Activation cross sections of the 169Tm(d,2n) reaction for production of the therapeutic radionuclide 169Yb

Activation cross sections of deuteron induced nuclear reactions on (169)Tm were measured up to 20 MeV by using the stacked-foil technique. Special emphasis was on production of the internal radiotherapy related radionuclide (169)Yb. No earlier experimental cross-section data on deuteron induced reactions on (169)Tm were found in the literature. The experimental data were compared with the results of the nuclear model codes ALICE-IPPE and EMPIRE-II. The integral yield of the (169)Tm(d,2n)(169)Yb reaction was deduced over the optimum energy range Ed = 20-->9 MeV. At 3.8 MBq/microA.h the yield is lower than that available from the commonly used (168)Yb(n,gamma) (169)Yb reactor method but on the other hand, it is higher than the yields from the earlier investigated (169)Tm(p,n)(169)Yb and (nat)Er(alpha,x) (169)Yb reactions

Glucocorticoids suppress bone formation by attenuating osteoblast differentiation via the monomeric glucocorticoid receptor

Development of osteoporosis severely complicates long-term glucocorticoid (GC) therapy. Using a Cre-transgenic mouse line, we now demonstrate that GCs are unable to repress bone formation in the absence of glucocorticoid receptor (GR) expression in osteoblasts as they become refractory to hormone-induced apoptosis, inhibition of proliferation, and differentiation. In contrast, GC treatment still reduces bone formation in mice carrying a mutation that only disrupts GR dimerization, resulting in bone loss in vivo, enhanced apoptosis, and suppressed differentiation in vitro. The inhibitory GC effects on osteoblasts can be explained by a mechanism involving suppression of cytokines, such as interleukin 11, via interaction of the monomeric GR with AP-1, but not NF-kappaB. Thus, GCs inhibit cytokines independent of GR dimerization and thereby attenuate osteoblast differentiation, which accounts, in part, for bone loss during GC therapy