List projects.

Fields

id (integer)

Primary key.

Expansions

To activate relation expansion add the desired fields as a comma separated list to the expand query parameter like this:

?expand=<field>,<field>,<field>,...

The following relational fields can be expanded:

  • organization
  • category
  • type
  • partner_function
  • manager
  • contact
  • status
  • grant
  • research
  • event
  • study
  • language
  • program
  • funders

Filters

To filter for exact value matches:

?<fieldname>=<value>

Possible exact filters:

  • organization
  • category
  • manager
  • contact
  • status
  • grant
  • research
  • study
  • language
  • funders
  • program

For advanced filtering use lookups:

?<fieldname>__<lookup>=<value>

All fields with advanced lookups can also be used for exact value matches as described above.

Possible advanced lookups:

  • begin_planned: gt, gte, lt, lte
  • begin_effective: gt, gte, lt, lte
  • end_planned: gt, gte, lt, lte
  • end_effective: gt, gte, lt, lte
GET /v1/research/project/?format=api&offset=2280&ordering=begin_planned
HTTP 200 OK
  Allow: GET, HEAD, OPTIONS
  Content-Type: application/json
  Vary: Accept
  
  {
    "count": 2323,
    "next": "https://api-test.medunigraz.at/v1/research/project/?format=api&limit=20&offset=2300&ordering=begin_planned",
    "previous": "https://api-test.medunigraz.at/v1/research/project/?format=api&limit=20&offset=2260&ordering=begin_planned",
    "results": [
        {
            "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": 7,
            "title": {
                "de": "Adenokarzinomentwicklung in der CCAM",
                "en": "Adenokarzinomentwicklung in der CCAM"
            },
            "short": "Adenokarzinomentwicklung in ",
            "url": null,
            "abstract": {
                "de": "Adenokarzinomentwicklung in der CCAM.",
                "en": "Adenokarzinomentwicklung in der CCAM."
            },
            "begin_planned": null,
            "begin_effective": "2003-06-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2004-01-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 81,
            "subprogram": null,
            "organization": 14020,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51523,
            "contact": 51523,
            "status": 2,
            "research": null,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                52
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "7-51523-10"
            ]
        },
        {
            "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": 116,
            "title": {
                "de": "Psychosomatik in Österreich",
                "en": "Psychosomatik in Österreich"
            },
            "short": "Psychosomatik in Österreich",
            "url": null,
            "abstract": {
                "de": "Für die zeitgemäße Organisation der Psychosomatik in Österreich wurde ein universitärer Fachbeirat gegründet, der in Abstimmung mit dem BM f.Soz.Sicherheit und Generationen wissenschaftliche Theorien zu prüfen und Qualitätsstandards für die Lehre, die Forschung und Krankenversorgung zu entwickeln hat.   \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": "Für die zeitgemäße Organisation der Psychosomatik in Österreich wurde ein universitärer Fachbeirat gegründet, der in Abstimmung mit dem BM f.Soz.Sicherheit und Generationen wissenschaftliche Theorien zu prüfen und Qualitätsstandards für die Lehre, die Forschung und Krankenversorgung zu entwickeln hat.   "
            },
            "begin_planned": null,
            "begin_effective": "2001-09-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2005-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 29447,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": null,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                102
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 319,
            "title": {
                "de": "Etiopathogenesis of Extranodal Marginal Zone B Cell Lymphoma of Mucosa Associated Lymphoid Tissue (=MALT lymphoma)",
                "en": "Etiopathogenesis of Extranodal Marginal Zone B Cell Lymphoma of Mucosa Associated Lymphoid Tissue (=MALT lymphoma)"
            },
            "short": "MALT lymphoma",
            "url": null,
            "abstract": {
                "de": "The four main questions this project will deal with are:\r\n*Are Lymphoma aberrantly somatic hypermutated?\r\n*Are Chlamydiae Species involved in thepathogenesis of nongastric MALT Lymphoma?\r\n*Is the novel translocation t(14;18)(q32;q21) involving the IGH and the MALT 1 gene a positive predictor for advanced disease and clinical outcome in nongastric MALT Lymphoma?\r\n*Are differentially expressed chemokine receptors responsible for the homing properties of nongastric MALT llmphoma?",
                "en": "The four main questions this project will deal with are:\r\n*Are Lymphoma aberrantly somatic hypermutated?\r\n*Are Chlamydiae Species involved in thepathogenesis of nongastric MALT Lymphoma?\r\n*Is the novel translocation t(14;18)(q32;q21) involving the IGH and the MALT 1 gene a positive predictor for advanced disease and clinical outcome in nongastric MALT Lymphoma?\r\n*Are differentially expressed chemokine receptors responsible for the homing properties of nongastric MALT llmphoma?"
            },
            "begin_planned": null,
            "begin_effective": "2004-10-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2005-10-01T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14046,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51930,
            "contact": 51930,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                52
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "319-50514-12",
                "319-50997-12",
                "319-50871-12",
                "319-51930-10"
            ]
        },
        {
            "id": 216,
            "title": {
                "de": "Nachweis und Charakterisierung epithelialer Tumorzellen im peripheren Blut und anderen Körperflüssigkeiten",
                "en": "Dedection, characterization and prognostic signifcance of circulating epithelial cells in peripherial blood and other body fluid specimens from patients with metastatic solid tumors"
            },
            "short": "Epitheliale Tumorz. im peripheren Blut",
            "url": null,
            "abstract": {
                "de": "Trotz wesentlicher Fortschritte in der Behandlung von Patienten mit Tumorerkrankungen, sterben weiterhin Patienten an dieser Erkrankung. Nicht der Primärtumor selbst gilt als Hauptursache für tumor-bedingte Mortalität, sondern die Entwicklung von Rezidiven und Metastasen. Eine kleine Anzahl von Tumorzellen (disseminierte Tumorzellen, DTC) breiten sich vom Primärtumor über den Blutkreislauf oder das Lymphsystem aus. Der Nachweis dieser minimalen Tumorresiduen (MRD) ist mit konventionellen bildgebenden Verfahren nicht möglich.\r\nDie Früherkennung dieser DTC ist bei Tumorpatienten hinsichtlich des Krankheitsverlaufes und der Therapie von besonderer Bedeutung.\r\nZiel dieses Projektes ist es, DTC im peripheren Blut und anderen Körperflüssigkeiten von Patienten mit soliden Tumoren mit einer möglichst sensitiven Methode nachzuweisen und zu charakterisieren. Als Techniken kommen neue molekularbiologische Verfahren wie die Real-time PCR und eine chromogene in situ Hybridisierung zum Einsatz. Die Ergebnisse werden mit der Standardtechnik der Zellanreicherung und anschließender Immunzytologie verglichen. Nachweis und Charakterisierung derartiger DTC könnte dazu beitragen, tumorbiologische Vorgänge besser zu verstehen und Therapieverfahren individueller und effektiver zu gestalten, sowie ein Monitoring der therapeutischen Wirksamkeit neuartiger Therapieformen zu ermöglichen.\r\n",
                "en": "Despite significant advances in treatment of patients with cancer, patients continue to die from this disease. The main cause for cancer-related death is no longer the primary tumor, but the development of recurrence and metastases. Small numbers of tumor cells are released from the primary tumor (disseminated tumor cells, DTC) and spread into the bloodstream or lymphatic vessels. This type of minimal residual disease (MRD) of solid tumors cannot be detected by conventional imaging. \r\nTherefore, early detection of DTC in patients with solid tumors is important for the evaluation of the tumor process and for monitoring therapy response.\r\nThe aim of this study is the detection and characterization of DTC in peripheral blood or other body fluids in patients with solid tumors by using sensitive techniques. Techniques to be applied are Real-time PCR and chromogenic in situ hybridization. The results will be compared with a standard enrichment technique, followed by immunocytochemical detection.\r\nDetection and characterization of these DTC might help to better understand tumor biology, to improve patient therapy and to identify new therapeutic targets.\r\n"
            },
            "begin_planned": null,
            "begin_effective": "2003-12-13T01:00:00+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": 14085,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 50563,
            "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": [
                "216-50229-12",
                "216-50539-12",
                "216-50563-10",
                "216-51692-12",
                "216-59188-12"
            ]
        },
        {
            "id": 292,
            "title": {
                "de": "AT-0042 Image Processing, Information Engineering & Interdisciplinary Knowledge Exchange",
                "en": "AT-0042 Image Processing, Information Engineering & Interdisciplinary Knowledge Exchange"
            },
            "short": "CEEPUS-Netzwerk AT-0042",
            "url": null,
            "abstract": {
                "de": "Virtual Endoscopy of Airways: \r\nApplying methods of virtual reality  to Spiral Computed Tomography investigations of airways, views can be generated similar to endoscopy . These views can be used to simulate endoscopic procedures for training of residents or for planing therapeutic interventions. Moreover, the virtual camera can be sent to positions, where a real endoscope fails.\r\n\r\nVirtual Dissection of the Colon: \r\nBesides endoscopy different imaging strategies are available for detection of colonic polyps. The medical goals is to detect those polyps as early as possible in order to prevent the development of a colonic cancer. Spiral Computed Tomography (S-CT) and Magnetic Resonance Tomography (MRT), augmented by virtual reality, have already demonstrated their effectivness in the detection of colonic polyps.\r\n\r\nComputer Aided Diagnosis of Breast Cancer:\r\nA system was programmed to support the reporting radiologist as a \"never tied second reader\" by using algorithms of artificial neural nets and image processing. In addition, a graphical user interface was developed to display the results of the \"never tired second reader\" to the radiologist in a convenient way. \r\n\r\n",
                "en": "Virtual Endoscopy of Airways: \r\nApplying methods of virtual reality  to Spiral Computed Tomography investigations of airways, views can be generated similar to endoscopy . These views can be used to simulate endoscopic procedures for training of residents or for planing therapeutic interventions. Moreover, the virtual camera can be sent to positions, where a real endoscope fails.\r\n\r\nVirtual Dissection of the Colon: \r\nBesides endoscopy different imaging strategies are available for detection of colonic polyps. The medical goals is to detect those polyps as early as possible in order to prevent the development of a colonic cancer. Spiral Computed Tomography (S-CT) and Magnetic Resonance Tomography (MRT), augmented by virtual reality, have already demonstrated their effectivness in the detection of colonic polyps.\r\n\r\nComputer Aided Diagnosis of Breast Cancer:\r\nA system was programmed to support the reporting radiologist as a \"never tied second reader\" by using algorithms of artificial neural nets and image processing. In addition, a graphical user interface was developed to display the results of the \"never tired second reader\" to the radiologist in a convenient way. \r\n\r\n"
            },
            "begin_planned": null,
            "begin_effective": "1997-01-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2050-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14106,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51913,
            "contact": 51913,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "292-51913-10"
            ]
        },
        {
            "id": 12,
            "title": {
                "de": "Schulsupport - wissenschaftlich begleitetes LehrerInnen-Training zum besseren Umgang mit Stress in der Schule",
                "en": "Schulsupport - wissenschaftlich begleitetes LehrerInnen-Training zum besseren Umgang mit Stress in der Schule"
            },
            "short": "Schulsupport",
            "url": null,
            "abstract": {
                "de": "Schulsupport - wissenschaftlich begleitetes LehrerInnen-Training zum besseren Umgang mit Stress in der Schule.",
                "en": "Schulsupport - wissenschaftlich begleitetes LehrerInnen-Training zum besseren Umgang mit Stress in der Schule."
            },
            "begin_planned": null,
            "begin_effective": "2003-02-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2005-02-28T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 75,
            "subprogram": null,
            "organization": 14010,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51671,
            "contact": 51671,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                55
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "12-51671-10"
            ]
        },
        {
            "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": 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": 203,
            "title": {
                "de": "Prävalenz von IGT und DM-2 in Graz",
                "en": "Prävalenz von IGT und DM-2 in Graz"
            },
            "short": "Prävalenz von IGT und DM-2",
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "2002-01-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2005-12-31T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14046,
            "category": 10,
            "type": 10,
            "partner_function": 1,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": null,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 438,
            "title": {
                "de": "The role of proteoglycans in the cellular metabolism of beta-amyloid peptides",
                "en": "The role of proteoglycans in the cellular metabolism of beta-amyloid peptides"
            },
            "short": "Beta-Amyloid Peptides",
            "url": null,
            "abstract": {
                "de": "The deposition of amyloid beta peptide (ABeta) in amyloid plaques is among the defining features of Alzheimer's Disease. Accumulation of Aâ may occur as a consequence of enhanced production or altered catabolism of ABeta. Recently, significant progress has been achieved regarding the determination of the mechnisms leading to the generation of ABeta. In contrast, virtually no information has been available as to whether and how ABeta is cleared by cells. We have shown that ABeta peptides are ligands of the LDL receptor-related protein (LRP) and/or heparan sulfate proteoglycans (HSPG), both of which are also involved in the clearance of apolipoprotein E, a major cholesterol transportin protein  in the central nervous system. Prolonged exposure of ABeta to apo E containing lipoproteins leads to the formation of ABeta/lipoprotein complexes. These complexes are avidly internalised by cells, but ar resistant to lysosomal degradation. HSPGs seem to be involved in this process. It will be the specific aims of the proposed project a) to identify the cellular mechanism responsible for ABeta internalisation, b) to elucidate the roles of proteoglycans and of LRP in the uptake of AB and c) to follow the subcellular trafficking of ABeta internalised by these cell surface molecules. ",
                "en": " The deposition of amyloid beta peptide (ABeta) in amyloid plaques is among the defining features of Alzheimer's Disease. Accumulation of Aâ may occur as a consequence of enhanced production or altered catabolism of ABeta. Recently, significant progress has been achieved regarding the determination of the mechnisms leading to the generation of ABeta. In contrast, virtually no information has been available as to whether and how ABeta is cleared by cells. We have shown that ABeta peptides are ligands of the LDL receptor-related protein (LRP) and/or heparan sulfate proteoglycans (HSPG), both of which are also involved in the clearance of apolipoprotein E, a major cholesterol transportin protein  in the central nervous system. Prolonged exposure of ABeta to apo E containing lipoproteins leads to the formation of ABeta/lipoprotein complexes. These complexes are avidly internalised by cells, but ar resistant to lysosomal degradation. HSPGs seem to be involved in this process. It will be the specific aims of the proposed project a) to identify the cellular mechanism responsible for ABeta internalisation, b) to elucidate the roles of proteoglycans and of LRP in the uptake of AB and c) to follow the subcellular trafficking of ABeta internalised by these cell surface molecules. "
            },
            "begin_planned": null,
            "begin_effective": "2005-04-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2007-03-31T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": null,
            "subprogram": null,
            "organization": 14028,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51906,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                35
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "438-51906-10"
            ]
        },
        {
            "id": 11,
            "title": {
                "de": "GOLD - Genomics of Lipid-associated Disorders' im Rahmen von 'GEN-AU Genomforschung in Österreich' des bm:bwk",
                "en": "GOLD - Genomics of Lipid-associated Disorders' im Rahmen von 'GEN-AU Genomforschung in Österreich' des bm:bwk"
            },
            "short": "GOLD (GEN-AU)",
            "url": null,
            "abstract": {
                "de": "The goal of this cluster-project is to discover novel genes, processes and pathways that regulate lipid homeostasis in humans and mice. Additionally, the analyses includes yeast as a prototype model organism in lipid metabolism.\r\nProject Description: http://gold.uni-graz.at/project_description.html.\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": "The goal of this cluster-project is to discover novel genes, processes and pathways that regulate lipid homeostasis in humans and mice. Additionally, the analyses includes yeast as a prototype model organism in lipid metabolism.\r\nProject Description: http://gold.uni-graz.at/project_description.html.\t"
            },
            "begin_planned": null,
            "begin_effective": "2002-11-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2005-11-30T01:00:00+01:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 73,
            "subprogram": null,
            "organization": 14013,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51669,
            "contact": 51669,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                152
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "11-51669-10"
            ]
        },
        {
            "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": 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": 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": 455,
            "title": {
                "de": "SonEnvir",
                "en": "SonEnvir"
            },
            "short": "SonEnvir",
            "url": null,
            "abstract": {
                "de": "SonEnvir ist ein Projekt mit dem Ziel, Sonifikation und ihre Anwendungen in verschiedenen wissenschaftlichen Disziplinen zu erforschen. Viele wissenschaftliche Forschungsgebiete arbeiten mit komplexen, multidimensionalen Daten. Die üblichen Verfahren, innere Strukturen dieser Daten darzustellen, sind Visualisierung und statistische Analyse. Beide Ansätze sind anerkannt, haben aber bekannte Nachteile: Visualisierung ist duch die perzeptuellen Schwächen des Sehsinns begrenzt (schlechte zeitliche Auflösung, nur wenige Dimenstionen darstellbar), und Statistik duch das mathematische Verständnis des Forschers, was die Komplexität der Verfahren betrifft - und deren Bedeutung für die zu analysierenden Daten. Sonifikation ist die Repräsentation und Analyse von Daten durch Klang und bietet eine zukunfswiesende Alternative und Ergänzung vom visuellen Modus. Während in den letzten 20 Jahren Sonifikation erfolgreich auf konkrete Einzelprobleme angewandt wurde, stellt SonEnvir den ersten generischen Ansatz dar, Sonifikation als fachübergreifendes Analyse- und Darstellungsverfahren zu etablieren. SonEnvir berücksichtigt erstmals alle relevanten Gebiete gleichermaßen:\r\n\r\n- Interdisziplinarität durch gleiche Gewichtung zwischen KlangspezialistInnen und ZielswissenschafterInnen\r\n- Verschiedene Zielwissenschaften mit sehr unterschiedlichen Datenstrukturen (Medizin/Neurologie, Teilchenphysik, Sozialwissenschaften, Nichtlineare Systeme).\r\n- Gestaltung von perzeptuell hochdifferenzierbaren Verfahren zur Klangsynthese und räumlichen wiedergabe in §D\r\n- Programmierung von praktisch nutzbarer Software, mit der WissenschafterInnen selbständig arbeiten können, und\r\n- Realisierte Anwendungen von Sonifikation in aktuellen Fragestellungen der Zielwissenschaften.\r\n",
                "en": "SonEnvir ist ein Projekt mit dem Ziel, Sonifikation und ihre Anwendungen in verschiedenen wissenschaftlichen Disziplinen zu erforschen. Viele wissenschaftliche Forschungsgebiete arbeiten mit komplexen, multidimensionalen Daten. Die üblichen Verfahren, innere Strukturen dieser Daten darzustellen, sind Visualisierung und statistische Analyse. Beide Ansätze sind anerkannt, haben aber bekannte Nachteile: Visualisierung ist duch die perzeptuellen Schwächen des Sehsinns begrenzt (schlechte zeitliche Auflösung, nur wenige Dimenstionen darstellbar), und Statistik duch das mathematische Verständnis des Forschers, was die Komplexität der Verfahren betrifft - und deren Bedeutung für die zu analysierenden Daten. Sonifikation ist die Repräsentation und Analyse von Daten durch Klang und bietet eine zukunfswiesende Alternative und Ergänzung vom visuellen Modus. Während in den letzten 20 Jahren Sonifikation erfolgreich auf konkrete Einzelprobleme angewandt wurde, stellt SonEnvir den ersten generischen Ansatz dar, Sonifikation als fachübergreifendes Analyse- und Darstellungsverfahren zu etablieren. SonEnvir berücksichtigt erstmals alle relevanten Gebiete gleichermaßen:\r\n\r\n- Interdisziplinarität durch gleiche Gewichtung zwischen KlangspezialistInnen und ZielswissenschafterInnen\r\n- Verschiedene Zielwissenschaften mit sehr unterschiedlichen Datenstrukturen (Medizin/Neurologie, Teilchenphysik, Sozialwissenschaften, Nichtlineare Systeme).\r\n- Gestaltung von perzeptuell hochdifferenzierbaren Verfahren zur Klangsynthese und räumlichen wiedergabe in §D\r\n- Programmierung von praktisch nutzbarer Software, mit der WissenschafterInnen selbständig arbeiten können, und\r\n- Realisierte Anwendungen von Sonifikation in aktuellen Fragestellungen der Zielwissenschaften.\r\n"
            },
            "begin_planned": null,
            "begin_effective": "2005-02-01T01:00:00+01:00",
            "end_planned": null,
            "end_effective": "2007-03-31T02:00:00+02:00",
            "assignment": "2005-10-26T02:00:00+02:00",
            "program": 75,
            "subprogram": null,
            "organization": 14051,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": null,
            "contact": null,
            "status": 2,
            "research": 2,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                55
            ],
            "funder_projectcode": null,
            "ethics_committee": null,
            "edudract_number": null,
            "persons": []
        },
        {
            "id": 1374,
            "title": {
                "de": "SFB LIPOTOX: Teilprojekt des Koordinationsprojekts (Pathophysiologischer Teil)",
                "en": "SFB LIPOTOX: Teilprojekt des Koordinationsprojekts (Pathophysiologischer Teil)"
            },
            "short": "SFB_LIPOTOX_Höfler",
            "url": null,
            "abstract": {
                "de": "The goal of the SFB-LIPOTOX is to elucidate the molecular and cellular\r\nprocesses and pathways behind the conversion of physiological substrates,\r\nsuch as FA and lipids into noxious compounds, their effects on cell and\r\norgan function and dysfunction, and their contribution to various forms of\r\ncell death. \r\nThe conversion of FA and lipids into lipotoxic substances occurs via two\r\nprocesses: First, substrate overload, as defined by the excessive cellular\r\nuptake of FA and lipids that exceeds the oxidative capacity of target cells.\r\nSecond, the chemical conversion and modification of FA and lipid substrates\r\ngenerating biologically active signaling molecules of high toxic potential,\r\ne.g. ceramide, lysophospholipids, lipid oxidation products, or ROS. Within\r\nthe SFB-LIPOTOX we propose to identify presently unknown lipotoxic compounds\r\nby a mass spectrometry (MS) based lipidomic approach, to study the molecular\r\nmechanisms of their biosynthesis and inactivation, and to elucidate the resulting biological responses in genetically modified model organisms. \r\nWe will:\r\n*identify and characterize enzymatic processes that generate or catabolize signalling lipids;\r\n*study the mechanisms by which FA and lipotoxic lipids affect cell signalling;\r\n*examine lipid modification processes and their role in lipotoxicity;\r\n*characterize the involvement of genes and their protein products in lipotoxic pathways;\r\n*uncover lipotoxic effects on cell and organ function and lipid-induced cell death;\r\nrelate our findings in model organisms to the pathogenesis of human diseases, such as insulin resistance, atherosclerosis, and neurodegenerative disorders.\r\n\r\nTo achieve these goals, it is necessary to combine a broad spectrum of\r\nscientific and methodological expertise from various fields in biomedicine:\r\nlipid biology, signal transduction, cell organelle function, and apoptosis\r\nresearch. Accordingly, we assembled an interdisciplinary research consortium\r\non the basis of scientific excellence, plus a keen interest in, and a strong\r\ncommitment to the goals of the SFB-LIPOTOX. All principal investigators have\r\na strong scientific track record, contribute important biological model\r\nsystems required for the project, and possess the technical expertise\r\nrequired for the proposed research. The combined expertise of the consortium\r\nmembers will provide a unique opportunity to investigate lipotoxic pathways\r\non a large scale across species, tissues, and conditions.\r\nWithin the initial funding period of the SFB-LIPOTOX (4 years) we expect to\r\ndiscover  unknown lipid species involved in signaling, enzymes and metabolic\r\nprocesses that generate or inactivate (degrade) signalling lipids, and the\r\nconsequences of lipid signalling on cell dysfunction and death. Long term\r\ngoals beyond the initial project period include the elucidation of the\r\ndetailed physiological function of our discoveries, their contribution to\r\nlipid and energy metabolism, and their potential application in the\r\ndiagnosis and treatment of human disease.\r\n",
                "en": "The goal of the SFB-LIPOTOX is to elucidate the molecular and cellular\r\nprocesses and pathways behind the conversion of physiological substrates,\r\nsuch as FA and lipids into noxious compounds, their effects on cell and\r\norgan function and dysfunction, and their contribution to various forms of\r\ncell death. \r\nThe conversion of FA and lipids into lipotoxic substances occurs via two\r\nprocesses: First, substrate overload, as defined by the excessive cellular\r\nuptake of FA and lipids that exceeds the oxidative capacity of target cells.\r\nSecond, the chemical conversion and modification of FA and lipid substrates\r\ngenerating biologically active signaling molecules of high toxic potential,\r\ne.g. ceramide, lysophospholipids, lipid oxidation products, or ROS. Within\r\nthe SFB-LIPOTOX we propose to identify presently unknown lipotoxic compounds\r\nby a mass spectrometry (MS) based lipidomic approach, to study the molecular\r\nmechanisms of their biosynthesis and inactivation, and to elucidate the resulting biological responses in genetically modified model organisms. \r\nWe will:\r\n*identify and characterize enzymatic processes that generate or catabolize signalling lipids;\r\n*study the mechanisms by which FA and lipotoxic lipids affect cell signalling;\r\n*examine lipid modification processes and their role in lipotoxicity;\r\n*characterize the involvement of genes and their protein products in lipotoxic pathways;\r\n*uncover lipotoxic effects on cell and organ function and lipid-induced cell death;\r\nrelate our findings in model organisms to the pathogenesis of human diseases, such as insulin resistance, atherosclerosis, and neurodegenerative disorders.\r\n\r\nTo achieve these goals, it is necessary to combine a broad spectrum of\r\nscientific and methodological expertise from various fields in biomedicine:\r\nlipid biology, signal transduction, cell organelle function, and apoptosis\r\nresearch. Accordingly, we assembled an interdisciplinary research consortium\r\non the basis of scientific excellence, plus a keen interest in, and a strong\r\ncommitment to the goals of the SFB-LIPOTOX. All principal investigators have\r\na strong scientific track record, contribute important biological model\r\nsystems required for the project, and possess the technical expertise\r\nrequired for the proposed research. The combined expertise of the consortium\r\nmembers will provide a unique opportunity to investigate lipotoxic pathways\r\non a large scale across species, tissues, and conditions.\r\nWithin the initial funding period of the SFB-LIPOTOX (4 years) we expect to\r\ndiscover  unknown lipid species involved in signaling, enzymes and metabolic\r\nprocesses that generate or inactivate (degrade) signalling lipids, and the\r\nconsequences of lipid signalling on cell dysfunction and death. Long term\r\ngoals beyond the initial project period include the elucidation of the\r\ndetailed physiological function of our discoveries, their contribution to\r\nlipid and energy metabolism, and their potential application in the\r\ndiagnosis and treatment of human disease.\r\n"
            },
            "begin_planned": null,
            "begin_effective": "2007-04-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "2011-03-31T02:00:00+02:00",
            "assignment": "2007-10-04T17:55:13+02:00",
            "program": 67,
            "subprogram": null,
            "organization": 14020,
            "category": 10,
            "type": 10,
            "partner_function": 2,
            "manager": 51691,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
            "study": null,
            "language": null,
            "funders": [
                9
            ],
            "funder_projectcode": "F30",
            "ethics_committee": null,
            "edudract_number": null,
            "persons": [
                "1374-51691-10"
            ]
        },
        {
            "id": 705,
            "title": {
                "de": "Humane Herzmuskelzellen",
                "en": "Humane Herzmuskelzellen"
            },
            "short": "P 11131",
            "url": null,
            "abstract": {
                "de": null,
                "en": null
            },
            "begin_planned": null,
            "begin_effective": "1995-08-01T02:00:00+02:00",
            "end_planned": null,
            "end_effective": "1998-11-11T01:00:00+01:00",
            "assignment": null,
            "program": null,
            "subprogram": null,
            "organization": 14011,
            "category": 10,
            "type": 10,
            "partner_function": 4,
            "manager": 51681,
            "contact": null,
            "status": 2,
            "research": 1,
            "grant": 10,
            "event": null,
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