On the Scale Uncertainties in the B→XsγB \to X_s \gamma Decay

We analyze the theoretical uncertainties in $Br(B\to X_s\gamma)$ due to the choice of the high energy matching scale \mu_W=\ord(\mw) and the scale $\mu_t$ at which the running top quark mass is defined: \mtb(\mu_t). To this end we have repeated the calculation of the initial conditions confirming the final results of Adel and Yao and Greub and Hurth and generalizing them to include the dependences on $\mu_t$ and $\mu_W$ with $\mu_t\not=\mu_W$. In the leading order the $\mu_W$ and $\mu_t$ uncertainties in $Br(B\to X_s\gamma)$ turn out to be $\pm 13$ and $\pm 3$ respectively. We show analytically how these uncertainties are reduced after including next-to-leading QCD corrections. They amount to $\pm 1.1$ and $\pm 0.4$ respectively. Reanalyzing the uncertainties due to the scale \mu_b=\ord(m_b) we find that after the inclusion of NLO effects they amount to $\pm 4.3$ which is a factor 2/3 smaller than claimed in the literature. Including the uncertainties due to input parameters as well as the non-perturbative $1/m_b^2$ and $1/m_c^2$ corrections we find $Br(B{\to}X_s \gamma) = (3.60 \pm 0.33) \times 10^{-4}$ where the error is dominated by uncertainties in the input parameters. This should be compared with $(3.28 \pm 0.33) \times 10^{-4}$ found by Chetyrkin et al. where the error is shared evenly between the scale and parametric uncertainties.Comment: 11 pages, Latex. The paper is updated by incorporating recently modified results of the literature that were used for the numerical evaluation of eq. (17). A term originally missing in eq. (22) is adde

Next-To-Leading-Order Matching for the Magnetic Photon-Penguin Operator in the B→XsγB \to X_s \gamma Decay

The initial condition at the matching scale $\mu_W = O(M_W)$ for the Wilson coefficient of the magnetic photon-penguin operator in the decay $B\to X_s \gamma$ is calculated in the next-to-leading-order approximation. The technical details of the necessary two-loop calculation in the full theory are described and the matching with the corresponding result in the effective theory is discussed in detail. Our outcome for the initial condition confirms the final results of Adel and Yao and Greub and Hurth. We show that --- contrary to the claims in the second of these papers --- the matching procedure can be properly performed for infrared divergent amplitudes, i.e. independently of contributions from gluon bremsstrahlung.Comment: 24 pages, Latex, 3 Figure

Bremsstrahlung corrections to the decay b→sγb \to s \gamma

We calculate the O($\alpha_s$) gluon Bremsstrahlung corrections to the inclusive decay $b \rightarrow s \gamma$, involving the full operator basis $\hat O_1$ -- $\hat O_8$. Confirming and extending earlier calculations of Ali and Greub, we give formulas for the total decay width as well as the perturbative photon spectrum, regarding the former as a necessary part of the forthcoming complete NLO analysis. We explore in detail the renormalization scale dependence of our results and find it considerably increased.Comment: 23 pages, LaTeX, uses epsf.sty and rotate.sty. 4 figures (uuencoded postscript) appended as seperate file. A complete postscript version may be obtained from URL ftp://feynman.t30.physik.tu-muenchen.de/pub/preprints/tum-93-95.ps.gz Final version as to appear in Physical Review D. Some minor errors corrected, without changes in the numerical results. One reference adde

Electroweak effects in the B0−Bˉ0B^0-{\bar B}^0 mixing

We compute analytically the complete electroweak two-loop corrections to the $B^0-{\bar B}^0$ mixing. These corrections fix the normalization of the electroweak coupling employed in the extraction of $|V_{td}|$ and reduce the theoretical uncertainty due to higher order electroweak effects from several percent to a few parts in a thousand. If the LO result is expressed in terms of $G_\mu$ or of the $\bar{MS}$ coupling $\hat{g}(M_Z)$, the two-loop corrections are $O(1$, the exact value depending on the mass of the Higgs boson. We discuss in detail the renormalization procedure and the scheme and scale dependence, and provide practical formulas for the numerical implementation of our results. We also consider the heavy top mass expansion and show that in the case at hand it converges very slowly.Comment: LaTeX, 29 pages, 6 postscript figures include

1/m_b^2 correction to the left-right lepton polarization asymmetry in the decay B -> X_s mu^+ mu^-

Using a known result by Falk et al. for the 1/m_b^2 correction to the dilepton invariant mass spectrum in the decay B \rightarrow X_s \mu^+ \mu^-, we calculate the 1/m_b^2 correction to the left-right muon polarization asymmetry in this decay. Employing an up-to-date range of values for the non-perturbative parameter \lambda_1, we find that the correction is much smaller than it should have been expected from the previous work by Falk et al.Comment: 8 pages, 2 figures included. Uses epsf.sty and rotate.sty. To appear in Physical Review D. The complete postscript file is also available from URL ftp://feynman.t30.physik.tu-muenchen.de/pub/preprints/ tum_t31_98_96.ps.g

SARS-CoV-2 variant Alpha has a spike-dependent replication advantage over the ancestral B.1 strain in human cells with low ACE2 expression

Epidemiological data demonstrate that Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) variants of concern (VOCs) Alpha and Delta are more transmissible, infectious, and pathogenic than previous variants. Phenotypic properties of VOC remain understudied. Here, we provide an extensive functional study of VOC Alpha replication and cell entry phenotypes assisted by reverse genetics, mutational mapping of spike in lentiviral pseudotypes, viral and cellular gene expression studies, and infectivity stability assays in an enhanced range of cell and epithelial culture models. In almost all models, VOC Alpha spread less or equally efficiently as ancestral (B.1) SARS-CoV-2. B.1. and VOC Alpha shared similar susceptibility to serum neutralization. Despite increased relative abundance of specific sgRNAs in the context of VOC Alpha infection, immune gene expression in infected cells did not differ between VOC Alpha and B.1. However, inferior spreading and entry efficiencies of VOC Alpha corresponded to lower abundance of proteolytically cleaved spike products presumably linked to the T716I mutation. In addition, we identified a bronchial cell line, NCI-H1299, which supported 24-fold increased growth of VOC Alpha and is to our knowledge the only cell line to recapitulate the fitness advantage of VOC Alpha compared to B.1. Interestingly, also VOC Delta showed a strong (595-fold) fitness advantage over B.1 in these cells. Comparative analysis of chimeric viruses expressing VOC Alpha spike in the backbone of B.1, and vice versa, showed that the specific replication phenotype of VOC Alpha in NCI-H1299 cells is largely determined by its spike protein. Despite undetectable ACE2 protein expression in NCI-H1299 cells, CRISPR/Cas9 knock-out and antibody-mediated blocking experiments revealed that multicycle spread of B.1 and VOC Alpha required ACE2 expression. Interestingly, entry of VOC Alpha, as opposed to B.1 virions, was largely unaffected by treatment with exogenous trypsin or saliva prior to infection, suggesting enhanced resistance of VOC Alpha spike to premature proteolytic cleavage in the extracellular environment of the human respiratory tract. This property may result in delayed degradation of VOC Alpha particle infectivity in conditions typical of mucosal fluids of the upper respiratory tract that may be recapitulated in NCI-H1299 cells closer than in highly ACE2-expressing cell lines and models. Our study highlights the importance of cell model evaluation and comparison for in-depth characterization of virus variant-specific phenotypes and uncovers a fine-tuned interrelationship between VOC Alpha- and host cell-specific determinants that may underlie the increased and prolonged virus shedding detected in patients infected with VOC Alpha

Tranexamic acid to reduce head injury death in people with traumatic brain injury: the CRASH-3 international RCT

Background Tranexamic acid safely reduces mortality in traumatic extracranial bleeding. Intracranial bleeding is common after traumatic brain injury and can cause brain herniation and death. We assessed the effects of tranexamic acid in traumatic brain injury patients. Objective To assess the effects of tranexamic acid on death, disability and vascular occlusive events in traumatic brain injury patients. We also assessed cost-effectiveness. Design Randomised trial and economic evaluation. Patients were assigned by selecting a numbered treatment pack from a box containing eight packs that were identical apart from the pack number. Patients, caregivers and those assessing outcomes were masked to allocation. All analyses were by intention to treat. We assessed the cost-effectiveness of tranexamic acid versus no treatment from a UK NHS perspective using the trial results and a Markov model. Setting 175 hospitals in 29 countries. Participants Adults with traumatic brain injury within 3 hours of injury with a Glasgow Coma Scale score of ≤ 12 or any intracranial bleeding on computerised tomography scan, and no major extracranial bleeding, were eligible. Intervention Tranexamic acid (loading dose 1 g over 10 minutes then infusion of 1 g over 8 hours) or matching placebo. Main outcome measures Head injury death in hospital within 28 days of injury in patients treated within 3 hours of injury. Secondary outcomes were early head injury deaths, all-cause and cause-specific mortality, disability, vascular occlusive events, seizures, complications and adverse events. Results Among patients treated within 3 hours of injury (n = 9127), the risk of head injury death was 18.5% in the tranexamic acid group versus 19.8% in the placebo group (855/4613 vs. 892/4514; risk ratio 0.94, 95% confidence interval 0.86 to 1.02). In a prespecified analysis excluding patients with a Glasgow Coma Scale score of 3 or bilateral unreactive pupils at baseline, the results were 12.5% in the tranexamic acid group versus 14.0% in the placebo group (485/3880 vs. 525/3757; risk ratio 0.89, 95% confidence interval 0.80 to 1.00). There was a reduction in the risk of head injury death with tranexamic acid in those with mild to moderate head injury (166/2846 vs. 207/2769; risk ratio 0.78, 95% confidence interval 0.64 to 0.95), but in those with severe head injury (689/1739 vs. 685/1710; risk ratio 0.99, 95% confidence interval 0.91 to 1.07) there was no apparent reduction (p-value for heterogeneity = 0.030). Early treatment was more effective in mild and moderate head injury (p = 0.005), but there was no obvious impact of time to treatment in cases of severe head injury (p = 0.73). The risk of disability, vascular occlusive events and seizures was similar in both groups. Tranexamic acid is highly cost-effective for mild and moderate traumatic brain injury (base case of £4288 per quality-adjusted life-year gained). Conclusion Early tranexamic acid treatment reduces head injury deaths. Treatment is cost-effective for patients with mild or moderate traumatic brain injury, or those with both pupils reactive. Future work Further trials should examine early tranexamic acid treatment in mild head injury. Research on alternative routes of administration is needed. Limitations Time to treatment may have been underestimated. Trial registration Current Controlled Trials ISRCTN15088122, ClinicalTrials.gov NCT01402882, EudraCT 2011-003669-14, Pan African Clinical Trial Registry PACTR20121000441277. Funding The project was funded by the National Institute for Health Research (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 25, No. 26. See the NIHR Journals Library website for further project information. In addition, funding was provided by JP Moulton Charitable Trust, Joint Global Health Trials (Medical Research Council, Department for International Development and the Wellcome Trust). This project was funded by the NIHR Global Health Trials programme

Bremsstrahlung Corrections to the Decay

We calculate the O(ff s ) gluon Bremsstrahlung corrections to the inclusive decay b ! sfl, involving the full operator basis O 1 -- O 8 . Confirming and extending earlier calculations of Ali and Greub, we give formulas for the total decay width as well as the perturbative photon spectrum, regarding the former as a necessary part of the forthcoming complete NLO analysis. We explore in detail the renormalization scale dependence of our results and find it considerably increased. 1 Introduction If we define rare weak decays of hadrons as weak decays which are rare because they are loopinduced (as opposed to CKM-suppressed), the analysis of these decays may shed light on at least three important topics: (i) Since they can proceed even at leading order only through diagrams with a loop of virtual particles, these decays do test the standard model of weak interactions as quantum field theory. (ii) Since they are decays of hadrons, they are of course strongly affected by QCD effects. If..