102 research outputs found

    Nietzsche & anarchism: an elective affinity, and a Nietzschean reading of the December 08 revolt in Athens

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    The aim of this research is to establish the bond between Friedrich Nietzsche and the anarchists, through the apparatus of elective affinity , and to challenge the boundaries of several anarchist trends especially classical and post anarchism and ideologies like anarchism and libertarian Marxism. Moreover, it highlights the importance of reading Nietzsche politically, in a radical way, to understand his utility for the contemporary anarchist movement. The review of the literature concerning the Nietzsche-anarchy relationship shows the hitherto limited bibliography and stresses the possibility of exploring this connection, with the methodological help of Michael Löwy s concept of elective affinity . The research opens with a discussion of anarchism, following the dominant model for categorizing anarchist traditions, presenting its basic features and currents and drawing on its historical development. This leads to the introduction of two points (the questioning of the anarchist canon and the exposure of the diversity that basic anarchist concepts bear among different anarchist currents) which contest the rigid ideological perception of anarchism in favour of a fluid and dynamic anarchy. There emerges the elective affinity with Nietzsche, serving a double goal: the unification of the distinct anarchist tendencies and the definition of the anarchist parameters in relation to other ideologies. The following section of the thesis examines Nietzsche, by presenting the evolution of his philosophical thought and the fundamental theses of his perception of politics. It, then, continues with a detailed analysis of the main concepts of his philosophy based on the interpretation made by Gilles Deleuze, Alexander Nehamas and Keith Ansell-Pearson, thus structuring its interpretative context for establishing the Nietzsche-anarchy connection. This establishment is realized in a dual way. Firstly, by exploring the elective affinity through the presence of Nietzsche in the thought and politics of anarchist/libertarian thinkers (Goldman, Landauer, Benjamin) and currents (post-anarchism), and secondly by recognizing the anarchist worldview in the Nietzschean philosophy. The first path (Nietzsche in anarchism) shows how Nietzsche has interacted with or has been absorbed by the anarchist way of thinking, whereas the second path (anarchism in Nietzsche) reveals the affinal worldview of the two parts by extensively using the interpretation context mentioned above. The final section of the thesis applies the whole analysis above on a Nietzschean reading of the December 08 revolt in Athens based on the Of the Three Metamorphoses discourse from Thus Spoke Zarathustra. What has been found is the existence of a clear bond, between Nietzsche and the anarchists, which even reaches the upper levels of Löwy s elective affinity , that is Nietzschean Anarchism as a result of the two parts interactive fusion. The significance of this finding is that the relevant affinity may contribute to an alternative, to the dominant, perception of anarchism as an ideology. It may also designate its special features together with its weaknesses, meaning the objections of Nietzsche to certain aspects of the anarchist practices and worldview (violence, resentment, bad conscience), thus opening a whole new road of self-criticism for the anarchists of the twenty first century. In addition, the location and analysis of the elective affinity serves the debunking of the Nietzschean concepts used by conservative and right-wing readings in order to appropriate Nietzsche, and of the accusations that the German philosopher had unleashed against anarchists, which reveals his misunderstanding of anarchist politics

    Establishment of computational biology in Greece and Cyprus: Past, present, and future.

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    We review the establishment of computational biology in Greece and Cyprus from its inception to date and issue recommendations for future development. We compare output to other countries of similar geography, economy, and size—based on publication counts recorded in the literature—and predict future growth based on those counts as well as national priority areas. Our analysis may be pertinent to wider national or regional communities with challenges and opportunities emerging from the rapid expansion of the field and related industries. Our recommendations suggest a 2-fold growth margin for the 2 countries, as a realistic expectation for further expansion of the field and the development of a credible roadmap of national priorities, both in terms of research and infrastructure funding

    Metagenomics : tools and insights for analyzing next-generation sequencing data derived from biodiversity studies

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    Advances in next-generation sequencing (NGS) have allowed significant breakthroughs in microbial ecology studies. This has led to the rapid expansion of research in the field and the establishment of “metagenomics”, often defined as the analysis of DNA from microbial communities in environmental samples without prior need for culturing. Many metagenomics statistical/computational tools and databases have been developed in order to allow the exploitation of the huge influx of data. In this review article, we provide an overview of the sequencing technologies and how they are uniquely suited to various types of metagenomic studies. We focus on the currently available bioinformatics techniques, tools, and methodologies for performing each individual step of a typical metagenomic dataset analysis. We also provide future trends in the field with respect to tools and technologies currently under development. Moreover, we discuss data management, distribution, and integration tools that are capable of performing comparative metagenomic analyses of multiple datasets using well-established databases, as well as commonly used annotation standards

    MicroRNA-124 Regulates STAT3 Expression and Is Down-regulated in Colon Tissues of Pediatric Patients With Ulcerative Colitis

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    Background & Aims - Altered levels and functions of microRNAs (miRs) have been associated with inflammatory bowel diseases (IBDs), although little is known about their roles in pediatric IBD. We investigated whether colonic mucosal miRs are altered in children with ulcerative colitis (UC). Methods - We used a library of 316 miRs to identify those that regulate phosphorylation of STAT3 in NCM460 human colonocytes incubated with interleukin-6. Levels of miR-124 were measured by real-time PCR analysis of colon biopsies from pediatric and adult patients with UC and patients without IBD (controls), and of HCT-116 colonocytes incubated with 5-aza-2’-deoxycytidine. Methylation of the MIR124 promoter was measured by quantitative methylation-specific PCR. Results - Levels of phosphorylated STAT3 and the genes it regulates (encoding VEGF, BCL2, BCLXL, and MMP9) were increased in pediatric patients with UC, compared to control tissues. Overexpression of miR-124, let-7, miR-125, miR-26, or miR-101 reduced STAT3 phosphorylation by ≥75% in NCM460 cells; miR-124 had the greatest effect. miR-124 was downregulated specifically in colon tissues from pediatric patients with UC and directly targeted STAT3 mRNA. Levels of miR-124 were decreased whereas levels of STAT3 phosphorylation increased in colon tissues from pediatric patients with active UC, compared to those with inactive disease. Furthermore, levels of miR-124 and STAT3 were inversely correlated in mice with experimental colitis. Downregulation of miR-124 in tissues from children with UC was attributed to hypermethylation of its promoter region. Incubation of HCT-116 colonocytes with 5-aza-2’ deoxycytidine upregulated miR-124 and reduced levels of STAT3 mRNA. Conclusions - MiR-124 appears to regulate the expression of STAT3. Reduced levels of miR-124 in colon tissues of children with active UC appear to increase expression and activity of STAT3, which could promote inflammation and pathogenesis of UC in children

    Lin28A and Lin28B Inhibit let-7 MicroRNA Biogenesis by Distinct Mechanisms

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    SummaryLin28A and Lin28B selectively block the expression of let-7 microRNAs and function as oncogenes in a variety of human cancers. Lin28A recruits a TUTase (Zcchc11/TUT4) to let-7 precursors to block processing by Dicer in the cell cytoplasm. Here we find that unlike Lin28A, Lin28B represses let-7 processing through a Zcchc11-independent mechanism. Lin28B functions in the nucleus by sequestering primary let-7 transcripts and inhibiting their processing by the Microprocessor. The inhibitory effects of Zcchc11 depletion on the tumorigenic capacity and metastatic potential of human cancer cells and xenografts are restricted to Lin28A-expressing tumors. Furthermore, the majority of human colon and breast tumors analyzed exclusively express either Lin28A or Lin28B. Lin28A is expressed in HER2-overexpressing breast tumors, whereas Lin28B expression characterizes triple-negative breast tumors. Overall our results illuminate the distinct mechanisms by which Lin28A and Lin28B function and have implications for the development of new strategies for cancer therapy

    Assessment of Circulating MicroRNAs for the Diagnosis and Disease Activity Evaluation in Patients with Ulcerative Colitis by Using the Nanostring Technology

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    Background: Clinical decision and patient care management in inflammatory bowel diseases is largely based on the assessment of clinical symptoms, while the biomarkers currently in use poorly reflect the actual disease activity. Therefore, the identification of novel biomarkers will serve an unmet clinical need for IBD screening and patient management. We examined the utility of circulating microRNAs for diagnosis and disease activity monitoring in ulcerative colitis (UC) patients. Methods: Blood serum microRNAs were isolated from UC patients with active and inactive disease and healthy donors. High-throughput microRNA profiling was performed using the Nanostring technology platform. Clinical disease activity was captured by calculating the partial Mayo score. C-reactive protein (CRP) was measured in UC patients as part of their clinical monitoring. The profiles of circulating microRNAs and CRP were correlated with clinical disease indices. Results: We have identified a signature of 12 circulating microRNAs that differentiate UC patients from control subjects. Moreover, six of these microRNAs significantly correlated with UC disease activity. Importantly, a set of four microRNAs (hsa-miR-4454, hsa-miR-223-3p, hsa-miR-23a-3p, and hsa-miR-320e) which correlated with UC disease activity, were found to have higher sensitivity and specificity values than CRP. Conclusions: Circulating microRNAs provide a novel diagnostic and prognostic marker for UC patients. The use of an FDA approved platform could accelerate the application of microRNA screening in a GI clinical setting. When used in combination with current diagnostic and disease activity assessment modalities, microRNAs could improve both IBD screening and care management

    Genome sequences and great expectations

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    To assess how automatic function assignment will contribute to genome annotation in the next five years, we have performed an analysis of 31 available genome sequences. An emerging pattern is that function can be predicted for almost two-thirds of the 73,500 genes that were analyzed. Despite progress in computational biology, there will always be a great need for large-scale experimental determination of protein function

    Phosphoproteomics Screen Reveals Akt Isoform-Specific Signals Linking RNA Processing to Lung Cancer

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    The three Akt isoforms are functionally distinct. Here we show that their phosphoproteomes also differ, suggesting that their functional differences are due to differences in target specificity. One of the top cellular functions differentially regulated by Akt isoforms is RNA processing. IWS1, an RNA processing regulator, is phosphorylated by Akt3 and Akt1 at Ser720/Thr721. The latter is required for the recruitment of SETD2 to the RNA Pol II complex. SETD2 trimethylates histone H3 at K36 during transcription, creating a docking site for MRG15 and PTB. H3K36me3-bound MRG15 and PTB regulate FGFR-2 splicing, which controls tumor growth and invasiveness downstream of IWS1 phosphorylation. Twenty-one of the twenty-four non-small-cell-lung carcinomas we analyzed express IWS1. More importantly, the stoichiometry of IWS1 phosphorylation in these tumors correlates with the FGFR-2 splicing pattern and with Akt phosphorylation and Akt3 expression. These data identify an Akt isoform-dependent regulatory mechanism for RNA processing and demonstrate its role in lung cancer
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