[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-study-detail:100454607":3},{"organization":4,"armGroups":7,"interventions":14,"overallOfficials":19,"centralContacts":24,"locations":34,"responsibleParty":50,"collaborators":10,"id":52,"slug":53,"hasResults":54,"nctId":55,"briefTitle":56,"officialTitle":57,"acronym":58,"eligibilityCriteria":59,"healthyVolunteers":54,"sex":60,"minAge":61,"maxAge":10,"enrollmentInfo":62,"targetDuration":10,"studyType":65,"phases":10,"briefSummary":66,"conditions":67,"keywords":10,"overallStatus":36,"whyStopped":10,"lastUpdateSubmitDate":69,"lastUpdatePostDateStruct":70,"startDateStruct":73,"completionDateStruct":75,"leadSponsor":77,"locationsCount":78},{"fullName":5,"class":6},"Maastricht University","OTHER",[8],{"label":9,"type":10,"description":11,"interventionNames":12},"mtDNA mutation carriers",null,"Carriers of a pathogenic mtDNA mutation",[13],"Other: in vitro analysis",[15],{"type":6,"name":16,"description":17,"armGroupLabels":18,"otherNames":10},"in vitro analysis","in vitro analysis of mesoangioblasts from mtDNA mutation carriers",[9],[20],{"name":21,"affiliation":22,"role":23},"Janneke Hoeijmakers, PhD, MD","Maastricht University Medical Center","PRINCIPAL_INVESTIGATOR",[25,30],{"name":26,"role":27,"phone":28,"phoneExt":10,"email":29},"Florence van Tienen, PhD","CONTACT","314332918","florence.vantienen@maastrichtuniversity.nl",{"name":31,"role":27,"phone":32,"phoneExt":10,"email":33},"Bert Smeets, Prof.","314331995","bert.smeets@maastrichtuniversity.nl",[35],{"facility":5,"status":36,"city":37,"state":10,"zip":10,"country":38,"countryCode":39,"cosmosGeoPoint":40,"geoPoint":45,"contacts":46},"RECRUITING","Maastricht","Netherlands","NL",{"type":41,"coordinates":42},"Point",[43,44],5.68889,50.84833,{"lat":44,"lon":43},[47],{"name":48,"role":27,"phone":49,"phoneExt":10,"email":29},"Florence Dept. Toxicogenomics, PhD","0433882918",{"type":51,"investigatorFullName":10,"investigatorTitle":10,"investigatorAffiliation":10,"oldNameTitle":10,"oldOrganization":10},"SPONSOR","100454607","mtdna-mutation-load-analysis-in-mesoangioblasts-100454607",false,"NCT05199740","mtDNA Mutation Load Analysis in Mesoangioblasts","Assess the mtDNA Mutation Load in Mesoangioblasts of mtDNA Mutation Carriers","MABS05","Inclusion Criteria all participants:\n\n* Written informed consent\n* Age: 18+\n* Sex: male\u002Ffemale\n* Carriers of a heteroplasmic mtDNA mutation load \\>20% in skeletal muscle or \\>1% in blood\n\nExclusion Criteria all participants:\n\n* No informed consent\n* Use of anti-coagulants, anti-thrombotics and other medication influencing coagulation\n* Have a weekly alcohol intake of ≥ 35 units (men) or ≥ 24 units (women)\n* Current history of drug abuse\n* A history of strokes\n* Significant concurrent illness\n* Ongoing participation in other clinical trials that contain an intervention\n* Major surgery within 4 weeks of the visit\n* Pregnant or lactating women\n* Patients unable and\u002For unwilling to comply with treatment and study instructions","ALL","18 Years",{"count":63,"type":64},30,"ESTIMATED","OBSERVATIONAL","Mitochondrial diseases caused by defects in oxidative phosphorylation (OXPHOS) due to heteroplasmic mitochondrial DNA (mtDNA) mutations are rare (frequency 1\u002F5,000), but severe multi-system disorders. Clinical manifestations are highly variable, but predominantly affect energy demanding tissues, like brain and muscle. Myopathy is a common feature of mtDNA disorders, being present in more than 50% of the mtDNA mutation carriers, and seriously affects patients' general well-being and quality of life. Currently, no treatment is available for these patients, although the induction of muscle regeneration by exercise treatment has been shown to alleviate their myopathy. This implies that these patients can produce muscle fibres that perform better, most likely because the mutation load is lower. Mesoangioblasts (MABs) are myogenic precursors that have been recognized as a source for development of a systemic myogenic stem-cell therapy. Autologous MABs may be feasible for half of the mtDNA mutation carriers of 6 different mtDNA mutations, as their mtDNA mutation load in mesoangioblasts was (nearly) absent (\\\u003C10%). However, there are many more mtDNA mutations in the 16.5kb mtDNA and the aim of this study is to determine the mtDNA mutation load in mesoangioblasts of other mtDNA mutation carriers and identify the patients or mutations for which this is a feasible approach.",[68],"Mitochondrial Myopathies","2024-01-22",{"date":71,"type":72},"2024-01-24","ACTUAL",{"date":74,"type":72},"2022-12-20",{"date":76,"type":64},"2026-07-01",{"name":5,"class":6},1]