{"count":2322,"next":"https://api-test.medunigraz.at/v1/research/project/?format=json&limit=20&offset=2320&ordering=end_planned","previous":"https://api-test.medunigraz.at/v1/research/project/?format=json&limit=20&offset=2280&ordering=end_planned","results":[{"id":326,"title":{"de":"Genetic analysis and functional studies of the RAB7, the SPTLC1 and HSN2 genes in patients with diabetic neuropathy","en":"Genetic analysis and functional studies of the RAB7, the SPTLC1 and HSN2 genes in patients with diabetic neuropathy"},"short":"Genes in diabetic neuropathy","url":null,"abstract":{"de":"Diabetic neuropathy is a frequent and challenging complication of diabetes mellitus type I and type II with an estimated prevalence up to 60% or even higher. Patients initially often complain of paresthesia, pain and dysthesia.\r\nChronic neuropathic foot ulceration is a severe and feared complication of diabetic neuropathy. It has to be dustinguished from necrosis and gangrene due to ischemia.\r\nHereditary neuropathies (HSN) are rare disorders of the peripheral nerves which are characterized by familial occurence of prominent sensory disturbances in the lower limbs, variable motor weakness and waisting, foot deformity and autonomic features. Very recently, molecular genetic studies have shown, that mutations in two genes, i.e. serine palmitoyltransferase long chain base subunit-1 (SPTLC1) and the small GTPase late endosomal protein RAB7 are responsible for two forms of ulcero-mutilating neuropathies which are genetically subclassified as HSN type 1 and CMT 2B, respectively.\r\nHioever, the mechanism how mutations in SPTLC2 and RAB7 lead to the motor and sensory neuropathy are still unknown. Also, no studies have been undertaken so far to investigate whether these two genes and their products do also play a role in diabetic neuropathies.","en":"Diabetic neuropathy is a frequent and challenging complication of diabetes mellitus type I and type II with an estimated prevalence up to 60% or even higher. Patients initially often complain of paresthesia, pain and dysthesia.\r\nChronic neuropathic foot ulceration is a severe and feared complication of diabetic neuropathy. It has to be dustinguished from necrosis and gangrene due to ischemia.\r\nHereditary neuropathies (HSN) are rare disorders of the peripheral nerves which are characterized by familial occurence of prominent sensory disturbances in the lower limbs, variable motor weakness and waisting, foot deformity and autonomic features. Very recently, molecular genetic studies have shown, that mutations in two genes, i.e. serine palmitoyltransferase long chain base subunit-1 (SPTLC1) and the small GTPase late endosomal protein RAB7 are responsible for two forms of ulcero-mutilating neuropathies which are genetically subclassified as HSN type 1 and CMT 2B, respectively.\r\nHioever, the mechanism how mutations in SPTLC2 and RAB7 lead to the motor and sensory neuropathy are still unknown. Also, no studies have been undertaken so far to investigate whether these two genes and their products do also play a role in diabetic neuropathies."},"begin_planned":null,"begin_effective":"2005-04-15T02:00:00+02:00","end_planned":null,"end_effective":"2006-04-15T02:00:00+02:00","assignment":"2005-10-26T02:00:00+02:00","program":null,"subprogram":null,"organization":14046,"category":10,"type":10,"partner_function":4,"manager":null,"contact":null,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[151],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["326-51831-12"]},{"id":295,"title":{"de":"Hereditäre spastische Paraparäse in Österreich","en":"Hereditäre spastische Paraparäse in Österreich"},"short":"Hereditäre spastische Paraparäse","url":null,"abstract":{"de":"Hereditäre spastische Paraparesen (HSP) sind eine heterogene Gruppe neurodegenerativer Erkrankungen, die mit einer langsam progredienten Spastizität der unteren Extremitäten einhergehen. Die Prävalenz wird mit 2.0 - 9.6 / 100000 geschätzt. Je nach dem klinischen Verlauf unterscheidet man zwei Hauptgruppen, die einfachen Formen, die lediglich eine Spastizität aufweisen und die komplizierten Formen, bei denen es zusätzlich zum Auftreten anderer neurologischer und nicht-neurologischer Ausfallssymptome kommt. \r\nJüngste molekulargenetische Untersuchungen haben gezeigt, dass sowohl die einfachen als auch die komplizierten Formen der HSP genetisch sehr heterogen sind. Bisher kennt man mindestens 15 genetische Subtypen, von denen sieben für autosomal dominant vererbte einfache Formen verantwortlich sind. Für die häufigste, am Chromosom 2p vererbte Form, wurde kürzlich das Gen (Spastin) identifiziert.\r\nIn diesem Forschungsprojekt planen wir klinische, elektrophysiologische, MRI und molekulargenetische Untersuchungen bei HSP-Patienten und -Familien aus Südost-Österreich. Im ersten Schritt wird ein Mutationsscreening des Spastin Gens durchgeführt werden. Danach werden in jenen Familien, in welchen Mutationen innerhalb dieses Gens ausgeschlossen wurden, Koppelungsstudien für bereits bekannte Genorte durchgeführt. In jenen Fällen, in denen dann Hinweise für eine Koppelung bestehen, werden Haplotypen konstruiert, um die kritische Region bei Vorhandensein von Rekombinationen zu verkleinern.\r\nUnsere Studie ist die erste Initiative zur Durchführung molekulargenetischer Untersuchungen bei HSP in Österreich und bezweckt die Erfassung der Frequenz verschiedener genetischer HSP-Subtypen in Südost-Österreich. Sie erlaubt weiters Phänotyp-Genotyp-Studien zur Abschätzung der Expressivität der Erkrankung. Die Möglichkeit der genetischen Testung von Patienten mit HSP ist von grosser Bedeutung für Patienten, Kliniker und Genetiker und wird in nächster Zukunft den diagnostischen Goldstandard dieser Krankheit darstellen. Die genaue Kenntnis eines die Krankheit auslösenden Gendefektes erleichtert die Diagnose, Differentialdiagnose und Ausschlussdiagnose bei sporadischen Fällen, ermöglicht eine gezielte genetische Beratung und eine pränatale Diagnose in schweren Fällen. ","en":"Hereditäre spastische Paraparesen (HSP) sind eine heterogene Gruppe neurodegenerativer Erkrankungen, die mit einer langsam progredienten Spastizität der unteren Extremitäten einhergehen. Die Prävalenz wird mit 2.0 - 9.6 / 100000 geschätzt. Je nach dem klinischen Verlauf unterscheidet man zwei Hauptgruppen, die einfachen Formen, die lediglich eine Spastizität aufweisen und die komplizierten Formen, bei denen es zusätzlich zum Auftreten anderer neurologischer und nicht-neurologischer Ausfallssymptome kommt. \r\nJüngste molekulargenetische Untersuchungen haben gezeigt, dass sowohl die einfachen als auch die komplizierten Formen der HSP genetisch sehr heterogen sind. Bisher kennt man mindestens 15 genetische Subtypen, von denen sieben für autosomal dominant vererbte einfache Formen verantwortlich sind. Für die häufigste, am Chromosom 2p vererbte Form, wurde kürzlich das Gen (Spastin) identifiziert.\r\nIn diesem Forschungsprojekt planen wir klinische, elektrophysiologische, MRI und molekulargenetische Untersuchungen bei HSP-Patienten und -Familien aus Südost-Österreich. Im ersten Schritt wird ein Mutationsscreening des Spastin Gens durchgeführt werden. Danach werden in jenen Familien, in welchen Mutationen innerhalb dieses Gens ausgeschlossen wurden, Koppelungsstudien für bereits bekannte Genorte durchgeführt. In jenen Fällen, in denen dann Hinweise für eine Koppelung bestehen, werden Haplotypen konstruiert, um die kritische Region bei Vorhandensein von Rekombinationen zu verkleinern.\r\nUnsere Studie ist die erste Initiative zur Durchführung molekulargenetischer Untersuchungen bei HSP in Österreich und bezweckt die Erfassung der Frequenz verschiedener genetischer HSP-Subtypen in Südost-Österreich. Sie erlaubt weiters Phänotyp-Genotyp-Studien zur Abschätzung der Expressivität der Erkrankung. Die Möglichkeit der genetischen Testung von Patienten mit HSP ist von grosser Bedeutung für Patienten, Kliniker und Genetiker und wird in nächster Zukunft den diagnostischen Goldstandard dieser Krankheit darstellen. Die genaue Kenntnis eines die Krankheit auslösenden Gendefektes erleichtert die Diagnose, Differentialdiagnose und Ausschlussdiagnose bei sporadischen Fällen, ermöglicht eine gezielte genetische Beratung und eine pränatale Diagnose in schweren Fällen. "},"begin_planned":null,"begin_effective":"2004-11-01T01:00:00+01:00","end_planned":null,"end_effective":"2006-03-31T02:00:00+02:00","assignment":"2005-10-26T02:00:00+02:00","program":72,"subprogram":null,"organization":14046,"category":10,"type":10,"partner_function":4,"manager":null,"contact":null,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[9],"funder_projectcode":"P17494","ethics_committee":null,"edudract_number":null,"persons":[]},{"id":131,"title":{"de":"PERILIP: Influence of dietary fatty acids on the pathophysiology of intrauterine foetal growth and neonatal development","en":"PERILIP: Influence of dietary fatty acids on the pathophysiology of intrauterine foetal growth and neonatal development"},"short":"PERILIP","url":null,"abstract":{"de":"Perinatal nutrition is known to affect the health and development of the newborn child. A foetus that suffers from intra-uterine growth restriction (IUGR) is more likely to suffer from cardiac or diabtetic problems in later life, an effect known as \"metabolic programming\". Particular fatty acids are required for development but the optimum composition of dietary lipids remains controversial. The project will compare normal and IUGR pregnancies in terms of matter, neonatal and placenta fatty acid profiles. Placental transfer of fatty acids in vivo and the funcional ability of trophoblasts in vitro will be measured. The effects of dietary fats, on maternal endocrine status, oxidative stress, milk composition, placental function and on the development of IUGR and normal foetuses in utero (or ex utero in the case of the pretern infants fed intravenously) will be assessed. Human's studies will be complemented with appropriate rat and pig animal-models. The results will be used to formulate improved dietary recommendations for mothers throughout pregnancy and lactation. ","en":"Perinatal nutrition is known to affect the health and development of the newborn child. A foetus that suffers from intra-uterine growth restriction (IUGR) is more likely to suffer from cardiac or diabtetic problems in later life, an effect known as \"metabolic programming\". Particular fatty acids are required for development but the optimum composition of dietary lipids remains controversial. The project will compare normal and IUGR pregnancies in terms of matter, neonatal and placenta fatty acid profiles. Placental transfer of fatty acids in vivo and the funcional ability of trophoblasts in vitro will be measured. The effects of dietary fats, on maternal endocrine status, oxidative stress, milk composition, placental function and on the development of IUGR and normal foetuses in utero (or ex utero in the case of the pretern infants fed intravenously) will be assessed. Human's studies will be complemented with appropriate rat and pig animal-models. The results will be used to formulate improved dietary recommendations for mothers throughout pregnancy and lactation. "},"begin_planned":null,"begin_effective":"2002-04-01T02:00:00+02:00","end_planned":null,"end_effective":"2005-09-30T02:00:00+02:00","assignment":"2005-10-26T02:00:00+02:00","program":20,"subprogram":"Quality of Life","organization":14038,"category":10,"type":10,"partner_function":2,"manager":51632,"contact":51632,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[10],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["131-51632-10"]},{"id":1771,"title":{"de":"Rett Disorder: The Pre-Regression Period","en":"Rett Disorder: The Pre-Regression Period"},"short":"RETT DISORDER","url":null,"abstract":{"de":null,"en":null},"begin_planned":null,"begin_effective":"2007-01-01T01:00:00+01:00","end_planned":null,"end_effective":"2011-12-31T01:00:00+01:00","assignment":"2009-03-30T17:24:34+02:00","program":null,"subprogram":null,"organization":14010,"category":10,"type":10,"partner_function":4,"manager":null,"contact":null,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[530],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":[]},{"id":325,"title":{"de":"SURVIVE-ICU: Role of the Subcutaneous Adipose Tissue as a Secretory Organ in Critically III Patients","en":"SURVIVE-ICU: Role of the Subcutaneous Adipose Tissue as a Secretory Organ in Critically III Patients"},"short":"Survive-ICU","url":null,"abstract":{"de":"Systemic inflammation conributes to the development of multiple organ dysfunction, the major cause of mortality in patients with septic shock. Systemic inflammation is a consequence of activation of the innate immune system. Recent studies have indicated that adipose tissue plays a major role in the secretion of inflammatory factors which have been called adipocytokines or adipokines. Also, the increased production rate of cytokines such as IL-6 or TNF-alpha have been implicated in the pathogenesis of cardiovascular complications and insulin resistance. However, the metabloic role and possible consequences of adipose tissue as a secretory organ in critically ill patients has not been investigated to date. For the present proposal we will test the hypothesis, that adipose tissue is one of the links between systemic inflammation causing insulin resistance in criticalla ill patients and low-grade inflammation causing insulin resistance in obesity. To test this obesity we will charaterize adipose tissue as a secretory organ using interstitial fluid sampling techniques and advanced pepide analysisi in critically ill patients and healthy controls.","en":"Systemic inflammation conributes to the development of multiple organ dysfunction, the major cause of mortality in patients with septic shock. Systemic inflammation is a consequence of activation of the innate immune system. Recent studies have indicated that adipose tissue plays a major role in the secretion of inflammatory factors which have been called adipocytokines or adipokines. Also, the increased production rate of cytokines such as IL-6 or TNF-alpha have been implicated in the pathogenesis of cardiovascular complications and insulin resistance. However, the metabloic role and possible consequences of adipose tissue as a secretory organ in critically ill patients has not been investigated to date. For the present proposal we will test the hypothesis, that adipose tissue is one of the links between systemic inflammation causing insulin resistance in criticalla ill patients and low-grade inflammation causing insulin resistance in obesity. To test this obesity we will charaterize adipose tissue as a secretory organ using interstitial fluid sampling techniques and advanced pepide analysisi in critically ill patients and healthy controls."},"begin_planned":null,"begin_effective":"2005-11-01T01:00:00+01:00","end_planned":null,"end_effective":"2007-10-31T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":21,"subprogram":"Marie Curie International Incoming Fellowship","organization":14046,"category":10,"type":10,"partner_function":2,"manager":null,"contact":null,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[10],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":[]},{"id":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":332,"title":{"de":"Investigation of the Effect of Physiological Hyperinsulinemia on the Access of Macromolecules to Insulin Sensitive Tissues","en":"Investigation of the Effect of Physiological Hyperinsulinemia on the Access of Macromolecules to Insulin Sensitive Tissues"},"short":"Access to Insulin-Sensitive Tissues","url":null,"abstract":{"de":"In recent years a rapid growing body of work has demonstrated that insulin, besides its metabolic effects, also stimulates systemic blood flow and tissue perfusion to enhance the delivery of nutrients to insulin sensitive tissues. It has benn suggested that these effects of insulin might support insulins primary mechanism at the cellular level to stimulate glucose disposal. The objective of the present grant application is to evaluate the effects of physiological hyperinsulinemia on the perfusion of insulin sensitive tissues by direct measurement of the distribution kinetics of the extracellular marker inulin in interstitial fluid of healthy volunteers. Results from the proposed study will add new knowledge about the potential of insulin to stimulate glucose uptake and other metabolic processes via hemodynamic as opposed to purely biochemical processes. The submitted project is a prerequisite for further planned studies investigating the hemodynamic effect of insulin during disease states such as obesity and type II diabetes.","en":"In recent years a rapid growing body of work has demonstrated that insulin, besides its metabolic effects, also stimulates systemic blood flow and tissue perfusion to enhance the delivery of nutrients to insulin sensitive tissues. It has benn suggested that these effects of insulin might support insulins primary mechanism at the cellular level to stimulate glucose disposal. The objective of the present grant application is to evaluate the effects of physiological hyperinsulinemia on the perfusion of insulin sensitive tissues by direct measurement of the distribution kinetics of the extracellular marker inulin in interstitial fluid of healthy volunteers. Results from the proposed study will add new knowledge about the potential of insulin to stimulate glucose uptake and other metabolic processes via hemodynamic as opposed to purely biochemical processes. The submitted project is a prerequisite for further planned studies investigating the hemodynamic effect of insulin during disease states such as obesity and type II diabetes."},"begin_planned":null,"begin_effective":"2005-03-01T01:00:00+01:00","end_planned":null,"end_effective":"2006-10-31T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":null,"subprogram":null,"organization":14046,"category":10,"type":10,"partner_function":4,"manager":null,"contact":null,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[151],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":[]},{"id":199,"title":{"de":"CLINICIP: Closed Loop Insulin Infusion for Critically Ill Patients","en":"CLINICIP: Closed Loop Insulin Infusion for Critically Ill Patients"},"short":"CLINICIP","url":null,"abstract":{"de":"Im Projekt Clinicip wird ein intelligentes System für eine verbesserte Überwachung und Behandlung von kritisch kranken Menschen, die sich auf Intensivstationen befinden, entwickelt. Durch Bio-sensoren werden die Blutzuckerwerte und andere Stoffwechselparameter kontinuierlich gemessen. In einer frühen Projektphase soll damit ein anpassungsfähiger Kontrollalgorithmus eine beratende Funktion für das Krankenhauspersonal ausüben; d.h. dieses System soll als Entscheidungshilfe für Ärzte und Krankenschwestern zum Einsatz kommen. In weiterer Folge wird aufgrund der aktuellen Messergebnisse des Blutzuckerspiegels und der anderen Stoffwechselparameter automatisch die richtige Menge Insulin verabreicht und damit der Stoffwechsel dieser schwer erkrankten Menschen optimiert. ","en":"Im Projekt Clinicip wird ein intelligentes System für eine verbesserte Überwachung und Behandlung von kritisch kranken Menschen, die sich auf Intensivstationen befinden, entwickelt. Durch Bio-sensoren werden die Blutzuckerwerte und andere Stoffwechselparameter kontinuierlich gemessen. In einer frühen Projektphase soll damit ein anpassungsfähiger Kontrollalgorithmus eine beratende Funktion für das Krankenhauspersonal ausüben; d.h. dieses System soll als Entscheidungshilfe für Ärzte und Krankenschwestern zum Einsatz kommen. In weiterer Folge wird aufgrund der aktuellen Messergebnisse des Blutzuckerspiegels und der anderen Stoffwechselparameter automatisch die richtige Menge Insulin verabreicht und damit der Stoffwechsel dieser schwer erkrankten Menschen optimiert"},"begin_planned":null,"begin_effective":"2004-01-01T01:00:00+01:00","end_planned":null,"end_effective":"2007-12-31T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":21,"subprogram":null,"organization":14046,"category":10,"type":10,"partner_function":2,"manager":51831,"contact":51831,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[10],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["199-51831-10"]},{"id":303,"title":{"de":"Wilson Disease: Creating a European Clinical Database and designing randomised controlled clinical trials","en":"Wilson Disease: Creating a European Clinical Database and designing randomised controlled clinical trials"},"short":"EuroWilson","url":null,"abstract":{"de":"Wilson disease is an autosomal recessive disorder in which deficiency of a copper-transporting trans-golgi P-type ATPase leads to intracellular retention of copper and hence hepatic, neurological & renal disease. Incidence estimates vary from 1:30000 to 1:100000. Mutation identification aids early diagnosis. Although there is encouraging single centre experience with copper-chelators (BAL in early work, now penicillamine or trientine), zinc sulfate of acetate, or ammonium tetrathiomolybdate, treatment dilemmas remain. We do not know how to treat pre-symptomatically diagnosed infants. There is a lack of randomised controlled clinical trials (RCTs). Initial neurological deterioration on starting treatment may not be reversible. Long term outlook is uncertain. A small survey of clinicians revealed wide differences in treatment choices and lack of certainty about optimum treatment. A Cochrane-style literature review found virtually no Level I evidence. A multicentre stratified RCT is necessary. In 2002 the European Society of Paediatric Gastroeneterology, Hepatology and Nutrition established a working group of paediatric and adult hepatologists and neurologists with representation from the European Society for the Study of the Liver and the Movement Disorder Society. This has concluded that mounting an RCT is not possible without data on the incidence, prevalence of sub-types, current treatments, and short term outcomes. The consortium wishes to establish a European Clinical Database, data from which will inform the process of setting up an RCT. Preliminary work has addressed diagnostic criteria, database items, choice of software, database host, and secure access. The aims of the project are to set up the database, collect and analyse 1 year's data, set up an RCT planning group and workshop, and to continue data collection and patient monitoring for 4 years.","en":"Wilson disease is an autosomal recessive disorder in which deficiency of a copper-transporting trans-golgi P-type ATPase leads to intracellular retention of copper and hence hepatic, neurological & renal disease. Incidence estimates vary from 1:30000 to 1:100000. Mutation identification aids early diagnosis. Although there is encouraging single centre experience with copper-chelators (BAL in early work, now penicillamine or trientine), zinc sulfate of acetate, or ammonium tetrathiomolybdate, treatment dilemmas remain. We do not know how to treat pre-symptomatically diagnosed infants. There is a lack of randomised controlled clinical trials (RCTs). Initial neurological deterioration on starting treatment may not be reversible. Long term outlook is uncertain. A small survey of clinicians revealed wide differences in treatment choices and lack of certainty about optimum treatment. A Cochrane-style literature review found virtually no Level I evidence. A multicentre stratified RCT is necessary. In 2002 the European Society of Paediatric Gastroeneterology, Hepatology and Nutrition established a working group of paediatric and adult hepatologists and neurologists with representation from the European Society for the Study of the Liver and the Movement Disorder Society. This has concluded that mounting an RCT is not possible without data on the incidence, prevalence of sub-types, current treatments, and short term outcomes. The consortium wishes to establish a European Clinical Database, data from which will inform the process of setting up an RCT. Preliminary work has addressed diagnostic criteria, database items, choice of software, database host, and secure access. The aims of the project are to set up the database, collect and analyse 1 year's data, set up an RCT planning group and workshop, and to continue data collection and patient monitoring for 4 years."},"begin_planned":null,"begin_effective":"2004-06-01T02:00:00+02:00","end_planned":null,"end_effective":"2008-08-31T02:00:00+02:00","assignment":"2005-10-26T02:00:00+02:00","program":21,"subprogram":null,"organization":14048,"category":10,"type":10,"partner_function":2,"manager":null,"contact":null,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[10],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":[]},{"id":437,"title":{"de":"Am Übergang vom Feten zum Neugeborenen: Neonatale Immunologie.","en":"At the crossing-point from fetus to newborn: neonatal immunology."},"short":"Neonatal immunology","url":null,"abstract":{"de":"During pregnancy TH1 immunity is downregulated favouring a TH2 driven immunresponse so that preeclampsia, premature delivery or even placental detachment and fetal soll are preventet. Furthermore, B cells express primarily IgM, but have not completed their maturation process in order to perform Ig switching. In addition to that, reduction in the available bone marrow reserve of granulocyte precursors, recuction in serum complement activity and deficient phagocytic cell function contribute to a physiologically immaturity of the neonate's immune system. An adult form of immune response is developed after live birth during the first yeaars of childhood by interaction with environmental stimuli (antigens). The reduced ability of the neonat's immune system to respond to bacterial, viral or fungal organisms is reflected by a higher rate of infections and septic events. The incidence of neonatal sepsis is still high, it varies from 1 to 8, 1 casses per 1.000 live births. The factor associated most significantly with development of septicaemia is low birth weight, therefore, preterm infants are essentially higher risk. Inflaamation and sepsis do not only contribute to a high mortality rate, but also to high morbidity. For example, neurological outcome, expecially occurrence of cerebral palsy, is strongly associated with neionatal infection. In order to reuce the resulting high mortality and morbidity, but also in order to study a model of primary immune response diverse studies have been performed by using umbilical cord blood. However, few investigations have been made with peripheral blood mononuclear cells of neonates, especially of lower gestational age. Peripheral blood represents another environment; so blood cells are exposed to other stimuli, resulting in other messages for B and T cells triggering activation and subsequent proliferation, differentntiation or even cell-death. Therefore, we want to examine absolute count of diverse lymphcyte subsets for different gestational ages in order to get reliable reference values, expression patterns of costimulatory molecules like CD40/CD40L, CD80, CD86, CD28, CD152, Interleukinsecretion of T cells, functional abilities conerning activation, proliferation and cell-death as read-out systems for activation and interactions of B and T cells immediately after life-birth.","en":"During pregnancy TH1 immunity is downregulated favouring a TH2 driven immunresponse so that preeclampsia, premature delivery or even placental detachment and fetal soll are preventet. Furthermore, B cells express primarily IgM, but have not completed their maturation process in order to perform Ig switching. In addition to that, reduction in the available bone marrow reserve of granulocyte precursors, recuction in serum complement activity and deficient phagocytic cell function contribute to a physiologically immaturity of the neonate's immune system. An adult form of immune response is developed after live birth during the first yeaars of childhood by interaction with environmental stimuli (antigens). The reduced ability of the neonat's immune system to respond to bacterial, viral or fungal organisms is reflected by a higher rate of infections and septic events. The incidence of neonatal sepsis is still high, it varies from 1 to 8, 1 casses per 1.000 live births. The factor associated most significantly with development of septicaemia is low birth weight, therefore, preterm infants are essentially higher risk. Inflaamation and sepsis do not only contribute to a high mortality rate, but also to high morbidity. For example, neurological outcome, expecially occurrence of cerebral palsy, is strongly associated with neionatal infection. In order to reuce the resulting high mortality and morbidity, but also in order to study a model of primary immune response diverse studies have been performed by using umbilical cord blood. However, few investigations have been made with peripheral blood mononuclear cells of neonates, especially of lower gestational age. Peripheral blood represents another environment; so blood cells are exposed to other stimuli, resulting in other messages for B and T cells triggering activation and subsequent proliferation, differentntiation or even cell-death. Therefore, we want to examine absolute count of diverse lymphcyte subsets for different gestational ages in order to get reliable reference values, expression patterns of costimulatory molecules like CD40/CD40L, CD80, CD86, CD28, CD152, Interleukinsecretion of T cells, functional abilities conerning activation, proliferation and cell-death as read-out systems for activation and interactions of B and T cells immediately after life-birth."},"begin_planned":null,"begin_effective":"2005-03-01T01:00:00+01:00","end_planned":null,"end_effective":"2008-02-28T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":79,"subprogram":null,"organization":14048,"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":["437-51743-12","437-51643-11"]},{"id":202,"title":{"de":"Endotheliale Dysfunktion bei Dm-2","en":"Endotheliale Dysfunktion bei Dm-2"},"short":"Endotheliale Dysfunktion bei 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":"2004-09-30T02:00:00+02:00","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":[12],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":[]},{"id":231,"title":{"de":"Transkapillärer Glukoseaustausch im Muskel- und Fettgewebe","en":"Transkapillärer Glukoseaustausch im Muskel- und Fettgewebe"},"short":"Transkapillärer Glukoseaustausch","url":null,"abstract":{"de":"In den letzten Jahren wurden mehrere Techniken zur kontinuierlichen Messung der Glukose in der menschlichen Gewebsflüssigkeit entwickelt (z.B.: Mikrodialyse, offene Mikroperfusion, implantierbare Glukosesensoren). Die mit diesen Techniken möglich gewordene Gewebsglukosemessung könnte die weitaus invasivere Glukosemessung im Blut ersetzen und dadurch eine wesentliche Verbesserung der Lebensqualität der Diabetespatienten erwirken. Die erfolgreiche Anwendung der Gewebsglukosemessung setzt aber voraus, dass die Zusammenhänge zwischen der Blutglukose und der Glukose in der Gewebsflüssigkeit bekannt sind, um dann ausgehend von den Gewebsglukosewerten die vorherrschenden Blutglukosewerte zu schätzen. Das Ziel der vorliegenden Studie ist es, die dynamischen Zusammenhänge zwischen der Blutglukose und der Glukose in der Gewebsflüssigkeit des menschlichen Muskel- und Fettgewebes zu erfassen. Glukosekonzentrationsverläufe sollen unter standardisierten Bedingungen gleichzeitig im Blut und Gewebsflüssigkeit in der Gegenwart von konstanten basalen Insulinwerten bei gesunden Menschen beobachtet werden. Um die Insulinsekretion stabil zu halten, sollen deshalb kleine Mengen verschiedener Glukoseisotope verabreicht und ihre Kinetiken in der Gewebsflüssigkeit des Muskel- und Fettgewebes mit Hilfe der offenen Mikroperfusionstechnik beobachtet werden. Die Zeitverläufe der Glukoseisotope im Plasma und Gewebsflüssigkeiten sollen hernach mit mathematischen Modellen analysiert werden. Die dabei gewonnenen Erkenntnisse sollen zur Verbesserung der Schätzung der Blutglukosekonzentration von den Gewebsglukosewerten herangezogen werden. \r\n\r\n","en":"In den letzten Jahren wurden mehrere Techniken zur kontinuierlichen Messung der Glukose in der menschlichen Gewebsflüssigkeit entwickelt (z.B.: Mikrodialyse, offene Mikroperfusion, implantierbare Glukosesensoren). Die mit diesen Techniken möglich gewordene Gewebsglukosemessung könnte die weitaus invasivere Glukosemessung im Blut ersetzen und dadurch eine wesentliche Verbesserung der Lebensqualität der Diabetespatienten erwirken. Die erfolgreiche Anwendung der Gewebsglukosemessung setzt aber voraus, dass die Zusammenhänge zwischen der Blutglukose und der Glukose in der Gewebsflüssigkeit bekannt sind, um dann ausgehend von den Gewebsglukosewerten die vorherrschenden Blutglukosewerte zu schätzen. Das Ziel der vorliegenden Studie ist es, die dynamischen Zusammenhänge zwischen der Blutglukose und der Glukose in der Gewebsflüssigkeit des menschlichen Muskel- und Fettgewebes zu erfassen. Glukosekonzentrationsverläufe sollen unter standardisierten Bedingungen gleichzeitig im Blut und Gewebsflüssigkeit in der Gegenwart von konstanten basalen Insulinwerten bei gesunden Menschen beobachtet werden. Um die Insulinsekretion stabil zu halten, sollen deshalb kleine Mengen verschiedener Glukoseisotope verabreicht und ihre Kinetiken in der Gewebsflüssigkeit des Muskel- und Fettgewebes mit Hilfe der offenen Mikroperfusionstechnik beobachtet werden. Die Zeitverläufe der Glukoseisotope im Plasma und Gewebsflüssigkeiten sollen hernach mit mathematischen Modellen analysiert werden. Die dabei gewonnenen Erkenntnisse sollen zur Verbesserung der Schätzung der Blutglukosekonzentration von den Gewebsglukosewerten herangezogen werden. "},"begin_planned":null,"begin_effective":"2003-01-01T01:00:00+01:00","end_planned":null,"end_effective":"2004-01-01T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":null,"subprogram":null,"organization":14046,"category":10,"type":10,"partner_function":1,"manager":51831,"contact":51831,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[9],"funder_projectcode":"P16228","ethics_committee":null,"edudract_number":null,"persons":["231-51831-10"]},{"id":48,"title":{"de":"Serverprojekt im Rahmen der \"Neue Medien in der Lehre an Fachhochschulen und Universitäten\"","en":"Serverprojekt im Rahmen der \"Neue Medien in der Lehre an Fachhochschulen und Universitäten\""},"short":"Severprojekt","url":null,"abstract":{"de":"Das Ziel des Gesamtprojektes \"Neue Medien in der Lehre\" liegt in der Vernetzung der bisherigen Aktivitäten auf diesem Gebiet und ihrer Entwickler/innen sowie in der Schaffung von Teams, die sich der neuen Herausforderung in der Lehre stellen und selbst zur weiteren Entwicklung beitragen. \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":"Das Ziel des Gesamtprojektes \"Neue Medien in der Lehre\" liegt in der Vernetzung der bisherigen Aktivitäten auf diesem Gebiet und ihrer Entwickler/innen sowie in der Schaffung von Teams, die sich der neuen Herausforderung in der Lehre stellen und selbst zur weiteren Entwicklung beitragen. "},"begin_planned":null,"begin_effective":"2000-11-01T01:00:00+01:00","end_planned":null,"end_effective":"2003-12-31T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":null,"subprogram":null,"organization":14026,"category":10,"type":10,"partner_function":2,"manager":51553,"contact":51553,"status":2,"research":null,"grant":null,"event":null,"study":null,"language":null,"funders":[],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["48-51344-12","48-51553-10","48-51050-10"]},{"id":47,"title":{"de":"Analyse der telemedizinischen Bildkommunikation in den Krankenhäusern der Steiermärkischen Krankenanstalten GesmbH mittels PACSview Software","en":"Analyse der telemedizinischen Bildkommunikation in den Krankenhäusern der Steiermärkischen Krankenanstalten GesmbH mittels PACSview Software"},"short":"PACSview Evaluation","url":null,"abstract":{"de":"Das Projektziel ist die Erhebung und Analyse des tatsächlichen Einsatzes der Bildverteilung und der Bildbetrachtung mit Hilfe der PACSview Software. Aufgeschlüsselt nach Anwendergruppen (Chirurgen, Internisten und Spitälern etc.) sollen Benutzerprofile erhoben werden, die sowohl über die Frequenz der Zugriffe als auch über die Art der Benutzung Aussagen erlauben (so wäre es interessant, welche Bildbearbeitungswerkzeuge wie oft eingesetzt werden). Schließlich soll auch eine subjektive Beurteilung der Benutzer über Vor- und Nachteile gegenüber dem konventionellen Film oder anderen Methoden erfasst werden. \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":"\t\t\t\t\t\t\t"},"begin_planned":null,"begin_effective":"2003-10-01T02:00:00+02:00","end_planned":null,"end_effective":"2005-04-30T02:00:00+02:00","assignment":"2005-10-26T02:00:00+02:00","program":null,"subprogram":null,"organization":14026,"category":10,"type":10,"partner_function":1,"manager":51553,"contact":51553,"status":2,"research":null,"grant":10,"event":null,"study":null,"language":null,"funders":[25],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["47-50487-12","47-51553-10"]},{"id":46,"title":{"de":"Integration von Randgruppen im Rahmen der Gemeinschaftsinitiative EQUAL in Österreich","en":"Integration von Randgruppen im Rahmen der Gemeinschaftsinitiative EQUAL in Österreich"},"short":"Randgruppenintegration","url":null,"abstract":{"de":"EQUAL-Randgruppenintegration.\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":"EQUAL-Randgruppenintegration."},"begin_planned":null,"begin_effective":"2002-09-01T02:00:00+02:00","end_planned":null,"end_effective":"2005-03-31T02:00:00+02:00","assignment":"2005-10-26T02:00:00+02:00","program":null,"subprogram":null,"organization":14024,"category":10,"type":10,"partner_function":4,"manager":51845,"contact":51845,"status":2,"research":null,"grant":10,"event":null,"study":null,"language":null,"funders":[40],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["46-51845-10"]},{"id":226,"title":{"de":"Identifizierung von Protein-Bindungs-Partner für die Endothel Lipase","en":"Identifizierung von Protein-Bindungs-Partner für die Endothel Lipase"},"short":"Endothel Lipase","url":null,"abstract":{"de":"Identifizierung von Protein-Bindungs-Partner für die Endothel Lipase.","en":"Identifizierung von Protein-Bindungs-Partner für die Endothel Lipase."},"begin_planned":null,"begin_effective":"2003-07-03T02:00:00+02:00","end_planned":null,"end_effective":"2005-07-31T02:00:00+02:00","assignment":"2005-10-26T02:00:00+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":["226-51988-10"]},{"id":261,"title":{"de":"European Leukemia Net","en":"European Leukemia Net"},"short":"European Leukemia Net","url":null,"abstract":{"de":"Leukemias are a challenge to society and a cost factor because of their frequency in all age groups.\r\nThe objective is to integrate the 78 leading leukemia trial groups (CML, AML, ALL, CLL, MDS, CMPD), their 83 interdisciplinary partners (diagnostic, treatment research, registry, guidelines), industry and SMEs across Europe to form a cooperative network for advancements in leukemia-related research and health care.\r\nThe proposed network will have the expertise and critical mass for European added value and world leadership. It will structure European research durably, spread European scientific excellence in the field of leukemias and can start immediately.","en":"Leukemias are a challenge to society and a cost factor because of their frequency in all age groups.\r\nThe objective is to integrate the 78 leading leukemia trial groups (CML, AML, ALL, CLL, MDS, CMPD), their 83 interdisciplinary partners (diagnostic, treatment research, registry, guidelines), industry and SMEs across Europe to form a cooperative network for advancements in leukemia-related research and health care.\r\nThe proposed network will have the expertise and critical mass for European added value and world leadership. It will structure European research durably, spread European scientific excellence in the field of leukemias and can start immediately."},"begin_planned":null,"begin_effective":"2004-01-01T01:00:00+01:00","end_planned":null,"end_effective":"2012-12-31T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":21,"subprogram":null,"organization":14026,"category":10,"type":10,"partner_function":2,"manager":51344,"contact":51344,"status":2,"research":2,"grant":10,"event":null,"study":null,"language":null,"funders":[10],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["261-51344-10","261-51553-10","261-52966-12"]},{"id":230,"title":{"de":"Rolle der Organellen in der endothelialen Calcium Homeostase (P16860-B09)","en":"Rolle der Organellen in der endothelialen Calcium Homeostase (P16860-B09)"},"short":"Calcium Homeostase","url":null,"abstract":{"de":"Wie in nahezu jedem Zelltyp dient Ca2+ als essentieller Regulator zahlreicher fundamentaler Zellfunktionen im Endothel. Diese faszinierende Vielseitigkeit ist umso eindrucksvoller wenn man die Präzision berücksichtigt, mit der Ca2+-sensitive Mechanismen kontrolliert werden. Doch wie kann ein einfaches Ion wie Ca2+ eine solch komplexe und präzise Maschinerie steuern und wie störanfällig ist diese unter pathologischen Bedingungen?\r\nIm Vorgängerprojekt konnte gezeigt werden, dass das Paradoxon der multiplen und dennoch hoch selektiven Funktionen von Ca2+ zumindest teilweise durch lokal begrenzte Ca2+ Gradienten im subplasmalemmalen Zytosol gelöst wird. Bei Stimulierung kommt es dort durch Teile des endoplasmatischen Retikulums zur lokalen Ca2+ Erhöhung auf bis zu >6.5 µM, wodurch Ca2+-aktivierte Ionenkanäle und Enzyme stimuliert werden. Im Gegensatz dazu, bleibt die Ca2+-Konzentration in der Umgebung membrannaher Mitochondrien nahezu unverändert (~0.2 µM), was essentiell für die Aufrechterhaltung des Ca2+-inhibierbaren kapazitativen Ca2+-Einstrom ist. Vorläufigen Daten zufolge ist die Kommunikation zwischen Organellen ein Eckpfeiler der zellulären Ca2+-Homöostase. Darüber hinaus verändert sich die Struktur von Organellen ständig durch Bewegungen, Fussionen und Abspaltungen. Die Bedeutung dieser Vorgänge und das Zusammenspiel mit Ionenströmen durch Organellen und die Zellmembran sind unklar und werden im Rahmen dieses Projektes erforscht.\r\nUm räumlich begrenzte Ca2+-Signale und die Dynamik und Interaktion von Organellen sowie deren Einfluss auf Ca2+-regulierte Zellfunktionen detailliert erfassen zu können, werden neue molekulare Sensoren entworfen und in Experimenten eingesetzt, in welchen Elektrophysiologie und Array Laser Scanning-Konfokalmikroskopie simultan zum Einsatz kommen.\r\nTrotz deutlicher Hinweise auf eine veränderte Ca2+-Homöostase als zumindest partielle Ursache der endothelialen Dysfunktion im Rahmen von z.B. Diabetes mellitus ist bislang eine detaillierte Analyse der molekularen und lokalen Aspekte pathologisch veränderter Ca2+-Signale ausständig. Basierend auf den neuesten Konzepten über die Regulation räumlich begrenzter Ca2+-Signale und mit Hilfe verbesserter technischer Möglichkeiten der lokalen Ca2+-Messung, wird dieses Projekt weiters die Mechanismen und Konsequenzen von Veränderungen im lokalen Ca2+-Signal und der Ca2+-Homöostase und Dynamik von Organellen in Endothelzellen unter Hyperglykämie untersuchen. ","en":"Wie in nahezu jedem Zelltyp dient Ca2+ als essentieller Regulator zahlreicher fundamentaler Zellfunktionen im Endothel. Diese faszinierende Vielseitigkeit ist umso eindrucksvoller wenn man die Präzision berücksichtigt, mit der Ca2+-sensitive Mechanismen kontrolliert werden. Doch wie kann ein einfaches Ion wie Ca2+ eine solch komplexe und präzise Maschinerie steuern und wie störanfällig ist diese unter pathologischen Bedingungen?\r\nIm Vorgängerprojekt konnte gezeigt werden, dass das Paradoxon der multiplen und dennoch hoch selektiven Funktionen von Ca2+ zumindest teilweise durch lokal begrenzte Ca2+ Gradienten im subplasmalemmalen Zytosol gelöst wird. Bei Stimulierung kommt es dort durch Teile des endoplasmatischen Retikulums zur lokalen Ca2+ Erhöhung auf bis zu >6.5 µM, wodurch Ca2+-aktivierte Ionenkanäle und Enzyme stimuliert werden. Im Gegensatz dazu, bleibt die Ca2+-Konzentration in der Umgebung membrannaher Mitochondrien nahezu unverändert (~0.2 µM), was essentiell für die Aufrechterhaltung des Ca2+-inhibierbaren kapazitativen Ca2+-Einstrom ist. Vorläufigen Daten zufolge ist die Kommunikation zwischen Organellen ein Eckpfeiler der zellulären Ca2+-Homöostase. Darüber hinaus verändert sich die Struktur von Organellen ständig durch Bewegungen, Fussionen und Abspaltungen. Die Bedeutung dieser Vorgänge und das Zusammenspiel mit Ionenströmen durch Organellen und die Zellmembran sind unklar und werden im Rahmen dieses Projektes erforscht.\r\nUm räumlich begrenzte Ca2+-Signale und die Dynamik und Interaktion von Organellen sowie deren Einfluss auf Ca2+-regulierte Zellfunktionen detailliert erfassen zu können, werden neue molekulare Sensoren entworfen und in Experimenten eingesetzt, in welchen Elektrophysiologie und Array Laser Scanning-Konfokalmikroskopie simultan zum Einsatz kommen.\r\nTrotz deutlicher Hinweise auf eine veränderte Ca2+-Homöostase als zumindest partielle Ursache der endothelialen Dysfunktion im Rahmen von z.B. Diabetes mellitus ist bislang eine detaillierte Analyse der molekularen und lokalen Aspekte pathologisch veränderter Ca2+-Signale ausständig. Basierend auf den neuesten Konzepten über die Regulation räumlich begrenzter Ca2+-Signale und mit Hilfe verbesserter technischer Möglichkeiten der lokalen Ca2+-Messung, wird dieses Projekt weiters die Mechanismen und Konsequenzen von Veränderungen im lokalen Ca2+-Signal und der Ca2+-Homöostase und Dynamik von Organellen in Endothelzellen unter Hyperglykämie untersuchen. "},"begin_planned":null,"begin_effective":"2003-12-01T01:00:00+01:00","end_planned":null,"end_effective":"2007-11-30T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":72,"subprogram":null,"organization":14013,"category":10,"type":10,"partner_function":4,"manager":51860,"contact":51860,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[9],"funder_projectcode":"P16860","ethics_committee":null,"edudract_number":null,"persons":["230-51860-10"]},{"id":6,"title":{"de":"Allelic imbalances in tonsillary squamous cell carcinomas","en":"Allelic imbalances in tonsillary squamous cell carcinomas"},"short":"Allelic imbalances ","url":null,"abstract":{"de":"Allelic imbalances in tonsillary squamous cell carcinomas.","en":"Allelic imbalances in tonsillary squamous cell carcinomas."},"begin_planned":null,"begin_effective":"2001-03-12T01:00:00+01:00","end_planned":null,"end_effective":"2004-12-31T01:00:00+01:00","assignment":"2005-10-26T02:00:00+02:00","program":81,"subprogram":null,"organization":14020,"category":10,"type":10,"partner_function":4,"manager":null,"contact":null,"status":2,"research":null,"grant":10,"event":null,"study":null,"language":null,"funders":[52],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":[]},{"id":1839,"title":{"de":"Mukosaschädigung und enterales Nervensystem","en":"Mukosaschädigung und enterales Nervensystem"},"short":"Mukosaschädigung und enterales Nervensys","url":null,"abstract":{"de":null,"en":null},"begin_planned":null,"begin_effective":"1999-06-24T02:00:00+02:00","end_planned":null,"end_effective":"2000-06-24T02:00:00+02:00","assignment":null,"program":79,"subprogram":null,"organization":14022,"category":10,"type":10,"partner_function":4,"manager":51832,"contact":51832,"status":2,"research":1,"grant":10,"event":null,"study":null,"language":null,"funders":[],"funder_projectcode":null,"ethics_committee":null,"edudract_number":null,"persons":["1839-51832-10"]}]}