921 resultados para Radial basis function network


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With this article we pretend to contribute, in a really modest way, to the liberation of a tenacious image of our society: which operates as an ideological basis of a group of current socio-political pseudocritics, with great success and diffusion. For this we will undertake the exposition and the analysis of the development group of Naissance de la biopolitique in which Foucault accomplishes the critic of all that number of inflationary speeches that represent our society like a “mass society” and a “estatalized space”. Facing these vague and disproportionate forms of consideration, the foucaltian critic, in its exquisite attention to what happens nowadays, it should reveal how our societies function as systems that optimize the difference –radically nominalists-, in which it is produced, beyond any phantasmatic of the oppressor and invasive estate, a regretion of the legal-estate structures that articulate the socio-politic groups, in benefit of the reconstitution and the social tissue as a communitarian network, suitable for the dynamics of market competence that characterise our enterprise societies. That will open to a new idea of the critic, and to a displacement of its object and objectives.

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Following and contributing to the ongoing shift from more structuralist, system-oriented to more pragmatic, socio-cultural oriented anglicism research, this paper verifies to what extent the global spread of English affects naming patterns in Flanders. To this end, a diachronic database of first names is constructed, containing the top 75 most popular boy and girl names from 2005 until 2014. In a first step, the etymological background of these names is documented and the evolution in popularity of the English names in the database is tracked. Results reveal no notable surge in the preference for English names. This paper complements these database-driven results with an experimental study, aiming to show how associations through referents are in this case more telling than associations through phonological form (here based on etymology). Focusing on the socio-cultural background of first names in general and of Anglo-American pop culture in particular, the second part of the study specifically reports on results from a survey where participants are asked to name the first three celebrities that leap to mind when hearing a certain first name (e.g. Lana, triggering the response Del Rey). Very clear associations are found between certain first names and specific celebrities from Anglo-American pop culture. Linking back to marketing research and the social turn in onomastics, we will discuss how these celebrities might function as referees, and how social stereotypes surrounding these referees are metonymically attached to their first names. Similar to the country-of-origin-effect in marketing, these metonymical links could very well be the reason why parents select specific “celebrity names”. Although further attitudinal research is needed, this paper supports the importance of including socio-cultural parameters when conducting onomastic research.

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The organizational and architectural configuration of white matter pathways connecting brain regions has ramifications for all facets of the human condition, including manifestations of incipient neurodegeneration. Although diffusion tensor imaging (DTI) has been used extensively to visualize white matter connectivity, due to the widespread presence of crossing fibres, the lateral projections of the corpus callosum are not normally detected using this methodology. Detailed knowledge of the transcallosal connectivity of the human cortical motor network has therefore remained elusive. We employed constrained spherical deconvolution (CSD) tractography - an approach that is much less susceptible to the influence of crossing fibres, in order to derive complete in-vivo characterizations of white matter pathways connecting specific motor cortical regions to their counterparts and other loci in the opposite hemisphere. The revealed patterns of connectivity closely resemble those derived from anatomical tracing in primates. It was established that dorsal premotor cortex (PMd) and supplementary motor area (SMA) have extensive interhemispheric connectivity - exhibiting both dense homologous projections, and widespread structural relations with every other region in the contralateral motor network. Through this in-vivo portrayal, the importance of non-primary motor regions for interhemispheric communication is emphasized. Additionally, distinct connectivity profiles were detected for the anterior and posterior subdivisions of primary motor cortex. The present findings provide a comprehensive representation of transcallosal white matter projections in humans, and have the potential to inform the development of models and hypotheses relating structural and functional brain connectivity.

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Enhancer regions and transcription start sites of estrogen-target regulated genes are connected by means of Estrogen Receptor long-range chromatin interactions. Yet, the complete molecular mechanisms controlling the transcriptional output of engaged enhancers and subsequent activation of coding genes remain elusive. Here, we report that CTCF binding to enhancer RNAs is enriched when breast cancer cells are stimulated with estrogen. CTCF binding to enhancer regions results in modulation of estrogen-induced gene transcription by preventing Estrogen Receptor chromatin binding and by hindering the formation of additional enhancer-promoter ER looping. Furthermore, the depletion of CTCF facilitates the expression of target genes associated with cell division and increases the rate of breast cancer cell proliferation. We have also uncovered a genomic network connecting loci enriched in cell cycle regulator genes to nuclear lamina that mediates the CTCF function. The nuclear lamina and chromatin interactions are regulated by estrogen-ER. We have observed that the chromatin loops formed when cells are treated with estrogen establish contacts with the nuclear lamina. Once there, the portion of CTCF associated with the nuclear lamina interacts with enhancer regions, limiting the formation of ER loops and the induction of genes present in the loop. Collectively, our results reveal an important, unanticipated interplay between CTCF and nuclear lamina to control the transcription of ER target genes, which has great implications in the rate of growth of breast cancer cells.

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The androgen receptor (AR) is required for prostate cancer (PCa) survival and progression, and ablation of AR activity is the first line of therapeutic intervention for disseminated disease. While initially effective, recurrent tumors ultimately arise for which there is no durable cure. Despite the dependence of PCa on AR activity throughout the course of disease, delineation of the AR-dependent transcriptional network that governs disease progression remains elusive, and the function of AR in mitotically active cells is not well understood. Analyzing AR activity as a function of cell cycle revealed an unexpected and highly expanded repertoire of AR-regulated gene networks in actively cycling cells. New AR functions segregated into two major clusters: those that are specific to cycling cells and retained throughout the mitotic cell cycle ('Cell Cycle Common'), versus those that were specifically enriched in a subset of cell cycle phases ('Phase Restricted'). Further analyses identified previously unrecognized AR functions in major pathways associated with clinical PCa progression. Illustrating the impact of these unmasked AR-driven pathways, dihydroceramide desaturase 1 was identified as an AR-regulated gene in mitotically active cells that promoted pro-metastatic phenotypes, and in advanced PCa proved to be highly associated with development of metastases, recurrence after therapeutic intervention and reduced overall survival. Taken together, these findings delineate AR function in mitotically active tumor cells, thus providing critical insight into the molecular basis by which AR promotes development of lethal PCa and nominate new avenues for therapeutic intervention.

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The cluster provides a greater commercial relationship between the companies that comprise it. This encourages companies to adopt competitive structures that allow solving problems that would hardly alone (Lubeck et. Al., 2011). With that this paper aims to describe the coopetition between companies operating on a commercial cluster planned, from the point of view of retailers, taking as a basis the theoretical models proposed by Bengtsson and Kock (1999) and Leon (2005) and operationalized by means of Social Network Analysis (SNA). Data collection consisted of two phases, the first exploratory aspect to identify the actors, and the second was characterized as descriptive as it aims to describe the coopetition among the enterprises. As a result we identified the companies that cooperate and compete simultaneously (coopetition), firms that only compete, companies just cooperate and businesses that do not compete and do not cooperate (coexistence).

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Thesis (Master's)--University of Washington, 2016-08

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The International Long-Term Ecological Research (ILTER) network comprises > 600 scientific groups conducting site-based research within 40 countries. Its mission includes improving the understanding of global ecosystems and informs solutions to current and future environmental problems at the global scales. The ILTER network covers a wide range of social-ecological conditions and is aligned with the Programme on Ecosystem Change and Society (PECS) goals and approach. Our aim is to examine and develop the conceptual basis for proposed collaboration between ILTER and PECS. We describe how a coordinated effort of several contrasting LTER site-based research groups contributes to the understanding of how policies and technologies drive either toward or away from the sustainable delivery of ecosystem services. This effort is based on three tenets: transdisciplinary research; cross-scale interactions and subsequent dynamics; and an ecological stewardship orientation. The overarching goal is to design management practices taking into account trade-offs between using and conserving ecosystems toward more sustainable solutions. To that end, we propose a conceptual approach linking ecosystem integrity, ecosystem services, and stakeholder well-being, and as a way to analyze trade-offs among ecosystem services inherent in diverse management options. We also outline our methodological approach that includes: (i) monitoring and synthesis activities following spatial and temporal trends and changes on each site and by documenting cross-scale interactions; (ii) developing analytical tools for integration; (iii) promoting trans-site comparison; and (iv) developing conceptual tools to design adequate policies and management interventions to deal with trade-offs. Finally, we highlight the heterogeneity in the social-ecological setting encountered in a subset of 15 ILTER sites. These study cases are diverse enough to provide a broad cross-section of contrasting ecosystems with different policy and management drivers of ecosystem conversion; distinct trends of biodiversity change; different stakeholders’ preferences for ecosystem services; and diverse components of well-being issues.

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Patients’ bowel dysfunction is a major factor that weakens the results of surgical care as it can cause pain and weaken patients’ rehabilitation. Bowel dysfunction is a common postoperative problem, yet most incidents remain undocumented. The nursing profession has a significant role in enhancing the bowel function postoperatively. However, studies of postoperative bowel function after hepatectomy are scarce and somewhat incongruous. Enhanced recovery protocols are innovative models of care aiming for better outcomes of surgical care. Enhanced recovery protocols can improve gastrointestinal function after surgery, yet patients are also known to be satisfied with their care. The aim was to investigate if postoperative bowel function day varies between patients in terms of age, gender, ASA score, type of surgery, histology, patients’ experienced pain and experienced satisfaction three days after discharge and three months after operation in patients undergoing hepatectomy. The goal was to produce information for basis of scientific research, to give nurses in clinical setting more tools to work with hepatectomy patients undergoing enhanced recovery protocol and to produce information to nurse managers to use in process management of patients undergoing enhanced recovery protocol. The design of this study is descriptive. Data was collected retrospectively from hepatectomy patients (n = 134) undergoing enhanced recovery protocol within the first year of enhanced recovery protocol implementation. The data was based on registers and analyzed statistically. Mean age of patients was 62 years and mean day of discharge was 4. Main (n = 72) histology of the patients was colorectal liver metastases. Mean bowel function day was 3. Most of the patients were very satisfied or satisfied with the care three days after discharge (99%) and three months (90%) after operation. Most of the patients (72%) experienced moderate pain three days after discharge, but three months after operation 47% of the patients did not experience pain and 48% experienced moderate pain. There were no statistically significant differences in bowel function between different age groups, genders, ASA score groups or histologies. Neither were there statistically significant differences in postoperative bowel function in terms of experienced satisfaction or pain. There were statistically significant differences in postoperative bowel function between different types of surgery (p < 0.01). Nurses should take into consideration hepatectomy patients’ type of surgery and pay special attention in supporting major open hepatectomy patients’ postoperative bowel function. Nurses should educate patients undergoing major open hepatectomy about prolonged postoperative bowel function.

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In this Letter we introduce a continuum model of neural tissue that include the effects of so-called spike frequency adaptation (SFA). The basic model is an integral equation for synaptic activity that depends upon the non-local network connectivity, synaptic response, and firing rate of a single neuron. A phenomenological model of SFA is examined whereby the firing rate is taken to be a simple state-dependent threshold function. As in the case without SFA classical Mexican-Hat connectivity is shown to allow for the existence of spatially localized states (bumps). Importantly an analysis of bump stability using recent Evans function techniques shows that bumps may undergo instabilities leading to the emergence of both breathers and traveling waves. Moreover, a similar analysis for traveling pulses leads to the conditions necessary to observe a stable traveling breather. Direct numerical simulations both confirm our theoretical predictions and illustrate the rich dynamic behavior of this model, including the appearance of self-replicating bumps.

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We present new methodologies to generate rational function approximations of broadband electromagnetic responses of linear and passive networks of high-speed interconnects, and to construct SPICE-compatible, equivalent circuit representations of the generated rational functions. These new methodologies are driven by the desire to improve the computational efficiency of the rational function fitting process, and to ensure enhanced accuracy of the generated rational function interpolation and its equivalent circuit representation. Toward this goal, we propose two new methodologies for rational function approximation of high-speed interconnect network responses. The first one relies on the use of both time-domain and frequency-domain data, obtained either through measurement or numerical simulation, to generate a rational function representation that extrapolates the input, early-time transient response data to late-time response while at the same time providing a means to both interpolate and extrapolate the used frequency-domain data. The aforementioned hybrid methodology can be considered as a generalization of the frequency-domain rational function fitting utilizing frequency-domain response data only, and the time-domain rational function fitting utilizing transient response data only. In this context, a guideline is proposed for estimating the order of the rational function approximation from transient data. The availability of such an estimate expedites the time-domain rational function fitting process. The second approach relies on the extraction of the delay associated with causal electromagnetic responses of interconnect systems to provide for a more stable rational function process utilizing a lower-order rational function interpolation. A distinctive feature of the proposed methodology is its utilization of scattering parameters. For both methodologies, the approach of fitting the electromagnetic network matrix one element at a time is applied. It is shown that, with regard to the computational cost of the rational function fitting process, such an element-by-element rational function fitting is more advantageous than full matrix fitting for systems with a large number of ports. Despite the disadvantage that different sets of poles are used in the rational function of different elements in the network matrix, such an approach provides for improved accuracy in the fitting of network matrices of systems characterized by both strongly coupled and weakly coupled ports. Finally, in order to provide a means for enforcing passivity in the adopted element-by-element rational function fitting approach, the methodology for passivity enforcement via quadratic programming is modified appropriately for this purpose and demonstrated in the context of element-by-element rational function fitting of the admittance matrix of an electromagnetic multiport.

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In this study the conodont multielement apparatus of Late Devonian (Famennian) Icriodus altematus is described which has been reconstructed from clustered group findings and separated elements. This apparatus is markedly different from classical ozarkodinid apparatuses and needs further consideration of its functional morphology. Since bedding plane assemblages of Icriodus altematus are yet unknown, a spatial reconstruction of this apparatus and a feeding mechanism are proposed which are based on the oropharyngal apparatus of recent lampreys. Though the extant representatives of petromyzontoids are not close phylogenetic relatives of extinct conodonts, there exist intriguing analogies concerning the morphology of the tooth types and the presumed spatial distribution within the oral cavity of both taxa.

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We study spatially localized states of a spiking neuronal network populated by a pulse coupled phase oscillator known as the lighthouse model. We show that in the limit of slow synaptic interactions in the continuum limit the dynamics reduce to those of the standard Amari model. For non-slow synaptic connections we are able to go beyond the standard firing rate analysis of localized solutions allowing us to explicitly construct a family of co-existing one-bump solutions, and then track bump width and firing pattern as a function of system parameters. We also present an analysis of the model on a discrete lattice. We show that multiple width bump states can co-exist and uncover a mechanism for bump wandering linked to the speed of synaptic processing. Moreover, beyond a wandering transition point we show that the bump undergoes an effective random walk with a diffusion coefficient that scales exponentially with the rate of synaptic processing and linearly with the lattice spacing.

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Artificial immune systems have previously been applied to the problem of intrusion detection. The aim of this research is to develop an intrusion detection system based on the function of Dendritic Cells (DCs). DCs are antigen presenting cells and key to the activation of the human immune system, behaviour which has been abstracted to form the Dendritic Cell Algorithm (DCA). In algorithmic terms, individual DCs perform multi-sensor data fusion, asynchronously correlating the fused data signals with a secondary data stream. Aggregate output of a population of cells is analysed and forms the basis of an anomaly detection system. In this paper the DCA is applied to the detection of outgoing port scans using TCP SYN packets. Results show that detection can be achieved with the DCA, yet some false positives can be encountered when simultaneously scanning and using other network services. Suggestions are made for using adaptive signals to alleviate this uncovered problem.

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Acute myeloid leukemia (AML) involves the proliferation, abnormal survival and arrest of cells at a very early stage of myeloid cell differentiation. The biological and clinical heterogeneity of this disease complicates treatment and highlights the significance of understanding the underlying causes of AML, which may constitute potential therapeutic targets, as well as offer prognostic information. Tribbles homolog 2 (Trib2) is a potent murine oncogene capable of inducing transplantable AML with complete penetrance. The pathogenicity of Trib2 is attributed to its ability to induce proteasomal degradation of the full length isoform of the transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα p42). The role of TRIB2 in human AML cells, however, has not been systematically investigated or targeted. Across human cancers, TRIB2 oncogenic activity was found to be associated with its elevated expression. In the context of AML, TRIB2 overexpression was suggested to be associated with the large and heterogeneous subset of cytogenetically normal AML patients. Based upon the observation that overexpression of TRIB2 has a role in cellular transformation, the effect of modulating its expression in human AML was examined in a human AML cell line that expresses high levels of TRIB2, U937 cells. Specific suppression of TRIB2 led to impaired cell growth, as a consequence of both an increase in apoptosis and a decrease in cell proliferation. Consistent with these in vitro results, TRIB2 silencing strongly reduced progression of the U937 in vivo xenografts, accompanied by detection of a lower spleen weight when compared with mice transplanted with TRIB2- expressing control cells. Gene expression analysis suggested that TRIB2 modulates apoptosis and cell-cycle sensitivity by influencing the expression of a subset of genes known to have implications on these phenotypes. Furthermore, TRIB2 was found to be expressed in a significant subset of AML patient samples analysed. To investigate whether increased expression of this gene could be afforded prognostic significance, primary AML cells with dichotomized levels of TRIB2 transcripts were evaluated in terms of their xenoengraftment potential, an assay reported to correlate with disease aggressiveness observed in humans. A small cohort of analysed samples with higher TRIB2 expression did not associate with preferential leukaemic cell engraftment in highly immune-deficient mice, hence, not predicting for an adverse prognosis. However, further experiments including a larger cohort of well characterized AML patients would be needed to clarify TRIB2 significance in the diagnostic setting. Collectively, these data support a functional role for TRIB2 in the maintenance of the oncogenic properties of human AML cells and suggest TRIB2 can be considered a rational therapeutic target. Proteasome inhibition has emerged as an attractive target for the development of novel anti-cancer therapies and results from translational research and clinical trials support the idea that proteasome inhibitors should be considered in the treatment of AML. The present study argued that proteasome inhibition would effectively inhibit the function of TRIB2 by abrogating C/EBPα p42 protein degradation and that it would be an effective pharmacological targeting strategy in TRIB2-positive AMLs. Here, a number of cell models expressing high levels of TRIB2 were successfully targeted by treatment with proteasome inhibitors, as demonstrated by multiple measurements that included increased cytotoxicity, inhibition of clonogenic growth and anti-AML activity in vivo. Mechanistically, it was shown that block of the TRIB2 degradative function led to an increase of C/EBPα p42 and that response was specific to the TRIB2-C/EBPα axis. Specificity was addressed by a panel of experiments showing that U937 cells (express detectable levels of endogenous TRIB2 and C/EBPα) treated with the proteasome inhibitor bortezomib (Brtz) displayed a higher cytotoxic response upon TRIB2 overexpression and that ectopic expression of C/EBPα rescued cell death. Additionally, in C/EBPα-negative leukaemia cells, K562 and Kasumi 1, Brtz-induced toxicity was not increased following TRIB2 overexpression supporting the specificity of the compound on the TRIB2-C/EBPα axis. Together these findings provide pre-clinical evidence that TRIB2- expressing AML cells can be pharmacologically targeted with proteasome inhibition due, in part, to blockage of the TRIB2 proteolytic function on C/EBPα p42. A large body of evidence indicates that AML arises through the stepwise acquisition of genetic and epigenetic changes. Mass spectrometry data has identified an interaction between TRIB2 and the epigenetic regulator Protein Arginine Methyltransferase 5 (PRMT5). Following assessment of TRIB2‟s role in AML cell survival and effective targeting of the TRIB2-C/EBPα degradation pathway, a putative TRIB2/PRMT5 cooperation was investigated in order to gain a deeper understanding of the molecular network in which TRIB2 acts as a potent myeloid oncogene. First, a microarray data set was interrogated for PRMT5 expression levels and the primary enzyme responsible for symmetric dimethylation was found to be transcribed at significantly higher levels in AML patients when compared to healthy controls. Next, depletion of PRMT5 in the U937 cell line was shown to reduce the transformative phenotype in the high expressing TRIB2 AML cells, which suggests that PRMT5 and TRIB2 may cooperate to maintain the leukaemogenic potential. Importantly, PRMT5 was identified as a TRIB2-interacting protein by means of a protein tagging approach to purify TRIB2 complexes from 293T cells. These findings trigger further research aimed at understanding the underlying mechanism and the functional significance of this interplay. In summary, the present study provides experimental evidence that TRIB2 has an important oncogenic role in human AML maintenance and, importantly in such a molecularly heterogeneous disease, provides the rational basis to consider proteasome inhibition as an effective targeting strategy for AML patients with high TRIB2 expression. Finally, the identification of PRMT5 as a TRIB2-interacting protein opens a new level of regulation to consider in AML. This work may contribute to our further understanding and therapeutic strategies in acute leukaemias.