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Raddatz, Dirk
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Raddatz, Dirk
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Raddatz, Dirk
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Raddatz, D.
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2009Journal Article [["dc.bibliographiccitation.firstpage","209"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","OSTEOLOGIE"],["dc.bibliographiccitation.lastpage","216"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Cortis, Judith"],["dc.contributor.author","Claus, Ch."],["dc.contributor.author","Funke, M."],["dc.contributor.author","Nolte, W."],["dc.contributor.author","Huefner, Michael"],["dc.contributor.author","Raddatz, Dirk"],["dc.date.accessioned","2018-11-07T08:35:18Z"],["dc.date.available","2018-11-07T08:35:18Z"],["dc.date.issued","2009"],["dc.description.abstract","Crohn's disease (CD) is associated with reduced bone mineral density and increased fracture risk. To assess the effects of the inflammatory process itself on bone parameters, we investigated patients with active CD and in remission without glucocorticoid treatment four weeks prior to analysis. Patients with active CD were compared to age- and sex-matched healthy volunteers and osteoporosis patients. Bone mineral density, bone formation and resorption markers were assessed, in addition to simple inflammatory markers and cytokines. Out of seven patients with active disease, three had osteopenia and one osteoporosis (WHO definition). The erythrocyte sedimentation rate (ESR) was associated with BMD at the femoral neck (R(2) = 0.853, p<0.01) and the spine (R(2)=0.772, p<0.05). ESR seems to influence bone formation, as shown by lower bone alkaline phosphatase with high ESR (R(2)=0.725, R=-0.852, p<0.05). The clinical disease activity score was not useful in determining patients' risk of acquiring bone disease. in conclusion, in patients with Crohn's disease, the degree of the inflammatory process as assessed by ESR indicates bone loss and might be of value in identifying patients at risk of developing osteoporosis."],["dc.identifier.isi","000271412000009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18032"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Verlag Hans Huber"],["dc.relation.issn","1019-1291"],["dc.title","Erythrocyte sedimentation rate as an osteoporosis risk factor in patients with active Crohn's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2001Conference Abstract [["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Bone"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Eidner, T."],["dc.contributor.author","Lehmann, G."],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Hein, G."],["dc.contributor.author","Hufner, M."],["dc.date.accessioned","2018-11-07T09:05:34Z"],["dc.date.available","2018-11-07T09:05:34Z"],["dc.date.issued","2001"],["dc.format.extent","S140"],["dc.identifier.isi","000168825000317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25351"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.issn","8756-3282"],["dc.title","Cytokines, osteoprotegerin and osteoprotegerin-ligand in vitro and histomorphometric indices of bone formation in patients with different bone diseases"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2003Journal Article [["dc.bibliographiccitation.firstpage","4206"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","The Journal of Clinical Endocrinology & Metabolism"],["dc.bibliographiccitation.lastpage","4213"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Grundker, Carsten"],["dc.contributor.author","Blaschke, S."],["dc.contributor.author","Niederkleine, B."],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Frosch, Karl-Heinz"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Emons, G."],["dc.contributor.author","Hofbauer, L. C."],["dc.date.accessioned","2018-11-07T10:36:37Z"],["dc.date.available","2018-11-07T10:36:37Z"],["dc.date.issued","2003"],["dc.description.abstract","Raloxifene reduces bone loss and prevents vertebral fractures in postmenopausal women. Its skeletal effects are mediated by estrogen receptors ( ER) and their modulation of paracrine osteoblastic factors. Receptor activator of nuclear factor-kappaB ligand is essential for osteoclasts and enhances bone resorption, whereas osteoprotegerin (OPG) neutralizes receptor activator of nuclear factor-kappaB ligand. Here, we assessed the effects of raloxifene on OPG production in human osteoblasts (hOB). Raloxifene enhanced gene expression of ER-alpha and progesterone receptor. Moreover, raloxifene increased OPG mRNA levels and protein secretion by hOB in a dose- and time-dependent fashion by 2- to 4-fold with a maximum effect at 10(-7) M and after 72 h ( P < 0.001). Treatment with the ER antagonist ICI 182,780 abrogated the effects of raloxifene on OPG production. Moreover, raloxifene enhanced osteoblastic differentiation markers, type 1 collagen secretion, and alkaline phosphatase activity by 3- and 2-fold, respectively ( P < 0.001). In addition, raloxifene inhibited expression of the bone-resorbing cytokine IL-6 by 25 - 45% ( P < 0.001). In conclusion, our data suggest that raloxifene stimulates OPG production and inhibits IL-6 production by hOB. Because OPG production increases with osteoblastic maturation, enhancement of OPG production by raloxifene could be related to its stimulatory effects on osteoblastic differentiation."],["dc.identifier.doi","10.1210/jc.2002-021877"],["dc.identifier.isi","000185258700031"],["dc.identifier.pmid","12970288"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45369"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Endocrine Soc"],["dc.relation.issn","0021-972X"],["dc.title","Raloxifene concurrently stimulates osteoprotegerin and inhibits interleukin-6 production by human trabecular osteoblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2009Conference Abstract [["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Bone"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Clasen, T. J."],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Schnell, R."],["dc.contributor.author","Nolte, W."],["dc.contributor.author","Press, A."],["dc.contributor.author","Siggelkow, Heide"],["dc.date.accessioned","2018-11-07T08:28:58Z"],["dc.date.available","2018-11-07T08:28:58Z"],["dc.date.issued","2009"],["dc.format.extent","S419"],["dc.identifier.doi","10.1016/j.bone.2009.03.349"],["dc.identifier.isi","000266348600559"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16540"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.conference","36th European Symposium on Calcified Tissues"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","8756-3282"],["dc.title","Influence of inflammation on bone density in patients with inflammatory bowel disease - Different effects on different structures within bone?"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2003Conference Paper [["dc.bibliographiccitation.firstpage","529"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Bone and Mineral Research"],["dc.bibliographiccitation.lastpage","538"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Eidner, T."],["dc.contributor.author","Lehmann, G."],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Munzel, U."],["dc.contributor.author","Hein, G."],["dc.contributor.author","Hufner, M."],["dc.date.accessioned","2018-11-07T10:40:33Z"],["dc.date.available","2018-11-07T10:40:33Z"],["dc.date.issued","2003"],["dc.description.abstract","Cytokines are supposed to play an essential role in the regulation of the bone metabolic unit. However, information on cytokine production of primary human osteoblasts from patients with metabolic bone disease is scarce, and few attempts have been made to correlate such data to histomorphometric parameters of individual patients. We investigated 11 patients with metabolic bone disease referred to our outpatient department for bone biopsy and analyzed interleukin (IL)-1, IL-6, and TNF-alpha protein release and gene expression in primary osteoblast cultures. Compared with four controls, five patients showed normal cytokine protein release, whereas six patients showed much higher levels of interleukin-6 (26-fold) and TNF-alpha (84-fold). All three cytokines were strongly correlated concerning gene expression and/or protein levels (r = 0.72-0.96). Histomorphometric analysis of the bone samples showed that eroded surface (ES/BS) as a parameter of bone resorption was significantly associated with TNF-alpha. In addition, RANKL gene expression was positively associated with ES/BS and osteoclast surface (Oc.S/BS). Finally, the formation parameters osteold volume and osteoid surface were negatively associated with TNF-alpha. In conclusion, in an in vitro-ex vivo model of bone cells obtained from a group of 11 patients with different forms of metabolic bone disease, cytokine release in conditioned medium was significantly associated with bone resorption and bone formation, as quantified by histomorphometry. TNF-alpha seemed to be the more important cytokine; its effect on bone resorption could be mediated by RANKL."],["dc.identifier.doi","10.1359/jbmr.2003.18.3.529"],["dc.identifier.isi","000181178400018"],["dc.identifier.pmid","12619938"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/46326"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Bone & Mineral Res"],["dc.publisher.place","Washington"],["dc.relation.conference","1st Joint Meeting of the International-Bone-and-Mineral-Society/European-Calcified-Tissue-Society"],["dc.relation.eventlocation","MADRID, SPAIN"],["dc.relation.issn","0884-0431"],["dc.title","Cytokines, osteoprotegerin, and RANKL in vitro and histomorphometric indices of bone turnover in patients with different bone diseases"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2002Journal Article [["dc.bibliographiccitation.firstpage","348"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cellular Biochemistry"],["dc.bibliographiccitation.lastpage","356"],["dc.bibliographiccitation.volume","86"],["dc.contributor.author","Viereck, Volker"],["dc.contributor.author","Siggelkow, Heide"],["dc.contributor.author","Tauber, S."],["dc.contributor.author","Raddatz, Dirk"],["dc.contributor.author","Schutze, N."],["dc.contributor.author","Hufner, M."],["dc.date.accessioned","2018-11-07T10:33:19Z"],["dc.date.available","2018-11-07T10:33:19Z"],["dc.date.issued","2002"],["dc.description.abstract","Core binding factor alpha 1 (Cbfa1) is air osteoblast-specific transcription factor essential to develop a mature osteoblast phenotype. However, its exact role in the sign a I in g of various osteotropic-differentiating agents is still unclear in this study, we assessed the effects of 1,25-(OH)(2)-D3 (D3), ascorbic acid, bone morphogenetic protein-2 (BMP-2), dexamethasone (Dex), and transforming growth factor-beta (TGF-beta) on Cbfa1 and osteocalcin (OCN) mRNA steady state levels (by semiquantitative RT-PCR) in an in vitro model of osteoblast differentiation. TGF-beta increased Cbfa1 mRNA levels in normal primary human osteoblasts (pHOB) by 2.6-fold in a time-dependent fashion with maximum effect on day 28 (P < 0.001). Similarly, the glucocorticoid Dex enhanced Cbfa1 gene expression by pHOB in a time-dependent fashion by up to 4.6-fold (P < 0.001). In contrast, Dex inhibited OCN gene expression levels by 68% (P < 0.01). Treatment with BMP-2 resulted in an earlier enhancement of Cbfa1 and led to a 4.2-fold increase with a maximum on day 21 (P < 0.001). Ascorbic acid did not modulate Cbfa1 and OCN gene expression, The effect of vitamin D (D3) on Cbfa1 mRNA expression was influenced by the duration of treatment, being inhibitory after 1 h and having a stimulatory effect after 48 h. Time course experiments indicated a stimulatory effect of D3 on Cbfa1 mRNA levels (by 2.5-fold after 48 h; P < 0.01). Analysis of the late cellular differentiation marker osteocalcin revealed that D3 increased OCN gene expression by 1 4-fold (P < 0.001). In conclusion, in normal primary human osteoblasts, the rapid and pronounced increase of OCN after treatment with D3 seems not to be mediated by Cbfa1. These data imply that Cbfa1 gene expression is differentially regulated by various osteoblastic differentiating agents and is dependent on the stage of maturation. (C) 2002 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jcb.10220"],["dc.identifier.isi","000176690400015"],["dc.identifier.pmid","12112004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44580"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0730-2312"],["dc.title","Differential regulation of Cbfa1/Runx2 and osteocalcin gene expression by vitamin-D3, dexamethasone, and local growth factors in primary human osteoblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS