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Books on the topic 'Gente de Arte (Association)'

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Published: 4 June 2021
Last updated: 4 March 2023

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1

del, Puerto Rafael, Peralta María José, Brom Diego, and Gente de Arte (Association), eds. Gente de Arte: Producción de los '90. Asunción, Paraguay: Gente de Arte, 2002.

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2

(Association), Gente de Arte. Gente de Arte: Producción de los '90. Asunción, Paraguay: FONDEC, 2002.

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3

Donni, Giovanni. Cologne: Storia, arte e gente. Cologne [Brescia]: Comune di Cologne, 2004.

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4

Arango, Biblioteca Luis-Angel, ed. Interpretación: El arte de la gente. [Colombia]: Banco de la República, Biblioteca Luis Ángel Arango, 1999.

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5

Baroja, Ricardo. Gente del 98 ; Arte, cine y ametralladora. Madrid: Cátedra, 1989.

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6

Kormann, Edith. Blumenau: Arte, cultura e as histórias de sua gente, 1850-1985. Florianópolis, Santa Catarina: edicao da autora, 1994.

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7

Colección Arte Contemporáneo (Association : Spain), ed. Arte en España, 1918-1994, en la Colección Arte Contemporáneo. Madrid: Alianza, 1995.

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8

Primieri, Rolando. Duesanti: Storia, arte e tradizioni di un paese e della sua gente. Todi (PG) [i.e. Perugia, Italy]: Edizioni dell'Anthurium, 2006.

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9

Maxwell, Richard. Convencer a la gente contando historias: El nuevo arte de la persuasión. México, D.F: Editorial Planeta, 2010.

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10

Spain), Colección Arte Contemporáneo (Association :. Colección Arte Contemporáneo. Madrid: La Colección, 1991.

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11

Artundo, Patricia. Amigos del Arte, 1924-1942. Buenos Aires, Argentina: Malba, Fundación Costantini, 2008.

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12

Museo de Arte Latinoamericano de Buenos Aires and Fundación Eduardo F. Costantini, eds. Amigos del Arte, 1924-1942. Buenos Aires, Argentina: Malba, Fundación Costantini, 2008.

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13

Fernández, Valeriano Bozal. Antes del informalismo: Arte español, 1940-1958, en la Colección Arte Contemporáneo. Madrid: Museo Nacional Centro de Arte Reina Sofía, 1996.

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14

Longoria, Josefina Rodríguez de. Cien años de arte y cultura en Monterrey: A través de su gente, museos y exposiciones. [México]: Value Casa de Bolsa, 1998.

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15

Hahn, Oliver. ARTE: Der europäische Kulturkanal : eine Fernsehsprache in vielen Sprachen. München: Verlag Reinhard Fischer, 1997.

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16

Vanguardia y renovación estética: Asociación Amigos del Arte. Buenos Aires: Fundación CICCUS, 2007.

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17

ARTE et le documentaire: De nouveaux enjeux pour la création. Lormont: Bord de l'eau, 2011.

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18

Hellmuth, Nathalie. ARTE - Europa auf Sendung: Verfassungsrechtliche Rahmenbedingungen für die Beteiligung von ARD und ZDF an supranationalen Gemeinschaftssendern am Beispiel des europäischen Kulturkanals ARTE. Frankfurt, M: P. Lang, 2007.

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19

Colección Arte Contemporáneo (Association : Spain), Museo Patio Herreriano, and Real Academia de Bellas Artes de San Fernando, eds. Experiencias de la modernidad: 1916-1956 / textos, Simón Marchán Fiz ... [and three others]. Valladolid, Spain: Museo Patio Herreriano, 2013.

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20

Grässle, Inge. Der europäische Fernseh-Kulturkanal ARTE: Deutsch-französische Medienpolitik zwischen europäischem Anspruch und nationaler Wirklichkeit. Frankfurt/Main: Campus, 1995.

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21

Le choix d'ARTE. Paris: Grasset, 2011.

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22

Colloque "50 ans de l'AICA" (1999 : Paris, France), ed. Histoires de 50 ans de l'Association internationale des critiques d'art/AICA: Historias de 50 años de la Asociación Internacional de Criticos de Arte/AICA = Histories of 50 years of the International Association of Art Critics/AICA. Paris: AICA Press, 2002.

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23

Jasper, Pat. Art among us =: Arte entre nosotros : Mexican American folk art of San Antonio : San Antonio Museum of Art, 27 April-15 June 1986, San Antonio Museum Association. [San Antonio, Tex.]: The Association, 1986.

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24

Jasper, Pat. Art among us =: Arte entre nosotros : Mexican American folk art of San Antonio : San Antonio Museum of Art, 27 April-15 June 1986, San Antonio Museum Association. [San Antonio, Tex.]: The Association, 1986.

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25

Sandy, Astolfo. Arte de Apreciar Gente Feia: Contos. Independently Published, 2019.

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26

Arte de Apreciar Gente Feia: Contos. Independently Published, 2021.

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27

Comunicación asociativa: No sólo hablando se entiende la gente. 2nd ed. Cádiz, Spain: CRAC, 2010.

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28

Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0043_update_002.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and large-scale genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now 17 JIA susceptibility loci which reach the genome-wide significance threshold for association and a further 7 regions with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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29

Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0043_update_003.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and large-scale genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now 17 JIA susceptibility loci which reach the genome-wide significance threshold for association and a further 7 regions with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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30

Siebert, Stefan, Sengupta Raj, and Alexander Tsoukas. The genetics of axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0004.

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Family and twin studies have long suggested a large genetic component in ankylosing spondylitis (AS). The genetic association with HLA-B27 remains one of the strongest single gene variant associations reported in any complex polygenic disease. The exact mechanism by which HLA-B27 contributes to AS remains unknown, with three main theories proposed: the arthritogenic peptide, endoplasmic reticulum stress with unfolded protein response, and homodimerization theories. Genome-wide association studies have identified a number of other important susceptibility genes for AS, several of which overlap with other spondyloarthritis conditions. Of these, ERAP1 and IL-23R, are covered in more detail, highlighting their functional importance.
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31

Hinks, Anne, and Wendy Thomson. Genetics of juvenile rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0043.

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Juvenile rheumatic diseases are heterogeneous, complex genetic diseases; to date only juvenile idiopathic arthritis (JIA) has been extensively studied in terms of identifying genetic risk factors. The MHC region is a well-established risk factor but in the last few years candidate gene and genome-wide association studies have been utilized in the search for non-HLA risk factors. There are now an additional 12 JIA susceptibility loci with evidence for association in more than one study. In addition, some subtype-specific associations are emerging. These risk loci now need to be investigated further using fine-mapping strategies and then appropriate functional studies to show how the variant alters the gene function. This knowledge will not only lead to a better understanding of disease pathogenesis for juvenile rheumatic diseases but may also aid in the classification of these heterogeneous diseases. It may identify new pathways for potential therapeutic targets and help in the prediction of disease outcome and response to treatment.
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32

Patenall, Philip. Aprende a dibujar gente/ Learn how to Draw People. Grupo Editorial Tomo, 2006.

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33

various and Colecci on Arte Contempor Aneo. Coleccion Arte Contemporaneo. Nuevas Estructuras, 1991.

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34

zitlol, minkhit. Notebook: Estrella Del Arte Conceptual 4, Gente Del Barrio 8. 5x11 Inch 100 Pages. Independently Published, 2020.

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35

Westberg, Lars, and Hasse Walum. Oxytocin and Vasopressin Gene Variation and the Neural Basis of Social Behaviors. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.011.

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Experimental studies in rodents and humans show that the neuropeptides oxytocin and vasopressin are important regulators of behaviors related to social interactions. Evidence for positive effects of oxytocin treatment on symptoms of psychiatric disorders characterized by impaired social functioning has emerged. Numerous studies report associations between various social behaviors, the risk of autism, and polymorphisms inOXTRandAVPR1A. This chapter provides an overview of these genetic association studies. Although many of the published findings are inconclusive and need replication in independent samples, the chapter concludes that variants ofOXTRandAVPR1Aseem to moderate individual variation in different aspects of social behavior. The challenges for future studies include replication of current findings, identification of the functional variants, and characterization of the neural mechanisms mediating the gene-behavior associations, as well as exploration of the pharmacogenetic potential ofOXTRandAVPR1Ain future clinical trials.
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36

Forme e colori, meccanismi ed esperimenti: Arslab : metodi ed emozioni : interazioni tra arte, scienza e tecnologia. Torino: Città di Torino, Assessorato per la cultura, 1992.

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37

Kormann, Edith. Blumenau: Arte, cultura e as historias de sua gente, 1850-1985 (v. 1: Serie Municipios catarinenses). edicao da autora, 1994.

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38

Gelbart, Matthew. Musical Genre and Romantic Ideology. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/oso/9780190646929.001.0001.

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Abstract European Romanticism gave rise to a powerful discourse equating genres to constrictive rules and forms that great art should transcend; and yet without the categories and intertextual references we hold in our minds, “music” would be meaningless noise. This book teases out that paradox, charting the workings and legacies of Romantic artistic values such as originality and anti-commercialism in relation to musical genre. Genre’s persistent power was amplified by music’s inevitably practical social, spatial, and institutional frames. Furthermore, starting in the nineteenth century, all music, even the most anti-commercial, was stamped by its relationship to the marketplace, entrenching associations between genres and target publics (whether based on ideas of nation, gender, class, or subtler aspects of identity). These newly strengthened correlations made genre, if anything, more potent rather than less, despite Romantic claims. In case studies from across nineteenth-century Europe engaging with canonical music by Bizet, Chopin, Verdi, Wagner, and Brahms, alongside representative genres such as opéra-comique and the piano ballade, Gelbart explores the processes through which composers, performers, critics, and listeners gave sounds, and themselves, a sense of belonging. He examines genre vocabulary and discourse, the force of generic titles, how avant-garde music is absorbed through and into familiar categories, and how interpretation can be bolstered or undercut by genre agreements. Even in a modern world where transcription and sound recording can take any music into an infinite array of new spatial and social situations, we are still locked in the Romantics’ ambivalent tussle with genre.
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39

Avomo, Javier Clemente Engonga. Alguna Gente Buena, el Libro de Los Inmortales : Don Carlos, Pura ProgramaciÓn Lineal: El Arte Del Éxito. Independently Published, 2021.

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40

Dalbeth, Nicola. Clinical features of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198748311.003.0005.

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About 60% of the variance in serum urate levels can be explained by inherited genetic factors, but the extent of the contribution of genetic factors to gout in the presence of hyperuricaemia is not known. Genome-wide association studies in Europeans have identified 28 loci controlling serum urate levels, although the molecular basis of the majority of these genetic associations is currently unknown. The SLC2A9 and ABCG2 renal and gut uric acid transporters have very strong effects on urate levels and the risk of gout. Other uric acid transporters (e.g. SLC22A11/OAT478, SLC22A12/URAT1) and a glycolysis gene (GCKR) are associated with urate levels. Environmental exposures such as sugar-sweetened beverages and alcohol interact with urate-associated genetic variants in an unpredictable fashion. Very little is known about the genetic control of gout in the presence of hyperuricaemia, formation of monosodium urate crystals, and the immune response.
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41

Arslab: Metodi ed emozioni : interazioni tra arte scienza tecnologia dall'Exploratorium di San Francisco ad Ars technica di Parigi : Torino, Mole Antonelliana, 19 marzo-26 aprile 1992. Umberto Allemandi, 1992.

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42

Arslab: Metodi ed emozioni : interazioni tra arte scienza tecnologia dall'Exploratorium di San Francisco ad Ars technica di Parigi : Torino, Mole Antonelliana, 19 marzo-26 aprile 1992. Torino: Umberto Allemandi, 1992.

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43

Heidet, Laurence, and Marie Claire Gubler. Nail patella syndrome. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0326_update_001.

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Nail patella syndrome can be recognized by its characteristic nail dystrophy and symmetrical skeletal abnormalities. Proteinuric renal disease is a variable part of the syndrome, usually mild but causing end-stage renal failure in up to 10%. An association with glaucoma has been recognized and this should be screened for. Underlying gene mutations are in a LIM homeodomain-containing transcription factor LMX1B, which seems to influence production of basement membrane proteins and other podocyte gene products.
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44

Merriman, Tony R. The genetic basis of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0040.

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An individual’s risk of gout is determined by a complex relationship between inherited genetic variants and environmental exposures. Genetic variants that control hyperuricaemia and subsequent progression to clinical gout specify pathogenic pathways that could be therapeutically targeted. Genome-wide association studies (GWAS) have provided novel insights into the pathways leading to hyperuricaemia. GWAS have identified the renal uric acid transporter SLC2A9/GLUT9 and the gut excretory molecule ABCG2, which each have very strong genetic effects in the control of urate levels and risk of gout. Histone deacetylase inhibitors are able to correct the genetically-determined ABCG2 dysfunction. Other renal uric acid transporters, such as SLC22A11/OAT4 and SLC22A12/URAT1 have been confirmed to be genetically associated with urate and the risk of gout. Genes that generate urate during glycolysis (e.g. GCKR) are also implicated. In contrast very little is known about genetic variants that control the progression from hyperuricaemia to gout with the toll-like receptor 4 gene being the only gene with replicated evidence of association.
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45

Distel, Marijn A., and Marleen H. M. de Moor. Genetic Influences on Borderline Personality Disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199997510.003.0007.

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Borderline personality disorder (BPD) tends to “run in families.” Twin and twin family studies show that BPD is moderately heritable, with some evidence for nonadditive gene action. BPD co-occurs with Axis I and other Axis II disorders, as well as with a certain profile of normal personality traits. Multivariate twin (family) studies have shown that these phenotypic associations are partly due to genetic associations, and this is observed most strongly for BPD and neuroticism. Candidate gene-finding studies for BPD suggest the possible role of genes in the serotonergic and dopaminergic system, but this needs to be confirmed in larger genome-wide studies. Future studies will complement the knowledge described in this chapter to enable us to move toward a comprehensive model of the development of BPD in which biological and environmental influences on BPD are integrated.
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46

Otowa, Takeshi, Roxann Roberson-Nay, Mandakh Bekhbat, Gretchen N. Neigh, and John M. Hettema. Genetics of Anxiety Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0033.

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This chapter provides a broad overview of the state of research in the genetics of the major anxiety disorders (ADs). They exhibit moderate familial aggregation and heritability due to genetic risk factors that are shared between them as well as those that are disorder-specific. Many candidate gene association studies have been published, with a small set of genes that have been consisted validated for their role in one or more anxiety phenotypes. Genome-wide association studies of ADs are in their infancy, with a handful of published studies for each disorder so far and more to come conducted by large consortia. Animal studies provide a promising complimentary approach that demonstrate concurring evidence across species supporting the involvement of particular biological systems in anxiety-related behaviors.
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47

Sumner, Jennifer A., Angela C. Bustamante, Karestan C. Koenen, and Monica Uddin. Genetics of PTSD. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0011.

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Trauma exposure and PTSD are heritable. However, the mechanisms of risk and resilience following trauma exposure are not yet well understood, suggesting that investigations into the genetic architecture of PTSD have much to contribute. This chapter reviews the rapidly growing literature on molecular genetic risk factors for PTSD, including findings from candidate gene and genome-wide association studies. Given the critical role of trauma exposure in the onset of PTSD, it also discusses gene-environment interplay, and highlights some recent findings from epigenetic studies. The chapter concludes by summarizing considerations for the field as it continues to move forward, and discusses exciting new developments in the search for genetic markers for PTSD.
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48

Steiger, Diego. Gente con Tatuajes Es Mucho Más Divertida de Ver Desnuda Calendario 2022: Calendario Anual para Aficionados a Los Tatuajes y Amigos Del Arte Corporal Colorido. Independently Published, 2021.

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49

Birch, Jonathan. Gene Mobility and the Concept of Relatedness. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198733058.003.0006.

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Social behaviour is widespread in the microbial world, yet social evolution theory was mostly developed with multicellular animals in mind. One difference between multicellular organisms and microbes is the prevalence of mobile genetic elements, such as plasmids, in microbial populations. Plasmids are often implicated in the production of so-called public goods, and relatedness may be at the heart of this phenomenon. However, gene mobility introduces a temporal aspect to relatedness: because genotypes can change over the life cycle, two bacteria may share a gene at one time point, but not at some earlier or later time point. This chapter argues that the best concept of relatedness in this context is a diachronic concept that captures the association between actor genotypes at the moment of gene expression and recipient genotypes at the end of the life cycle.
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50

Inteligencia Emocional - el Arte de Leer a la Gente: Cómo Aprender a Percibir, Entender y Controlar Los Sentimientos a Través de la Atención y la Empatía. Independently Published, 2020.

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