Successful Prediction of Total α-Induced Reaction Cross Sections at Astrophysically Relevant Sub-Coulomb Energies Using a Novel Approach

The prediction of stellar ($\gamma$,$\alpha$) reaction rates for heavy nuclei is based on the calculation of ($\alpha$,$\gamma$) cross sections at sub-Coulomb energies. These rates are essential for modeling the nucleosynthesis of so-called $p$-nuclei. The standard calculations in the statistical model show a dramatic sensitivity to the chosen $\alpha$-nucleus potential. The present study explains the reason for this dramatic sensitivity which results from the tail of the imaginary $\alpha$-nucleus potential in the underlying optical model calculation of the total reaction cross section. As an alternative to the optical model, a simple barrier transmission model is suggested. It is shown that this simple model in combination with a well-chosen $\alpha$-nucleus potential is able to predict total $\alpha$-induced reaction cross sections for a wide range of heavy target nuclei above $A \gtrsim 150$ with uncertainties below a factor of two. The new predictions from the simple model do not require any adjustment of parameters to experimental reaction cross sections whereas in previous statistical model calculations all predictions remained very uncertain because the parameters of the $\alpha$-nucleus potential had to be adjusted to experimental data. The new model allows to predict the reaction rate of the astrophysically important $^{176}$W($\alpha$,$\gamma$)$^{180}$Os reaction with reduced uncertainties, leading to a significantly lower reaction rate at low temperatures. The new approach could also be validated for a broad range of target nuclei from $A \approx 60$ up to $A \gtrsim 200$.Comment: 6 pages, 3 figures; 6 pages supplement with 3 additional figures and 3 tables; Physical Review Letters, accepted for publicatio

BMP9 Mutations Cause a Vascular-Anomaly Syndrome with Phenotypic Overlap with Hereditary Hemorrhagic Telangiectasia

Hereditary hemorrhagic telangiectasia (HHT), the most common inherited vascular disorder, is caused by mutations in genes involved in the transforming growth factor beta (TGF-β) signaling pathway (ENG, ACVRL1, and SMAD4). Yet, approximately 15% of individuals with clinical features of HHT do not have mutations in these genes, suggesting that there are undiscovered mutations in other genes for HHT and possibly vascular disorders with overlapping phenotypes. The genetic etiology for 191 unrelated individuals clinically suspected to have HHT was investigated with the use of exome and Sanger sequencing; these individuals had no mutations in ENG, ACVRL1, and SMAD4. Mutations in BMP9 (also known as GDF2) were identified in three unrelated probands. These three individuals had epistaxis and dermal lesions that were described as telangiectases but whose location and appearance resembled lesions described in some individuals with RASA1-related disorders (capillary malformation-arteriovenous malformation syndrome). Analyses of the variant proteins suggested that mutations negatively affect protein processing and/or function, and a bmp9-deficient zebrafish model demonstrated that BMP9 is involved in angiogenesis. These data confirm a genetic cause of a vascular-anomaly syndrome that has phenotypic overlap with HHT