Prospects of forming ultracold molecules in double-Sigma states by magnetoassociation of alkali-metal atoms with Yb

We explore the feasibility of producing ultracold diatomic molecules with nonzero electric and magnetic dipole moments by magnetically associating two atoms, one with zero electron spin and one with nonzero spin. Feshbach resonances arise through the dependence of the hyperfine coupling on internuclear distance.We survey the Feshbach resonances in diatomic systems combining the nine stable alkali-metal isotopes with those of Yb, focusing on the illustrative examples of RbYb and CsYb. We show that the resonance widths may expressed as a product of physically comprehensible terms in the framework of Fermi’s golden rule. The resonance widths depend strongly on the background scattering length, which may be adjusted by selecting the Yb isotope, and on the hyperfine coupling constant and the magnetic field. In favorable cases the resonances may be over 100 mG wide

Magnetically Tunable Feshbach Resonances in Ultracold Li-Yb Mixtures

We investigate the possibility of forming Li+Yb ultracold molecules by magnetoassociation in mixtures of ultracold atoms. We find that magnetically tunable Feshbach resonances exist, but are extremely narrow for even-mass ytterbium isotopes, which all have zero spin. For odd-mass Yb isotopes, however, there is a new mechanism due to hyperfine coupling between the electron spin and the Yb nuclear magnetic moment. This mechanism produces Feshbach resonances for fermionic Yb isotopes that can be more than 2 orders of magnitude larger than for the bosonic counterparts

Nfkb2

NF-κB2/p100 (p100) is an inhibitor of κB (IκB) protein that is partially degraded to produce the NF-κB2/p52 (p52) transcription factor. Heterozygous NFKB2 mutations cause a human syndrome of immunodeficiency and autoimmunity, but whether autoimmunity arises from insufficiency of p52 or IκB function of mutated p100 is unclear. Here, we studied mice bearing mutations in the p100 degron, a domain that harbors most of the clinically recognized mutations and is required for signal-dependent p100 degradation. Distinct mutations caused graded increases in p100-degradation resistance. Severe p100-degradation resistance, due to inheritance of one highly degradation-resistant allele or two subclinical alleles, caused thymic medullary hypoplasia and autoimmune disease, whereas the absence of p100 and p52 did not. We inferred a similar mechanism occurs in humans, as the T cell receptor repertoires of affected humans and mice contained a hydrophobic signature of increased self-reactivity. Autoimmunity in autosomal dominant NFKB2 syndrome arises largely from defects in nonhematopoietic cells caused by the IκB function of degradation-resistant p100