Differential Cross Section for Higgs Boson Production Including All-Orders Soft Gluon Resummation

The transverse momentum $Q_T$ distribution is computed for inclusive Higgs boson production at the energy of the CERN Large Hadron Collider. We focus on the dominant gluon-gluon subprocess in perturbative quantum chromodynamics and incorporate contributions from the quark-gluon and quark-antiquark channels. Using an impact-parameter $b$-space formalism, we include all-orders resummation of large logarithms associated with emission of soft gluons. Our resummed results merge smoothly at large $Q_T$ with the fixed-order expectations in perturbative quantum chromodynamics, as they should, with no need for a matching procedure. They show a high degree of stability with respect to variation of parameters associated with the non-perturbative input at low $Q_T$. We provide distributions $d\sigma/dy dQ_T$ for Higgs boson masses from $M_Z$ to 200 GeV. The average transverse momentum at zero rapidity $y$ grows approximately linearly with mass of the Higgs boson over the range $M_Z < m_h \simeq 0.18 m_h + 18$~GeV. We provide analogous results for $Z$ boson production, for which we compute $\simeq 25$ GeV. The harder transverse momentum distribution for the Higgs boson arises because there is more soft gluon radiation in Higgs boson production than in $Z$ production.Comment: 42 pages, latex, 26 figures. All figures replaced. Some changes in wording. Published in Phys. Rev. D67, 034026 (2003

a review of methodological design choices

Publisher Copyright: © 2023 Cambridge University Press. All rights reserved.This systematic literature review aimed to provide an overview of the characteristics and methods used in studies applying the Disability-Adjusted Life Years (DALY) concept for infectious diseases within European Union (EU)/European Economic Area (EEA)/European Free Trade Association (EFTA) countries and the United Kingdom. Electronic databases and grey literature were searched for articles reporting the assessment of DALY and its components. We considered studies in which researchers performed DALY calculations using primary epidemiological data input sources. We screened 3,053 studies of which 2,948 were excluded and 105 studies met our inclusion criteria. Of these studies, 22 were multi-country and 83 were single-country studies, of which 46 were from the Netherlands. Food- and water-borne diseases were the most frequently studied infectious diseases. Between 2015 and 2022, the number of burden of infectious disease studies was 1.6 times higher compared to that published between 2000 and 2014. Almost all studies (97%) estimated DALYs based on the incidence- and pathogen-based approach and without social weighting functions; however, there was less methodological consensus with regards to the disability weights and life tables that were applied. The number of burden of infectious disease studies undertaken across Europe has increased over time. Development and use of guidelines will promote performing burden of infectious disease studies and facilitate comparability of the results.publishersversionepub_ahead_of_prin

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease