The emerging structure of the Extended Evolutionary Synthesis: where does Evo-Devo fit in?

The Extended Evolutionary Synthesis (EES) debate is gaining ground in contemporary evolutionary biology. In parallel, a number of philosophical standpoints have emerged in an attempt to clarify what exactly is represented by the EES. For Massimo Pigliucci, we are in the wake of the newest instantiation of a persisting Kuhnian paradigm; in contrast, Telmo Pievani has contended that the transition to an EES could be best represented as a progressive reformation of a prior Lakatosian scientific research program, with the extension of its Neo-Darwinian core and the addition of a brand-new protective belt of assumptions and auxiliary hypotheses. Here, we argue that those philosophical vantage points are not the only ways to interpret what current proposals to ‘extend’ the Modern Synthesis-derived ‘standard evolutionary theory’ (SET) entail in terms of theoretical change in evolutionary biology. We specifically propose the image of the emergent EES as a vast network of models and interweaved representations that, instantiated in diverse practices, are connected and related in multiple ways. Under that assumption, the EES could be articulated around a paraconsistent network of evolutionary theories (including some elements of the SET), as well as models, practices and representation systems of contemporary evolutionary biology, with edges and nodes that change their position and centrality as a consequence of the co-construction and stabilization of facts and historical discussions revolving around the epistemic goals of this area of the life sciences. We then critically examine the purported structure of the EES—published by Laland and collaborators in 2015—in light of our own network-based proposal. Finally, we consider which epistemic units of Evo-Devo are present or still missing from the EES, in preparation for further analyses of the topic of explanatory integration in this conceptual framework

KLauS – A charge readout and fast discrimination chip for silicon photomultipliers

KLauS is an application specific integrated circuit (ASIC) for the readout of silicon photomultipliers. The chip has been designed for the application in the analog hadronic calorimeter developed by the CALICE collaboration for the next linear collider experiment . To address the severe power constraints introduced by the highly granular design of the calorimeter, the chip has been designed for low power consumption while maintaining the high dynamic range and timing precision required by the experiment. In addition, a power gating scheme has been implemented to further decrease the average power consumption. For a duty cycle of 1% a value of 25µW per channel is achieved without affecting the readout capabilities of the chip. The chip has been designed in the 0.35µm SiGe technology and provides a low power readout channel for SiPMs with low gain for the input stage of the existing readout chip SPIROC. The analog channel of KLauS will be implemented in a future version of the SPIROC chip

Thyroid function, morphology and autoimmunity in children and adolescents with type 1 diabetes mellitus

info:eu-repo/semantics/publishe

Downregulation of HIF-1a sensitizes U251 glioma cells to the temozolomide (TMZ) treatment

PURPOSE: The aim of this study was to investigate the effect of downregulation of HIF-1alpha gene on human U251 glioma cells and examine the consequent changes of TMZ induced effects and explore the molecular mechanisms. METHODS: U251 cell line stably expressing HIF-1alpha shRNA was acquired via lentiviral vector transfection. The mRNA and protein expression alterations of genes involved in our study were determined respectively by qRT-PCR and Western blot. Cell proliferation was measured by MTT assay and colony formation assay, cell invasion/migration capacity was determined by transwell invasion assay/wound healing assay, and cell apoptosis was detected by flow cytometry. RESULTS: We successfully established a U251 cell line with highly efficient HIF-1alpha knockdown. HIF-1a downregulation sensitized U251 cells to TMZ treatment and enhanced the proliferation-inhibiting, invasion/migration-suppressing, apoptosis-inducing and differentiation-promoting effects exerted by TMZ. The related molecular mechanisms demonstrated that expression of O6-methylguanine DNA methyltransferase gene (MGMT) and genes of Notch1 pathway were significantly upregulated by TMZ treatment. However, this upregulation was abrogated by HIF-1alpha knockdown. We further confirmed important regulatory roles of HIF-1alpha in the expression of MGMT and activation of Notch1 pathways. CONCLUSION: HIF-1alpha downregulation sensitizes U251 glioma cells to the temozolomide treatment via inhibiting MGMT expression and Notch1 pathway activation