{"count":2329,"next":"https://api-test.medunigraz.at/v1/research/project/?format=json&limit=20&offset=320&ordering=begin_planned","previous":"https://api-test.medunigraz.at/v1/research/project/?format=json&limit=20&offset=280&ordering=begin_planned","results":[{"id":1573,"title":{"de":"Identification of the causative gene for a notable type of hereditary motor neuropathy","en":"Identification of the causative gene for a notable type of hereditary motor neuropathy"},"short":"HERED_NEURP_OENB08","url":null,"abstract":{"de":"Hauptmerkmale distaler hereditärer Neuropathien (dHMN) sind eine distale Muskelatrophie, häufig verbunden mit Zusatzsymptomen. Bisher wurden fünf ursächliche Gene für die dHMN beschrieben. Eine besondere Verlaufsform mit oft kongenitalem Beginn der Muskelschwäche und Kontrakturen wurden auf Chromosom 12q23-q24 lokalisiert. Zur selben Lokalisation wurde auch in einer Familie mit dominant vererbter skapuloperonealer spinaler Muskelatrophe (SPSMA) sowie in Familien mit hereditärer motorisch-sensibler Neuropathie mit zusätzlicher Stimmband- und Zwerchfelllähmung (HMSN2C) eine Koppelung gezeigt. Daher wurde spekuliert, dass diese Erkrankungen durch Mutationen im selben Gen bedingt sind, das bis heute nicht identifiziert wurde.\r\nIn diesem Forschungsprojekt möchten wir das Gen der dHMN, HMSN2C bzw. SPSMA in einer Familie, in der betroffene Personen alle beschriebenen Phänotypen aufweisen und der Genort auf Chromosom 12q23-q24 lokalisiert wurde, identifizieren.","en":"Hauptmerkmale distaler hereditärer Neuropathien (dHMN) sind eine distale Muskelatrophie, häufig verbunden mit Zusatzsymptomen. Bisher wurden fünf ursächliche Gene für die dHMN beschrieben. Eine besondere Verlaufsform mit oft kongenitalem Beginn der Muskelschwäche und Kontrakturen wurden auf Chromosom 12q23-q24 lokalisiert. Zur selben Lokalisation wurde auch in einer Familie mit dominant vererbter skapuloperonealer spinaler Muskelatrophe (SPSMA) sowie in Familien mit hereditärer motorisch-sensibler Neuropathie mit zusätzlicher Stimmband- und Zwerchfelllähmung (HMSN2C) eine Koppelung gezeigt. Daher wurde spekuliert, dass diese Erkrankungen durch Mutationen im selben Gen bedingt sind, das bis heute nicht identifiziert wurde.\r\nIn diesem Forschungsprojekt möchten wir das Gen der dHMN, HMSN2C bzw. SPSMA in einer Familie, in der betroffene Personen alle beschriebenen Phänotypen aufweisen und der Genort auf Chromosom 12q23-q24 lokalisiert wurde, identifizieren."},"begin_planned":"2008-07-01T02:00:00+02:00","begin_effective":"2008-07-01T02:00:00+02:00","end_planned":"2009-06-30T02:00:00+02:00","end_effective":"2009-12-31T01:00:00+01:00","assignment":"2008-07-07T19:03:21+02:00","program":79,"subprogram":null,"organization":14021,"category":10,"type":10,"partner_function":4,"manager":null,"contact":null,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[12],"funder_projectcode":"13010","ethics_committee":null,"edudract_number":null,"persons":[]},{"id":1617,"title":{"de":"Phase 4 development EORTC Quality of Life module specific to Endometrail Cancer (EORTC QLQ-EN34)","en":"Phase 4 development EORTC Quality of Life module specific to Endometrail Cancer (EORTC QLQ-EN34)"},"short":"EORTC QLQ-EN34","url":null,"abstract":{"de":"Endometrial cancer rates have risen over the last two decades, in some countries very significantly due to a combination of factors that includes an ageing population, increased obesity, and exposure to oestrogens.\r\nWith this burgeoning research agenda there is an urgent need to develop a specific quality of life measure for women with endometrial cancer that is sensitive to the impact of treatments so that their affect on quality of life can be assessed. In addition patients are increasingly encouraged to seek information about the impact of treatment on their quality of life so that they can make informed choices about their treatment and care.","en":"Endometrial cancer rates have risen over the last two decades, in some countries very significantly due to a combination of factors that includes an ageing population, increased obesity, and exposure to oestrogens.\r\nWith this burgeoning research agenda there is an urgent need to develop a specific quality of life measure for women with endometrial cancer that is sensitive to the impact of treatments so that their affect on quality of life can be assessed. In addition patients are increasingly encouraged to seek information about the impact of treatment on their quality of life so that they can make informed choices about their treatment and care."},"begin_planned":"2008-07-01T02:00:00+02:00","begin_effective":"2008-07-01T02:00:00+02:00","end_planned":"2010-09-30T02:00:00+02:00","end_effective":"2010-09-30T02:00:00+02:00","assignment":"2008-09-16T16:47:26+02:00","program":null,"subprogram":null,"organization":14038,"category":10,"type":10,"partner_function":1,"manager":null,"contact":null,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[442],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["1617-57392-12"]},{"id":1722,"title":{"de":"Determining the Hierarchy of EMTRs in Malignant Melanoma","en":"Determining the Hierarchy of EMTRs in Malignant Melanoma"},"short":"DETERMINING_HIERARCHY_EMTR_MELANOMA","url":null,"abstract":{"de":"Epithelial-mesenchymal transition (EMT) is a hallmark of cellular transformation in solid tumors. A similar process is thought to be relevant for melanomgenesis. The exact mechanisms how this is accomplished with respect to stage specific effects of epilthelial-mesenchymal transcriptional regulation, however, are unknown for many tumor entities and melanoma in particular. \r\nThe intent of this project is to decipher targets of EMT inducing regulators at the transcriptional level as exemplified by modulation of cadherins through hepatocyte growth factor (HGF), an important growth factor in melanomagenesis. Our previous data show that the effect of HGF on epithelial-mesenchymal transcriptional regulators (EMTRs) is stage-dependent in melanoma cell lines. Based on these observations we want to pinpoint EMTRs specific binding to E-boxes in cadherins, investigate on HGF-mediated regulation of Snail and Slug and study overexpression of Slug and Twist in melanoma cell lines. We expect to uncover the hierachical sequence of EMTRs activation in early versus late stage melanomas, the preferential binding of EMRTs to cadherins and in vitro and in vivo effects of over-expressed or down-regulated EMRTs. The following hypothesis:\r\n\"Hierachy of epithelial-mesenchymal transcriptional regulators in malignant melanoma\"\r\nwill be tested in two specific aims:\r\n*Continuing investigations on E-box binding EMRTs and the functional effects of Slug and Twist in melanocytic cells \r\n*Scrutinizing HGF mediated modulation of Snail, Slug and Twist through regulation by NF-kB and GSK -3ß.","en":"Epithelial-mesenchymal transition (EMT) is a hallmark of cellular transformation in solid tumors. A similar process is thought to be relevant for melanomgenesis. The exact mechanisms how this is accomplished with respect to stage specific effects of epilthelial-mesenchymal transcriptional regulation, however, are unknown for many tumor entities and melanoma in particular. \r\nThe intent of this project is to decipher targets of EMT inducing regulators at the transcriptional level as exemplified by modulation of cadherins through hepatocyte growth factor (HGF), an important growth factor in melanomagenesis. Our previous data show that the effect of HGF on epithelial-mesenchymal transcriptional regulators (EMTRs) is stage-dependent in melanoma cell lines. Based on these observations we want to pinpoint EMTRs specific binding to E-boxes in cadherins, investigate on HGF-mediated regulation of Snail and Slug and study overexpression of Slug and Twist in melanoma cell lines. We expect to uncover the hierachical sequence of EMTRs activation in early versus late stage melanomas, the preferential binding of EMRTs to cadherins and in vitro and in vivo effects of over-expressed or down-regulated EMRTs. The following hypothesis:\r\n\"Hierachy of epithelial-mesenchymal transcriptional regulators in malignant melanoma\"\r\nwill be tested in two specific aims:\r\n*Continuing investigations on E-box binding EMRTs and the functional effects of Slug and Twist in melanocytic cells \r\n*Scrutinizing HGF mediated modulation of Snail, Slug and Twist through regulation by NF-kB and GSK -3ß."},"begin_planned":"2008-08-01T02:00:00+02:00","begin_effective":"2009-01-15T01:00:00+01:00","end_planned":"2009-07-31T02:00:00+02:00","end_effective":"2011-01-14T01:00:00+01:00","assignment":"2009-01-16T14:06:24+01:00","program":72,"subprogram":null,"organization":14047,"category":10,"type":10,"partner_function":4,"manager":53662,"contact":53662,"status":2,"research":5,"grant":10,"event":null,"study":null,"language":null,"funders":[9],"funder_projectcode":"P21156","ethics_committee":null,"edudract_number":null,"persons":["1722-53662-10"]},{"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":"2008-08-01T02:00:00+02:00","begin_effective":"2008-08-01T02:00:00+02:00","end_planned":"2011-07-31T02:00:00+02:00","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":1586,"title":{"de":"Predictive markers of spontaneous preterm delivery","en":"Predictive markers of spontaneous preterm delivery"},"short":"PREDICTIVE_MARKERS","url":null,"abstract":{"de":"Frühgeburtlichkeit ist eine Hauptursache für perinatale Morbidität und Mortalität. In Bezug auf die neurologische Langzeitprognose ist die periventrikuläre Leukoenzephalomalazie (PVL) und die daraus resultierende Zerebralparese eine der häufigsten Ursachen für Behinderungen. Das Problem des Screenings und der Diagnostik liegt darin, dass die Frühgeburt ein Endpunkt verschiedener Ätiologien ist. In diesem Projekt wollen wir Marker evaluieren, die unterschiedlichen ätiologischen Kategorien entsprechen: Polymorphismen von Interleukin-10 und Interleukin-4 (Entzündung), SERPINE1 (uteroplazentare Vaskulopathie), messenger RNA von Cortikotropin-releasing-Hormon (Wehenauslösung) und Pentraxin 3 (Entzündung). Das Screeningpotential dieses Marker-Sets wird dabei sowohl für die Frühgeburt als auch für Frühgeburt mit Entwicklung einer PVL evaluiert. Diese Marker sollen den Einsatz prophylaktischer und therapeutischer Interventionen (Progesteron, anti-inflammatorische Interleukine) ermöglichen.","en":"Frühgeburtlichkeit ist eine Hauptursache für perinatale Morbidität und Mortalität. In Bezug auf die neurologische Langzeitprognose ist die periventrikuläre Leukoenzephalomalazie (PVL) und die daraus resultierende Zerebralparese eine der häufigsten Ursachen für Behinderungen. Das Problem des Screenings und der Diagnostik liegt darin, dass die Frühgeburt ein Endpunkt verschiedener Ätiologien ist. In diesem Projekt wollen wir Marker evaluieren, die unterschiedlichen ätiologischen Kategorien entsprechen: Polymorphismen von Interleukin-10 und Interleukin-4 (Entzündung), SERPINE1 (uteroplazentare Vaskulopathie), messenger RNA von Cortikotropin-releasing-Hormon (Wehenauslösung) und Pentraxin 3 (Entzündung). Das Screeningpotential dieses Marker-Sets wird dabei sowohl für die Frühgeburt als auch für Frühgeburt mit Entwicklung einer PVL evaluiert. Diese Marker sollen den Einsatz prophylaktischer und therapeutischer Interventionen (Progesteron, anti-inflammatorische Interleukine) ermöglichen."},"begin_planned":"2008-09-01T02:00:00+02:00","begin_effective":"2008-09-01T02:00:00+02:00","end_planned":"2010-08-31T02:00:00+02:00","end_effective":"2011-02-28T01:00:00+01:00","assignment":"2008-07-25T13:12:34+02:00","program":79,"subprogram":null,"organization":14064,"category":10,"type":10,"partner_function":4,"manager":null,"contact":null,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[12],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":[]},{"id":1645,"title":{"de":"Influence of Antioxidative Agents like Resveratrol, Quercetin-dihydrate, and Seleno-L-Methionine on Human Synoviocytes of Osteoarthritis (OA), Rheumatoid Arthritis (RA) and Psoriasis Arthritis (PsA) Patients","en":"Influence of Antioxidative Agents like Resveratrol, Quercetin-dihydrate, and Seleno-L-Methionine on Human Synoviocytes of Osteoarthritis (OA), Rheumatoid Arthritis (RA) and Psoriasis Arthritis (PsA) Patients"},"short":"Influence of Antioxidative Agents","url":null,"abstract":{"de":"Osteoarthritis is the most prevalent disorder of the musculoskeletal system and has a very high socioeconomic impact. Current treatments for Osteoarthritis are only symptomatic, because they do not act on the causes of Arthritis and do not stop the progression of the disease. This study is designed to investigate the effect of Resveratrol, Quercetin, and Selenium on healthy human synovial cells compared to synovial cells from OA and RA patients. We propose that these chemo preventive agents cause a growth rate decrease in synovial tissue and furthermore an inhibition of proinflammatory factors as well as an increase in factors favouring apoptosis and cell death. \r\nEspecially Resveratrol is known as a potent specific inhibitor of inflammation, but its potency has not been tested on human synovial cells. If the potency in decreasing inflammatory Interleukins is similar to the results of animal experiments, it would be an enormous effort for treatment of Osteoarthritis and Rheumatoid Arthritis. This study should be undertaken to define a possible systemic or local application of Resveratrol compared to Quercetin and Selenium. A close interaction between clinicians and basic scientists is necessary because of the combination of analytical, functional and molecular methods.\r\n","en":"Osteoarthritis is the most prevalent disorder of the musculoskeletal system and has a very high socioeconomic impact. Current treatments for Osteoarthritis are only symptomatic, because they do not act on the causes of Arthritis and do not stop the progression of the disease. This study is designed to investigate the effect of Resveratrol, Quercetin, and Selenium on healthy human synovial cells compared to synovial cells from OA and RA patients. We propose that these chemo preventive agents cause a growth rate decrease in synovial tissue and furthermore an inhibition of proinflammatory factors as well as an increase in factors favouring apoptosis and cell death. \r\nEspecially Resveratrol is known as a potent specific inhibitor of inflammation, but its potency has not been tested on human synovial cells. If the potency in decreasing inflammatory Interleukins is similar to the results of animal experiments, it would be an enormous effort for treatment of Osteoarthritis and Rheumatoid Arthritis. This study should be undertaken to define a possible systemic or local application of Resveratrol compared to Quercetin and Selenium. A close interaction between clinicians and basic scientists is necessary because of the combination of analytical, functional and molecular methods.\r\n"},"begin_planned":"2008-09-01T02:00:00+02:00","begin_effective":"2008-08-01T02:00:00+02:00","end_planned":"2009-08-31T02:00:00+02:00","end_effective":"2010-08-31T02:00:00+02:00","assignment":"2008-10-29T16:01:05+01:00","program":79,"subprogram":null,"organization":14052,"category":10,"type":10,"partner_function":4,"manager":null,"contact":null,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[12],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["1645-50696-12","1645-57343-12"]},{"id":1748,"title":{"de":"Anbahnungsfinanzierung Healthcare integrated Biobanking RP7 Health 1. Stufe","en":"Anbahnungsfinanzierung Healthcare integrated Biobanking RP7 Health 1. Stufe"},"short":"HEALTHCARE_INTEGR_BIOBANKING","url":null,"abstract":{"de":null,"en":null},"begin_planned":"2008-09-03T02:00:00+02:00","begin_effective":"2008-09-03T02:00:00+02:00","end_planned":"2008-12-31T01:00:00+01:00","end_effective":"2008-12-31T01:00:00+01:00","assignment":"2009-02-17T13:36:04+01:00","program":54,"subprogram":null,"organization":14020,"category":10,"type":10,"partner_function":4,"manager":51663,"contact":51663,"status":2,"research":5,"grant":10,"event":null,"study":null,"language":null,"funders":[416],"funder_projectcode":"821139","ethics_committee":null,"edudract_number":null,"persons":["1748-51663-10"]},{"id":1640,"title":{"de":"Effect of ivabradine, a novel If-blocker, on human atrial myocytes under elevated endotoxin levels","en":"Effect of ivabradine, a novel If-blocker, on human atrial myocytes under elevated endotoxin levels"},"short":"IVABRADINE_FWF08","url":null,"abstract":{"de":"Endotoxine (Lipopolysaccharide, LPSe), die Auslöser von gram-negativer Sepsis, führen durch Interaktion mit den Wirtszellen zu einer Vielzahl von biologischen Reaktionen. Kürzlich konnten wir in einer Publikation zeigen, dass LPS den Schrittmacherstrom If in humanen Vorhofzellen, nach 6-stündiger Inkubation hemmt, ein Ereignis, das für das Verständnis der bei Sepsis auftretenden Reduktion der Herzfrequenzvariabilität von großer Relevanz ist.\r\nAusgehend von der hemmenden LPS-Wirkung auf If sollen 2 große Themenschwerpunkte untersucht werden:\r\n*Interaktion von Ivabradine und Endotoxin auf den humanen If\r\n*Mechanismus der Endotoxinwirkung","en":"Endotoxine (Lipopolysaccharide, LPSe), die Auslöser von gram-negativer Sepsis, führen durch Interaktion mit den Wirtszellen zu einer Vielzahl von biologischen Reaktionen. Kürzlich konnten wir in einer Publikation zeigen, dass LPS den Schrittmacherstrom If in humanen Vorhofzellen, nach 6-stündiger Inkubation hemmt, ein Ereignis, das für das Verständnis der bei Sepsis auftretenden Reduktion der Herzfrequenzvariabilität von großer Relevanz ist.\r\nAusgehend von der hemmenden LPS-Wirkung auf If sollen 2 große Themenschwerpunkte untersucht werden:\r\n*Interaktion von Ivabradine und Endotoxin auf den humanen If\r\n*Mechanismus der Endotoxinwirkung"},"begin_planned":"2008-10-01T02:00:00+02:00","begin_effective":"2009-10-01T02:00:00+02:00","end_planned":"2011-09-30T02:00:00+02:00","end_effective":"2013-09-30T02:00:00+02:00","assignment":"2008-10-13T14:02:42+02:00","program":72,"subprogram":null,"organization":14011,"category":10,"type":10,"partner_function":4,"manager":50615,"contact":50615,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[9],"funder_projectcode":"P21159","ethics_committee":null,"edudract_number":null,"persons":["1640-50615-10","1640-50417-12","1640-50969-12","1640-51592-12"]},{"id":2033,"title":{"de":"Mit autologen Thrombozyten angereichertes körpereigenes Fibrin zur Förderung der Wundheilung bei chronischem Ulcus cruris venosum (kontrollierte prospektive randomisierte klinische Studie)","en":"Mit autologen Thrombozyten angereichertes körpereigenes Fibrin zur Förderung der Wundheilung bei chronischem Ulcus cruris venosum (kontrollierte prospektive randomisierte klinische Studie)"},"short":" Ulcus cruris venosum Studie","url":null,"abstract":{"de":null,"en":null},"begin_planned":"2008-10-01T02:00:00+02:00","begin_effective":"2010-01-01T01:00:00+01:00","end_planned":"2009-09-30T02:00:00+02:00","end_effective":"2011-12-31T01:00:00+01:00","assignment":"2010-01-12T17:36:20+01:00","program":null,"subprogram":null,"organization":14073,"category":10,"type":10,"partner_function":4,"manager":51612,"contact":51612,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[135],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["2033-51612-10"]},{"id":2161,"title":{"de":"BM.W_Fa-Zusatzfinanzierung 7. RP zu EU Projekt \"HEALTH-F5-2008-22916\" (SPIDIA)","en":"BM.W_Fa-funding to the 7th EU FP \"HEALTH-F5-2008-22916\" (SPIDIA)"},"short":"BM.W_Fa Zusatzfinanzierung SPIDIA","url":null,"abstract":{"de":null,"en":null},"begin_planned":"2008-10-01T02:00:00+02:00","begin_effective":"2008-10-01T02:00:00+02:00","end_planned":"2012-09-30T02:00:00+02:00","end_effective":"2012-09-30T02:00:00+02:00","assignment":"2010-03-15T13:01:21+01:00","program":90,"subprogram":null,"organization":14020,"category":10,"type":10,"partner_function":4,"manager":51663,"contact":51663,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[25],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["2161-51663-10"]},{"id":1936,"title":{"de":"CII-AT-0042-04-0809 - Medical Imaging & Medical Information Processing","en":"CII-AT-0042-04-0809 - Medical Imaging & Medical Information Processing"},"short":"CEEPUS Medical Imaging","url":null,"abstract":{"de":null,"en":null},"begin_planned":"2008-10-01T02:00:00+02:00","begin_effective":"2008-10-01T02:00:00+02:00","end_planned":"2009-09-30T02:00:00+02:00","end_effective":"2009-09-30T02:00:00+02:00","assignment":null,"program":null,"subprogram":null,"organization":14106,"category":10,"type":10,"partner_function":2,"manager":51913,"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":["1936-83445-12","1936-51824-12","1936-51709-12","1936-51913-10"]},{"id":1581,"title":{"de":"Identification and functional characterisation of Nuclear Orphan Receptors as Tumor Suppressor Genes in aggressive non-Hodgkin`s Lymphomas and acute lymphoblastic leukemia","en":"Identification and functional characterisation of Nuclear Orphan Receptors as Tumor Suppressor Genes in aggressive non-Hodgkin`s Lymphomas and acute lymphoblastic leukemia"},"short":"non-Hodgkin`s Lymphoma","url":null,"abstract":{"de":"NR4A1 (also called Nur77, TR3, or NGFI-B), NR4A2 (Nurr1 or RNR-1) and NR4A3 (Nor-1 or Minor) are three members of an orphan nuclear hormone receptor family referred to as Nur77 family. They are all transcription factors belonging to the superfamily of steroid nuclear hormone receptors. These nuclear hormone receptors (NR) are classified as early response genes, are induced by a diverse range of signals, including fatty acids, stress, growth factors, cytokines, peptide hormones, neurotransmitters, and physical stimuli for example magnetic fields or shear stress. In line with the pleiotropic physiological stimuli that induce the NR4A subgroup, these orphan NRs have been implicated in cell cycle regulation, apoptosis, inflammation, atherogenesis and more recently in carcinogenesis. \r\nThe ultimate growth of a tumour depends on not only the rate of tumour cell proliferation, but also the rate of tumour cell death (=apoptosis). NR4A1 controls both survival and death of cancer cells. \r\nIn contrast to NR4A1, only pro-survival effects, but not pro-apoptotic effects, have been reported for NR4A2. \r\nNR4A3 has been shown to be functionally redundant with NR4A1 in T-cell apoptosis. Results also suggest that NR4A1 and NR4A3 have non-redundant functions as well.\r\nThe most convincing evidence that nuclear orphan receptors function as critical tumor suppressors is the observation that the abrogation of nuclear receptors Nr4a3 and Nr4a1 leads to rapid development of acute myeloid leukemia. Evidence of nuclear orphan receptors acting as tumor suppressor genes in B-cell malignancies comes from the observation that Epstein-Barr virus EBNA 2 blocks NR4A1 mediated apoptosis in B-cells and from gene expression profiling in diffuse large B-cell lymphoma (DLBCL) in which over expression of NR4A3 is found in cured or refractory DLBCL, as opposed to a fatal course of disease. Hence, it is speculated that NR4A3 increases the apoptotic response to chemotherapy in curable DLBCL.\r\n\r\nThe aim of our study was to comprehensively study NR expression and function in B-cell malignancies and to define the nuclear orphan receptors NR4A1 and NR4A1 as cooperative putative tumor suppressor genes (TSG) in B-cell malignancies.\r\n\r\n","en":"NR4A1 (also called Nur77, TR3, or NGFI-B), NR4A2 (Nurr1 or RNR-1) and NR4A3 (Nor-1 or Minor) are three members of an orphan nuclear hormone receptor family referred to as Nur77 family. They are all transcription factors belonging to the superfamily of steroid nuclear hormone receptors. These nuclear hormone receptors (NR) are classified as early response genes, are induced by a diverse range of signals, including fatty acids, stress, growth factors, cytokines, peptide hormones, neurotransmitters, and physical stimuli for example magnetic fields or shear stress. In line with the pleiotropic physiological stimuli that induce the NR4A subgroup, these orphan NRs have been implicated in cell cycle regulation, apoptosis, inflammation, atherogenesis and more recently in carcinogenesis. \r\nThe ultimate growth of a tumour depends on not only the rate of tumour cell proliferation, but also the rate of tumour cell death (=apoptosis). NR4A1 controls both survival and death of cancer cells. \r\nIn contrast to NR4A1, only pro-survival effects, but not pro-apoptotic effects, have been reported for NR4A2. \r\nNR4A3 has been shown to be functionally redundant with NR4A1 in T-cell apoptosis. Results also suggest that NR4A1 and NR4A3 have non-redundant functions as well.\r\nThe most convincing evidence that nuclear orphan receptors function as critical tumor suppressors is the observation that the abrogation of nuclear receptors Nr4a3 and Nr4a1 leads to rapid development of acute myeloid leukemia. Evidence of nuclear orphan receptors acting as tumor suppressor genes in B-cell malignancies comes from the observation that Epstein-Barr virus EBNA 2 blocks NR4A1 mediated apoptosis in B-cells and from gene expression profiling in diffuse large B-cell lymphoma (DLBCL) in which over expression of NR4A3 is found in cured or refractory DLBCL, as opposed to a fatal course of disease. Hence, it is speculated that NR4A3 increases the apoptotic response to chemotherapy in curable DLBCL.\r\n\r\nThe aim of our study was to comprehensively study NR expression and function in B-cell malignancies and to define the nuclear orphan receptors NR4A1 and NR4A1 as cooperative putative tumor suppressor genes (TSG) in B-cell malignancies."},"begin_planned":"2008-10-01T02:00:00+02:00","begin_effective":"2008-10-01T02:00:00+02:00","end_planned":"2010-09-30T02:00:00+02:00","end_effective":"2010-09-30T02:00:00+02:00","assignment":"2008-07-17T12:24:53+02:00","program":null,"subprogram":null,"organization":14082,"category":10,"type":10,"partner_function":4,"manager":51930,"contact":51930,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[836],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["1581-51930-10"]},{"id":1577,"title":{"de":"Identification of specific endothelial binding-sites for inflammatory carbamylated low-density lipoproteins","en":"Identification of specific endothelial binding-sites for inflammatory carbamylated low-density lipoproteins"},"short":"CARBAMYL_LDL_FWF08","url":null,"abstract":{"de":"In renal disease, elevated levels of urea lead to an increased concentration of cyanate that reacts irreversible with amino groups of proteins through carbamylation reactions. High concentrations of carbamylated low-density-lipoproteins (cLDL) have recently been reported to accumulate in plasma of pateints with chronic renal failure, indicating that cLDL is by far the most abundant modified LDL found in human plasa. Of importance, carbamylated proteins may also be formed directly at sites of inflammation - even in the absence of renal disease- via the phagocyte derived inflammatory mediator myeloperoxidase (MPO). Active MPO is present in human atherosclerotic lesion material and has been shown to bind to low- and high-density lipoproteins. Thus, it can be assumed that MPO derived cyanate contributes to lipoprotein carbamylation at sites of inflammation. Recent clinical studies demonstrated that carbamylated proteins predict increased risk of coronary artery disease, future myocardial infarction, stroke and death.\r\n\r\nNo endothelial receptors of binding proteins that might trigger the potent pro-atherosclerotic effects of carbamylated LDL have yet been identified. Therefore, the aim of the proposed project is to identify endothelial receptors for carbamylated LDL and to systemically examine the impact of carbamylated LDL on the expression of inflammatory genes in human derived vascular endothelial cells.","en":"In renal disease, elevated levels of urea lead to an increased concentration of cyanate that reacts irreversible with amino groups of proteins through carbamylation reactions. High concentrations of carbamylated low-density-lipoproteins (cLDL) have recently been reported to accumulate in plasma of pateints with chronic renal failure, indicating that cLDL is by far the most abundant modified LDL found in human plasa. Of importance, carbamylated proteins may also be formed directly at sites of inflammation - even in the absence of renal disease- via the phagocyte derived inflammatory mediator myeloperoxidase (MPO). Active MPO is present in human atherosclerotic lesion material and has been shown to bind to low- and high-density lipoproteins. Thus, it can be assumed that MPO derived cyanate contributes to lipoprotein carbamylation at sites of inflammation. Recent clinical studies demonstrated that carbamylated proteins predict increased risk of coronary artery disease, future myocardial infarction, stroke and death.\r\n\r\nNo endothelial receptors of binding proteins that might trigger the potent pro-atherosclerotic effects of carbamylated LDL have yet been identified. Therefore, the aim of the proposed project is to identify endothelial receptors for carbamylated LDL and to systemically examine the impact of carbamylated LDL on the expression of inflammatory genes in human derived vascular endothelial cells."},"begin_planned":"2008-10-01T02:00:00+02:00","begin_effective":"2008-10-01T02:00:00+02:00","end_planned":"2011-09-30T02:00:00+02:00","end_effective":"2013-09-30T02:00:00+02:00","assignment":"2008-07-14T14:41:55+02:00","program":72,"subprogram":null,"organization":14022,"category":10,"type":10,"partner_function":4,"manager":53252,"contact":53252,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[9],"funder_projectcode":"P21004","ethics_committee":null,"edudract_number":null,"persons":["1577-53252-10"]},{"id":1543,"title":{"de":"Expression und Lokalisierung der Endothel Lipase in stabilen und unstabilen atherosklerotischen Plaques","en":"Expression and localization of endothelial lipase in stable and unstable atherosclerotic plaques"},"short":"EXPRESS_LOKALIS_ENDOTHEL_LIPASE","url":null,"abstract":{"de":"Atherosklerose im Bereich der Karotiden ist Hauptverursacher des Schlaganfalles, einer der häufigsten Invaliditäts- und Todesursachen in den westlichen Industrieländern. Das Auftreten von neurologischen Symptomen bei betroffenen Patienten geht mit der Destabilisierung der atherosklerotischen Plaques einher. Da die Endothel Lipase in den Plaque-assoziierten Zellen exprimiert wird, wollen wir im Rahmen des beantragten Projektes untersuchen ob sich die Expressionsrate und die zellspezifische Lokalisierung der Endothel Lipase zwischen stabilen und unstabilen atherosklerotischen Plaques von Patienten nach operativer Endarterektomie unterscheidet. Die Ergebnisse dieser Studie versprechen neue Erkenntnisse über die Rolle von Endothel Lipase in der Entwicklung und Destabilisierung von karotidalen atherosklerotischen Plaques und stellen die Basis für die Entwicklung neuer Medikamente zur Prävention von Plaque-Destabilisierung dar.","en":"Atherosklerose im Bereich der Karotiden ist Hauptverursacher des Schlaganfalles, einer der häufigsten Invaliditäts- und Todesursachen in den westlichen Industrieländern. Das Auftreten von neurologischen Symptomen bei betroffenen Patienten geht mit der Destabilisierung der atherosklerotischen Plaques einher. Da die Endothel Lipase in den Plaque-assoziierten Zellen exprimiert wird, wollen wir im Rahmen des beantragten Projektes untersuchen ob sich die Expressionsrate und die zellspezifische Lokalisierung der Endothel Lipase zwischen stabilen und unstabilen atherosklerotischen Plaques von Patienten nach operativer Endarterektomie unterscheidet. Die Ergebnisse dieser Studie versprechen neue Erkenntnisse über die Rolle von Endothel Lipase in der Entwicklung und Destabilisierung von karotidalen atherosklerotischen Plaques und stellen die Basis für die Entwicklung neuer Medikamente zur Prävention von Plaque-Destabilisierung dar."},"begin_planned":"2008-10-01T02:00:00+02:00","begin_effective":"2008-10-01T02:00:00+02:00","end_planned":"2011-09-30T02:00:00+02:00","end_effective":"2011-09-30T02:00:00+02:00","assignment":"2008-05-29T11:09:47+02:00","program":79,"subprogram":null,"organization":14013,"category":10,"type":10,"partner_function":4,"manager":51988,"contact":51988,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[12],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["1543-51988-10"]},{"id":1613,"title":{"de":"Glukose Monitoring bei der Hemodialyse","en":"Glucose monitoring in hemodialysis"},"short":"GLUCOSEMONITORING_BRIDGE08","url":null,"abstract":{"de":"Ziel des Projekts ist die Entwicklung eines Systems zur automatischen und kontinuierlichen Messung der Glukose bei der Hämodialyse und bei verwandten extrakorporalen Blutbehandlungsverfahren, sowie zur indirekten Bestimmung der Glukosekonzentration im Blut und davon abgeleiteter Größen.","en":"To develop a system for automatic and continuous glucose measurements during hemodialysis and other related extracorporeal blood treatments for indirect estimation of arterial blood glucose and related entities."},"begin_planned":"2008-10-01T02:00:00+02:00","begin_effective":"2008-10-01T02:00:00+02:00","end_planned":"2010-11-30T01:00:00+01:00","end_effective":"2011-03-31T02:00:00+02:00","assignment":"2008-09-02T18:21:16+02:00","program":60,"subprogram":null,"organization":14010,"category":10,"type":10,"partner_function":4,"manager":51834,"contact":51834,"status":2,"research":3,"grant":10,"event":null,"study":null,"language":null,"funders":[416],"funder_projectcode":"818127","ethics_committee":null,"edudract_number":null,"persons":["1613-50404-12","1613-51834-10"]},{"id":1714,"title":{"de":"GOLD3 - Genomics Of Lipid Droplet Biology, Component 5: Discovery of lipolytic activities by in vivo proteomic profiling","en":"GOLD3 - Genomics Of Lipid Droplet Biology, Component 5: Discovery of lipolytic activities by in vivo proteomic profiling"},"short":"GOLD3_BIRNER_GRUENBERGER","url":null,"abstract":{"de":"Lipid-associated disorders constitute a major health treat wordlwide. Currently more than one billion individuals are overweight or obese and it is estimated that by 2010 more than 300 million patients will be affected by insulin resistance and type-II diabetes.\r\nThe general aim of GOLD 3 is to elucidate processes that govern the biology of lipid droplets (LD), their synthesis and mobilization under normal and pathological conditions.\r\nThe proposed project will discover genes, proteins, and metabolites involved in the generation and catabolsim of LD in human cells. The characterization of their biochemical function, regulation od their expression, and 3-D structure will reveal currently unknown mechanisms and pathways that control the generation of lipid signalling molecules, energy substrates and membrane components affecting cell tissue function as well as energy homeostasis.","en":"Lipid-associated disorders constitute a major health treat wordlwide. Currently more than one billion individuals are overweight or obese and it is estimated that by 2010 more than 300 million patients will be affected by insulin resistance and type-II diabetes.\r\nThe general aim of GOLD 3 is to elucidate processes that govern the biology of lipid droplets (LD), their synthesis and mobilization under normal and pathological conditions.\r\nThe proposed project will discover genes, proteins, and metabolites involved in the generation and catabolsim of LD in human cells. The characterization of their biochemical function, regulation od their expression, and 3-D structure will reveal currently unknown mechanisms and pathways that control the generation of lipid signalling molecules, energy substrates and membrane components affecting cell tissue function as well as energy homeostasis."},"begin_planned":"2008-12-01T01:00:00+01:00","begin_effective":"2009-02-01T01:00:00+01:00","end_planned":"2011-11-30T01:00:00+01:00","end_effective":"2012-04-30T02:00:00+02:00","assignment":"2009-01-14T12:15:11+01:00","program":73,"subprogram":null,"organization":28394,"category":10,"type":10,"partner_function":2,"manager":58794,"contact":58794,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[152],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["1714-58794-10"]},{"id":1735,"title":{"de":"GOLD3 - Genomics Of Lipid Droplet Biology, Component 8: Lipid droplet-associated proteins regulating lipid storage and release in macrophages and foam cells","en":"GOLD3 - Genomics Of Lipid Droplet Biology, Component 8: Lipid droplet-associated proteins regulating lipid storage and release in macrophages and foam cells"},"short":"GOLD3_KRATKY","url":null,"abstract":{"de":"Lipid-associated disorders constitute a major health treat wordlwide. Currently more than one billion individuals are overweight or obese and it is estimated that by 2010 more than 300 million patients will be affected by insulin resistance and type-II diabetes.\r\nThe general aim of GOLD 3 is to elucidate processes that govern the biology of lipid droplets (LD), their synthesis and mobilization under normal and pathological conditions.\r\nThe proposed project will discover genes, proteins, and metabolites involved in the generation and catabolsim of LD in human cells. The characterization of their biochemical function, regulation od their expression, and 3-D structure will reveal currently unknown mechanisms and pathways that control the generation of lipid signalling molecules, energy substrates and membrane components affecting cell tissue function as well as energy homeostasis.","en":"Lipid-associated disorders constitute a major health treat wordlwide. Currently more than one billion individuals are overweight or obese and it is estimated that by 2010 more than 300 million patients will be affected by insulin resistance and type-II diabetes.\r\nThe general aim of GOLD 3 is to elucidate processes that govern the biology of lipid droplets (LD), their synthesis and mobilization under normal and pathological conditions.\r\nThe proposed project will discover genes, proteins, and metabolites involved in the generation and catabolsim of LD in human cells. The characterization of their biochemical function, regulation od their expression, and 3-D structure will reveal currently unknown mechanisms and pathways that control the generation of lipid signalling molecules, energy substrates and membrane components affecting cell tissue function as well as energy homeostasis."},"begin_planned":"2008-12-01T01:00:00+01:00","begin_effective":"2009-02-01T01:00:00+01:00","end_planned":"2011-11-30T01:00:00+01:00","end_effective":"2012-04-30T02:00:00+02:00","assignment":"2009-01-22T11:56:26+01:00","program":73,"subprogram":null,"organization":14013,"category":10,"type":10,"partner_function":2,"manager":51904,"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":["1735-51904-10","1735-58794-11"]},{"id":1957,"title":{"de":"Genetics of the Dopaminergic System and Smoking Behavior","en":"Genetics of the Dopaminergic System and Smoking Behavior"},"short":"Genetics of the Dopaminergic System","url":null,"abstract":{"de":null,"en":null},"begin_planned":"2009-01-01T01:00:00+01:00","begin_effective":"2009-01-01T01:00:00+01:00","end_planned":"2010-12-30T01:00:00+01:00","end_effective":"2010-12-30T01:00:00+01:00","assignment":"2009-10-23T12:55:40+02:00","program":null,"subprogram":null,"organization":14028,"category":10,"type":10,"partner_function":4,"manager":50910,"contact":50910,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[135],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["1957-50910-10"]},{"id":1734,"title":{"de":"Verkalkung von Gefäßen und Knochen bei NierentransplantationspatientInnen [Regulierung der Kalzifizierung bei NierentransplantationspatientInnen]","en":"Verkalkung von Gefäßen und Knochen bei NierentransplantationspatientInnen [Regulierung der Kalzifizierung bei NierentransplantationspatientInnen]"},"short":"Verkalkung bei Nierentransplantationen","url":null,"abstract":{"de":"Kalzifizierung tritt physiologisch im Knochen und pathophysiologisch im Gefäßsystem auf. Kardiovaskuläre Erkrankungen sind eine Haupt-Todesursache von Nierenerkrankten und sind entscheidend für die Durchführbarkeit von Nierentransplantationen (RTX). Das derezeitige Wissen um die Regulation der Kalzifizierung in Knochen und Gefäßsystem bei RTX-Patienten ist fragmentarisch.\r\n\r\nDiese offene, kontrollierte, monozentrische Studie untersucht die Regulation der Kalzifizierung im Knochen- und Gefäßsystem bei PatientInnen mit RTX.\r\nUnsere Fragestellung zielt auf Unterschiede der Expressionslevels von Regulatoren der Kalzifizierung in beiden Gewebstypen und im Vergleich von athero- und mediasklerotischen Gefäßen.\r\nWir erwarten uns Einblick in Kalzifizierungsmechanismen und mögliche klinische Aspekte für Diagnose und Therapie bei diesen HochrisikopatientInnen.","en":"Kalzifizierung tritt physiologisch im Knochen und pathophysiologisch im Gefäßsystem auf. Kardiovaskuläre Erkrankungen sind eine Haupt-Todesursache von Nierenerkrankten und sind entscheidend für die Durchführbarkeit von Nierentransplantationen (RTX). Das derezeitige Wissen um die Regulation der Kalzifizierung in Knochen und Gefäßsystem bei RTX-Patienten ist fragmentarisch.\r\n\r\nDiese offene, kontrollierte, monozentrische Studie untersucht die Regulation der Kalzifizierung im Knochen- und Gefäßsystem bei PatientInnen mit RTX.\r\nUnsere Fragestellung zielt auf Unterschiede der Expressionslevels von Regulatoren der Kalzifizierung in beiden Gewebstypen und im Vergleich von athero- und mediasklerotischen Gefäßen.\r\nWir erwarten uns Einblick in Kalzifizierungsmechanismen und mögliche klinische Aspekte für Diagnose und Therapie bei diesen HochrisikopatientInnen."},"begin_planned":"2009-01-01T01:00:00+01:00","begin_effective":"2009-01-01T01:00:00+01:00","end_planned":"2011-12-31T01:00:00+01:00","end_effective":"2012-12-31T01:00:00+01:00","assignment":"2009-01-21T15:49:20+01:00","program":79,"subprogram":null,"organization":14073,"category":10,"type":10,"partner_function":4,"manager":51982,"contact":51982,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[12],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["1734-51982-10","1734-57544-12"]},{"id":1721,"title":{"de":"Influence of Resveratrol, Quercetin-dihydrate und Seleno-L-Methoionine an Matrix Metalloproteinases and RANKL Levels in Human Osteoarthritis Rheumatoid Arthritis Synovial Fluids","en":"Influence of Resveratrol, Quercetin-dihydrate und Seleno-L-Methoionine an Matrix Metalloproteinases and RANKL Levels in Human Osteoarthritis Rheumatoid Arthritis Synovial Fluids"},"short":"Metalloproteinases and RANKL Levels ","url":null,"abstract":{"de":"Osteoarthritis (OA) is the most prevalent disorder of the musculoskeletal system and has a very high socioeconomic impact. Current treatments for Osteoarthritis are only symptomatic, because they do not act on the causes of Arthritis and do not stop the progression of the disease. This study is designed to investigate the effect of Resveratrol, Quercetin, and Selenium on special inflammation enzymes and factors in human synovial fluid. \r\nEspecially Resveratrol is known as a potent specific inhibitor of inflammation, but its potency has not been tested on human synovial fluid. If the protective potency on Osteoarthritis is similar to the results of animal experiments, it would be an enormous effort. Previous studies indicate that elevated levels of matrix metalloproteinases (MMPs) and receptor activator of nuclear factor NFkB ligand (RANKL) play an important role in cartilage degeneration in OA Rheumatic Arthritis (RA) and Psoriatic Arthritis (PsA) [1, 2]. \r\nThis study should be undertaken to define a possible influence of Resveratrol compared to other antioxidants like Quercetin and Selenium on synovial fluid and these factors. A close interaction between clinicians and basic scientists is necessary because of the combination of analytical, functional and molecular methods. \r\n","en":"Osteoarthritis (OA) is the most prevalent disorder of the musculoskeletal system and has a very high socioeconomic impact. Current treatments for Osteoarthritis are only symptomatic, because they do not act on the causes of Arthritis and do not stop the progression of the disease. This study is designed to investigate the effect of Resveratrol, Quercetin, and Selenium on special inflammation enzymes and factors in human synovial fluid. \r\nEspecially Resveratrol is known as a potent specific inhibitor of inflammation, but its potency has not been tested on human synovial fluid. If the protective potency on Osteoarthritis is similar to the results of animal experiments, it would be an enormous effort. Previous studies indicate that elevated levels of matrix metalloproteinases (MMPs) and receptor activator of nuclear factor NFkB ligand (RANKL) play an important role in cartilage degeneration in OA Rheumatic Arthritis (RA) and Psoriatic Arthritis (PsA) [1, 2]. \r\nThis study should be undertaken to define a possible influence of Resveratrol compared to other antioxidants like Quercetin and Selenium on synovial fluid and these factors. A close interaction between clinicians and basic scientists is necessary because of the combination of analytical, functional and molecular methods. \r\n"},"begin_planned":"2009-01-01T01:00:00+01:00","begin_effective":"2009-01-01T01:00:00+01:00","end_planned":"2009-12-31T01:00:00+01:00","end_effective":"2009-12-31T01:00:00+01:00","assignment":"2009-01-15T11:27:46+01:00","program":null,"subprogram":null,"organization":14052,"category":10,"type":10,"partner_function":4,"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":["1721-50696-12","1721-57343-12","1721-50826-12"]}]}