1,720,962 research outputs found
Measurement of air activity concentrations and comparison with meteorological variables in surface air at Palermo , Italy.
No full textAutophagy and glutamate signaling in the onset of Huntington’s Disease
No full textHuntington’s Disease is an inherited disease caused by the expansion of CAG trinucleotide, which results in translation of a protein containing an enlarged polyglutamine (polyQ) domain. HD is characterized by the progressive degeneration of neurons, resulting in involuntary movement and death. Neuronal cell death is caused by an excess of glutamate, that is maintained and
physiological level by a non autonomous cycle between glia and neurons, also called the glutamate-glutamine cycle. Glutamate removal from the synaptic cleft by neuroglia is reduced in a mouse model of Huntington's disease (HD) and in HD patients, suggesting that glial cells actively participate in the survival of neuronal cells. Is possible to manipulate components of the glutamate-glutamine
to ameliorate to neuronal death in HD? To answer this question we are taking advantage of a Drosophila model that has been successfully used to dissect the cellular and molecular events of neurodegenerative disorders including HD. Our preliminary data show that modulation of the enzyme GS1 that converts glutamate into glutamine, in Drosophila’s neurons expressing the human mutant HttQ93, ameliorate animal motility and reduces neuronal loss in the adults. On the contrary, using enzymes that increase the concentration of glutamate has the opposite effect. Growth factor signaling play a dual role in the onset of HD and both in flies and mammals it was shown that while activation of IGF/Akt signaling in neuroglia ameliorates neuronal degeneration induced by HD, the opposite was seen when autophagy was inhibited by activation of the amino TOR signaling pathway. We are using genetics and biochemistry assays to better understand how components of the Insulin/ and TOR pathways act in the regulation of the glutamate-glutamine cycle, and in controlling autophagy in neuronal and glial cells
Autophagy and glutamate signaling in the onset of Huntington's disease
No full textNeuronal cell death is often caused by an excess of glutamate that is maintained and physiological level by an equilibrium of signaling between glia and neurons, also called the glutamate-glutamine cycle. Glutamate removal from the synaptic cleft by neuroglia is reduced in a mouse model of Huntington's disease (HD) and in HD patients, suggesting that glial cells actively participate in the survival of neurons cells in HD. But is the glutamate-glutamine cycle contributing to neuronal death in HD? To answer this question we are taking advantage of a Drosophila model that has been successfully used to dissect the cellular and molecular events of neurodegenerative disorders including HD. HD, an inherited disease caused by expansion of CAG trinucleotide, which results in translation of a protein containing an enlarged polyglutamine (polyQ) domain. HD is characterized by the progressive degeneration of neurons, resulting in involuntary movement and death. Our preliminary data show that modulation of the enzyme GS1 that converts glutamate into glutamine, in Drosophila’s neurons expressing the human mutant HttQ93 ameliorate animal motility. On the contrary, using enzymes that increase the concentration of glutamate has the opposite effect. Growth factor signaling play a dual role in the onset of HD and both in flies and mammals it was shown that while activation of IGF/Akt signaling in neuroglia ameliorates neuronal degeneration induced by HD, the opposite was seen when autophagy was inhibited by activation of the amino TOR signaling pathway.
We would like to better understand how components of the TOR pathways act in the regulation of the glutamate-glutamine cycle, and the potential new role of components of the cycle in controlling autophagy in neuronal and glial cells. With this approach we hope to provide novel insights into the processes that cause neuronal degeneration not only in Huntington's disease but also in other neuronal pathologies
Autophagy and glutamate signaling in the onset of Huntington’s Disease
No full textHuntington’s Disease is an inherited disease caused by the expansion of CAG trinucleotide, which results in translation of a protein containing an enlarged polyglutamine (polyQ) domain. HD is characterized by the progressive degeneration of neurons, resulting in involuntary movement and death. Neuronal cell death is caused by an excess of glutamate, that is maintained and
physiological level by a non autonomous cycle between glia and neurons, also called the glutamate-glutamine cycle. Glutamate removal from the synaptic cleft by neuroglia is reduced in a mouse model of Huntington's disease (HD) and in HD patients, suggesting that glial cells actively participate in the survival of neuronal cells. Is possible to manipulate components of the glutamate-glutamine
to ameliorate to neuronal death in HD? To answer this question we are taking advantage of a Drosophila model that has been successfully used to dissect the cellular and molecular events of neurodegenerative disorders including HD. Our preliminary data show that modulation of the enzyme GS1 that converts glutamate into glutamine, in Drosophila’s neurons expressing the human mutant HttQ93, ameliorate animal motility and reduces neuronal loss in the adults. On the contrary, using enzymes that increase the concentration of glutamate has the opposite effect. Growth factor signaling play a dual role in the onset of HD and both in flies and mammals it was shown that while activation of IGF/Akt signaling in neuroglia ameliorates neuronal degeneration induced by HD, the opposite was seen when autophagy was inhibited by activation of the amino TOR signaling pathway. We are using genetics and biochemistry assays to better understand how components of the Insulin/ and TOR pathways act in the regulation of the glutamate-glutamine cycle, and in controlling autophagy in neuronal and glial cells. We are also analyzing if the expression of GS1 can ameliorate other polyQ induced-neuronal diseases such as the Spinocerebellar Ataxia 3 (SC3) to provide novel insights into the processes that cause neuronal degeneration not only in Huntington's disease but also in other neurodegenetive pathologies
The role of the glutamine-glutamate cycle in neuronal degeneration induced by the mutant human Huntington PolyQ protein
No full textHuntington's disease (HD) is an inherited neurodegenerative disease caused by expansion of a CAG trinucleotide repeat in the Huntingtin gene (Htt), which results in translation of a protein containing an enlarged CAG- encoded polyglutamine (polyQ) characterized by the progressive degeneration of neurons in the brain during aging. This results in chorea (involuntary movement), death. The glutamate-glutamine cycle is fundamental in maintaining neuronal function and survival. When glutamate homeostasis levels in neurons increase, resulting in neuronal death. Glial cells also have an important function in maintaining this homeostasis, removal from the synaptic cleft by glial cells is reduced in a mouse HD model suggesting that glia actively participate in the HD. But how does the glutamate-glutamine cycle contribute to neuronal death? And how does signaling in glial cells contribute pathogenesis in HD? To answer these questions we are using a Drosophila model that has been successfully used to dissect the events in polyQ-related diseases including HD. Our preliminary data show that manipulation of components of the glutamine-neuronal death and ameliorate the motility of animals expressing the HttQ93 in neurons using ELAV. Activation of TOR signaling functions in neurons as a cleaning/survival mechanism. We would like to understand how components of the TOR pathway act glutamate-glutamine cycle, and what controls autophagy in neuronal cells. With this approach we hope to provide novel insights that cause neuronal degeneration not only in Huntington's diseases but also in other neuronal pathologies related to the aging work was sponsored by the Ministero degli Affari Esteri e Cooperazione Internazionale
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Get PDF“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Get PDFWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Dispelling the Myths Behind First-author Citation Counts
Get PDFWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
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