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  1. Article ; Online: Carlos Somigliana

    Alba Saura Clares

    Pensamiento al Margen, Iss 5, Pp 391-

    sátira, ironía y parodia teatral contra la última dictadura argentina

    2016  Volume 410

    Abstract: En esta investigación nos adentramos en la obra del dramaturgo Carlos Somigliana (1932-1987 ... principal de este trabajo es acercarnos a las obras de Somigliana para el festival Teatro Abierto, evento ... escénico contra la dictadura del Proceso, y a la estética elegida por el dramaturgo ...

    Abstract En esta investigación nos adentramos en la obra del dramaturgo Carlos Somigliana (1932-1987), una de las figuras más destacadas de la escena argentina del siglo XX. Con una producción marcada por la inestabilidad sociopolítica vivida en el país, profundizaremos en los textos que escribió durante la última dictadura militar argentina, el autodenominado Proceso de Reorganización Nacional (1976-1983). El objetivo principal de este trabajo es acercarnos a las obras de Somigliana para el festival Teatro Abierto, evento escénico contra la dictadura del Proceso, y a la estética elegida por el dramaturgo para las mismas, donde percibimos un predominio de la sátira, la ironía y la parodia unido al carácter político de los textos. Nuestro corpus lo compondrán El Nuevo Mundo (1981), El oficial primero (1982) y La democracia en el tocador (1984).
    Keywords Carlos Somigliana ; Proceso de Reorganización Nacional ; Argentina ; Teatro ; Dictadura ; Political science ; J ; Political theory ; JC11-607
    Language Spanish
    Publishing date 2016-12-01T00:00:00Z
    Publisher Ateneo Cantonal de Estudios Políticos
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Book: Carlos Saura's Tango

    Schifrin, Lalo / Saura, Carlos

    original motion picture soundtrack

    1998  

    Author's details original music by Lalo Schifrin
    Language English ; Spanish
    Size 1 CD (64 Min.), DDD, stereo, 12 cm
    Publisher Dt. Grammophon
    Publishing place Hamburg
    Document type Book
    Note Text des Beih. engl. und span.
    Accompanying material Beih.
    Database Former special subject collection: coastal and deep sea fishing

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  3. Book: Carlos Saura

    Arnold, Frank / Saura, Carlos

    (Reihe Film ; 26)

    1981  

    Author's details mit Beitr. von Frank Arnold
    Series title Reihe Film ; 26
    Language German
    Size 151 S, Ill
    Publisher Hanser
    Publishing place München u.a.
    Document type Book
    Note Filmogr. u. Bibliogr. C. Saura S. 125 - 151
    ISBN 3446133704 ; 9783446133709
    Database Former special subject collection: coastal and deep sea fishing

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  4. Book: Carlos Saura

    Brasó, Enrique / Saura, Carlos

    (Taller dos : Ser. Cine ; 5)

    1974  

    Series title Taller dos : Ser. Cine ; 5
    Language Spanish
    Size 346 S, zahlr. Ill
    Publisher Taller de Ed. Josefina Betancor
    Publishing place Madrid
    Document type Book
    ISBN 8473300068 ; 9788473300063
    Database Former special subject collection: coastal and deep sea fishing

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  5. Book: Sobre "Elisa vida mía" de Carlos Saura

    Beceyro, Raúl / Saura, Carlos

    1983  

    Author's details Raúl Beceyro
    Language Spanish
    Size 60 leaves, 21 cm
    Publisher Centre d'études hispaniques et hispano-américaines, Université de Rennes
    Publishing place Rennes
    Document type Book
    ISBN 2900055032 ; 9782900055038
    Database Former special subject collection: coastal and deep sea fishing

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  6. Article ; Online: Is phosphorylated tau a good biomarker of synapse pathology in Alzheimer's disease?

    Saura, Carlos A / Parra-Damas, Arnaldo

    Brain communications

    2023  Volume 5, Issue 3, Page(s) fcad142

    Abstract: This scientific commentary refers to 'Distinct brain pathologies associated with Alzheimer's disease biomarker-related phospho-tau 181 and phospho-tau 217 ... ...

    Abstract This scientific commentary refers to 'Distinct brain pathologies associated with Alzheimer's disease biomarker-related phospho-tau 181 and phospho-tau 217 in
    Language English
    Publishing date 2023-04-27
    Publishing country England
    Document type Journal Article ; Comment
    ISSN 2632-1297
    ISSN (online) 2632-1297
    DOI 10.1093/braincomms/fcad142
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Indoxyl Sulfate-Induced Valve Endothelial Cell Endothelial-to-Mesenchymal Transition and Calcification in an Integrin-Linked Kinase-Dependent Manner.

    Delgado-Marin, Maria / Sánchez-Esteban, Sandra / Cook-Calvete, Alberto / Jorquera-Ortega, Sara / Zaragoza, Carlos / Saura, Marta

    Cells

    2024  Volume 13, Issue 6

    Abstract: Calcific Aortic Valve Disease (CAVD) is a significant concern for cardiovascular health and is closely associated with chronic kidney disease (CKD). Aortic valve endothelial cells (VECs) play a significant role in the onset and progression of CAVD. ... ...

    Abstract Calcific Aortic Valve Disease (CAVD) is a significant concern for cardiovascular health and is closely associated with chronic kidney disease (CKD). Aortic valve endothelial cells (VECs) play a significant role in the onset and progression of CAVD. Previous research has suggested that uremic toxins, particularly indoxyl sulfate (IS), induce vascular calcification and endothelial dysfunction, but the effect of IS on valve endothelial cells (VECs) and its contribution to CAVD is unclear. Our results show that IS reduced human VEC viability and increased pro-calcific markers RUNX2 and alkaline phosphatase (ALP) expression. Additionally, IS-exposed VECs cultured in pro-osteogenic media showed increased calcification. Mechanistically, IS induced endothelial-to-mesenchymal transition (EndMT), evidenced by the loss of endothelial markers and increased expression of mesenchymal markers. IS triggered VEC inflammation, as revealed by NF-kB activation, and decreased integrin-linked kinase (ILK) expression. ILK overexpression reversed the loss of endothelial phenotype and RUNX2, emphasizing its relevance in the pathogenesis of CAVD in CKD. Conversely, a lower dose of IS intensified some of the effects in EndMT caused by silencing ILK. These findings imply that IS affects valve endothelium directly, contributing to CAVD by inducing EndMT and calcification, with ILK acting as a crucial modulator.
    MeSH term(s) Humans ; Indican ; Core Binding Factor Alpha 1 Subunit/metabolism ; Endothelial Cells/metabolism ; Cells, Cultured ; Vascular Calcification/metabolism ; Renal Insufficiency, Chronic/pathology ; Aortic Valve/pathology ; Aortic Valve Stenosis ; Calcinosis ; Protein Serine-Threonine Kinases
    Chemical Substances integrin-linked kinase (EC 2.7.1.-) ; Indican (N187WK1Y1J) ; Core Binding Factor Alpha 1 Subunit ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2024-03-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells13060481
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Editorial: Bidirectional Communication Between Synapses and Nucleus in Brain Physiology and Disease.

    Parra-Damas, Arnaldo / Ch'ng, Toh Hean / Jordan, Bryen A / Saura, Carlos A

    Frontiers in molecular neuroscience

    2022  Volume 15, Page(s) 909036

    Language English
    Publishing date 2022-05-06
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2452967-9
    ISSN 1662-5099
    ISSN 1662-5099
    DOI 10.3389/fnmol.2022.909036
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The Expression of Cellular Prion Protein, PrPC, Favors pTau Propagation and Blocks NMDAR Signaling in Primary Cortical Neurons.

    Rivas-Santisteban, Rafael / Raïch, Iu / Aguinaga, David / Saura, Carlos A / Franco, Rafael / Navarro, Gemma

    Cells

    2023  Volume 12, Issue 2

    Abstract: Background: The N-methyl-D-aspartate receptor (NMDAR) is a target in current treatments for Alzheimer's disease (AD). The human prion protein (PrPC) has an important role in the pathophysiology of AD. We hypothesized that PrPC modulates NMDA signaling, ... ...

    Abstract Background: The N-methyl-D-aspartate receptor (NMDAR) is a target in current treatments for Alzheimer's disease (AD). The human prion protein (PrPC) has an important role in the pathophysiology of AD. We hypothesized that PrPC modulates NMDA signaling, thus being a process associated with Alzheimer's disease.
    Methods: NMDAR signaling was characterized in the absence or presence of PrPC in cAMP level determination, mitogen-activated protein kinase (MAPK) pathway and label-free assays in homologous and heterologous systems. Bioluminescence resonance energy transfer was used to detect the formation of NMDAR-PrPC complexes. AXIS™ Axon Isolation Devices were used to determine axonal transport of Tau and pTau proteins in cortical primary neurons in the absence or presence of PrPC. Finally, proximity ligation assays were used to quantify NMDA-PrPC complex formation in neuronal primary cultures isolated from APP
    Results: We discovered a direct interaction between the PrPC and the NMDAR and we found a negative modulation of NMDAR-mediated signaling due to the NMDAR-PrPC interaction. In mice primary neurons, we identified NMDA-PrPC complexes where PrPC was capable of blocking NMDAR-mediated effects. In addition, we observed how the presence of PrPC results in increased neurotoxicity and neuronal death. Similarly, in microglial primary cultures, we observed that PrPC caused a blockade of the NMDA receptor link to the MAPK signaling cascade. Interestingly, a significant increase in NMDA-PrPC macromolecular complexes was observed in cortical neurons isolated from the APP
    Conclusions: PrPC can interact with the NMDAR, and the interaction results in the alteration of the receptor functionality. NMDAR-PrPC complexes are overexpressed in neurons of APP
    MeSH term(s) Mice ; Humans ; Animals ; Alzheimer Disease/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Prion Proteins/metabolism ; N-Methylaspartate/pharmacology ; N-Methylaspartate/metabolism ; Phosphorylation ; Neurons/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Mice, Transgenic
    Chemical Substances Receptors, N-Methyl-D-Aspartate ; Prion Proteins ; N-Methylaspartate (6384-92-5) ; Amyloid beta-Protein Precursor
    Language English
    Publishing date 2023-01-11
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12020283
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Loss of presenilin function enhances tau phosphorylation and aggregation in mice.

    Soto-Faguás, Carlos M / Sanchez-Molina, Paula / Saura, Carlos A

    Acta neuropathologica communications

    2021  Volume 9, Issue 1, Page(s) 162

    Abstract: Mutations in the presenilin (PS/PSEN) genes encoding the catalytic components of γ-secretase accelerate amyloid-β (Aβ) and tau pathologies in familial Alzheimer's disease (AD). Although the mechanisms by which these mutations affect Aβ are well defined, ... ...

    Abstract Mutations in the presenilin (PS/PSEN) genes encoding the catalytic components of γ-secretase accelerate amyloid-β (Aβ) and tau pathologies in familial Alzheimer's disease (AD). Although the mechanisms by which these mutations affect Aβ are well defined, the precise role PS/γ-secretase on tau pathology in neurodegeneration independently of Aβ is largely unclear. Here we report that neuronal PS deficiency in conditional knockout (cKO) mice results in age-dependent brain atrophy, inflammatory responses and accumulation of pathological tau in neurons and glial cells. Interestingly, genetic inactivation of presenilin 1 (PS1) or both PS genes in mutant human Tau transgenic mice exacerbates memory deficits by accelerating phosphorylation and aggregation of tau in excitatory neurons of vulnerable AD brain regions (e.g., hippocampus, cortex and amygdala). Remarkably, neurofilament (NF) light chain (NF-L) and phosphorylated NF are abnormally accumulated in the brain of Tau mice lacking PS. Synchrotron infrared microspectroscopy revealed aggregated and oligomeric β-sheet structures in amyloid plaque-free PS-deficient Tau mice. Hippocampal-dependent memory deficits are associated with synaptic tau accumulation and reduction of pre- and post-synaptic proteins in Tau mice. Thus, partial loss of PS/γ-secretase in neurons results in temporal- and spatial-dependent tau aggregation associated with memory deficits and neurodegeneration. Our findings show that tau phosphorylation and aggregation are key pathological processes that may underlie neurodegeneration caused by familial AD-linked PSEN mutations.
    MeSH term(s) Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Animals ; Brain/pathology ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Neurons/pathology ; Phosphorylation ; Presenilins/genetics ; Presenilins/metabolism ; Protein Aggregation, Pathological/genetics ; tau Proteins/metabolism
    Chemical Substances Presenilins ; tau Proteins
    Language English
    Publishing date 2021-09-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2715589-4
    ISSN 2051-5960 ; 2051-5960
    ISSN (online) 2051-5960
    ISSN 2051-5960
    DOI 10.1186/s40478-021-01259-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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