foundation for further investigation into the response of biotechnologically important filamentous fungi to glucose

    Evaluation of the use and need of dental prosthesis in a school clinic: a cross-study / Avaliação do uso e necessidade de prótese dentåria numa clínica escola: um estudo transversal

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    Objective: This paper aims to identify the use and need of prosthesis, age and gender of users of the dental service of the school clinic of a private university in Recife. Methodology: A descriptive cross-sectional study was performed through analysis of medical records. From 2,294 records of the semesters 2016.2 and 2017.1, 790 were analyzed that met the inclusion and exclusion criteria. The study was divided into three groups according to the age of the patients (35 - 44, 45 - 64 and 65 - 74 years old) and were analyzed according to gender, prosthesis use, need of prosthesis or use and need of prosthesis. Data were tabulated in Microsoft Excel © and submitted to statistics. Results: Females were the most expressive in the search of the service (66.1%); besides that, 86.8% of the patients did not wear prosthesis and 71.1% needed to use it. Total Prosthesis was the most used (50%) and the Removable Partial Prosthesis presented the greatest need of use (74%). Conclusion: It was concluded that women from 45 – 64 years old seek more the rehabilitation service, and the need is greater in one arcade, showing an evolution to access the dentist. 

    Hippocampal Astrocytes in Migrating and Wintering Semipalmated Sandpiper

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    Seasonal migratory birds return to the same breeding and wintering grounds year after year, and migratory long-distance shorebirds are good examples of this. These tasks require learning and long-term spatial memory abilities that are integrated into a navigational system for repeatedly locating breeding, wintering, and stopover sites. Previous investigations focused on the neurobiological basis of hippocampal plasticity and numerical estimates of hippocampal neurogenesis in birds but only a few studies investigated potential contributions of glial cells to hippocampal-dependent tasks related to migration. Here we hypothesized that the astrocytes of migrating and wintering birds may exhibit significant morphological and numerical differences connected to the long-distance flight. We used as a model the semipalmated sandpipe

    Aberrant upregulation of the glycolytic enzyme PFKFB3 in CLN7 neuronal ceroid lipofuscinosis

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    CLN7 neuronal ceroid lipofuscinosis is an inherited lysosomal storage neurodegenerative disease highly prevalent in children. CLN7/MFSD8 gene encodes a lysosomal membrane glycoprotein, but the biochemical processes affected by CLN7-loss of function are unexplored thus preventing development of potential treatments. Here, we found, in the Cln7∆ex2 mouse model of CLN7 disease, that failure in autophagy causes accumulation of structurally and bioenergetically impaired neuronal mitochondria. In vivo genetic approach reveals elevated mitochondrial reactive oxygen species (mROS) in Cln7∆ex2 neurons that mediates glycolytic enzyme PFKFB3 activation and contributes to CLN7 pathogenesis. Mechanistically, mROS sustains a signaling cascade leading to protein stabilization of PFKFB3, normally unstable in healthy neurons. Administration of the highly selective PFKFB3 inhibitor AZ67 in Cln7∆ex2 mouse brain in vivo and in CLN7 patients-derived cells rectifies key disease hallmarks. Thus, aberrant upregulation of the glycolytic enzyme PFKFB3 in neurons may contribute to CLN7 pathogenesis and targeting PFKFB3 could alleviate this and other lysosomal storage diseases
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