Project List

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  {
    "count": 2213,
    "next": "https://api-test.medunigraz.at/v1/research/project/?format=api&limit=20&offset=2060&ordering=-begin_effective",
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    "results": [
        {
            "id": 757,
            "title": {
                "de": " GATiB: Genome Austria Tissue Bank (Koordinationsprojekt, SP1)",
                "en": " GATiB: Genome Austria Tissue Bank (Koordinationsprojekt, SP1)"
            },
            "short": "Genome-Austria Tissue Bank (GATiB)",
            "url": null,
            "abstract": {
                "de": "Biobanken, die menschliche biologische Proben wie Gewebe, Blut oder Körperflüssigkeiten sowie damit\r\nassoziierte Daten beinhalten, sind eine essentielle Ressource um die Funktion und medizinische Relevanz\r\nvon menschlichen Genen zu bestimmen. Besonders bedeutend sind Biobanken, welche qualitativ\r\nhochwertige normale als auch erkrankte Gewebe beinhalten. In diesen Geweben sind die Informationen über\r\njene genetischen und epigenetischen Veränderungen, sowie Veränderungen der Genprodukte, die eine\r\nErkrankung verursacht und ihren Verlauf bestimmt haben, noch enthalten. Umfangreiche\r\nGewebesammlungen gewähren einen Einblick in die große Variabilität von menschlichen Erkrankungen\r\nsowie deren unterschiedliches Ansprechen auf Behandlungen. Sie sind somit eine essentielle Grundlage für\r\ndie Weiterentwicklung einer individualisierten Medizin. Die Etablierung von Biobanken hat sich weltweit\r\nbisher auf Blutproben konzentriert, während Gewebebanken nur fragmentarisch, in unterschiedlicher Größe,\r\nmit uneinheitlicher Probenzusammensetzung sowie nach unterschiedlichen Standards und Zielen aufgebaut\r\nwurden. Auf Grund dieser Mängel von isoliert aufgebauten Biobanken wurde der Etablierung eines\r\ninternationalen Netzwerkes von Bio(Gewebe)banken eine hohe strategische Priorität eingeräumt; nicht nur\r\num den wachsenden Bedarf an derartigen Ressourcen zu decken, sondern auch um die Effizienz der\r\nmedizinischen Genomforschung zu steigern und Forschungskosten zu reduzieren.\r\nWir planen eine der weltweit größten Sammlungen von erkrankten humanen Geweben, die bereits an der\r\nMed. Universität Graz besteht, zu einem OECD Biologischen Ressourcenzentrum weiterzuentwickeln, das\r\nspezifisch auf die Unterstützung von systembiologischen Forschungsansätzen, die Entwicklung von\r\nMedikamenten und die Verbesserung der Volksgesundheit ausgerichtet ist. Da menschliches Gewebe eine\r\näußerst begrenzt verfügbare Ressource ist, wird besonderes Augenmerk auf eine gut koordinierte Analyse\r\nder Proben gelegt, so dass zukünftig qualitativ hochwertige Daten, die aus den Geweben gewonnen wurden,\r\nanstelle des Gewebes selbst für Forschungszwecke zur Verfügung gestellt werden können.\r\nDie zentralen Komponenten von GATiB umfassen: 1) archivierte Gewebeproben, die mit Daten über den\r\nKrankheitsverlauf und weiteren medizinischen Daten assoziiert sind, 2) prospektiv gesammelte Gewebe und\r\nBlutproben mit dazugehörigen Daten über die Erkrankung des Patienten sowie über einwirkende\r\nUmweltfaktoren, 3) Tiermodelle, die auf molekularer Ebene hinsichtlich ihrer Relevanz für menschliche\r\nErkrankungen überprüft wurden und 4) IT-Werkzeuge, die Probendokumentation, Datenspeicherung und\r\nDatensuchen unterstützen sowie die Anonymität der Probenspender schützen. Die Entwicklung von GATiB\r\nwird von Erfahrungen geleitet, die aus Forschungsprojekten über Brustkrebs und stoffwechselbedingte\r\nLebererkrankungen, sowie aus Analysen der wichtigsten Biobanken in Europa, USA, Asien und Australien\r\ngewonnen werden. Besonders beachtet wird auch das soziale, ethische und politische Umfeld von GATiB,\r\num eine gute Integration dieser wichtigen Ressource auf nationaler und internationaler Ebene zu\r\nermöglichen.",
                "en": "Biobanks containing human biological samples, such as tissues, blood or body fluids as well as related data\r\nare essential resources for the establishment of the function and medical relevance of human genes. Biobanks\r\ncontaining both high quality normal and diseased human tissues are particularly valuable since they contain\r\ninformation on the genetic and epigenetic alterations as well as on modification of gene products that caused\r\na disease and influenced its outcome. Large tissue collections provide insights into the great variability of\r\nhuman diseases and of responses to medical treatment and, therefore, provide an essential basis for the\r\nadvancement of individualized medicine. To date, biobank development worldwide has focused on blood\r\nsamples whereas tissue collections have been established in a fragmented manner, resulting in tissue banks\r\nof variable size, composition, standards and with different goals. In recognition of the limitations of the\r\ncurrent stand-alone biobank model, the establishment of international networks of bio(tissue)banks have\r\nbeen recently assigned a very high strategic priority, not only to cover the emerging demands for such\r\nresources but also to increase efficacy in medical genomics and to reduce research costs\r\nWe plan to develop, in an internationally oriented context, one of the largest collections of diseased human\r\ntissues already established at the Medical University of Graz to qualify as an OECD Biological Resource\r\nCentre specifically designed to support the needs of systems biology approaches to human diseases, of drug\r\ndiscovery, and public health. Since human tissues are a very limited resource and to minimise the\r\ninternational distribution of human samples, special emphasis will be placed on well-coordinated analysis of\r\nsamples, allowing in the future the distribution of high quality tissue-derived data rather than original tissues\r\nthemselves. Key components of GATiB will comprise (i) archival tissue samples associated with long-term\r\nfollow up and medical data, (ii) prospectively collected tissue and blood samples associated with\r\nstandardized information on the patient’s disease and environmental exposure, (iii) animal models\r\nmolecularly validated for their human disease relevance, and (iv) IT-tools supporting sample tracking, data\r\nstorage, data mining and protecting sample donor privacy. The development of GATiB will be guided by\r\nexperiences obtained from research projects performed in the field of breast cancer and metabolic liver\r\ndiseases and by investigation of major biobank projects in Europe, USA, Asia, and Australia. Furthermore\r\nwe will carefully consider the social, ethical and political issues related to GATiB to ensure proper\r\nembedding of this important resource at the national and international levels."
            },
            "begin_planned": "2005-11-01T01:00:00+01:00",
            "begin_effective": "2006-05-01T02:00:00+02:00",
            "end_planned": "2008-10-31T01:00:00+01:00",
            "end_effective": "2009-09-30T02:00:00+02:00",
            "assignment": "2006-03-28T12:13:27+02:00",
            "program": 73,
            "subprogram": null,
            "organization": 14020,
            "category": 10,
            "type": 10,
            "partner_function": 3,
            "manager": 51663,
            "contact": 51663,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                152
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "757-51663-10",
                "757-51515-12",
                "757-51532-12"
            ]
        },
        {
            "id": 763,
            "title": {
                "de": "GASP & zellulaerer Transport viraler Chemokinrezeptoren",
                "en": "GASP and post-endocytic trafficking of virally encoded chemokine receptors"
            },
            "short": "GASP",
            "url": null,
            "abstract": {
                "de": "Eine relativ große Anzahl von Herpes- und Pockenviren (HHV4-8) kodiert für G protein gekoppelte\r\nRezeptoren (GPCRs) mit 7 transmembranaeren Helices (7TM) der Chemokinfamilie. Diese viralen Rezeptoren\r\nwerden vom Virus zur Evasion des Immunsystems, zellulaeren Transformation, Gewebelokalisation und\r\nwahrscheinlich auch fuer das Eintreten des Virus in eine Zelle verwendet. Fuer einige dieser Rezeptoren konnte\r\nsogar ein direkter Zusammenhang mit pathologischen Phaenotypen wie Kaposi Sarcoma, Arteriosklerose und\r\nHIV-Infektion gezeigt werden. Nach wie vor aber ist die Rolle dieser Rezeptoren im viralen Lebenszyklus bzw.\r\nder viralen Pathogenese wenig verstanden.\r\nTypischerweise befindet sich ein Grossteil dieser viralen Rezeptoren in den Membranen intrazellulaerer\r\nOrganellen von Zellen des 'Wirtorganismus' (=Mensch). Diese Organellen sind ein Teil der post-endozytotischen\r\nKaskade, welche normalerweise fuer den Abbau von nicht mehr benoetigten Proteinen verantwortlich ist, also\r\nz.Bsp. multivesikulaere Endosomen und Lysosomen. Interessanterweise sind es aber genau diese lysosomalen\r\nOrganellen in denen waehrend des viralen Lebenszyklus die viralen Rezeptoren in die Viruswand inkorporiert\r\nwerden.\r\nZiel dieses Projektes ist, den Mechanismus bzw. den Interaktionspartner zu finden, den die viralen\r\nRezeptoren verwenden, um in die lysosomalen Organellen zu gelangen und sukzessive in das Virus inkorporiert\r\nzu werden. Ein vielversprechendes Kandidatenprotein ist das kuerzlich identifizierte Protein GASP (GPCRassoziiertes-\r\nsortierendes-Protein), welches spezifisch an 7TM/GPCRs bindet und in der Lage ist, solche\r\nRezeptoren in post-endozytaere Organellen zu transportieren.\r\nDurch die genaue Charakterisierung der post-endozytotischen Eigenschaften dieser viralen Rezeptoren und\r\nderen Interaktion mit dem Protein GASP hoffen wir, wichtige Einblicke in die Funktion und die Pathogenese dieser\r\nviralen Rezeptoren zu erlangen.",
                "en": "A number of human and animal herpes (HHV4-8) and pox viruses encode G -protein coupled receptors\r\n(GPCRs) with seven transmembrane (7TM) segments - most of which are clearly related to human chemokine\r\nreceptors. It appears, that these receptors are used by the virus for either immune evasion, cellular transformation,\r\ntissue targeting, and possibly for cell entry. In addition, many virally-encoded chemokine 7TM/GPCRs have been\r\nsuggested to be causally involved in pathogenic phenotypes like Kaposi sarcoma, atherosclerosis and HIVinfection.\r\nHowever, to date, the role of these receptors during the viral life cycle and in viral pathogenesis is poorly\r\nunderstood. The majority of these receptors is found in the membranes of intracellular organelles that include\r\ncomponents of the endocytotic pathway, i.e. multivesicular endosomes/lysosomes. It was suggested that this is the\r\nplace where the viral receptors are incorporated into the viral membranes during the final stages virus assembly.\r\nHere, we set out to elucidate the mechanisms by which these viral receptors are endocytosed and targeted\r\nto these intracellular lysosomal compartments. One protein has recently been identified that specifically targets\r\n7TM/GPCRs - typically by interaction with their carboxy-terminal domains – to the degradative pathways. This\r\nprotein is the GPCR-associated sorting protein GASP. By addressing the post-endocytic trafficking properties of\r\nthese viral receptors and their possible interaction with GASP, we hope to gain important insights in the function\r\nand pathology of these viral proteins."
            },
            "begin_planned": "2006-04-01T02:00:00+02:00",
            "begin_effective": "2006-04-01T02:00:00+02:00",
            "end_planned": "2009-03-31T02:00:00+02:00",
            "end_effective": "2011-03-31T02:00:00+02:00",
            "assignment": "2006-03-28T13:39:17+02:00",
            "program": 72,
            "subprogram": null,
            "organization": 14022,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                9
            ],
            "funder_projectcode": "P18723",
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 827,
            "title": {
                "de": "Abberant Somatic Hypermutation in Hodgkin Lymphoma",
                "en": "Abberant Somatic Hypermutation in Hodgkin Lymphoma"
            },
            "short": "HODGKIN LYMPHOMA",
            "url": null,
            "abstract": {
                "de": "The present study is aimed at investigating the role of abberrant somatic hypermutation in different types of Hodgkin Lymphoma and its relation to Hodgkin lymphomagenesis. We will perform a comprehensive analysis exploring the mutation profile throughout the clinicopathologic spectrum of Hodgkin lymphoma correlating the mutation frequency with the expression level of AID in tumor cells. These results will aid in the correct diagnosis of these disorders leading to an optimized therapy.",
                "en": "The present study is aimed at investigating the role of abberrant somatic hypermutation in different types of Hodgkin Lymphoma and its relation to Hodgkin lymphomagenesis. We will perform a comprehensive analysis exploring the mutation profile throughout the clinicopathologic spectrum of Hodgkin lymphoma correlating the mutation frequency with the expression level of AID in tumor cells. These results will aid in the correct diagnosis of these disorders leading to an optimized therapy."
            },
            "begin_planned": "2006-04-01T02:00:00+02:00",
            "begin_effective": "2006-04-01T02:00:00+02:00",
            "end_planned": "2008-03-31T02:00:00+02:00",
            "end_effective": "2008-03-31T02:00:00+02:00",
            "assignment": "2006-05-16T18:45:22+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14082,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                140
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 762,
            "title": {
                "de": "Die Rolle von c-Jun und JunB für die Lymphomenstehung",
                "en": "Die Rolle von c-Jun und JunB für die Lymphomenstehung"
            },
            "short": "c-Jun and JunB in lymphoma formation",
            "url": null,
            "abstract": {
                "de": "ALCL sind hoch maligne Lymphome und häufig mit einer chromosomalen Translokation assoziiert, wobei das onkogene Fusionsprotein NPM-ALK entsteht. Vor kurzem wurde ein NPM-ALK transgenes Mausmodell generiert. Diese Mäuse erkranken an T-Zell Lymphomen, aber auch an B-zelligen Plasmoblastischen Lymphomen. In humanen ALCL wurde vor kurzem eine selektive Überexpression von c-Jun and JunB nachgewiesen. Die Rolle dieser beiden AP-1 Komponeten für die T-Zell Lymphomentstehung ist noch nicht nicht geklärt. Interessanterweise wurde eine tumorsuppressive Rolle von JunB kürzlich in Mäusen denen JunB in der myeloiden Linie fehlt gezeigt, die eine CML-ähnliche Erkrankung entwickeln. Wir werden Mäuse mit gefloxten Allelen von JUNB and c-JUN mit Lck-Cre or CD4-Cre Mäusen kreuzen, um diese Gene spezifisch in T-Zellen zu deletieren. Dadurch können wir die Rolle des proto-Onkogens c-JUN und des anti-Onkogens JUNB in NPM-ALK assozierten T-Zell Lymphomen in vivo untersuchen.\r\nDer Effekt von NPM-ALK auf den MAPK Signaltransduktionsweg und auf AP-1 Aktivität soll mittels NPM-ALK positiver and negativer Lymphomzellinien untersucht werden. Wir wollen die Zusammensetzung der AP-1 Dimere bestimmen, die an die AP-1 Consensus Oligonucleotidsequenz in NPM-ALK positiven Lymphomazelllinien binden.\r\nDanach soll c-Jun in NPM-ALK induzierten Lymphomzellen konditional deletiert werden, um die Rolle von c-Jun für die Lymphomentstehung zu untersuchen. In diesem Zusammenhang sollen die Latenzzeit, Proliferation und der apoptotische Index der transformierten Zellen studiert werden. Diese Experimente könnten c-Jun als potentielles therapeutisches Target in der T-Zell Lymphomagenese definieren. Wir wollen c-Jun and JunB in humanen ALCL Zelllinien stabil ausschalten. Xenograft Experimente mit diesen Zellen sollen die Relevanz unserer in Mäusen durchgeführten Studien für die menschliche Lymphomentstehung demonstrieren.\r\n",
                "en": "ALCL, a highly malignant form of Non-Hodgkin’s lymphoma, is frequently associated with a chromosomal translocation generating the oncogenic fusion protein NPM-ALK. A NPM-ALK transgenic mouse model of lymphomagenesis was recently described. These mice develop thymic T-cell lymphomas and also B-cell neoplasms with plasmablastic differentiation. Human ALCLs were recently shown to constitutively overexpress the AP-1 proteins c-Jun and JunB. The role of c-Jun and JunB in T-cell lymphomas has not been fully understood. Interestingly, a tumor suppressive role of JunB was recently demonstrated in mice lacking JunB in the myeloid lineage which develop a CML-like disease. In the proposed project we take advantage of mice carrying floxed alleles of JUNB and c-JUN and the Lck-Cre or CD4-Cre mice which specifically delete these genes in T-cells. Therefore we will be able to further investigate the role of proto-oncogene c-JUN and the anti-oncogene JUNB in NPM-ALK mediated T-cell malignancies in vivo. \r\nHere we further want to analyse the effect of NPM-ALK on the MAPK signal transduction pathway and on AP-1 activity using NPM-ALK positive and negative lymphoma cell lines. We determine also the composition of AP-1 dimers that bind to AP-1 DNA binding elements in cell lines. \r\nNext we are using conditional deletion of c-Jun in NPM-ALK induced lymphomas to study the requirement for c-Jun in lymphoma formation. In this context we want to analyse the latency, proliferation and the apoptotic index of transformed cells. These experiments will define the function of c-Jun as a potential therapeutic target in T-cell lymphomas before or after lymphoma formation. A conditional loss of function approach whereby JunB and/or c-Jun are specifically deleted in T-cells of NPM-ALK transgenic mice will be employed to define the functions of these two proteins in T cell transformation. \r\nWe also intend to stably knock down the expression of c-Jun and JunB in human ALCL derived cell lines. To elucidate the relevance of our studies done in mice on human lymphoma formation, we will then perform Xenograft experiments using these cell lines. \r\n"
            },
            "begin_planned": "2006-04-01T02:00:00+02:00",
            "begin_effective": "2006-04-01T02:00:00+02:00",
            "end_planned": "2008-09-30T02:00:00+02:00",
            "end_effective": "2009-03-31T02:00:00+02:00",
            "assignment": "2006-03-28T13:28:34+02:00",
            "program": 72,
            "subprogram": null,
            "organization": 14020,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51691,
            "contact": 51691,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                9
            ],
            "funder_projectcode": "P18478",
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "762-51691-10"
            ]
        },
        {
            "id": 1228,
            "title": {
                "de": "Probiotika bei alkoholischer Hepatitis",
                "en": "Probiotika bei alkoholischer Hepatitis"
            },
            "short": "Probiotika bei alkoholischer Hepatitis",
            "url": null,
            "abstract": {
                "de": "Die alkoholische Hepatitis ist ein lebensbedrohliches Krankheitsbild mit einer Sterblichkeitsrate von über 50% nach einem Jahr. Patienten mit alkoholischer Hepatitis sind überdurchschnittlich anfällig gegenüber bakteriellen Infektionen. Mögliche Ursachen für die erhöhte Infektionsneigung dieser Patienten sind eine bakterielle Translokation aus dem Darm (Invasion von Bakterien durch die Darmwand) sowie eine verminderte zelluläre Immunantwort. Neutrophile Granulozyten (eine Untergruppe der weißen Blutkörperchen) sind bei alkoholischer Hepatitis aktiviert (\"priming\"), wodurch sie bakterielle Infektionen besser bekämpfen können. Doch trotz des erhöhten \"priming\" ist die Funktion der neutrophilen Granulozyten eingeschränkt, wie anhand einer verringerten Phagozytose-Kapazität gezeigt wurde. \"Priming\" kann durch Endotoxin (toxische Produkte bestimmter Bakterien) verursacht werden. Bei Patienten mit alkoholischer Hepatitis wurden erhöhte Serumspiegel von Endotoxin gemessen. Die erhöhten Endotoxinspiegel sind durch bakterielle Translokation aus dem Darm infolge bakterieller Überwucherung und erhöhter Darmpermeabilität (gestörte Barrierefunktion des Darms) bedingt.\r\nDiese Studie untersucht den Effekt einer Therapie mit Probiotika (lebensfähige Mikroorganismen, die die Zusammensetzung der Darmflora verändern und dadurch positive Auswirkungen auf die Gesundheit haben) auf die Funktion neutrophiler Granulozyten bei Patienten mit alkoholischer Hepatitis. Wir postulieren, dass eine Veränderung der Darmflora durch Probiotika die bakterielle Translokation verminden und damit die Endotoxinspiegel senken kann. Dadurch sollte das inadäquate \"priming\" der neutrophilen Granulozyten herabgesetzt und die Funktion dieser Zellen im Blut wiederhergestellt werden. In weiterer Folge würde das Infektionsrisiko dieser Patienten sinken und möglicherweise das Überleben verbessert werden. \r\nDas Hauptziel des beantragten Projektes ist die Untersuchung des Effekts einer speziellen Probiotika-Mischung beziehungsweise Plazebo auf die lokale und systemische Funktion neutrophiler Granulozyten bei Patienten mit alkoholischer Hepatitis. Dazu werden verschiedene Tests zur Untersuchung der Aktivität (\"priming\") und Funktion (Phagozytose) neutrophiler Granulozyten, der Darmpermeabilität sowie Messungen von Zytokinen und Endotoxinspiegeln vor und nach Probiotikagabe durchgeführt. Sollte sich die oben erwähnte Hypothese bewahrheiten, wäre die Behandlung mit Probiotika eine einfache und kostengünstige Behandlungsmöglichkeit der alkoholischen Hepatitis.\r\n\r\n\r\n",
                "en": "Die alkoholische Hepatitis ist ein lebensbedrohliches Krankheitsbild mit einer Sterblichkeitsrate von über 50% nach einem Jahr. Patienten mit alkoholischer Hepatitis sind überdurchschnittlich anfällig gegenüber bakteriellen Infektionen. Mögliche Ursachen für die erhöhte Infektionsneigung dieser Patienten sind eine bakterielle Translokation aus dem Darm (Invasion von Bakterien durch die Darmwand) sowie eine verminderte zelluläre Immunantwort. Neutrophile Granulozyten (eine Untergruppe der weißen Blutkörperchen) sind bei alkoholischer Hepatitis aktiviert (\"priming\"), wodurch sie bakterielle Infektionen besser bekämpfen können. Doch trotz des erhöhten \"priming\" ist die Funktion der neutrophilen Granulozyten eingeschränkt, wie anhand einer verringerten Phagozytose-Kapazität gezeigt wurde. \"Priming\" kann durch Endotoxin (toxische Produkte bestimmter Bakterien) verursacht werden. Bei Patienten mit alkoholischer Hepatitis wurden erhöhte Serumspiegel von Endotoxin gemessen. Die erhöhten Endotoxinspiegel sind durch bakterielle Translokation aus dem Darm infolge bakterieller Überwucherung und erhöhter Darmpermeabilität (gestörte Barrierefunktion des Darms) bedingt.\r\nDiese Studie untersucht den Effekt einer Therapie mit Probiotika (lebensfähige Mikroorganismen, die die Zusammensetzung der Darmflora verändern und dadurch positive Auswirkungen auf die Gesundheit haben) auf die Funktion neutrophiler Granulozyten bei Patienten mit alkoholischer Hepatitis. Wir postulieren, dass eine Veränderung der Darmflora durch Probiotika die bakterielle Translokation verminden und damit die Endotoxinspiegel senken kann. Dadurch sollte das inadäquate \"priming\" der neutrophilen Granulozyten herabgesetzt und die Funktion dieser Zellen im Blut wiederhergestellt werden. In weiterer Folge würde das Infektionsrisiko dieser Patienten sinken und möglicherweise das Überleben verbessert werden. \r\nDas Hauptziel des beantragten Projektes ist die Untersuchung des Effekts einer speziellen Probiotika-Mischung beziehungsweise Plazebo auf die lokale und systemische Funktion neutrophiler Granulozyten bei Patienten mit alkoholischer Hepatitis. Dazu werden verschiedene Tests zur Untersuchung der Aktivität (\"priming\") und Funktion (Phagozytose) neutrophiler Granulozyten, der Darmpermeabilität sowie Messungen von Zytokinen und Endotoxinspiegeln vor und nach Probiotikagabe durchgeführt. Sollte sich die oben erwähnte Hypothese bewahrheiten, wäre die Behandlung mit Probiotika eine einfache und kostengünstige Behandlungsmöglichkeit der alkoholischen Hepatitis.\r\n\r\n\r\n"
            },
            "begin_planned": "2006-03-01T01:00:00+01:00",
            "begin_effective": "2006-03-01T01:00:00+01:00",
            "end_planned": "2008-03-01T01:00:00+01:00",
            "end_effective": "2008-03-01T01:00:00+01:00",
            "assignment": "2007-04-18T15:50:14+02:00",
            "program": 69,
            "subprogram": null,
            "organization": 14081,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 50989,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                9
            ],
            "funder_projectcode": "J2547",
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "1228-50989-10"
            ]
        },
        {
            "id": 684,
            "title": {
                "de": "Modeling the cardiopulmonary-arterial baroreflexes: pressure and volume control with clinical applications to hypovolemic stress",
                "en": "Modeling the cardiopulmonary-arterial baroreflexes: pressure and volume control with clinical applications to hypovolemic stress"
            },
            "short": "Modeling baroreflexes",
            "url": null,
            "abstract": {
                "de": "The objective of this project ist to develop a physiologically based mathematical model of the cardiovascular system (CVS) that can be applied to stydy the short-term control of hypovolemic stress. Hypovolemic stress refers to disturbances to the DVS caused by the loss or sequestration of blood volume. Specifically, we propose to develop a model that can quantitatively reflect the interacteion to the cardiopulmonary and arterial baroreflexes which are key elements in the short-term response to hypovolemic stress. ",
                "en": "The objective of this project ist to develop a physiologically based mathematical model of the cardiovascular system (CVS) that can be applied to stydy the short-term control of hypovolemic stress. Hypovolemic stress refers to disturbances to the DVS caused by the loss or sequestration of blood volume. Specifically, we propose to develop a model that can quantitatively reflect the interacteion to the cardiopulmonary and arterial baroreflexes which are key elements in the short-term response to hypovolemic stress. "
            },
            "begin_planned": "2006-03-01T01:00:00+01:00",
            "begin_effective": "2006-03-01T01:00:00+01:00",
            "end_planned": "2009-03-31T02:00:00+02:00",
            "end_effective": "2009-02-28T01:00:00+01:00",
            "assignment": "2006-01-31T09:56:45+01:00",
            "program": 72,
            "subprogram": null,
            "organization": 14010,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51683,
            "contact": 51683,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                9
            ],
            "funder_projectcode": "P18778",
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "684-51683-10"
            ]
        },
        {
            "id": 2540,
            "title": {
                "de": "Modellierung des kardiopulmonal-arteriellen Baroreflexes ",
                "en": "Modellierung des kardiopulmonal-arteriellen Baroreflexes "
            },
            "short": "Baroreflex",
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2006-02-15T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2009-03-14T01:00:00+01:00",
            "assignment": null,
            "program": 72,
            "subprogram": null,
            "organization": 14010,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 737,
            "title": {
                "de": "GOLDII - Genomics of Lipid-associated Disorders",
                "en": "GOLDII - Genomics of Lipid-associated Disorders"
            },
            "short": "GOLDII",
            "url": null,
            "abstract": {
                "de": "Despite the general opinion, that obesity and other lipid-associated disorders are to a large extent the result of misbehaviour, it is evident that overeating in humans is mostly \"hard-wired\" and that adipose tissue mass is genetically determined. Numerous twin/adoption and family studies confirm a major contribution of genes to the development of obesity. This fact, combined with the \"Obesogenic environment\" that we face in developed countries, with adopting a sedentary life style and an abundance of high-fat, high-calorie food at low cost, results in the tremendous rate at which obesity and related disorders increase in today's world.\r\n\r\nThis project will identify subsets of genes that are involved in the development of adipocytes, the regulation of lipid deposition and lipid mobilization, and the maintenance of cellular cholesterol homeostasis.\r\nWe expect to discover important components of the eukaryotic proteo-lipidome. Our results will significantly advance the understanding of lipid and energy metabolism and may provide novel durg targets for the treatment of metabolic diseases.",
                "en": "Despite the general opinion, that obesity and other lipid-associated disorders are to a large extent the result of misbehaviour, it is evident that overeating in humans is mostly \"hard-wired\" and that adipose tissue mass is genetically determined. Numerous twin/adoption and family studies confirm a major contribution of genes to the development of obesity. This fact, combined with the \"Obesogenic environment\" that we face in developed countries, with adopting a sedentary life style and an abundance of high-fat, high-calorie food at low cost, results in the tremendous rate at which obesity and related disorders increase in today's world.\r\n\r\nThis project will identify subsets of genes that are involved in the development of adipocytes, the regulation of lipid deposition and lipid mobilization, and the maintenance of cellular cholesterol homeostasis.\r\nWe expect to discover important components of the eukaryotic proteo-lipidome. Our results will significantly advance the understanding of lipid and energy metabolism and may provide novel durg targets for the treatment of metabolic diseases."
            },
            "begin_planned": "2005-12-01T01:00:00+01:00",
            "begin_effective": "2006-02-01T01:00:00+01:00",
            "end_planned": "2008-11-30T01:00:00+01:00",
            "end_effective": "2008-11-30T01:00:00+01:00",
            "assignment": "2006-03-02T10:14:41+01:00",
            "program": 73,
            "subprogram": null,
            "organization": 14019,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51974,
            "contact": 51974,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                152
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "737-51974-10"
            ]
        },
        {
            "id": 1454,
            "title": {
                "de": "CONTICA: Control of Intracellular Calcium and Arrhythmias",
                "en": "Control of Intracellular Calcium and Arrhythmias"
            },
            "short": "CONTICA",
            "url": null,
            "abstract": {
                "de": "Ventricular arrhythmias are a major cause of mortality. Currently there is no effective treatment available, largely because our understanding of their molecular basis is poor. Altered intracellular Ca handling may be a final common pathway predisposing to ventricular tachycardias and sudden death in acquired or congenital heart disease.\r\nUnderstanding the complex function of the RyR2 Ca channel and its regulatory mechanisms, therefore, holds the promise to develop new diagnostic and therapeutic strategies for effective treatment of these lethal arrhythmias. \r\nThe goal pursued by the CONTICA group is the elucidation of the molecular mechanisms linking defective RyR2 function to the generation of arrhythmias.\r\nThe combined knowledge gained from these studies will be used to develop and test novel diagnostic approaches and antiarrhythmic drugs to help alleviate one of the largest health burdens to the European society, i.e. malignant ventricular arrhythmias.",
                "en": "Ventricular arrhythmias are a major cause of mortality. Currently there is no effective treatment available, largely because our understanding of their molecular basis is poor. Altered intracellular Ca handling may be a final common pathway predisposing to ventricular tachycardias and sudden death in acquired or congenital heart disease.\r\nUnderstanding the complex function of the RyR2 Ca channel and its regulatory mechanisms, therefore, holds the promise to develop new diagnostic and therapeutic strategies for effective treatment of these lethal arrhythmias. \r\nThe goal pursued by the CONTICA group is the elucidation of the molecular mechanisms linking defective RyR2 function to the generation of arrhythmias.\r\nThe combined knowledge gained from these studies will be used to develop and test novel diagnostic approaches and antiarrhythmic drugs to help alleviate one of the largest health burdens to the European society, i.e. malignant ventricular arrhythmias."
            },
            "begin_planned": "2007-02-01T01:00:00+01:00",
            "begin_effective": "2006-02-01T01:00:00+01:00",
            "end_planned": "2009-01-31T01:00:00+01:00",
            "end_effective": "2009-07-31T02:00:00+02:00",
            "assignment": "2008-01-22T11:15:08+01:00",
            "program": 21,
            "subprogram": null,
            "organization": 14083,
            "category": 10,
            "type": 10,
            "partner_function": 3,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                10
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "1454-60041-12"
            ]
        },
        {
            "id": 671,
            "title": {
                "de": "DISMAL: Molecular signatures as diagnostic and therapeutic targets for disseminated epithelial malignancies",
                "en": "DISMAL: Molecular signatures as diagnostic and therapeutic targets for disseminated epithelial malignancies"
            },
            "short": "DISMAL",
            "url": null,
            "abstract": {
                "de": "Disseminated tumour cells (DTC) occur at very low numbers and can be detected using sensitive immunostaining and PCR methods. However, sensitivity and in particular specificity of this approach need to be improved. Combining the expertise of 11 academic partners with long-term expertise in mi-crometastasis research the DISMAL-project will establish an improved platform for DTC detection with an increased sensitivity and – in particular – with a largely improved specificity. Besides DTC detection also analysis of circulating tumour DNA and RNA, and expression profiling of tumours are being ex-plored for assessment of minimal disease. We will focus on epithelial tumours as the most common types of solid tumours in the EU, investigating the carcinoma types that display different modes of metastatic spread. Dissemination via the blood circulation will be analyzed, using bone marrow as an important indicator organ to which epithelial tumour cells home. Using genomics-based approaches, novel diagnos-tic target molecules will be identified and validated in functional models. We will complement immuno-cytochemical DTC detection by additional genotypic and phenotypic markers relevant for metastatic progression. To further increase diagnostic precision we will analyze whether this improved platform can be combined with analysis of tumour characteristics that were revealed by the microarray analysis, and with evaluation of circulating tumour-associated DNA or RNA. Besides the primary focus on improve-ment of DTC-based diagnostic platforms, it is important to realize that these cells are the target cells for adjuvant chemotherapy and radiotherapy. In innovative DTC models, the efficacy of DTC treatment will therefore be analyzed and potential improvements studied. The translation of scientific knowledge into commercial products will be ensured by 3 SMEs with unique technological capabilities.",
                "en": "Disseminated tumour cells (DTC) occur at very low numbers and can be detected using sensitive immunostaining and PCR methods. However, sensitivity and in particular specificity of this approach need to be improved. Combining the expertise of 11 academic partners with long-term expertise in mi-crometastasis research the DISMAL-project will establish an improved platform for DTC detection with an increased sensitivity and – in particular – with a largely improved specificity. Besides DTC detection also analysis of circulating tumour DNA and RNA, and expression profiling of tumours are being ex-plored for assessment of minimal disease. We will focus on epithelial tumours as the most common types of solid tumours in the EU, investigating the carcinoma types that display different modes of metastatic spread. Dissemination via the blood circulation will be analyzed, using bone marrow as an important indicator organ to which epithelial tumour cells home. Using genomics-based approaches, novel diagnos-tic target molecules will be identified and validated in functional models. We will complement immuno-cytochemical DTC detection by additional genotypic and phenotypic markers relevant for metastatic progression. To further increase diagnostic precision we will analyze whether this improved platform can be combined with analysis of tumour characteristics that were revealed by the microarray analysis, and with evaluation of circulating tumour-associated DNA or RNA. Besides the primary focus on improve-ment of DTC-based diagnostic platforms, it is important to realize that these cells are the target cells for adjuvant chemotherapy and radiotherapy. In innovative DTC models, the efficacy of DTC treatment will therefore be analyzed and potential improvements studied. The translation of scientific knowledge into commercial products will be ensured by 3 SMEs with unique technological capabilities."
            },
            "begin_planned": "2006-01-01T01:00:00+01:00",
            "begin_effective": "2006-02-01T01:00:00+01:00",
            "end_planned": "2008-10-31T01:00:00+01:00",
            "end_effective": "2009-04-30T02:00:00+02:00",
            "assignment": "2006-01-21T19:45:22+01:00",
            "program": 21,
            "subprogram": "Biowissenschaften",
            "organization": 14021,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                10
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 733,
            "title": {
                "de": "Regulation of G-CSF receptor ubiquitination: Implications on granulopoieses and pathogenesis in myeloid disorders.",
                "en": "Regulation of G-CSF receptor ubiquitination: Implications on granulopoieses and pathogenesis in myeloid disorders."
            },
            "short": "Regulat of G-CSF receptor ubiquitination",
            "url": null,
            "abstract": {
                "de": "Myelodysplastic syndromes (MDS) and severe congenital neutropenia (SCN) are myeloid disorders characterized by defective myeloid differentiation. We and others have identified mutations within the granulocyte colony-stimulation factor receptor (G-CSF-R), which es the mamor transducer of signals regulating granulopoiesis, in SCN or MDS patients prone to develop acute myeloid leukemia (AML). Many of the Phenotypic features conferred by these mutations can be explained by defects in negative regulation of G-CSF-R signaling. Modulation and, finally, termination of signaling is largely influenced by receptor routing from the plasma membrane, a process that is controlled by ubiquitination. Two ubiquitin ligases, SOCS3 and WSB-1/2, habe recently been shown to bind to the G-CSF-R and to modulate its signaling suggesting an important role of ubiquitination on G-CSF-R signaling. In addition, preliminary experiments in myelid progenitor cells suggest that the candidate targets for ubiquitination, i.e. conserved lysine residues in the cytoplasmic domain of the G-CSF-R, regulate the G-CSF response.\r\nThe aim of this projet ist to thoroughly investigate the mechanisms of G-CSF-R ubiqutination and to determine their impact on intracellular receptor routing and signaling functions. For this purpose, a series of lysine substitution as well as the sisease specific mutant G-CSF-R construckts will be generated. Tu study the individual contribution of SOCS3 and WSB-1/2 to receptor ubiquination, mutants which in addition lack SOCS3 recruitment site Y729 or the C-terminal WSB-binding domain will bei included. Introduction of these G-CSF-R mutants into myeloid progenitor cells form G-CSF-R deficient mice, myeloid 32D cells and HEK293 human embryonic kidney cells will elucidate the mechanisms regulating G-CSF-R ubiquitination and their impact on receptor routing and signaling pathways in al cellular context. This project will therefore provied insights in the mechanisms whereby receptor ubiquitination and their impact on receptor routing and signaling pathways in al cellular context. This project  will therefore provide insights in the mechanisms whereby receptor ubiquitination modulates G-CSF-controlled granulopoiesis and will reveal the significance of their deregulation in myeloid disorders. This knowledge may contribute to the design of therapeutic modalities aimed at restoring the signaling network in human myeloid disorders, such as MDS and AML.",
                "en": "Myelodysplastic syndromes (MDS) and severe congenital neutropenia (SCN) are myeloid disorders characterized by defective myeloid differentiation. We and others have identified mutations within the granulocyte colony-stimulation factor receptor (G-CSF-R), which es the mamor transducer of signals regulating granulopoiesis, in SCN or MDS patients prone to develop acute myeloid leukemia (AML). Many of the Phenotypic features conferred by these mutations can be explained by defects in negative regulation of G-CSF-R signaling. Modulation and, finally, termination of signaling is largely influenced by receptor routing from the plasma membrane, a process that is controlled by ubiquitination. Two ubiquitin ligases, SOCS3 and WSB-1/2, habe recently been shown to bind to the G-CSF-R and to modulate its signaling suggesting an important role of ubiquitination on G-CSF-R signaling. In addition, preliminary experiments in myelid progenitor cells suggest that the candidate targets for ubiquitination, i.e. conserved lysine residues in the cytoplasmic domain of the G-CSF-R, regulate the G-CSF response.\r\nThe aim of this projet ist to thoroughly investigate the mechanisms of G-CSF-R ubiqutination and to determine their impact on intracellular receptor routing and signaling functions. For this purpose, a series of lysine substitution as well as the sisease specific mutant G-CSF-R construckts will be generated. Tu study the individual contribution of SOCS3 and WSB-1/2 to receptor ubiquination, mutants which in addition lack SOCS3 recruitment site Y729 or the C-terminal WSB-binding domain will bei included. Introduction of these G-CSF-R mutants into myeloid progenitor cells form G-CSF-R deficient mice, myeloid 32D cells and HEK293 human embryonic kidney cells will elucidate the mechanisms regulating G-CSF-R ubiquitination and their impact on receptor routing and signaling pathways in al cellular context. This project will therefore provied insights in the mechanisms whereby receptor ubiquitination and their impact on receptor routing and signaling pathways in al cellular context. This project  will therefore provide insights in the mechanisms whereby receptor ubiquitination modulates G-CSF-controlled granulopoiesis and will reveal the significance of their deregulation in myeloid disorders. This knowledge may contribute to the design of therapeutic modalities aimed at restoring the signaling network in human myeloid disorders, such as MDS and AML."
            },
            "begin_planned": "2006-02-01T01:00:00+01:00",
            "begin_effective": "2006-02-01T01:00:00+01:00",
            "end_planned": "2008-01-31T01:00:00+01:00",
            "end_effective": "2008-01-31T01:00:00+01:00",
            "assignment": "2006-02-24T17:33:52+01:00",
            "program": 69,
            "subprogram": null,
            "organization": 14082,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51911,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                9
            ],
            "funder_projectcode": "J2536",
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "733-51911-10"
            ]
        },
        {
            "id": 584,
            "title": {
                "de": "Cloning, sequencing, expression, and intracellular localization of an undescribed 34-kDa protein constitutent of the triglyceride-droplet surface in adipocytes",
                "en": "Cloning, sequencing, expression, and intracellular localization of an undescribed 34-kDa protein constitutent of the triglyceride-droplet surface in adipocytes"
            },
            "short": "localization of  undescr. 34-kDa protein",
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": "2006-01-01T01:00:00+01:00",
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": "2006-12-31T01:00:00+01:00",
            "end_effective": "2006-12-31T01:00:00+01:00",
            "assignment": "2005-11-13T20:57:56+01:00",
            "program": null,
            "subprogram": null,
            "organization": 14013,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                150
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "584-50712-12"
            ]
        },
        {
            "id": 558,
            "title": {
                "de": "Kernrezeptoren als therapeutische Targets bei Cholestase",
                "en": "Molecular Regulation of Alternative Bile Acid Transport and Detoxification Mechanisms by Nuclear Receptor (PXR, CAR, VDR) Ligands in the Treatment of Cholestasis"
            },
            "short": "Nuclear Receptor Ligands (Cholestasis)",
            "url": null,
            "abstract": {
                "de": "Ziel dieses Projekts ist die Identifizierung neuer Therapiestrategien für cholestatische Lebererkrankungen, welche auf der Stimulation alternativer Gallensäuren-Transport- und Entgiftungssysteme in Leber und Niere mittels Kernrezeptor (PXR, CAR und VDR)-Agonisten basieren. Es soll untersucht werden, ob dieser therapeutische Zugang zu einer Verbesserung der Cholestase, der Cholestase assoziierten Leberschädigung und biliärer Leberfibrose führt. Diese Fragestellungen werden sowohl in vivo (Mausmodelle für Cholestase, Lebergewebe von Patienten mit cholestatischen Lebererkrankungen wie der primär biliären Leberzirrhose und primär sklerosierenden Cholangitis) als auch in vitro (primäre Hepatozytenkulturen) durch die Gabe etablierter und spezifischer Kernrezeptor-Liganden und die nachfolgende Analyse deren Effekte auf die Leberzellschädigung, biliäre Fibrose, sowie auf die Expression und Funktion der für die Entgiftung und Elimination von Gallensäuren verantwortlichen Genprodukte untersucht. PXR, CAR and VDR wurden als therapeutische Targets ausgewählt, da bisher vorliegende Ergebnisse und Daten in der Literatur darauf hinweisen, dass diese Kernrezeptoren Gene regulieren, welche an der Entgiftung und Elimination von potentiell hepatotoxischen Gallensäuren beteiligt sind. Das therapeutische Targeting von Kernrezeptoren \"über den klassischen nukleären Gallensäurenrezeptor FXR hinaus\" stellt (insbesondere für die beiden Xenobiotika Kernrezeptoren PXR und CAR) einen neuen Ansatz in der Behandlung cholestatischer Lebererkrankungen dar. Dieses Projekt versucht eine Verbindung zwischen den Forschungsgebieten des hepatobiliären Transportes/Cholestase und der Leberschädigung/biliären Fibrose herzustellen. Die Fibrose stellt die prognostisch wichtigste Cholestasefolge bzw. Komplikation dar. Weiters spielt die biliäre Fibrose bereits früh in der Entstehung der primär sklerosierenden Cholangitis eine wichtige Rolle. Der kombinierte experimentelle Ansatz in tiermodellen der Cholestase und Untersuchungen im humanen Lebergewebe von Patienten mit cholestatischen Lebererkrankungen sollte wesentliche mechanistische Einblicke in die therapeutische Transporter Regulation über Spezies-Grenzen hinweg erlauben. Die derzeitige pharmakologische Therpie cholestatischer Lebererkrankungen ist nur wenig zufriedenstellend und effektiv. Die Ergebnisse dieses Projekts werden wichtige Implikationen für die Entwicklung efektiverer Therapieformen für für die Cholestase haben. Aufgrund der Untersuchungen im humanen Gewebe sind klinisch-relevante therapeutische Implikationen zu erwarten. Weiters sind Auswirkungen auf andere Fachgebiete über das der Hepatologie hinaus (zB Atherosklerose, Colon-Carcinom, Medikamentenstoffwechsel, Chemotherapieresistenz) möglich.",
                "en": "The overall objective of the proposed research project is to identify novel therapeutic strategies for cholestasis aimed at stimulating alternative bile acid transport and detoxification in liver and kidney via nuclear receptor (PXR, CAR and VDR) agonists and to determine whether this approach results in improvement of cholestasis and cholestasis-associated liver injury and biliary fibrosis. this will be addressed in vivo (mouse models of cholestasis, liver tissue from patients with cholestatic liver diseases such as primary biliary cirrhosis and primary sclerosing cholangitis) and in vitro (primary hepatocyte cultures) by administration of established and specific agonistic nuclear receptor ligands and subsequent analysis of liver injury biliary fibrosis, as well as expression and function of genes involved in bile acid detoxification and elimination. PXR, CAR and VDR have been chosen as therapeutic targets since these nuclear receptors coordinately regulate genes/gene products predected to detoxify and eliminate bile acids and other potentially toxic biliary constituents. Targeting nuclear receptors \"beyound the classic bile acid receptro FXR\" (in particular the \"xenobiotic sensors\" CAR and VDR) for the treatment of cholestatic liver diseases is novel. This project attempts to provide potential links between the research area of hepatobiliary transport/cholestasis and liver injyry/biliary fibrosis, the latter being the prognostically most relevant consequence of cholestasis. Moreover, biliary fibrosis is an early and important feature of chronic bile duct disorders such as primary sclerosing cholangitis. The combined approach in animal models of cholestasis and human liver tisue form patients with cholestatic disorders both treated with respective nuclear receptor agonists which will provede major mechanistic insights into the therapeutic effects across species diferences. Currently, medical treatment options for cholestatic liver diseases are unsatisfactory and of limited efficacy. The results of this study will have major implications for understanding and developing future therapeutic strategies against cholestatic liver diseases. Based on the results in the human arm of the study, the proposed project should directly contribute to new knowledge in an area of liver research with potential importance to clinical therapeutics. Moreover, the results of this study should also impact on other research areas beyound the field of hepatology (e.g., atherosclerosis, colon cancer, hepatic drug metabolism and multidrug resistance)."
            },
            "begin_planned": "2005-07-01T02:00:00+02:00",
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": "2007-07-31T02:00:00+02:00",
            "end_effective": "2010-01-01T01:00:00+01:00",
            "assignment": "2005-11-04T01:00:00+01:00",
            "program": 72,
            "subprogram": null,
            "organization": 14081,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                9
            ],
            "funder_projectcode": "P19118",
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 691,
            "title": {
                "de": "Netzwerk Psychosomatik in Österreich (Teilprojekt 1 des Projektes \"Standards für stationäre Psychosomatik in Österreich).",
                "en": "Netzwerk Psychosomatik in Österreich (Teilprojekt 1 des Projektes \"Standards für stationäre Psychosomatik in Österreich)."
            },
            "short": "Netzwerk Psychosomatik in Österreich. ",
            "url": null,
            "abstract": {
                "de": "Psychosomatische Krankheitsbilder fordern den sozialen Kulturraum spezifisch heraus. Um zu heilen müssen sie in ihrem Appell erkannt und in ihren Impulsen für kulturelle Erneuerung verstanden werden. Wo dies nicht gelingt, kommt es zur Chronifizierung oder zur Verschlimmerung des Krankheitsbildes. Diese hohe Relevanz der psychosozialen \"Übersetzung der Klage\" führt dazu, dass die Schnittstellenproblematik zwischen stationärer und niedergelassener medizinischer Versorgung besonders bedeutsam wird. Die oft mangelnde Kooperation zwischen diesen Ebenen stellt im Gesundheitssystem insgesamt einen Problembereich dar und wird gerade für psychosomatische Erkrankungen besonders aktuell. Das Netzwerk Psychosomatik soll  als virtueller Raum Personen und Institutionen mit bestehender psychosomatischer Fachkompetenz sowohl untereinander lebendig vernetzen als auch mit den befassten politischen Verantwortungsträgern aber auch konkreten Patientenanliegen in Austausch bringen. Es ist als Forum für die Entwicklung und die Umsetzung von nationalen Standards der Qualitätssicherung und zugleich als Weiterbildungsplattform im Bereich Psychosomatik konzipiert. Für die Österreichische Gesundheitsversorgung bietet es eine gute Möglichkeit regional wie überregional und themenbezogen psychosomatisch kompetente Ansprechpersonen zu kontaktieren, Beratungs- und Behandlungsempfehlungen einzuholen und eine gezielete psychosomatische Fachbehandlung in die Wege zu leiten.",
                "en": "Psychosomatische Krankheitsbilder fordern den sozialen Kulturraum spezifisch heraus. Um zu heilen müssen sie in ihrem Appell erkannt und in ihren Impulsen für kulturelle Erneuerung verstanden werden. Wo dies nicht gelingt, kommt es zur Chronifizierung oder zur Verschlimmerung des Krankheitsbildes. Diese hohe Relevanz der psychosozialen \"Übersetzung der Klage\" führt dazu, dass die Schnittstellenproblematik zwischen stationärer und niedergelassener medizinischer Versorgung besonders bedeutsam wird. Die oft mangelnde Kooperation zwischen diesen Ebenen stellt im Gesundheitssystem insgesamt einen Problembereich dar und wird gerade für psychosomatische Erkrankungen besonders aktuell. Das Netzwerk Psychosomatik soll  als virtueller Raum Personen und Institutionen mit bestehender psychosomatischer Fachkompetenz sowohl untereinander lebendig vernetzen als auch mit den befassten politischen Verantwortungsträgern aber auch konkreten Patientenanliegen in Austausch bringen. Es ist als Forum für die Entwicklung und die Umsetzung von nationalen Standards der Qualitätssicherung und zugleich als Weiterbildungsplattform im Bereich Psychosomatik konzipiert. Für die Österreichische Gesundheitsversorgung bietet es eine gute Möglichkeit regional wie überregional und themenbezogen psychosomatisch kompetente Ansprechpersonen zu kontaktieren, Beratungs- und Behandlungsempfehlungen einzuholen und eine gezielete psychosomatische Fachbehandlung in die Wege zu leiten."
            },
            "begin_planned": "2006-01-01T01:00:00+01:00",
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": "2007-01-31T01:00:00+01:00",
            "end_effective": "2009-05-31T02:00:00+02:00",
            "assignment": "2006-02-03T15:29:55+01:00",
            "program": null,
            "subprogram": null,
            "organization": 29447,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 50774,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                472
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "691-50774-10"
            ]
        },
        {
            "id": 2990,
            "title": {
                "de": "Interaktion von TRPC-Ionenkanälen mit Membranlipiden",
                "en": "Interaktion von TRPC-Ionenkanälen mit Membranlipiden"
            },
            "short": "TRPC",
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2009-06-30T02:00:00+02:00",
            "assignment": null,
            "program": 69,
            "subprogram": null,
            "organization": 14011,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                9
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 1506,
            "title": {
                "de": "PRIVILEGED",
                "en": "PRIVILEGED"
            },
            "short": "PRIVILEGED",
            "url": null,
            "abstract": {
                "de": "PRIVILEGED (Privacy in Law, Ethics and Genetic Data) will make recommendations for research practice and public policy-making, including regulatory options at the national and European level, to promote the optimal relation between research using genetic data and bio-banks and ethical interests in privacy. PRIVILEGED will identify, analyse and compare plural ethical, cultural and social concepts of legitimate privacy interest engaged by research using genetic database and bio-banks. It will articulate the relation between such concepts and the current regulation of research using genetic data and bio-banks.\r\nPRIVILEGED will bring together experts in medicine, public health, philosophy, ethics, sience and law from across the whole research area. A series of workshops, web-resources, national and comparaive papers will be co-ordinated through three centres (Lthuania, Portugal and the UK) to address points of both potential conflict and synergy within and between the interests of science and privacy, individual and groups, and diverse cultures and fundamental ethical principles.",
                "en": "PRIVILEGED (Privacy in Law, Ethics and Genetic Data) will make recommendations for research practice and public policy-making, including regulatory options at the national and European level, to promote the optimal relation between research using genetic data and bio-banks and ethical interests in privacy. PRIVILEGED will identify, analyse and compare plural ethical, cultural and social concepts of legitimate privacy interest engaged by research using genetic database and bio-banks. It will articulate the relation between such concepts and the current regulation of research using genetic data and bio-banks.\r\nPRIVILEGED will bring together experts in medicine, public health, philosophy, ethics, sience and law from across the whole research area. A series of workshops, web-resources, national and comparaive papers will be co-ordinated through three centres (Lthuania, Portugal and the UK) to address points of both potential conflict and synergy within and between the interests of science and privacy, individual and groups, and diverse cultures and fundamental ethical principles."
            },
            "begin_planned": "2006-01-01T01:00:00+01:00",
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": "2008-12-31T01:00:00+01:00",
            "end_effective": "2008-12-31T01:00:00+01:00",
            "assignment": "2008-04-03T17:43:24+02:00",
            "program": 21,
            "subprogram": null,
            "organization": 14045,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                10
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 675,
            "title": {
                "de": "SNPs im VEGF Gen und deren Einfluss auf das Prostatakarzinom ",
                "en": "Candidate single nucleotide polymorphisms (SNPs) in the gene for vascular endothelial growth factor (VEGF) and prostata cancer risk "
            },
            "short": "SNPs im VEGF Gen",
            "url": null,
            "abstract": {
                "de": "Tumorwachstum erfordert die Bildung von neuen Gefäßen, ein Prozess, der als Angiogenese bezeichnet wird. Eine Schlüsselrolle in der Regulation der Angiogenese spielt der vascular endothelial growth factor (VEGF). Für verschiedene Tumorentitäten konnte bereits ein Zusammenhang zwischen erhöhten VEGF Spiegeln und ungünstiger Prognose gezeigt werden. Im VEGF Gen sind verschiedene single nucleotide polymorphisms (SNPs) bekannt, von denen einige die VEGF Expression beeinflussen. Die Bedeutung von Varianten im VEGF Gen für das Prostatakarzinomrisiko ist noch weitgehend unbekannt. In der vorliegenden populationsbasierten Fall-Kontroll-Studie möchten wir der Frage nachgehen, ob das Prostatakarzinomrisiko durch bestimmte VEGF Geno- oder Haplotypen beeinflusst wird. Dazu sollen an insgesamt 1000 Probanden (500 Prostatakarzinompatienten und 500 gesunde Kontrollpersonen) 8 SNPs analysiert und Haplotypenberechnungen durchgeführt werden. Die Untersuchung von VEGF Geno- und Haplotypen wird zu einem besseren Verständnis für die Krankheitsentstehung führen. Zusätzlich kann das Wissen über genetische Risikofaktoren für das Prostatakarzinom dazu beitragen, Personen mit hereditärer Prädisposition zu identifizieren und diese frühzeitig prophylaktischen Maßnahmen zuzuführen. ",
                "en": null
            },
            "begin_planned": "2006-01-01T01:00:00+01:00",
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": "2007-06-30T02:00:00+02:00",
            "end_effective": "2007-06-30T02:00:00+02:00",
            "assignment": "2006-01-25T14:38:27+01:00",
            "program": 79,
            "subprogram": null,
            "organization": 14060,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 50495,
            "contact": 50495,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                12
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "675-50495-10",
                "675-51045-12"
            ]
        },
        {
            "id": 557,
            "title": {
                "de": "PULMOTENSION: \"Pulmonary Hypertension: Functional Genomics and Therapy of Lung Vascular Remodelling\"",
                "en": "PULMOTENSION: \"Pulmonary Hypertension: Functional Genomics and Therapy of Lung Vascular Remodelling\""
            },
            "short": "PULMOTENSION",
            "url": null,
            "abstract": {
                "de": "Pulmonary hypertension (PH) describes a group of devastating diseases, comprising idiopathic and secondary forms, which cause breathlessness and premature death, representing a major burden on healthcare systems. Extensive lung vascular remodelling with loss of vessel patency is the underlying pathomechanism in PH. PULMOTENSION integrates the top EU Centres in PH and lung vascular biology in a multidisciplinary approach, with the aim to combat and finally cure PH. The expertise of all members fully extends from the initially discovery of gene mutations causative of PH to having established new therapeutic regimen of PH. We will uncover underlying molecular pathways, identify distinct targets for anti-remodelling therapy, foster drug development based on these targets, and test these new treatment options in preclinical and clinical trials.\r\nGender issues will be particularly addressed, as many PH forms have a female preponderance. Hence, this ambitious translational research programme will span \"from molecules to patients\" to the benefit of molecular understanding and new treatments of PH, a prototype disease of vascular remodelling.",
                "en": "Pulmonary hypertension (PH) describes a group of devastating diseases, comprising idiopathic and secondary forms, which cause breathlessness and premature death, representing a major burden on healthcare systems. Extensive lung vascular remodelling with loss of vessel patency is the underlying pathomechanism in PH. PULMOTENSION integrates the top EU Centres in PH and lung vascular biology in a multidisciplinary approach, with the aim to combat and finally cure PH. The expertise of all members fully extends from the initially discovery of gene mutations causative of PH to having established new therapeutic regimen of PH. We will uncover underlying molecular pathways, identify distinct targets for anti-remodelling therapy, foster drug development based on these targets, and test these new treatment options in preclinical and clinical trials.\r\nGender issues will be particularly addressed, as many PH forms have a female preponderance. Hence, this ambitious translational research programme will span \"from molecules to patients\" to the benefit of molecular understanding and new treatments of PH, a prototype disease of vascular remodelling."
            },
            "begin_planned": "2006-01-01T01:00:00+01:00",
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": "2009-12-31T01:00:00+01:00",
            "end_effective": "2009-12-31T01:00:00+01:00",
            "assignment": "2005-11-04T01:00:00+01:00",
            "program": 21,
            "subprogram": "Biowissenschaften",
            "organization": 14087,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                10
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 734,
            "title": {
                "de": "Somatic Hypermutation of multiple proto-oncogenes in diffuse large b-cell lymphoma may constitute distinct clinical subtypes",
                "en": "Somatic Hypermutation of multiple proto-oncogenes in diffuse large b-cell lymphoma may constitute distinct clinical subtypes"
            },
            "short": "Somatic Hypermutation ",
            "url": null,
            "abstract": {
                "de": "Hochmaligne Lymphome sind der häufigste Lymphomtyp und können in nur 35 - 40 % geheilt werden. Wir konnten zeigen, dass eine aberrante Hypermutationaktivität in über 50 % multiple Onkogene mutiert. Ein Ziel ist die Frage zu klären, warum 50 % der Lymphome mutiert sind, die verbleibenden jedoch nicht. Wir beabsichtigen mittels Microarray Gene zu identifizieren, die differentiell in beiden Gruppen (mutiert vs unmutiert) experimentiert werden. Im zweiten Teil werden wir Genexpressionsprofile erstellen, um eine bestimmte \"Gensignatur\" jeder Gruppe zuordnen zu können. Anschließend werden diese Signaturen mit klinischen Daten korreliert um einen Überlebensprädikator zu definieren. Der letzte Teil geht der Frage nach den molekularen Grundlagen der aberranten SHM nach. Das Enzym AID spielt eine zentrale Rolle in der SHM. Viele Untersuchungen deuten daruaf hin, dass AID kein \"unkontrollierter\" Mutator ist, sondern dass es einen spezifischen \"targeting\" mechanismus gibt, der die unterschiedlichen Funktionen von AID reguliert. Ziel ist, Kofaktoren, die durch die Microarrayanalyse identifiziert wurden funktionell zu charakterisieren. Die Aufklärung dieses Mechanismus wäre ein wesentlicher Fortschritt in der Erforschung der Entstehungsursachen maligner Lymphome und eine wesentliche Grundvoraussetzung für die Konzeption innovativer Therapiestrategien. ",
                "en": "Hochmaligne Lymphome sind der häufigste Lymphomtyp und können in nur 35 - 40 % geheilt werden. Wir konnten zeigen, dass eine aberrante Hypermutationaktivität in über 50 % multiple Onkogene mutiert. Ein Ziel ist die Frage zu klären, warum 50 % der Lymphome mutiert sind, die verbleibenden jedoch nicht. Wir beabsichtigen mittels Microarray Gene zu identifizieren, die differentiell in beiden Gruppen (mutiert vs unmutiert) experimentiert werden. Im zweiten Teil werden wir Genexpressionsprofile erstellen, um eine bestimmte \"Gensignatur\" jeder Gruppe zuordnen zu können. Anschließend werden diese Signaturen mit klinischen Daten korreliert um einen Überlebensprädikator zu definieren. Der letzte Teil geht der Frage nach den molekularen Grundlagen der aberranten SHM nach. Das Enzym AID spielt eine zentrale Rolle in der SHM. Viele Untersuchungen deuten daruaf hin, dass AID kein \"unkontrollierter\" Mutator ist, sondern dass es einen spezifischen \"targeting\" mechanismus gibt, der die unterschiedlichen Funktionen von AID reguliert. Ziel ist, Kofaktoren, die durch die Microarrayanalyse identifiziert wurden funktionell zu charakterisieren. Die Aufklärung dieses Mechanismus wäre ein wesentlicher Fortschritt in der Erforschung der Entstehungsursachen maligner Lymphome und eine wesentliche Grundvoraussetzung für die Konzeption innovativer Therapiestrategien. "
            },
            "begin_planned": "2006-01-01T01:00:00+01:00",
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": "2008-01-01T01:00:00+01:00",
            "end_effective": "2010-02-28T01:00:00+01:00",
            "assignment": "2006-02-24T17:34:13+01:00",
            "program": 79,
            "subprogram": null,
            "organization": 14082,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51930,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                12
            ],
            "funder_projectcode": "11181",
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "734-51930-10"
            ]
        },
        {
            "id": 826,
            "title": {
                "de": "Quantifizierung der Expression des GLUT 4 Gens im atrialen humanen Myocard unter experimenteller Ischämie",
                "en": "Quantitative Assessment of GLUT4 Gene Expression in Human Atrial Myocardium: An Experimental Study on the Effects of Ischemia"
            },
            "short": "Assessment of GLUT4 ",
            "url": null,
            "abstract": {
                "de": "Ischemic heart disease is still the main cause of death in the western hemisphere despite considerable improvement of primary and secondary prevention, diagnostic techniques and treatment during the recent years. Like hypertension and dyslipidemia, dysfunctional glucose metabolism contributes largely to cardiovascular disease morbidity and mortality. Ample epidemiologic and clinical evidence suggests that these cardiovascular disease risk factors tend to cluster within individuals with even mild disturbances in glucose metabolism (glucose tolerance, insulin resistance, insulin secretion). In this context, comparatively little is known about insulin-dependent trans-membrane glucose transport in human heart. The investigation of insulin-dependent trans-membrane glucose transport (via GLUT4) and its implications on CHD as well as on ischemia, hence, appears to be of high priority in thwarding coronary death.\r\n\r\nWhile it has been shown by a number of authors that in experimental/clinical diabetes, hypertension and related disorders, GLUT4-gene expression is altered, GLUT4-gene expression in coronary/ischemic heart disease has not been looked at as yet. Hence, it has remained unknown, whether or not ischemia, like DM and hypertension can be related to altered GLUT4 gene expression.\r\n\r\nThe present project is designed to study GLUT4-gene expression under ischemic conditions using an apropriate experimental chamber various techniques of experimental ischemia and RT (real-time) - GLUT4-PCR (Light Cycler). We wish to see whether or not there is a difference in GLUT4-gene expression in patients with and without coronary heart disease under ischemic conditions. \r\n We expect to learn from these results whether or not ischemic myocardial tissue from patients with and without CHD shows altered pattern of GLUT4-gene expression in order to improve understanding of ischemic glucose metabolism.  \r\n\r\nFrom our experiments, we expect to learn about insulin dependent myocardial transmembrane glucose transport both in ischemic heart disease. In the long run, our results may provide new approaches in primary prevention as well as in direct myocardial tissue protection. ",
                "en": "Ischemic heart disease is still the main cause of death in the western hemisphere despite considerable improvement of primary and secondary prevention, diagnostic techniques and treatment during the recent years. Like hypertension and dyslipidemia, dysfunctional glucose metabolism contributes largely to cardiovascular disease morbidity and mortality. Ample epidemiologic and clinical evidence suggests that these cardiovascular disease risk factors tend to cluster within individuals with even mild disturbances in glucose metabolism (glucose tolerance, insulin resistance, insulin secretion). In this context, comparatively little is known about insulin-dependent trans-membrane glucose transport in human heart. The investigation of insulin-dependent trans-membrane glucose transport (via GLUT4) and its implications on CHD as well as on ischemia, hence, appears to be of high priority in thwarding coronary death.\r\n\r\nWhile it has been shown by a number of authors that in experimental/clinical diabetes, hypertension and related disorders, GLUT4-gene expression is altered, GLUT4-gene expression in coronary/ischemic heart disease has not been looked at as yet. Hence, it has remained unknown, whether or not ischemia, like DM and hypertension can be related to altered GLUT4 gene expression.\r\n\r\nThe present project is designed to study GLUT4-gene expression under ischemic conditions using an apropriate experimental chamber various techniques of experimental ischemia and RT (real-time) - GLUT4-PCR (Light Cycler). We wish to see whether or not there is a difference in GLUT4-gene expression in patients with and without coronary heart disease under ischemic conditions. \r\n We expect to learn from these results whether or not ischemic myocardial tissue from patients with and without CHD shows altered pattern of GLUT4-gene expression in order to improve understanding of ischemic glucose metabolism.  \r\n\r\nFrom our experiments, we expect to learn about insulin dependent myocardial transmembrane glucose transport both in ischemic heart disease. In the long run, our results may provide new approaches in primary prevention as well as in direct myocardial tissue protection. "
            },
            "begin_planned": "2006-01-01T01:00:00+01:00",
            "begin_effective": "2006-01-01T01:00:00+01:00",
            "end_planned": "2006-12-31T01:00:00+01:00",
            "end_effective": "2006-12-31T01:00:00+01:00",
            "assignment": "2006-05-16T18:41:17+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14083,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51533,
            "contact": 51533,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                468
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "826-51533-10"
            ]
        }
    ]
}