Two-electron QED contributions to the ground-state binding energy in He-like Kr34+ ions

The two-electron QED contributions to the ground-state binding energy of Kr34+ ions have been determined in two independent experiments performed with electron beam ion traps (EBIT) in Heidelberg (HD) and Tokyo (BT, Belfast-Tokyo collaboration). X rays arising from radiative recombination (RR) of free electrons to the ground state of initially bare Kr36+ and hydrogenlike Kr35+ ions were observed as a function of the interacting electron energy. The K edge absorption by thin Eu and W foils provided fixed photon energy references used to measure the difference in binding energy Delta E-2e between the H- and He-like Kr ions (Kr35+ and Kr34+, respectively). The two values agree well, yielding a final result of Delta E-2e=641.8 +/- 1.7 eV, confirming recent results of rigorous QED calculations. This accuracy is just of the order required to access screened radiative QED contributions.

Agelastatin A: a novel inhibitor of osteopontin-mediated adhesion, invasion, and colony formation

Effective inhibitors of osteopontin (OPN)-mediated neoplastic transformation and metastasis are still lacking. (-)-Agelastatin A is a naturally occurring oroidin alkaloid with powerful antitumor effects that, in many cases, are superior to cisplatin in vitro. In this regard, past comparative assaying of the two agents against a range of human tumor cell lines has revealed that typically (-)-agelastatin A is 1.5 to 16 times more potent than cisplatin at inhibiting cell growth, its effects being most pronounced against human bladder, skin, colon, and breast carcinomas. In this study, we have investigated the effects of (-)-agelastatin A on OPN-mediated malignant transformation using mammary epithelial cell lines. Treatment with (-)-agelastatin A inhibited OPN protein expression and enhanced expression of the cellular OPN inhibitor, Tcf-4. (-)-Agelastatin A treatment also reduced beta-catenin protein expression and reduced anchorage-independent growth, adhesion, and invasion in R37 OPN pBK-CMV and C9 cell lines. Similar effects were observed in MDA-MB-231 and MDA-MB-435s human breast cancer cell lines exposed to (-)-agelastatin A. Suppression of Tcf-4 by RNA interference (short interfering RNA) induced malignant/invasive transformation in parental benign Rama 37 cells; significantly, these events were reversed by treatment with (-)-agelastatin A. Our study reveals, for the very first time, that (-)-agelastatin A down-regulates beta-catenin expression while simultaneously up-regulating Tcf-4 and that these combined effects cause repression of OPN and inhibition of OPN-mediated malignant cell invasion, adhesion, and colony formation in vitro. We have also shown that (-)-agelastatin A inhibits cancer cell proliferation by causing cells to accumulate in the G(2) phase of cell cycle.