We review the parameter regions allowed by measurements of R(D ( * ) ) and by a theoretical limit on B(B c → τ ν) in terms of generic scalar and pseudoscalar new physics couplings, g s and g p . We then use these regions as constraints to predict the ranges for additional observables in b → cτ ν including the differential decay distributions dΓ/dq 2 ; the ratios R(J/ψ) and R(Λ c ); and the tau-lepton polarisation in B → D ( ) τ ν, with emphasis on the CP violating normal polarisation. Finally we map the allowed regions in g s and g p into the parameters of four versions of the Yukawa couplings of the general 2HDM-III model. We find that the model is still viable but could be ruled out by a confirmation of a large R(J/ψ).
We present a likelihood analysis of the general two Higgs doublet model, using the most important currently measured flavour observables, in view of the anomalies in charged current tree-level and neutral current one-loop rare decays of B mesons in b → cl$$ \overline{\nu} $$
ν
¯
and b → sμ+μ− transitions, respectively. We corroborate that the model explains the latter and it is able to simultaneously fit the experimental values of the R(D) charged current ratio at 1σ, but it can not accommodate the D* charmed meson observables R(D*) and FL(D*). We find that the fitted values for the angular observables in b → sμ+μ− transitions exhibit better agreement with the general two Higgs double model in comparison to the SM. We also make predictions for future collider observables BR(t → ch), BR(h → bs), BR(h → τμ), BR(Bs → τ+τ−), BR(B+ → K+τ+τ−) and the flavour violating decays of the τ lepton, BR(τ → 3μ) and BR(τ → μγ). The model predicts values of BR(t → ch), BR(Bs → τ+τ−) and BR(B+ → K+τ+τ−) that are out of reach of future experiments, but its predictions for BR(h → bs) and BR(h → τμ) are within the future sensitivity of the HL-LHC or the ILC. We also find that the predictions for the τ → 3μ and τ → μγ decays are well within the projected limits of the Belle II experiment. Finally, using the latest measurement of the Fermilab Muon g − 2 Collaboration, we performed a simultaneous fit to ∆aμ constrained by the charged anomalies, finding solutions at the 1σ level. Once the neutral anomalies are included, however, a simultaneous explanation is unfeasible.
Due to their capacity to proliferate, migrate, and differentiate, mesenchymal stem cells (MSCs) are considered to be good candidates for regenerative medicine applications. The mechanisms underlying proliferation and differentiation of MSCs have been studied. However, much less is known about the mechanisms regulating the migration of MSCs. Platelet lysate (PL), a supplement used to promote cell expansion, has been shown to promote MSCs migration; however, the underlying mechanism are unknown. Here, by using adipose-derived rat MSCs (rMSCs) and the scratch assay in the absence and presence of various BK channels modulators, we evaluated the role of BK channels in mediating the PL-stimulated migration of rMSCs. We found that 5% PL increased rMSCs migration, and this effect was blocked by the addition of the BK channel selective antagonist Iberiotoxin (IBTX). In the absence of PL, the BK channel agonist NS1619, stimulated rMSCs migration to similar level as 5% PL. Addition of both NS1619 and 5% PL resulted in an increase in rMSCs migration, that was higher than when either one was added individually. From whole-cell recordings, it was found that the addition of 5% PL increased the magnitude of BK current density. By using Western blot and flow cytometry, it was found that PL did not affect the expression of BK channels. Together, our results indicate that as shown in other cell types, activation of BK channels by themselves also promote rMSC migration, and show that activation of BK channels contribute to the observed PL-induced increase in migration of rMSC.
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