Spontaneous two photon emission from a single quantum dot

Spontaneous two photon emission from a solid-state single quantum emitter is observed. We investigated photoluminescence from the neutral biexciton in a single semiconductor quantum dot coupled with a high Q photonic crystal nanocavity. When the cavity is resonant to the half energy of the biexciton, the strong vacuum field in the cavity inspires the biexciton to simultaneously emit two photons into the mode, resulting in clear emission enhancement of the mode. Meanwhile, suppression was observed of other single photon emission from the biexciton, as the two photon emission process becomes faster than the others at the resonance.Comment: 13 pages, 4 figure

LHC Benchmarks from Flavored Gauge Mediation

We present benchmark points for LHC searches from flavored gauge mediation models, in which messenger-matter couplings give flavor-dependent squark masses. Our examples include spectra in which a single squark - stop, scharm, or sup - is much lighter than all other colored superpartners, motivating improved quark flavor tagging at the LHC. Many examples feature flavor mixing; in particular, large stop-scharm mixing is possible. The correct Higgs mass is obtained in some examples by virtue of the large stop A-term. We also revisit the general flavor and CP structure of the models. Even though the A-terms can be substantial, their contributions to EDM's are very suppressed, because of the particular dependence of the A-terms on the messenger coupling. This holds regardless of the messenger-coupling texture. More generally, the special structure of the soft terms often leads to stronger suppression of flavor- and CP-violating processes, compared to naive estimates.Comment: 32 pages, 11 figures. Updated to published versio

Hypertension, Na+/Ca2+ exchanger, and Na+, K+-ATPase

Hypertension is the most prevalent risk factor for stroke, myocardial infarction, or end-stage renal failure. The critical importance of excess salt intake in the pathogenesis of hypertension is widely recognized, but the mechanisms whereby salt intake elevates blood pressure have puzzled researchers. Recent studies using Na+/Ca2+ exchange inhibitors and genetically engineered mice provide evidence that vascular Na+/Ca2+ exchanger type 1 (NCX1) is involved in the development of salt-dependent hypertension. Endogenous cardiac glycosides, which may contribute to salt-dependent hypertension, seem to be necessary for NCX1-mediated hypertension. Intriguingly, studies using knock-in mice with modified cardiac glycoside binding affinity of Na+,K+-ATPases provide a clear demonstration that this cardiac glycoside-binding site plays an important role in blood pressure regulation. Taken all together: (1) endogenous cardiac glycosides are secreted after high salt intake; (2) these cardiac glycosides inhibit Na+,K+-ATPase in vascular smooth muscle cells; (3) this inhibition results in the elevation of local Na+ on the submembrane area; and (4) this elevation of local Na+ facilitates Ca2+ entry through NCX1, resulting in vasoconstriction. This proposed pathway may have enabled us to explain how to link dietary salt to hypertension