CP-safe Gravity Mediation and Muon g-2

We propose a CP-safe gravity mediation model, where the phases of the Higgs B parameter, scalar trilinear couplings and gaugino mass parameters are all aligned. Since all dangerous CP violating phases are suppressed, we are now safe to consider low-energy SUSY scenarios. As an application, we consider a gravity mediation model explaining the observed muon $g-2$ anomaly. The CP-safe property originates in two simple assumptions: SUSY breaking in the K\"ahler potential and a shift symmetry of a SUSY breaking field $Z$. As a result of the shift symmetry, the imaginary part of $Z$ behaves as a QCD axion, leading to an intriguing possibility: the strong CP problem in QCD and the SUSY CP problem are solved simultaneously.Comment: 23 pages, 2 figures; v2 with additional explanation

Spin-dependent observables in surrogate reactions

Observables emitted from various spin states in compound U nuclei are investigated to validate usefulness of the surrogate reaction method. It was found that energy spectrum of cascading $\gamma$-rays and their multiplicities, spectrum of evaporated neutrons, and mass-distribution of fission fragments show clear dependence on the spin of decaying nuclei. The present results indicate that they can be used to infer populated spin distributions which significantly affect the decay branching ratio of the compound system produced by the surrogate reactions

Participation of Cbfa1 in regulation of chondrocyte maturation

AbstractObjective Cbfa1 is a transcription factor, which is classified into the runt family. The mice lacking this gene display complete loss of bone formation, indicating that Cbfa1 is an essential factor for osteoblast differentiation. The Cbfa1-deficient mice also show an abnormality in cartilage development. Although cartilage anlagens are well formed in these mice, endochondral ossification is blocked, and most of chondrocytes fail to differentiate into their maturation form as characterized by the absence of type X collagen and low levels of alkaline phosphatase activity. It is suggested that Cbfa1 may participate in chondrocyte differentiation. In this study, we have investigated the role of Cbfa1 in chondrocytes during their cytodifferentiation in vitro.Design To investigate the role of Cbfa1 in regulation of chondrocyte differentiation, we over-expressed Cbfa1 or its dominant negative form in cultured chick chondrocytes using a retrovirus (RCAS)system and examined changes in chondrocyte behaviour induced by the introduced genes.Results Mature chondrocytes isolated form the cephalic portion of sterna seemed to express Cbfa1 more prominently than immature chondrocytes isolated from the one-third caudal portion of sterna. Over-expression of Cbfa1 in immature chondrocytes strongly stimulated alkaline phosphatase activity and matrix calcification. In contrast, expression of a dominant negative form of Cbfa1, which lacks the C-terminal PST domain, severely inhibited alkaline phosphatase activity and matrix calcification in mature chondrocytes.Conclusion Taken together with the observation that Cbfa1 transcripts dominantly localized in hypertrophic chondrocytes as well as in osteoblasts, it is suggested that Cbfa1 plays an important role in the progression of chondrocyte maturation

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