Rare Decays of \Lambda_b->\Lambda + \gamma and \Lambda_b ->\Lambda + l^{+} l^{-} in the Light-cone Sum Rules

Within the Standard Model, we investigate the weak decays of $\Lambda_b \to \Lambda + \gamma$ and $\Lambda_b \to \Lambda + l^{+} l^{-}$ with the light-cone sum rules approach. The higher twist distribution amplitudes of $\Lambda$ baryon to the leading conformal spin are included in the sum rules for transition form factors. Our results indicate that the higher twist distribution amplitudes almost have no influences on the transition form factors retaining the heavy quark spin symmetry, while such corrections can result in significant impacts on the form factors breaking the heavy quark spin symmetry. Two phenomenological models (COZ and FZOZ) for the wave function of $\Lambda$ baryon are also employed in the sum rules for a comparison, which can give rise to the form factors approximately 5 times larger than that in terms of conformal expansion. Utilizing the form factors calculated in LCSR, we then perform a careful study on the decay rate, polarization asymmetry and forward-backward asymmetry, with respect to the decays of $\Lambda_b \to \Lambda \gamma$, $\Lambda l^{+}l^{-}$.Comment: 38 pages, 15 figures, some typos are corrected and more references are adde

Familial thrombocytopenia due to a complex structural variant resulting in a WAC-ANKRD26 fusion transcript

Advances in genome sequencing have resulted in the identification of the causes for numerous rare diseases. However, many cases remain unsolved with standard molecular analyses. We describe a family presenting with a phenotype resembling inherited thrombocytopenia 2 (THC2). THC2 is generally caused by single nucleotide variants that prevent silencing of ANKRD26 expression during hematopoietic differentiation. Short-read whole-exome and genome sequencing approaches were unable to identify a causal variant in this family. Using long-read whole-genome sequencing, a large complex structural variant involving a paired-duplication inversion was identified. Through functional studies, we show that this structural variant results in a pathogenic gain-of-function WAC-ANKRD26 fusion transcript. Our findings illustrate how complex structural variants that may be missed by conventional genome sequencing approaches can cause human disease

Neuro4Neuro: A neural network approach for neural tract segmentation using large-scale population-based diffusion imaging

Subtle changes in white matter (WM) microstructure have been associated with normal aging and neurodegeneration. To study these associations in more detail, it is highly important that the WM tracts can be accurately and reproducibly characterized from brain diffusion MRI. In addition, to enable analysis of WM tracts in large datasets and in clinical practice it is essential to have methodology that is fast and easy to apply. This work therefore presents a new approach for WM tract segmentation: Neuro4Neuro, that is capable of direct extraction of WM tracts from diffusion tensor images using convolutional neural network (CNN). This 3D end-to-end method is trained to segment 25 WM tracts in aging individuals from a large population-based study (N=9752, 1.5T MRI). The proposed method showed good segmentation performance and high reproducibility, i.e., a high spatial agreement (Cohen's kappa, k = 0.72 ~ 0.83) and a low scan-rescan error in tract-specific diffusion measures (e.g., fractional anisotropy: error = 1% ~ 5%). The reproducibility of the proposed method was higher than that of a tractography-based segmentation algorithm, while being orders of magnitude faster (0.5s to segment one tract). In addition, we showed that the method successfully generalizes to diffusion scans from an external dementia dataset (N=58, 3T MRI). In two proof-of-principle experiments, we associated WM microstructure obtained using the proposed method with age in a normal elderly population, and with disease subtypes in a dementia cohort. In concordance with the literature, results showed a widespread reduction of microstructural organization with aging and substantial group-wise microstructure differences between dementia subtypes. In conclusion, we presented a highly reproducible and fast method for WM tract segmentation that has the potential of being used in large-scale studies and clinical practice.Comment: Preprint to be published in NeuroImag

Nonleptonic Λb\Lambda_b decays to Ds(2317)D_s(2317), Ds(2460)D_s(2460) and other final states in Factorization

We consider nonleptonic Cabibbo--allowed $\Lambda_b$ decays in the factorization approximation. We calculate nonleptonic decays of the type $\Lambda_b \to \Lambda_c P$ and $\Lambda_b \to \Lambda_c V$ relative to $\bar{B}_d \to D^+ P$ and $\bar{B}_d \to D^+ V$ where we include among the pseudoscalar states(P) and the vector states(V) the newly discovered $D_s$ resonances, $D_s(2317)$ and $D_s(2460)$. In the ratio of $\Lambda_b$ decays to $D_s(2317)$ and $D_s(2460)$ relative to the $\bar{B}_d$ decays to these states, the poorly known decay constants of $D_s(2317)$ and $D_s(2460)$ cancel leading to predictions that can shed light on the nature of these new states. In general, we predict the $\Lambda_b$ decays to be larger than the corresponding $\bar{B}_d$ decays and in particular we find the branching ratio for $\Lambda_b \to \Lambda_c D_s(2460)$ can be between four to five times the branching ratio for $\bar{B}_d \to D^+ D_s(2460)$. This enhancement of $\Lambda_b$ branching ratios follows primarily from the fact that more partial waves contribute in $\Lambda_b$ decays than in $\bar{B}_d$ decays. Our predictions are largely independent of model calculations of hadronic inputs like form factors and decay constants.Comment: 16 pages LaTe

Size Doesn't Matter: Towards a More Inclusive Philosophy of Biology

notes: As the primary author, O’Malley drafted the paper, and gathered and analysed data (scientific papers and talks). Conceptual analysis was conducted by both authors.publication-status: Publishedtypes: ArticlePhilosophers of biology, along with everyone else, generally perceive life to fall into two broad categories, the microbes and macrobes, and then pay most of their attention to the latter. ‘Macrobe’ is the word we propose for larger life forms, and we use it as part of an argument for microbial equality. We suggest that taking more notice of microbes – the dominant life form on the planet, both now and throughout evolutionary history – will transform some of the philosophy of biology’s standard ideas on ontology, evolution, taxonomy and biodiversity. We set out a number of recent developments in microbiology – including biofilm formation, chemotaxis, quorum sensing and gene transfer – that highlight microbial capacities for cooperation and communication and break down conventional thinking that microbes are solely or primarily single-celled organisms. These insights also bring new perspectives to the levels of selection debate, as well as to discussions of the evolution and nature of multicellularity, and to neo-Darwinian understandings of evolutionary mechanisms. We show how these revisions lead to further complications for microbial classification and the philosophies of systematics and biodiversity. Incorporating microbial insights into the philosophy of biology will challenge many of its assumptions, but also give greater scope and depth to its investigations

Integrated analysis of environmental and genetic influences on cord blood DNA methylation in new-borns

Epigenetic processes, including DNA methylation (DNAm), are among the mechanisms allowing integration of genetic and environmental factors to shape cellular function. While many studies have investigated either environmental or genetic contributions to DNAm, few have assessed their integrated effects. Here we examine the relative contributions of prenatal environmental factors and genotype on DNA methylation in neonatal blood at variably methylated regions (VMRs) in 4 independent cohorts (overall n = 2365). We use Akaike’s information criterion to test which factors best explain variability of methylation in the cohort-specific VMRs: several prenatal environmental factors (E), genotypes in cis (G), or their additive (G + E) or interaction (GxE) effects. Genetic and environmental factors in combination best explain DNAm at the majority of VMRs. The CpGs best explained by either G, G + E or GxE are functionally distinct. The enrichment of genetic variants from GxE models in GWAS for complex disorders supports their importance for disease risk