Nonperturbative m_X cut effects in B -> Xs l+ l- observables

Recently, it was shown that in inclusive B -> Xs l+ l- decay, an angular decomposition provides three independent (q^2 dependent) observables. A strategy was formulated to extract all measurable Wilson coefficients in B -> Xs l+ l- from a few simple integrals of these observables in the low q^2 region. The experimental measurements in the low q^2 region require a cut on the hadronic invariant mass, which introduces a dependence on nonperturbative b quark distribution functions. The associated hadronic uncertainties could potentially limit the sensitivity of these decays to new physics. We compute the nonperturbative corrections to all three observables at leading and subleading order in the power expansion in \Lambda_QCD/m_b. We find that the subleading power corrections give sizeable corrections, of order -5% to -10% depending on the observable and the precise value of the hadronic mass cut. They cause a shift of order -0.05 GeV^2 to -0.1 GeV^2 in the zero of the forward-backward asymmetry.Comment: 11 pages, 4 figures, v2: corrected typos and Eq. (25), v3: journal versio

Universality and m_X cut effects in B -> Xs l+ l-

The most precise comparison between theory and experiment for the B -> Xs l+ l- rate is in the low q^2 region, but the hadronic uncertainties associated with an experimentally required cut on m_X potentially spoil the search for new physics in these decays. We show that a 10-30% reduction of d\Gamma(B -> Xs l+ l-) / dq^2 due to the m_X cut can be accurately computed using the B -> X_s gamma shape function. The effect is universal for all short distance contributions in the limit m_X^2 << m_B^2, and this universality is spoiled neither by realistic values of the m_X cut nor by alpha_s corrections. Both the differential decay rate and forward-backward asymmetry with an m_X cut are computed.Comment: 5 pages, journal versio

Extracting short distance information from b-->s[script-l]+[script-l]- effectively

We point out that in inclusive B-->Xs[script-l]+[script-l]- decay an angular decomposition provides a third (q2 dependent) observable sensitive to a different combination of Wilson coefficients than the rate and the forward-backward asymmetry. Since a precise measurement of q2 dependence requires large data sets, it is important to consider the data integrated over regions of q2. We develop a strategy to extract all measurable Wilson coefficients in B-->Xs[script-l]+[script-l]- from a few simple integrated rates in the low q2 region. A similar decomposition in B-->K*[script-l]+[script-l]-, together with the B-->K*gamma rate, also provides a determination of the Wilson coefficients, without reliance on form factor models and without having to measure the zero of the forward-backward asymmetry

An engineered cardiac reporter cell line identifies human embryonic stem cell-derived myocardial precursors.

Unlike some organs, the heart is unable to repair itself after injury. Human embryonic stem cells (hESCs) grow and divide indefinitely while maintaining the potential to develop into many tissues of the body. As such, they provide an unprecedented opportunity to treat human diseases characterized by tissue loss. We have identified early myocardial precursors derived from hESCs (hMPs) using an α-myosin heavy chain (αMHC)-GFP reporter line. We have demonstrated by immunocytochemistry and quantitative real-time PCR (qPCR) that reporter activation is restricted to hESC-derived cardiomyocytes (CMs) differentiated in vitro, and that hMPs give rise exclusively to muscle in an in vivo teratoma formation assay. We also demonstrate that the reporter does not interfere with hESC genomic stability. Importantly, we show that hMPs give rise to atrial, ventricular and specialized conduction CM subtypes by qPCR and microelectrode array analysis. Expression profiling of hMPs over the course of differentiation implicate Wnt and transforming growth factor-β signaling pathways in CM development. The identification of hMPs using this αMHC-GFP reporter line will provide important insight into the pathways regulating human myocardial development, and may provide a novel therapeutic reagent for the treatment of cardiac disease

A Physical Interaction between the Dopamine Transporter and DJ-1 Facilitates Increased Dopamine Reuptake

The regulation of the dopamine transporter (DAT) impacts extracellular dopamine levels after release from dopaminergic neurons. Furthermore, a variety of protein partners have been identified that can interact with and modulate DAT function. In this study we show that DJ-1 can potentially modulate DAT function. Co-expression of DAT and DJ-1 in HEK-293T cells leads to an increase in [3H] dopamine uptake that does not appear to be mediated by increased total DAT expression but rather through an increase in DAT cell surface localization. In addition, through a series of GST affinity purifications and co-immunoprecipitations, we provide evidence that the DAT can be found in a complex with DJ-1, which involve distinct regions within both DAT and DJ-1. Using in vitro binding experiments we also show that this complex can be formed in part by a direct interaction between DAT and DJ-1. Co-expression of a mini-gene that can disrupt the DAT/DJ-1 complex appears to block the increase in [3H] dopamine uptake by DJ-1. Mutations in DJ-1 have been linked to familial forms of Parkinson’s disease, yet the normal physiological function of DJ-1 remains unclear. Our study suggests that DJ-1 may also play a role in regulating dopamine levels by modifying DAT activity