@article{KlotzMentrupRegensburgeretal.2012,
  author    = {Klotz, Barbara and Mentrup, Birgit and Regensburger, Martina and Zeck, Sabine and Schneidereit, Jutta and Schupp, Nicole and Linden, Christian and Merz, Cornelia and Ebert, Regina and Jakob, Franz},
  title     = {1,25-Dihydroxyvitamin D3 Treatment Delays Cellular Aging in Human Mesenchymal Stem Cells while Maintaining Their Multipotent Capacity},
  series = {PLoS ONE},
  volume    = {7},
  journal   = {PLoS ONE},
  number    = {1},
  doi       = {10.1371/journal.pone.0029959},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133392},
  pages     = {e29959},
  year      = {2012},
  abstract  = {1,25-dihydroxyvitamin D3 (1,25D3) was reported to induce premature organismal aging in fibroblast growth factor-23 (Fgf23) and klotho deficient mice, which is of main interest as 1,25D3 supplementation of its precursor cholecalciferol is used in basic osteoporosis treatment. We wanted to know if 1,25D3 is able to modulate aging processes on a cellular level in human mesenchymal stem cells (hMSC). Effects of 100 nM 1,25D3 on hMSC were analyzed by cell proliferation and apoptosis assay, beta-galactosidase staining, VDR and surface marker immunocytochemistry, RT-PCR of 1,25D3-responsive, quiescence-and replicative senescence-associated genes. 1,25D3 treatment significantly inhibited hMSC proliferation and apoptosis after 72 h and delayed the development of replicative senescence in long-term cultures according to beta-galactosidase staining and P16 expression. Cell morphology changed from a fibroblast like appearance to broad and rounded shapes. Long term treatment did not induce lineage commitment in terms of osteogenic pathways but maintained their clonogenic capacity, their surface marker characteristics (expression of CD73, CD90, CD105) and their multipotency to develop towards the chondrogenic, adipogenic and osteogenic pathways. In conclusion, 1,25D3 delays replicative senescence in primary hMSC while the pro-aging effects seen in mouse models might mainly be due to elevated systemic phosphate levels, which propagate organismal aging.},
  language  = {en}
}
@article{VandeKerkhofFeenstravanderHeijdenetal.2012,
  author    = {Van de Kerkhof, Noortje W. A. and Feenstra, Ilse and van der Heijden, Frank M. M. A. and de Leeuw, Nicole and Pfundt, Rolph and St{\"o}ber, Gerald and Egger, Jos I. M. and Verhoeven, Willem M. A.},
  title     = {Copy number variants in a sample of patients with psychotic disorders: is standard screening relevant for actual clinical practice?},
  series = {Neuropsychiatric Disease and Treatment},
  volume    = {8},
  journal   = {Neuropsychiatric Disease and Treatment},
  doi       = {10.2147/NDT.S32903},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-134769},
  pages     = {295-300},
  year      = {2012},
  abstract  = {With the introduction of new genetic techniques such as genome-wide array comparative genomic hybridization, studies on the putative genetic etiology of schizophrenia have focused on the detection of copy number variants (CNVs), ie, microdeletions and/or microduplications, that are estimated to be present in up to 3\% of patients with schizophrenia. In this study, out of a sample of 100 patients with psychotic disorders, 80 were investigated by array for the presence of CNVs. The assessment of the severity of psychiatric symptoms was performed using standardized instruments and ICD-10 was applied for diagnostic classification. In three patients, a submicroscopic CNV was demonstrated, one with a loss in 1q21.1 and two with a gain in 1p13.3 and 7q11.2, respectively. The association between these or other CNVs and schizophrenia or schizophrenia-like psychoses and their clinical implications still remain equivocal. While the CNV affected genes may enhance the vulnerability for psychiatric disorders via effects on neuronal architecture, these insights have not resulted in major changes in clinical practice as yet. Therefore, genome-wide array analysis should presently be restricted to those patients in whom psychotic symptoms are paired with other signs, particularly dysmorphisms and intellectual impairment.},
  language  = {en}
}