@article{WuertzKozakRoszkowskiCambriaetal.2020,
  author    = {Wuertz-Kozak, Karin and Roszkowski, Martin and Cambria, Elena and Block, Andrea and Kuhn, Gisela A. and Abele, Thea and Hitzl, Wolfgang and Drießlein, David and M{\"u}ller, Ralph and Rapp, Michael Armin and Mansuy, Isabelle M. and Peters, Eva M. J. and Wippert, Pia-Maria},
  title     = {Effects of Early Life Stress on Bone Homeostasis in Mice and Humans},
  series = {International Journal of Molecular Sciences},
  volume    = {21},
  journal   = {International Journal of Molecular Sciences},
  number    = {18},
  publisher = {Molecular Diversity Preservation International},
  address   = {Basel},
  issn      = {1422-0067},
  doi       = {10.3390/ijms21186634},
  pages     = {24},
  year      = {2020},
  abstract  = {Bone pathology is frequent in stressed individuals. A comprehensive examination of mechanisms linking life stress, depression and disturbed bone homeostasis is missing. In this translational study, mice exposed to early life stress (MSUS) were examined for bone microarchitecture (μCT), metabolism (qPCR/ELISA), and neuronal stress mediator expression (qPCR) and compared with a sample of depressive patients with or without early life stress by analyzing bone mineral density (BMD) (DXA) and metabolic changes in serum (osteocalcin, PINP, CTX-I). MSUS mice showed a significant decrease in NGF, NPYR1, VIPR1 and TACR1 expression, higher innervation density in bone, and increased serum levels of CTX-I, suggesting a milieu in favor of catabolic bone turnover. MSUS mice had a significantly lower body weight compared to control mice, and this caused minor effects on bone microarchitecture. Depressive patients with experiences of childhood neglect also showed a catabolic pattern. A significant reduction in BMD was observed in depressive patients with childhood abuse and stressful life events during childhood. Therefore, future studies on prevention and treatment strategies for both mental and bone disease should consider early life stress as a risk factor for bone pathologies.},
  language  = {en}
}
@misc{WuertzKozakRoszkowskiCambriaetal.2020,
  author    = {Wuertz-Kozak, Karin and Roszkowski, Martin and Cambria, Elena and Block, Andrea and Kuhn, Gisela A. and Abele, Thea and Hitzl, Wolfgang and Drießlein, David and M{\"u}ller, Ralph and Rapp, Michael Armin and Mansuy, Isabelle M. and Peters, Eva M. J. and Wippert, Pia-Maria},
  title     = {Effects of Early Life Stress on Bone Homeostasis in Mice and Humans},
  series = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  number    = {670},
  issn      = {1866-8364},
  doi       = {10.25932/publishup-48532},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-485324},
  pages     = {26},
  year      = {2020},
  abstract  = {Bone pathology is frequent in stressed individuals. A comprehensive examination of mechanisms linking life stress, depression and disturbed bone homeostasis is missing. In this translational study, mice exposed to early life stress (MSUS) were examined for bone microarchitecture (μCT), metabolism (qPCR/ELISA), and neuronal stress mediator expression (qPCR) and compared with a sample of depressive patients with or without early life stress by analyzing bone mineral density (BMD) (DXA) and metabolic changes in serum (osteocalcin, PINP, CTX-I). MSUS mice showed a significant decrease in NGF, NPYR1, VIPR1 and TACR1 expression, higher innervation density in bone, and increased serum levels of CTX-I, suggesting a milieu in favor of catabolic bone turnover. MSUS mice had a significantly lower body weight compared to control mice, and this caused minor effects on bone microarchitecture. Depressive patients with experiences of childhood neglect also showed a catabolic pattern. A significant reduction in BMD was observed in depressive patients with childhood abuse and stressful life events during childhood. Therefore, future studies on prevention and treatment strategies for both mental and bone disease should consider early life stress as a risk factor for bone pathologies.},
  language  = {en}
}
@article{ChupeerachTungtrongchitrPhonratetal.2012,
  author    = {Chupeerach, Chaowanee and Tungtrongchitr, Anchalee and Phonrat, Benjaluck and Schweigert, Florian J. and Tungtrongchitr, Rungsunn and Preutthipan, Sangchai},
  title     = {Association of Thr420Lys polymorphism in DBP gene with fat-soluble vitamins and low radial bone mineral density in postmenopausal Thai women},
  series = {Biomarkers in medicine},
  volume    = {6},
  journal   = {Biomarkers in medicine},
  number    = {1},
  publisher = {Future Medicine},
  address   = {London},
  issn      = {1752-0363},
  doi       = {10.2217/BMM.11.88},
  pages     = {103 -- 108},
  year      = {2012},
  abstract  = {Aims: To investigate the genetic markers for osteoporosis bone mineral density by the genotyping of rs7041, rs4588 and rs1352845 in the DBP gene with either bone mineral density or serum 25-hydroxycholecalciferol, retinol and alpha-tocopherol, among 365 postmenopausal Thai women. Materials \& methods: The DBP genotypes were analyzed by a PCR restriction fragment-length polymorphism method. Serum 25-hydroxycholecalciferol was assessed using a commercial chemiluminescent immunoassay. Serum retinol and alpha-tocopherol were measured by reverse-phase high-performance liquid chromatography. Results: After adjustment for age >50 years, elder Thai subjects with low BMI (<= 25 kg/m(2)) and carrying the rs4588 CC genotype had a higher risk of radial bone mineral density osteoporosis (odds ratio: 6.29; p = 0.048). The rs1352845 genotype also had a statistical association with total hip bone mineral density; however, it disappeared after adjustment for age and BMI. No association was found in fat-soluble vitamins with bone mineral density. Conclusion: DBP genotypes may influence the osteoporosis bone mineral density in postmenopausal Thai women.},
  language  = {en}
}