Paul–Straubel–Kingdon trap for true zero-point confinement of an individual ion and reservoir

A modification of the Paul–Straubel trap previously described by us may profitably be operated in a Paul–Straubel–Kingdon (PSK) mode during the initial loading of an individual ion into the trap. Thereby the coating of the trap ring electrode by the atomic beam directed upon it in earlier experiments is eliminated, as is the ionization of an already trapped ion. Coating created serious problems as it spot-wise changed the work function of the ring electrode, which caused large, uncontrolled dc fields in the trap center that prevented zero-point confinement. Operating the Paul–Straubel trap with a small negative bias on the ring electrode wire is all that is required to realize the PSK mode. In this mode the tiny ring trap in the center of the long, straight wire section is surrounded by a second trapping well shaped like a long, thin-walled cylindrical shell and extending to the end-caps. There, ions may be conveniently created in this well without danger of coating the ring with barium. In addition, the long second well is useful as a multi-ion reservoir.

Mouse model of human beta zero thalassemia: targeted deletion of the mouse beta maj- and beta min-globin genes in embryonic stem cells.

beta zero-Thalassemia is an inherited disorder characterized by the absence of beta-globin polypeptides derived from the affected allele. The molecular basis for this deficiency is a mutation of the adult beta-globin structural gene or cis regulatory elements that control beta-globin gene expression. A mouse model of this disease would enable the testing of therapeutic regimens designed to correct the defect. Here we report a 16-kb deletion that includes both adult beta-like globin genes, beta maj and beta min, in mouse embryonic stem cells. Heterozygous animals derived from the targeted cells are severely anemic with dramatically reduced hemoglobin levels, abnormal red cell morphology, splenomegaly, and markedly increased reticulocyte counts. Homozygous animals die in utero; however, heterozygous mice are fertile and transmit the deleted allele to progeny. The anemic phenotype is completely rescued in progeny derived from mating beta zero-thalassemic animals with transgenic mice expressing high levels of human hemoglobin A. The beta zero-thalassemic mice can be used to test genetic therapies for beta zero-thalassemia and can be bred with transgenic mice expressing high levels of human hemoglobin HbS to produce an improved mouse model of sickle cell disease.