Nonfactorizable contributions in B decays to charmonium: the case of B−→K−hcB^- \to K^- h_c

Nonleptonic $B$ to charmonium decays generally show deviations from the factorization predictions. For example, the mode $B^- \to K^- \chi_{c0}$ has been experimentally observed with sizeable branching fraction while its factorized amplitude vanishes. We investigate the role of rescattering effects mediated by intermediate charmed meson production in this class of decay modes, and consider $B^- \to K^- h_c$ with $h_c$ the $J^{PC}=1^{+-}$ $\bar c c$ meson. Using an effective lagrangian describing interactions of pairs of heavy-light $Q{\bar q}$ mesons with a quarkonium state, we relate this mode to the analogous mode with $\chi_{c0}$ in the final state. We find ${\cal B}(B^- \to K^- h_c)$ large enough to be measured at the $B$ factories, so that this decay mode could be used to study the poorly known $h_c$.Comment: RevTex, 16 pages, 2 eps figure

Feasibility of a subcutaneous gluteal turnover flap without donor site scar for perineal closure after abdominoperineal resection for rectal cancer

Background: Abdominoperineal resection (APR) carries a high risk of perineal wound morbidity. Perineal wound closure using autologous tissue flaps has been shown to be advantageous, but there is no consensus as to the optimal method. The aim of this study was to evaluate the feasibility of a novel gluteal turnover flap (GT-flap) without donor site scar for perineal closure after APR. Methods: Consecutive patients who underwent APR for primary or recurrent

A connection between inclusive semileptonic decays of bound and free heavy quarks

A relativistic constituent quark model, formulated on the light-front, is used to derive a new parton approximation for the inclusive semileptonic decay width of the B-meson. A simple connection between the decay rate of a free heavy-quark and the one of a heavy-quark bound in a meson or in a baryon is established. The main features of the new approach are the treatment of the b-quark as an on-mass-shell particle and the inclusion of the effects arising from the b-quark transverse motion in the B-meson. In a way conceptually similar to the deep-inelastic scattering case, the B-meson inclusive width is expressed as the integral of the free b-quark partial width multiplied by a bound-state factor related to the b-quark distribution function in the B-meson. The non-perturbative meson structure is described through various quark-model wave functions, constructed via the Hamiltonian light-front formalism using as input both relativized and non-relativistic potential models. A link between spectroscopic quark models and the B-meson decay physics is obtained in this way. Our predictions for the B -> X_c l nu_l and B -> X_u l nu_l decays are used to extract the CKM parameters |V_cb| and |V_ub| from available inclusive data. After averaging over the various quark models adopted and including leading-order perturbative QCD corrections, we obtain |V_cb| = (43.0 +/- 0.7_exp +/- 1.8_th) 10^-3 and |V_ub| = (3.83 +/- 0.48_exp +/- 0.14_th) 10^-3, implying |V_ub / V_cb| = 0.089 +/- 0.011_exp +/- 0.005_th, in nice agreement with existing predictions.Comment: revised version with pQCD corrections included, to appear in Physical Review

A Phenomenological Analysis of Heavy Hadron Lifetimes

A phenomenological analysis of lifetimes of bottom and charmed hadrons within the framework of the heavy quark expansion is performed. The baryon matrix element is evaluated using the bag model and the nonrelativistic quark model. We find that bottom-baryon lifetimes follow the pattern $\tau(\Omega_b)\simeq\tau(\Xi_b^-)>\tau(\Lambda_b)\simeq\tau(\Xi_b^0)$. However, neither the lifetime ratio $\tau(\Lambda_b)/\tau( B_d)$ nor the absolute decay rates of the $\Lambda_b$ baryon and $B$ mesons can be explained. One way of solving both difficulties is to allow the presence of linear $1/m_Q$ corrections by scaling the inclusive nonleptonic width with the fifth power of the hadron mass $m_{H_Q}$ rather than the heavy quark mass $m_Q$. The hierarchy of bottom baryon lifetimes is dramatically modified to $\tau(\Lambda_b)>\tau(\Xi_b^-)>\tau(\Xi_b^0)>\tau( \Omega_b)$: The longest-lived $\Omega_b$ among bottom baryons in the OPE prescription now becomes shortest-lived. The replacement of $m_Q$ by $m_{H_Q}$ in nonleptonic widths is natural and justified in the PQCD-based factorization approach formulated in terms of hadron-level kinematics. For inclusive charmed baryon decays, we argue that since the heavy quark expansion does not converge, local duality cannot be tested in this case. We show that while the ansatz of substituting the heavy quark mass by the hadron mass provides a much better description of the charmed-baryon lifetime {\it ratios}, it appears unnatural and unpredictive for describing the {\it absolute} inclusive decay rates of charmed baryons, contrary to the bottom case.Comment: 35 pages, to appear in Phys. Rev. The CDF result on the lifetime ratio of Lambda_b and B_d is discusse

Nonresonant Semileptonic Heavy Quark Decay

In both the large N_c limit and the valence quark model, semileptonic decays are dominated by resonant final states. Using Bjorken's sum rule in an "unquenched" version of the quark model, I demonstrate that in the heavy quark limit nonresonant final states should also be produced at a significant rate. By calculating the individual strengths of a large number of exclusive two-body nonresonant channels, I show that the total rate for such processes is highly fragmented. I also describe some very substantial duality-violating suppression factors which reduce the inclusive nonresonant rate to a few percent of the total semileptonic rate for the finite quark masses of B decay, and comment on the importance of nonresonant decays as testing grounds for very basic ideas on the structure, strength, and significance of the quark-antiquark sea and on quark-hadron duality in QCD.Comment: 51 pages, 2 Postscript figure

Perineal wound closure using gluteal turnover flap or primary closure after abdominoperineal resection for rectal cancer: study protocol of a randomised controlled multicentre trial (BIOPEX-2 study)

BACKGROUND: Abdominoperineal resection (APR) for rectal cancer is associated with high morbidity of the perineal wound, and controversy exists about the optimal closure technique. Primary perineal wound closure is still the standard of care in the Netherlands. Biological mesh closure did not improve wound healing in our previous randomised controlled trial (BIOPEX-study). It is suggested, based on meta-analysis of cohort studies, that filling of the perineal defect with well-vascularised tissue improves perineal wound healing. A gluteal turnover flap seems to be a promising method for this purpose, and with the advantage of not having a donor site scar. The aim of this study is to investigate whether a gluteal turnover flap improves the uncomplicated perineal wound healing after APR for rectal cancer. METHODS: Patients with primary or recurrent rectal cancer who are planned for APR will be considered eligible in this multicentre randomised controlled trial. Exclusion criteria are total exenteration, sacral resection above S4/S5, intersphincteric APR, biological mesh closure of the pelvic floor, collagen disorders, and severe systemic diseases. A total of 160 patients will be randomised between gluteal turnover flap (experimental arm) and primary closure (control arm). The total follow-up duration is 12 months, and outcome assessors and patients will be blinded for type of perineal wound closure. The primary outcome is the percentage of uncomplicated perineal wound healing on day 30, defined as a Southampton wound score of less than two. Secondary outcomes include time to perineal wound closure, incidence of perineal hernia, the number, duration and nature of the complications, re-interventions, quality of life and urogenital function. DISCUSSION: The uncomplicated perineal wound healing rate is expected to increase from 65 to 85% by using the gluteal turnover flap. With proven effectiveness, a quick implementation of this relatively simple surgical technique is expected to take place. TRIAL REGISTRATION: The trial was retrospectively registered at Clinicaltrials.gov NCT04004650 on July 2, 2019

Pathogenic neurofibromatosis type 1 (NF1) RNA splicing resolved by targeted RNAseq

Neurofibromatosis type 1 (NF1) is caused by loss-of-function variants in the NF1 gene. Approximately 10% of these variants affect RNA splicing and are either missed by conventional DNA diagnostics or are misinterpreted by in silico splicing predictions. Therefore, a targeted RNAseq-based approach was designed to detect pathogenic RNA splicing and associated pathogenic DNA variants. For this method RNA was extracted from lymphocytes, followed by targeted RNAseq. Next, an in-house developed tool (QURNAs) was used to calculate the enrichment score (ERS) for each splicing event. This method was thoroughly tested using two different patient cohorts with known pathogenic splice-variants in NF1. In both cohorts all 56 normal reference transcript exon splice junctions, 24 previously described and 45 novel non-reference splicing events were detected. Additionally, all expected pathogenic splice-variants were detected. Eleven patients with NF1 symptoms were subsequently tested, three of which have a known NF1 DNA variant with a putative effect on RNA splicing. This effect could be confirmed for all 3. The other eight patients were previously without any molecular confirmation of their NF1-diagnosis. A deep-intronic pathogenic splice variant could now be identified for two of them (25%). These results suggest that targeted RNAseq can be successfully used to detect pathogenic RNA splicing variants in NF1

Pathogenic neurofibromatosis type 1 (NF1) RNA splicing resolved by targeted RNAseq

Neurofibromatosis type 1 (NF1) is caused by loss-of-function variants in the NF1 gene. Approximately 10% of these variants affect RNA splicing and are either missed by conventional DNA diagnostics or are misinterpreted by in silico splicing predictions. Therefore, a targeted RNAseq-based approach was designed to detect pathogenic RNA splicing and associated pathogenic DNA variants. For this method RNA was extracted from lymphocytes, followed by targeted RNAseq. Next, an in-house developed tool (QURNAs) was used to calculate the enrichment score (ERS) for each splicing event. This method was thoroughly tested using two different patient cohorts with known pathogenic splice-variants in NF1. In both cohorts all 56 normal reference transcript exon splice junctions, 24 previously described and 45 novel non-reference splicing events were detected. Additionally, all expected pathogenic splice-variants were detected. Eleven patients with NF1 symptoms were subsequently tested, three of which have a known NF1 DNA variant with a putative effect on RNA splicing. This effect could be confirmed for all 3. The other eight patients were previously without any molecular confirmation of their NF1-diagnosis. A deep-intronic pathogenic splice variant could now be identified for two of them (25%). These results suggest that targeted RNAseq can be successfully used to detect pathogenic RNA splicing variants in NF1.Genetics of disease, diagnosis and treatmen