Project List

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  {
    "count": 2260,
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    "results": [
        {
            "id": 210,
            "title": {
                "de": "Selektive exokrine Hyperstimulierung des Pankreas zur Untersuchung akuter Pankreatitis",
                "en": "Selektive exokrine Hyperstimulierung des Pankreas zur Untersuchung akuter Pankreatitis"
            },
            "short": "Hyperstimulierung des Pankreas",
            "url": null,
            "abstract": {
                "de": "Cholecystokinin CCK1 receptors have two affinity states, which are activated by appropriate concentrations of CCK or analogs like caerulein. Activation of high affinity sites stimulates enzyme secretion into the pancreatic ducts, while activation of low affinity sites inhibits this effect and induces acute pancreatitis in vivo. We have investigated whether the selective CCK1 agonist SR146131 would discriminate between the two affinity states of the receptor. Intraperitoneal injection of caerulein (0.25–7.5 nmol/kg) in anesthetized rats stimulated amylase output via the biliopancreatic duct in a dose-dependent manner, but enzyme secretion was completely blocked at a supramaximal dose (25 nmol/kg). SR146131 (18–180 nmol/kg) also dose-dependently stimulated amylase secretion; however, secretion did not decline even at doses of 1800 nmol/kg. The effect of SR146131 was blocked by a CCK1 antagonist dexloxiglumide, but not by the CCK2 antagonist itriglumide. A supramaximal dose of caerulein (25 nmol/kg given twice i.p. at an interval of 1 h) induced acute oedematous pancreatitis, quantified by water content of the pancreatic tissue and increases in amylase activities in the blood serum and in the pancreatic interstitial space. The effects of caerulein were prevented by dexloxiglumide, but not by itriglumide. SR146131 (60–1800 nmol/kg twice i.p.) did not induce any signs of inflammation, as all measured parameters remained at values obtained in rats without pancreatitis. Histological evaluation showed that even the highest dose of SR146141 did not induce any signs of acinar cell damage. In summary, the CCK1 agonist SR146131 stimulates pancreatic exocrine function in vivo without exhibiting inhibition at supramaximal doses. Unlike the CCK analog caerulein, SR146131 does not induce acute pancreatitis even when applied at excessive dose levels. We conclude that in contrast to CCK and caerulein, SR146131 is an agonist only at the high affinity site of the CCK1 receptor.",
                "en": "Cholecystokinin CCK1 receptors have two affinity states, which are activated by appropriate concentrations of CCK or analogs like caerulein. Activation of high affinity sites stimulates enzyme secretion into the pancreatic ducts, while activation of low affinity sites inhibits this effect and induces acute pancreatitis in vivo. We have investigated whether the selective CCK1 agonist SR146131 would discriminate between the two affinity states of the receptor. Intraperitoneal injection of caerulein (0.25–7.5 nmol/kg) in anesthetized rats stimulated amylase output via the biliopancreatic duct in a dose-dependent manner, but enzyme secretion was completely blocked at a supramaximal dose (25 nmol/kg). SR146131 (18–180 nmol/kg) also dose-dependently stimulated amylase secretion; however, secretion did not decline even at doses of 1800 nmol/kg. The effect of SR146131 was blocked by a CCK1 antagonist dexloxiglumide, but not by the CCK2 antagonist itriglumide. A supramaximal dose of caerulein (25 nmol/kg given twice i.p. at an interval of 1 h) induced acute oedematous pancreatitis, quantified by water content of the pancreatic tissue and increases in amylase activities in the blood serum and in the pancreatic interstitial space. The effects of caerulein were prevented by dexloxiglumide, but not by itriglumide. SR146131 (60–1800 nmol/kg twice i.p.) did not induce any signs of inflammation, as all measured parameters remained at values obtained in rats without pancreatitis. Histological evaluation showed that even the highest dose of SR146141 did not induce any signs of acinar cell damage. In summary, the CCK1 agonist SR146131 stimulates pancreatic exocrine function in vivo without exhibiting inhibition at supramaximal doses. Unlike the CCK analog caerulein, SR146131 does not induce acute pancreatitis even when applied at excessive dose levels. We conclude that in contrast to CCK and caerulein, SR146131 is an agonist only at the high affinity site of the CCK1 receptor."
            },
            "begin_planned": null,
            "begin_effective": "2001-12-13T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2003-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 79,
            "subprogram": null,
            "organization": 14022,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51661,
            "contact": 51661,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                12
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "210-51661-10"
            ]
        },
        {
            "id": 220,
            "title": {
                "de": "Molekular-epidemiologische Mutationsanalyse an p16INK4a, p14ARF, p53, und Ha-ras bei Psoralen+PUVA-assozierten Hauttumoren",
                "en": "Molekular-epidemiologische Mutationsanalyse an p16INK4a, p14ARF, p53, und Ha-ras bei Psoralen+PUVA-assozierten Hauttumoren"
            },
            "short": "Mutationsanalyse",
            "url": null,
            "abstract": {
                "de": "Die orale Psoralen UVA (PUVA)-Photochemotherapie stellt eine hocheffektive Behandlungsform für ausgeprägte Formen der Psoriasis vulgaris (Schuppenflechte), einer sehr häufig auftretenden, etwa 1 bis 3% der Bevölkerung betreffenden entzündlichen Hauterkrankung, dar. Patienten, die über Jahre aufgrund chronischer psoriatischer Hautveränderungen immer wieder mit PUVA therapiert werden, weisen ein erhöhtes Hautkrebsrisiko auf. Die genauen Ursachen und Mechanismen der Hautkrebsentstehung nach PUVA sind nicht geklärt, zumal PUVA nicht nur tumorinitierende und –promovierende, sondern auch immunsuppressive Eigenschaften hat und Psoriasis-Patienten nicht selten auch andere potentielle (ko-)karzinogene Faktoren und/oder Behandlungen, z.B. mit topischen Teerpräparaten, UV-Bestrahlungen, Röntgenbestrahlungen, Arsen, antiproliferativen und/oder immunsuppressiven Medikamenten, aufweisen. Im vorliegenden Projekt untersuchten wir auf molekularer Ebene mittels Polymerasekettenreaktion und nachfolgender DNA-Sequenzierung, ob PUVA-assoziierte Karzinome und sog. PUVA-Keratosen, potentielle Karzinomvorläufer, Fingerabdruckmutationen an bestimmten Tumorsuppressor- und/oder Onkogenen zeigen. Unsere Analysen am INK-4-ARF Tumorsuppressor-Locus (für p14 und p16 kodierend) ergaben, dass 11 von 26 (42%) Plattenepithelkarzinomen der Haut bei 7 von 11 (64%) PUVA-behandelten Patienten Mutationen an diesem Gen aufwiesen, wobei die Mehrzahl der Mutationen (58%) typisch für eine Verursachung durch ultraviolette Strahlung (C-T-Transitionen am Dipyrimidin-Sequenzen) war. Nur 16% der Mutationen am INK-4-ARF-Locus traten an möglichen Psoralen-Bindungsstellen auf und waren somit vermutlich auf eine PUVA-Behandlung zurückzuführen. Dies ist in Übereinstimmung mit Ergebnissen früherer Studien unserer Arbeitsgruppe am p53 Tumorsuppressorgen und Ha-Ras Protoonkogen von PUVA-assoziierten Karzinomen, bei denen ebenso die UV-typischen Mutationen in der Häufigkeit die PUVA-bedingten Mutationen deutlich übertrafen. Die Mutationsanalyse an 28 PUVA-Keratosen hatte ergeben, dass 44% der untersuchten Proben ein in 72% der Fälle UV-typisch mutiertes Ha-ras Protoonkogen und 28% ein meist UV-typisch mutiertes p53 Gen aufwiesen. Zusammenfassend ergibt sich, dass es bei der PUVA-Karzinogenese beim Menschen offensichtlich zu einer komplexen Interaktion und Mutationen an unterschiedlichen Onkogenen und Tumorsuppressorgenen kommt. Nicht PUVA selbst, sondern ultraviolette Strahlung, sei es therapeutischer Herkunft oder vom natürlichen Sonnenlicht stammend, scheint auf molekular-genetischer Ebene den Hauptfaktor der PUVA-Karzinogenese darzustellen. ",
                "en": "Die orale Psoralen UVA (PUVA)-Photochemotherapie stellt eine hocheffektive Behandlungsform für ausgeprägte Formen der Psoriasis vulgaris (Schuppenflechte), einer sehr häufig auftretenden, etwa 1 bis 3% der Bevölkerung betreffenden entzündlichen Hauterkrankung, dar. Patienten, die über Jahre aufgrund chronischer psoriatischer Hautveränderungen immer wieder mit PUVA therapiert werden, weisen ein erhöhtes Hautkrebsrisiko auf. Die genauen Ursachen und Mechanismen der Hautkrebsentstehung nach PUVA sind nicht geklärt, zumal PUVA nicht nur tumorinitierende und –promovierende, sondern auch immunsuppressive Eigenschaften hat und Psoriasis-Patienten nicht selten auch andere potentielle (ko-)karzinogene Faktoren und/oder Behandlungen, z.B. mit topischen Teerpräparaten, UV-Bestrahlungen, Röntgenbestrahlungen, Arsen, antiproliferativen und/oder immunsuppressiven Medikamenten, aufweisen. Im vorliegenden Projekt untersuchten wir auf molekularer Ebene mittels Polymerasekettenreaktion und nachfolgender DNA-Sequenzierung, ob PUVA-assoziierte Karzinome und sog. PUVA-Keratosen, potentielle Karzinomvorläufer, Fingerabdruckmutationen an bestimmten Tumorsuppressor- und/oder Onkogenen zeigen. Unsere Analysen am INK-4-ARF Tumorsuppressor-Locus (für p14 und p16 kodierend) ergaben, dass 11 von 26 (42%) Plattenepithelkarzinomen der Haut bei 7 von 11 (64%) PUVA-behandelten Patienten Mutationen an diesem Gen aufwiesen, wobei die Mehrzahl der Mutationen (58%) typisch für eine Verursachung durch ultraviolette Strahlung (C-T-Transitionen am Dipyrimidin-Sequenzen) war. Nur 16% der Mutationen am INK-4-ARF-Locus traten an möglichen Psoralen-Bindungsstellen auf und waren somit vermutlich auf eine PUVA-Behandlung zurückzuführen. Dies ist in Übereinstimmung mit Ergebnissen früherer Studien unserer Arbeitsgruppe am p53 Tumorsuppressorgen und Ha-Ras Protoonkogen von PUVA-assoziierten Karzinomen, bei denen ebenso die UV-typischen Mutationen in der Häufigkeit die PUVA-bedingten Mutationen deutlich übertrafen. Die Mutationsanalyse an 28 PUVA-Keratosen hatte ergeben, dass 44% der untersuchten Proben ein in 72% der Fälle UV-typisch mutiertes Ha-ras Protoonkogen und 28% ein meist UV-typisch mutiertes p53 Gen aufwiesen. Zusammenfassend ergibt sich, dass es bei der PUVA-Karzinogenese beim Menschen offensichtlich zu einer komplexen Interaktion und Mutationen an unterschiedlichen Onkogenen und Tumorsuppressorgenen kommt. Nicht PUVA selbst, sondern ultraviolette Strahlung, sei es therapeutischer Herkunft oder vom natürlichen Sonnenlicht stammend, scheint auf molekular-genetischer Ebene den Hauptfaktor der PUVA-Karzinogenese darzustellen. "
            },
            "begin_planned": null,
            "begin_effective": "2002-06-27T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2004-06-30T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 79,
            "subprogram": null,
            "organization": 14047,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51618,
            "contact": 51618,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                12
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "220-51618-10"
            ]
        },
        {
            "id": 281,
            "title": {
                "de": "Activation of a nuclear receptor impairs cycloocygenase-2expression but induces apoptosis in human choriocarcinoma cell lines: A possible therapeutic approach for treatment",
                "en": "Activation of a nuclear receptor impairs cycloocygenase-2expression but induces apoptosis in human choriocarcinoma cell lines: A possible therapeutic approach for treatment"
            },
            "short": "Cycloocygenase-2expression ",
            "url": null,
            "abstract": {
                "de": "Cyclooxygenase-2 (COX-2), the inducible isoform of COX is the enzyme that catalyzes the rate-limiting step in prostaglandin synthesis from arachidonic acid. Various prostaglandins are produced in a cell type-specific manner, and they elicit cellular functions via signaling through G-protein-coupled membrane receptors, and in some cases, through the nuclear receptor peroxisome proliferator-activated receptor (PPAR) e.g. PPARgamma. In a number of cell and animal models, induction of COX-2 has been shown to promote cell growth, inhibit apoptosis and enhance cell motility and adhesion. Compelling eidence from genetic and clinical studies indicate that COX-2 upregulation is a key step in carcinogenesis. Overexpression of COX-2 is sufficient to cause tumorigenesis in animal models and inhibition of the COX-2 pathway results in reduction in tumor incidence and progression, but increased apoptosis (programmed cell death), in parallel. Recent findings revealed that PPARgamma-agonists induce apoptosis in cancer cells via down-regulation of COX-2. PPARgamma binds to specific response elements as heterodimers with the retinoid X receptor and activates transcription in response to a variety of endogenous and exogenous ligands. PPARgamma is needed for plasental development and modulates differentiation of human trophoblast. As the trophoblast may also give rise to choriocarcinomas -malignant tumors of epithelial origin- the present application is aimed to focus on PPARgamma-dependent activities mediating expression and regulation of COX-2 and subsequent induction of apoptotic pathways in choriocarcinoma celll lines in vitro. In this scenario, COX-2 inhibition could afford its effects against choriocarcinoma by modulating COX-2 expression and activity. An exciting corollary to this ongoing pathway is that the parallel increase in apoptotic events via PPARgamma-dependent modulation of COX-2 may exhibit chemoprotective and even chemotherapeutive effects against choriocarcinoma in humans.",
                "en": "Cyclooxygenase-2 (COX-2), the inducible isoform of COX is the enzyme that catalyzes the rate-limiting step in prostaglandin synthesis from arachidonic acid. Various prostaglandins are produced in a cell type-specific manner, and they elicit cellular functions via signaling through G-protein-coupled membrane receptors, and in some cases, through the nuclear receptor peroxisome proliferator-activated receptor (PPAR) e.g. PPARgamma. In a number of cell and animal models, induction of COX-2 has been shown to promote cell growth, inhibit apoptosis and enhance cell motility and adhesion. Compelling eidence from genetic and clinical studies indicate that COX-2 upregulation is a key step in carcinogenesis. Overexpression of COX-2 is sufficient to cause tumorigenesis in animal models and inhibition of the COX-2 pathway results in reduction in tumor incidence and progression, but increased apoptosis (programmed cell death), in parallel. Recent findings revealed that PPARgamma-agonists induce apoptosis in cancer cells via down-regulation of COX-2. PPARgamma binds to specific response elements as heterodimers with the retinoid X receptor and activates transcription in response to a variety of endogenous and exogenous ligands. PPARgamma is needed for plasental development and modulates differentiation of human trophoblast. As the trophoblast may also give rise to choriocarcinomas -malignant tumors of epithelial origin- the present application is aimed to focus on PPARgamma-dependent activities mediating expression and regulation of COX-2 and subsequent induction of apoptotic pathways in choriocarcinoma celll lines in vitro. In this scenario, COX-2 inhibition could afford its effects against choriocarcinoma by modulating COX-2 expression and activity. An exciting corollary to this ongoing pathway is that the parallel increase in apoptotic events via PPARgamma-dependent modulation of COX-2 may exhibit chemoprotective and even chemotherapeutive effects against choriocarcinoma in humans."
            },
            "begin_planned": null,
            "begin_effective": "2004-10-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2006-10-01T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14017,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51714,
            "contact": 51714,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                142
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "281-51714-10"
            ]
        },
        {
            "id": 9576,
            "title": {
                "de": "Synthese und Modifizierung von Briciclib-Phosphonat-Analoga zur topischen Behandlung der Psoriasis",
                "en": "Synthesis and modification of Briciclib phosphonate analogs for the topical treatment of psoriasis"
            },
            "short": null,
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2026-02-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2027-01-31T01:00:00+01:00",
            "assignment": "2026-02-02T10:10:25+01:00",
            "program": null,
            "subprogram": null,
            "organization": 14047,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 84167,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                1743
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "9576-84167-10"
            ]
        },
        {
            "id": 7299,
            "title": {
                "de": "OES Gewebeproben – Phase 2",
                "en": "OES Gewebeproben – Phase 2"
            },
            "short": null,
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2022-12-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2025-09-30T02:00:00+02:00",
            "assignment": "2022-12-12T14:54:22+01:00",
            "program": null,
            "subprogram": null,
            "organization": 14020,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 86408,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "7299-86408-10"
            ]
        },
        {
            "id": 1804,
            "title": {
                "de": "European network of paediatric Hodgkin´s lymphoma- European-wide organisation of quality controlled treatment (Paediaric Hodgkin network)",
                "en": "European network of paediatric Hodgkin´s lymphoma- European-wide organisation of quality controlled treatment (Paediaric Hodgkin network)"
            },
            "short": "Paediaric Hodgkin network",
            "url": null,
            "abstract": {
                "de": "Build on the experience from national trials for paediatric Hodgkin's lymphoma (PHL) experts from 12 EU countries decided on a common protocol to individualise PHL treatment.\r\n\r\nThe general objective of this proposal is to ensure a high-quality teatment for all affected patients from paediatric Hodgkin's lymphoma independent of their social or geographical origin by establishing a shared case management and expert system using a medical image and communication network. Aim of the high-quality treatment planning algorithm is to achieve high rates for event-free survival with the least necessary treatment toxicity in every child.",
                "en": "Build on the experience from national trials for paediatric Hodgkin's lymphoma (PHL) experts from 12 EU countries decided on a common protocol to individualise PHL treatment.\r\n\r\nThe general objective of this proposal is to ensure a high-quality teatment for all affected patients from paediatric Hodgkin's lymphoma independent of their social or geographical origin by establishing a shared case management and expert system using a medical image and communication network. Aim of the high-quality treatment planning algorithm is to achieve high rates for event-free survival with the least necessary treatment toxicity in every child."
            },
            "begin_planned": null,
            "begin_effective": "2008-08-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2011-07-31T02:00:00+02:00",
            "assignment": "2009-04-30T19:27:24+02:00",
            "program": 21,
            "subprogram": null,
            "organization": 14107,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51727,
            "contact": 51727,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                10
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "1804-51727-10"
            ]
        },
        {
            "id": 170,
            "title": {
                "de": "Freie Radikale",
                "en": "Freie Radikale"
            },
            "short": "Freie Radikale",
            "url": null,
            "abstract": {
                "de": "Extensive Fibrose rund um totale Hüftendoprothesen wird unregelmäßig bei Revisionen gefunden. Der Zweck unserer Studie war es zu untersuchen, ob die aseptische Hüftprothesenlockerung mit oxidativem Stress verbunden ist. \r\n\r\nLevel von oxidiertem (GSSG) und reduziertem Gluthation (GSH) und Malondialdehyd (MDA) wurden in Gewebe von 28 Patienten mit aseptischen Hüftprothesenlockerungen (Gruppe I) und in 12 Hüften, die aufgrund vermehrten Abriebs revidiert wurden, analysiert (Gruppe II). In den periprothetischen Geweben wurde Kollagen sowie eine genaue Metallabriebanalyse durchgeführt. \r\n\r\nErhöhter oxidativer Stress, gemessen anhand eines niedrigen GSH/GSSG Verhältnisses sowie eine erhöhte MDA Konzentration wurde in der Gruppe II im Vergleich zur Gruppe I gefunden (p<0.05). Die Evaluierung von Hydroxyprolin zeigte eine signifikant höhere Konzentration von Kollagen in der Gruppe II im Vergleich zur Gruppe I (p<0.05). Signifikant höhere Werte von Eisen, Chrom und Nickel wurden im Gewebe von 32 Hüften mit Osteolyse im Vergleich zu 8 Hüften ohne Osteolyse gefunden. MDA und GSH wie GSSG Konzentrationen korrelierten signifikant mit der Hydroxyprolin Konzentration. \r\n\r\nDiese Daten sind ein Hinweis, dass hoher oxidativer Stress eine Rolle in der aseptischen Hüftprothesenlockerung spielen dürfte. Der Beginn dieses Prozesses dürfte mit exzessiver Fibrose beginnen. \r\n \r\n \r\n \r\n",
                "en": "Extensive Fibrose rund um totale Hüftendoprothesen wird unregelmäßig bei Revisionen gefunden. Der Zweck unserer Studie war es zu untersuchen, ob die aseptische Hüftprothesenlockerung mit oxidativem Stress verbunden ist. \r\n\r\nLevel von oxidiertem (GSSG) und reduziertem Gluthation (GSH) und Malondialdehyd (MDA) wurden in Gewebe von 28 Patienten mit aseptischen Hüftprothesenlockerungen (Gruppe I) und in 12 Hüften, die aufgrund vermehrten Abriebs revidiert wurden, analysiert (Gruppe II). In den periprothetischen Geweben wurde Kollagen sowie eine genaue Metallabriebanalyse durchgeführt. \r\n\r\nErhöhter oxidativer Stress, gemessen anhand eines niedrigen GSH/GSSG Verhältnisses sowie eine erhöhte MDA Konzentration wurde in der Gruppe II im Vergleich zur Gruppe I gefunden (p<0.05). Die Evaluierung von Hydroxyprolin zeigte eine signifikant höhere Konzentration von Kollagen in der Gruppe II im Vergleich zur Gruppe I (p<0.05). Signifikant höhere Werte von Eisen, Chrom und Nickel wurden im Gewebe von 32 Hüften mit Osteolyse im Vergleich zu 8 Hüften ohne Osteolyse gefunden. MDA und GSH wie GSSG Konzentrationen korrelierten signifikant mit der Hydroxyprolin Konzentration. \r\n\r\nDiese Daten sind ein Hinweis, dass hoher oxidativer Stress eine Rolle in der aseptischen Hüftprothesenlockerung spielen dürfte. Der Beginn dieses Prozesses dürfte mit exzessiver Fibrose beginnen. \r\n"
            },
            "begin_planned": null,
            "begin_effective": "2003-07-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2004-07-31T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14052,
            "category": 10,
            "type": 10,
            "partner_function": 1,
            "manager": 53237,
            "contact": 53237,
            "status": 2,
            "research": null,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                12
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "170-53237-10"
            ]
        },
        {
            "id": 296,
            "title": {
                "de": "Peripheral glutamate receptors as target for drug therapy of human melanoma",
                "en": "Peripheral glutamate receptors as target for drug therapy of human melanoma"
            },
            "short": "Periph glutamate recept (human melanoma)",
            "url": null,
            "abstract": {
                "de": "Glutamate is a widely distributed peiotropic molecule with many functions in mammals (metabolic intermediary, taste stimulus, the major excitatory neurotransmitter in the brain, neurotoxin if released in excess): Besides the broad distribution in the central nervous system (CNS), inotropic (ligand-gated ion channels) as well as metabotropic (G-protein coupled) glutamate receptors have also been found in a number of peripheral non-excitable cells (e.g. taste buds, intestine, heart, lung, spleen, thymus, pancreas, adrenal gland, skin, bone, hepatocytes, megakaryocytes, platelets and lymphocytes).\r\nSo it became apparent that glutamate, in addition to eliciting excitatory currents, can regulate other biological responses as well. Of particular interest is the discovery that excessive glutamate release promotes tumor growth.\r\nIn the present project we want to systemically analyze the therapeutic potential of glutamate receptor ligands specific for mGluR1 and 5 to establish novel therapeutic concepts of melanocytic neoplasia. Tumor cell lines will be exposed to metabotropic receptor agonists/antagonists, and tumor cell growth, morphology, differentiation and apoptosis will be evaluated. In addition, by combining metabotropic glutamate receptor reagents with established chemotherapeutic drugs, we want to define optimal combinations to achieve superior cytostatic effects as compared to either treatment alone.",
                "en": "Glutamate is a widely distributed peiotropic molecule with many functions in mammals (metabolic intermediary, taste stimulus, the major excitatory neurotransmitter in the brain, neurotoxin if released in excess): Besides the broad distribution in the central nervous system (CNS), inotropic (ligand-gated ion channels) as well as metabotropic (G-protein coupled) glutamate receptors have also been found in a number of peripheral non-excitable cells (e.g. taste buds, intestine, heart, lung, spleen, thymus, pancreas, adrenal gland, skin, bone, hepatocytes, megakaryocytes, platelets and lymphocytes).\r\nSo it became apparent that glutamate, in addition to eliciting excitatory currents, can regulate other biological responses as well. Of particular interest is the discovery that excessive glutamate release promotes tumor growth.\r\nIn the present project we want to systemically analyze the therapeutic potential of glutamate receptor ligands specific for mGluR1 and 5 to establish novel therapeutic concepts of melanocytic neoplasia. Tumor cell lines will be exposed to metabotropic receptor agonists/antagonists, and tumor cell growth, morphology, differentiation and apoptosis will be evaluated. In addition, by combining metabotropic glutamate receptor reagents with established chemotherapeutic drugs, we want to define optimal combinations to achieve superior cytostatic effects as compared to either treatment alone."
            },
            "begin_planned": null,
            "begin_effective": "2005-01-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2006-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14014,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                52
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 10,
            "title": {
                "de": "An improved in vitro model of the blood-brain barrier based on the use of procine brains, a valuable 'waste' from t. slaughterhouse",
                "en": "An improved in vitro model of the blood-brain barrier based on the use of procine brains, a valuable 'waste' from t. slaughterhouse"
            },
            "short": "Blut-Hirn-Schranke",
            "url": null,
            "abstract": {
                "de": "Optimization of culture conditions for primary brain capillary endothelial cells, definition of transport routes of essential long chain PUFAs, and identification of novel transcytosis pathways via caveolaex.\t\t\t\t\t\t\t\t\t\t\t\t\t\r\n\t\t\t\t\t\t\t\t\t\t\t\t\t\r\n",
                "en": "Optimization of culture conditions for primary brain capillary endothelial cells, definition of transport routes of essential long chain PUFAs, and identification of novel transcytosis pathways via caveolaex.\t\t\t\t\t\t\t\t\t\t"
            },
            "begin_planned": null,
            "begin_effective": "2004-01-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2005-09-30T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14013,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51669,
            "contact": 51705,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                25
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "10-51669-10"
            ]
        },
        {
            "id": 13,
            "title": {
                "de": "RISE Subcontract n°UWIEN.BMEP/01",
                "en": "RISE Subcontract n°UWIEN.BMEP/01"
            },
            "short": "EU-RISE (Subkontraktor)",
            "url": null,
            "abstract": {
                "de": "Use of electrical stimulation to restore standing in paraplegics with long-term denervated degenerated muscles (DDM).\t\t\t\t\t\t\t\t\t\t\t\t\t\r\n\t\t\t\t\t\t\t\t\t\t\t\t\t\r\n",
                "en": "Use of electrical stimulation to restore standing in paraplegics with long-term denervated degenerated muscles (DDM)."
            },
            "begin_planned": null,
            "begin_effective": "2001-02-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2005-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 20,
            "subprogram": null,
            "organization": 14010,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51814,
            "contact": 51814,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                10
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "13-51814-10"
            ]
        },
        {
            "id": 298,
            "title": {
                "de": "In vivo aging as regenerative defect. Effects of adrenergic and oxidative stress on stem cell functions",
                "en": "In vivo aging as regenerative defect. Effects of adrenergic and oxidative stress on stem cell functions"
            },
            "short": "In vivo aging as regenerative defect",
            "url": null,
            "abstract": {
                "de": "We plan to study stem cell biology in the context of the aging process. Besides a gross characterization of stem cells with regard to tissue regeneration, we will also investigate, if and how oxidative stress and catecholamines influence the growth and regenartive capcity of adult stem cells in the bone marrow, and, by the same token, affect aging, age-associated disease and life span. Experimentally, this will be tested in the Senescence-Accelerated-Mouse-Prone/Resistant Model. Several substrains with differing in age-associated pathology are available.\r\nIn particular, we will determine *the regenerative capacity of b one marrow stem cells in the context of aging and age-associated pathology, *if stem cell survival and functions can be affected by catecholamines and/or oxidative stress, *if aging and age associated pathology can be reduced by transplantation of bone marrow cells from young but not old donors.",
                "en": "We plan to study stem cell biology in the context of the aging process. Besides a gross characterization of stem cells with regard to tissue regeneration, we will also investigate, if and how oxidative stress and catecholamines influence the growth and regenartive capcity of adult stem cells in the bone marrow, and, by the same token, affect aging, age-associated disease and life span. Experimentally, this will be tested in the Senescence-Accelerated-Mouse-Prone/Resistant Model. Several substrains with differing in age-associated pathology are available.\r\nIn particular, we will determine *the regenerative capacity of b one marrow stem cells in the context of aging and age-associated pathology, *if stem cell survival and functions can be affected by catecholamines and/or oxidative stress, *if aging and age associated pathology can be reduced by transplantation of bone marrow cells from young but not old donors."
            },
            "begin_planned": null,
            "begin_effective": "2005-01-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2007-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 72,
            "subprogram": null,
            "organization": 14014,
            "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": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "298-50379-12"
            ]
        },
        {
            "id": 482,
            "title": {
                "de": "Defective DNA-Repair in acute myeloid leukemia",
                "en": "Defective DNA-Repair in acute myeloid leukemia"
            },
            "short": "Defective DNA-Repair ",
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2005-09-05T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2009-09-03T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14082,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51857,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                423
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "482-51857-10"
            ]
        },
        {
            "id": 309,
            "title": {
                "de": "Vermindert NADH-Zusatz Ischämie bzw. Reperfusionsschäden? Untersuchungen an isolierten Herzmuskelzellen und im herzchirurgischen Tiermodell",
                "en": "Vermindert NADH-Zusatz Ischämie bzw. Reperfusionsschäden? Untersuchungen an isolierten Herzmuskelzellen und im herzchirurgischen Tiermodell"
            },
            "short": "NADH bei Ischämie & Reperfusionsschäden",
            "url": null,
            "abstract": {
                "de": "Gewebe- bzw. Zellschädigung, die durch Ischämie und Reperfusion hervorgerufen wird, stellt ein zentrales Problem für die Herztransplantation dar. Minimierung von pathologischen Änderungen und Erhaltung der Funktionsfähigkeit von Herzmuskelzellen hat eine Verlängerung der vom Herzen tolerierten Ischämiedauer, eine verringerte Abstoßungsreaktion und somit ein verbessertes Langzeitergebnis der Herzchirurgie zur Folge. NADH, ein Enzym, das eine zentrale Stellung im Energiehaushalt der Zelle einnimmt, stellt einen potentiellen Kandidaten als Zusatzstoff zu kardioplegischenLösungen dar, da es einerseits den Adenosintriphosphat (ATP)-Gehalt einer Herzmuskelzelle zu erhöhen vermag und darüberhinaus als Schutz vor durch Ischämie/Reperfussion erzeugten reaktiven Sauerstoffverbindungen gilt. Im Rahmen des Forschungsprojektes soll unter Anwendung elektrophysiologischer, biochemischer sowie histologischer Methoden untersucht werden, ob der Zusatz von NADH Schutz vor Gewebe- bzw. Zellschädigung, hervorgerufen durch Ischämie/Reperfusion, bietet. Isolierte Herzmuskelzellen (tierischen und humanen Ursprungs) sowie ein Tiermodell stellen hierfür sich ergänzende Untersuchungsobjekte dar, und es ist zu erwarten, dass die im Rahmen des Projektes erzielten Ergebnisse praktische klinische Anwendung erlangen werden.",
                "en": "Gewebe- bzw. Zellschädigung, die durch Ischämie und Reperfusion hervorgerufen wird, stellt ein zentrales Problem für die Herztransplantation dar. Minimierung von pathologischen Änderungen und Erhaltung der Funktionsfähigkeit von Herzmuskelzellen hat eine Verlängerung der vom Herzen tolerierten Ischämiedauer, eine verringerte Abstoßungsreaktion und somit ein verbessertes Langzeitergebnis der Herzchirurgie zur Folge. NADH, ein Enzym, das eine zentrale Stellung im Energiehaushalt der Zelle einnimmt, stellt einen potentiellen Kandidaten als Zusatzstoff zu kardioplegischenLösungen dar, da es einerseits den Adenosintriphosphat (ATP)-Gehalt einer Herzmuskelzelle zu erhöhen vermag und darüberhinaus als Schutz vor durch Ischämie/Reperfussion erzeugten reaktiven Sauerstoffverbindungen gilt. Im Rahmen des Forschungsprojektes soll unter Anwendung elektrophysiologischer, biochemischer sowie histologischer Methoden untersucht werden, ob der Zusatz von NADH Schutz vor Gewebe- bzw. Zellschädigung, hervorgerufen durch Ischämie/Reperfusion, bietet. Isolierte Herzmuskelzellen (tierischen und humanen Ursprungs) sowie ein Tiermodell stellen hierfür sich ergänzende Untersuchungsobjekte dar, und es ist zu erwarten, dass die im Rahmen des Projektes erzielten Ergebnisse praktische klinische Anwendung erlangen werden."
            },
            "begin_planned": null,
            "begin_effective": "2004-03-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2005-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 79,
            "subprogram": null,
            "organization": 14011,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51681,
            "contact": 51681,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                12
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "309-50615-12",
                "309-50417-12",
                "309-50969-12",
                "309-52012-12",
                "309-51592-11",
                "309-51681-10"
            ]
        },
        {
            "id": 299,
            "title": {
                "de": "Chemotherapie von Phäochromocytomen: In vitro and in vivo Modelle als neue Testsysteme",
                "en": "Chemotherapie von Phäochromocytomen: In vitro and in vivo Modelle als neue Testsysteme"
            },
            "short": "Chemotherapie von Phäochromocytomen",
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2004-08-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2007-08-31T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 81,
            "subprogram": null,
            "organization": 14014,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                52
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 310,
            "title": {
                "de": "Endotoxinwirkung auf Schrittmacherströme",
                "en": "Endotoxin effects on pacemaker currrents"
            },
            "short": "Endotoxinwirkung auf Schrittmacherströme",
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2004-10-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2006-06-30T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14011,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51681,
            "contact": 51681,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "310-50615-12",
                "310-50417-12",
                "310-50969-12",
                "310-51592-12",
                "310-51681-10"
            ]
        },
        {
            "id": 7963,
            "title": {
                "de": "Academia-2-Entrepreneurs",
                "en": "Academia-2-Entrepreneurs"
            },
            "short": null,
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2023-03-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2023-09-30T02:00:00+02:00",
            "assignment": "2024-01-11T15:44:50+01:00",
            "program": null,
            "subprogram": null,
            "organization": 23646,
            "category": 10,
            "type": 10,
            "partner_function": 1,
            "manager": 51154,
            "contact": null,
            "status": 2,
            "research": 10,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "7963-51154-10"
            ]
        },
        {
            "id": 287,
            "title": {
                "de": "PEROXISOMES: Integrated Project to decipher the biological function of peroxisomes in health and disease",
                "en": "PEROXISOMES: Integrated Project to decipher the biological function of peroxisomes in health and disease"
            },
            "short": "Peroxisomes",
            "url": null,
            "abstract": {
                "de": "Although peroxisomes are essential for life, the various functions and dynamics of this organelle in health and disease are only poorly understood. Most inherited peroxisomal disorders in humans have a low incidence but collectively they represent an enormous burden on affected individuals, families and society. A detailed understanding of biogenesis and function of this organelle is required for developing therapeutic strategies. To bridge the gap between the scarce knowledge about peroxisomes and their importance for living organisms, we will establish genomic, proteomic and metabolomic platforms focussed on peroxisomes. We will identify novel peroxisomal matrix and membrane proteins and gather comprehensive knowledge about their functions. Using this information, we should be able to decipher the molecular mechanism of so far uncharacterised peroxisomal disorders and open up novel diagnostic and therapeutic opportunities. Genome-wide gene expression and biochemical analyses of 14 different mouse models of  peroxisomal deficiencies will reveal why differing phenotypes occur even when the same metabolic pathway is disturbed. Mouse genetics will be used to evaluate the role of peroxisomes in different cell types during development and in adulthood. Because evidence is emerging for a role of peroxisomes as modulators in diseases of complex inheritance, such as arteriosclerosis, cancer and Alzheimer's disease, we will screen appropriate databases to detect dysregulation of genes encoding peroxisomal proteins. Tissue microarray analysis, cDNA chip and quantitative RT-PCR analysis will be used to verify the results with the final goal to develop diagnostic tools. The role of peroxisomes in Alzheimer's disease and in chronic metabolic liver diseases will be analysed and the biogenesis and dynamics of this organelle deciphered. Only with this integrated EU project will we be able to elucidate the role of peroxisomes in living organisms in the near future.",
                "en": "Although peroxisomes are essential for life, the various functions and dynamics of this organelle in health and disease are only poorly understood. Most inherited peroxisomal disorders in humans have a low incidence but collectively they represent an enormous burden on affected individuals, families and society. A detailed understanding of biogenesis and function of this organelle is required for developing therapeutic strategies. To bridge the gap between the scarce knowledge about peroxisomes and their importance for living organisms, we will establish genomic, proteomic and metabolomic platforms focussed on peroxisomes. We will identify novel peroxisomal matrix and membrane proteins and gather comprehensive knowledge about their functions. Using this information, we should be able to decipher the molecular mechanism of so far uncharacterised peroxisomal disorders and open up novel diagnostic and therapeutic opportunities. Genome-wide gene expression and biochemical analyses of 14 different mouse models of  peroxisomal deficiencies will reveal why differing phenotypes occur even when the same metabolic pathway is disturbed. Mouse genetics will be used to evaluate the role of peroxisomes in different cell types during development and in adulthood. Because evidence is emerging for a role of peroxisomes as modulators in diseases of complex inheritance, such as arteriosclerosis, cancer and Alzheimer's disease, we will screen appropriate databases to detect dysregulation of genes encoding peroxisomal proteins. Tissue microarray analysis, cDNA chip and quantitative RT-PCR analysis will be used to verify the results with the final goal to develop diagnostic tools. The role of peroxisomes in Alzheimer's disease and in chronic metabolic liver diseases will be analysed and the biogenesis and dynamics of this organelle deciphered. Only with this integrated EU project will we be able to elucidate the role of peroxisomes in living organisms in the near future."
            },
            "begin_planned": null,
            "begin_effective": "2005-01-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2008-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 21,
            "subprogram": "Life sciences, genomics and biotechnology for health",
            "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": [
                10
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "287-51691-10"
            ]
        },
        {
            "id": 54,
            "title": {
                "de": "Molekulargenetische Analysen von Knochen- und Weichteiltumoren",
                "en": "Molekulargenetische Analysen von Knochen- und Weichteiltumoren"
            },
            "short": "Molekulargenetik",
            "url": null,
            "abstract": {
                "de": "Analysiert sollen verschiedene Tumore und tumorartige Läsionen werden, bei denen entweder die Klonalität unklar ist oder ungenügende Daten über Chromosomenaberrationen vorliegen. Weiters ist zu überprüfen, ob bestimmte Chromosomenaberrationen als prognostischer Faktor dienen könnten. \t\t\t\t\t\t\t\t\t\t\t\t\t\r\n\t\t\t\t\t\t\t\t\t\t\t\t\t\r\n",
                "en": "Analysiert sollen verschiedene Tumore und tumorartige Läsionen werden, bei denen entweder die Klonalität unklar ist oder ungenügende Daten über Chromosomenaberrationen vorliegen. Weiters ist zu überprüfen, ob bestimmte Chromosomenaberrationen als prognostischer Faktor dienen könnten. "
            },
            "begin_planned": null,
            "begin_effective": "2003-07-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2004-07-31T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14052,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 53237,
            "contact": 53237,
            "status": 2,
            "research": null,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                1270
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "54-53237-10"
            ]
        },
        {
            "id": 480,
            "title": {
                "de": "GRAM - Genetic Response According to the Type of Microbial Infection during Sepsis",
                "en": "GRAM - Genetic Response According to the Type of Microbial Infection during Sepsis"
            },
            "short": "GRAM",
            "url": null,
            "abstract": {
                "de": "Sepsis stellt weiterhin ein großes klinisches Problem dar und ist Ursache vieler Todesfälle bzw. langwieriger Morbidität. Dabei komm es zu einem vermehrtem Auftreten Gram positiver Bakterien. Im Gegensatz zum umfangreichen Wissen über Infektionen durch Gram negative Bakterien ist deutlich weniger über die durch Gram positive Bakterien induzierten Vorgänge bekannt. Ein Problem von Studien, die mit humanem Probenmaterial arbeiten, ist die Heterogenität des jeweiligen Patientenkollektivs. Aus diesem Grund soll diese Genexpressionsstudie mit Gewebeproben aus kontrollierten experimentellen Studien, in denen Gram positive und Gram negative Stimulantien verabreicht wurden, durchgeführt werden. Durch den Einsatz von cDNA-Microarrays kann eine Vielzahs durch Sepsis regulierter Gene entdeckt werden. Neu entwickelte Gewebe-Microarrays (tissue microarrays, TMA), die den Probendurchsatz der immunhistochemischen Analysen dramatisch erhöhen, erlauben die Untersuchung der Relevanz dieser Gene in Geweben verschiedener Organe. ",
                "en": "Sepsis stellt weiterhin ein großes klinisches Problem dar und ist Ursache vieler Todesfälle bzw. langwieriger Morbidität. Dabei komm es zu einem vermehrtem Auftreten Gram positiver Bakterien. Im Gegensatz zum umfangreichen Wissen über Infektionen durch Gram negative Bakterien ist deutlich weniger über die durch Gram positive Bakterien induzierten Vorgänge bekannt. Ein Problem von Studien, die mit humanem Probenmaterial arbeiten, ist die Heterogenität des jeweiligen Patientenkollektivs. Aus diesem Grund soll diese Genexpressionsstudie mit Gewebeproben aus kontrollierten experimentellen Studien, in denen Gram positive und Gram negative Stimulantien verabreicht wurden, durchgeführt werden. Durch den Einsatz von cDNA-Microarrays kann eine Vielzahs durch Sepsis regulierter Gene entdeckt werden. Neu entwickelte Gewebe-Microarrays (tissue microarrays, TMA), die den Probendurchsatz der immunhistochemischen Analysen dramatisch erhöhen, erlauben die Untersuchung der Relevanz dieser Gene in Geweben verschiedener Organe. "
            },
            "begin_planned": null,
            "begin_effective": "2004-02-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2008-07-31T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 73,
            "subprogram": null,
            "organization": 14020,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51663,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                152
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "480-51663-10"
            ]
        },
        {
            "id": 481,
            "title": {
                "de": "ESBIC-D European Systems Biology Initiative for combating Complex Diseases",
                "en": "ESBIC-D European Systems Biology Initiative for combating Complex Diseases"
            },
            "short": "ESBIC-D",
            "url": null,
            "abstract": {
                "de": "Primary targets of FP6 are activities for the combat of multigenic complex diseases such as cancer, diabetes and heart diseases. These diseases, like many others, are caused by disturbances in the complex networks of biological processes in the organisms. Prevention, diagnosis and therapy of these diseases require a detailed understanding of these processes in health and disease, based on the application of techniques from the area of functional genomics on the individual patient, combined with the development of modelling systems, that are able to model the disease process, based on available information as well as the information gained on the individual (genetic factors, chromosomal changes, expression patterns on the RNA and protein levels etc.).\r\n\r\nIn this coordination action (CA) we propose to develop a European infrastructure for such a systems biology approach to combat complex diseases. While we plan to focus on cancer in our initial work, we expect this approach and infrastructure component to become a key instrument in improving diagnosis and therapy of many other complex diseases.\r\n\r\nThis proposal will unite the effort of groups at the forefront of systems biology and modelling, of functional genomics and some of the foremost centres of cancer research.\r\n\r\nMajor goals will be to integrate data and analysis resources available at the participating centres, as well as other centres world wide, to develop and use new mechanisms to identify the pathways likely to be most relevant to the problem domain (cancer), to incorporate these into the models, and to carry out benchmarking studies on the pilot scale to identify strength and weaknesses of current approaches. A major effort will be also invested into a strong outreach component, designed to create local networks contributing to the work of each center, and to educate researchers throughout Europe to the new possibilities and concepts.\r\n",
                "en": "Primary targets of FP6 are activities for the combat of multigenic complex diseases such as cancer, diabetes and heart diseases. These diseases, like many others, are caused by disturbances in the complex networks of biological processes in the organisms. Prevention, diagnosis and therapy of these diseases require a detailed understanding of these processes in health and disease, based on the application of techniques from the area of functional genomics on the individual patient, combined with the development of modelling systems, that are able to model the disease process, based on available information as well as the information gained on the individual (genetic factors, chromosomal changes, expression patterns on the RNA and protein levels etc.).\r\n\r\nIn this coordination action (CA) we propose to develop a European infrastructure for such a systems biology approach to combat complex diseases. While we plan to focus on cancer in our initial work, we expect this approach and infrastructure component to become a key instrument in improving diagnosis and therapy of many other complex diseases.\r\n\r\nThis proposal will unite the effort of groups at the forefront of systems biology and modelling, of functional genomics and some of the foremost centres of cancer research.\r\n\r\nMajor goals will be to integrate data and analysis resources available at the participating centres, as well as other centres world wide, to develop and use new mechanisms to identify the pathways likely to be most relevant to the problem domain (cancer), to incorporate these into the models, and to carry out benchmarking studies on the pilot scale to identify strength and weaknesses of current approaches. A major effort will be also invested into a strong outreach component, designed to create local networks contributing to the work of each center, and to educate researchers throughout Europe to the new possibilities and concepts.\r\n"
            },
            "begin_planned": null,
            "begin_effective": "2005-11-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2007-10-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 21,
            "subprogram": "Life Sciences, Genomics and Biotechnology for Health, TP1, 3rd Call ",
            "organization": 14020,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51663,
            "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": [
                "481-51663-10"
            ]
        }
    ]
}