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R. Adam Rebeles,A. Hermanne 한국물리학회 2011 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.59 No.23
Excitation functions of deuteron induced reactions on natural thallium, leading to the formation of the ^(204m,203,202m)Pb, ^(202)Tl isotopes, were studied by the stacked foil activation technique. Reaction cross sections were measured from their respective thresholds up to E_d = 21 MeV. Quantification of induced isotopes has been made by gamma spectrometry. Where available, the experimental cross sections are compared with values reported previously in literature. Based on the discrete values of the measured cross section, thick target yield for the medically interesting radionuclide ^(203)Pb is calculated.
Shim, Jae-Hyuck,Greenblatt, Matthew B,Singh, Anju,Brady, Nicholas,Hu, Dorothy,Drapp, Rebecca,Ogawa, Wataru,Kasuga, Masato,Noda, Tetsuo,Yang, Sang-Hwa,Lee, Sang-Kyou,Rebel, Vivienne I,Glimcher, Laurie American Society for Clinical Investigation 2012 The Journal of clinical investigation Vol.122 No.1
<P>Mutations in the coactivator CREB-binding protein (CBP) are a major cause of the human skeletal dysplasia Rubinstein-Taybi syndrome (RTS); however, the mechanism by which these mutations affect skeletal mineralization and patterning is unknown. Here, we report the identification of 3-phosphoinositide-dependent kinase 1 (PDK1) as a key regulator of CBP activity and demonstrate that its functions map to both osteoprogenitor cells and mature osteoblasts. In osteoblasts, PDK1 activated the CREB/CBP complex, which in turn controlled runt-related transcription factor 2 (RUNX2) activation and expression of bone morphogenetic protein 2 (BMP2). These pathways also operated in vivo, as evidenced by recapitulation of RTS spectrum phenotypes with osteoblast-specific Pdk1 deletion in mice (Pdk1osx mice) and by the genetic interactions observed in mice heterozygous for both osteoblast-specific Pdk1 deletion and either Runx2 or Creb deletion. Finally, treatment of Pdk1osx and Cbp+/- embryos with BMPs in utero partially reversed their skeletal anomalies at birth. These findings illustrate the in vivo function of the PDK1-AKT-CREB/CBP pathway in bone formation and provide proof of principle for in utero growth factor supplementation as a potential therapy for skeletal dysplasias.</P>