Global Finance and Environmental Politics:

Summary This article outlines how insurance companies have so far responded to climate change. Such change threatens the viability of much of their business, by disrupting the actuarial data on which insurance risks are calculated. At the same time, insurance companies are an important component of global finance, and thus their political?economic power has led many observers to suggest that their involvement in climate politics is encouraging from an environmentalist point of view. The article critically analyses whether such optimism is justified

Track E Implementation Science, Health Systems and Economics

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138412/1/jia218443.pd

Carboniferous and Permian Rugosochonetidae (Brachiopoda) from West Spitsbergen

The rugosochonetid brachiopod species Lissochonetes geinitzianus from the Kazimovian of the Nordenskioldbreen Formation, and Dyoros (Dyoros) mucronata sp. nov., Dyoros (Dyoros) spitzbergianus and Lissochonetes superba from the Artinskian to latest Permian Kapp Starostin Formation in West Spitsbergen are described and figured. Dyoros is generally restricted to the Boreal Realm, whereas Lissochonetes is mostly distributed in the Boreal Realm, but occasionally present in the Palaeoequatorial and Gondwanan Realms<br /

Post-acute COVID-19 neuropsychiatric symptoms are not associated with ongoing nervous system injury

A proportion of patients infected with severe acute respiratory syndrome coronavirus 2 experience a range of neuropsychiatric symptoms months after infection, including cognitive deficits, depression and anxiety. The mechanisms underpinning such symptoms remain elusive. Recent research has demonstrated that nervous system injury can occur during COVID-19. Whether ongoing neural injury in the months after COVID-19 accounts for the ongoing or emergent neuropsychiatric symptoms is unclear. Within a large prospective cohort study of adult survivors who were hospitalized for severe acute respiratory syndrome coronavirus 2 infection, we analysed plasma markers of nervous system injury and astrocytic activation, measured 6 months post-infection: neurofilament light, glial fibrillary acidic protein and total tau protein. We assessed whether these markers were associated with the severity of the acute COVID-19 illness and with post-acute neuropsychiatric symptoms (as measured by the Patient Health Questionnaire for depression, the General Anxiety Disorder assessment for anxiety, the Montreal Cognitive Assessment for objective cognitive deficit and the cognitive items of the Patient Symptom Questionnaire for subjective cognitive deficit) at 6 months and 1 year post-hospital discharge from COVID-19. No robust associations were found between markers of nervous system injury and severity of acute COVID-19 (except for an association of small effect size between duration of admission and neurofilament light) nor with post-acute neuropsychiatric symptoms. These results suggest that ongoing neuropsychiatric symptoms are not due to ongoing neural injury

Search for dark mesons decaying to top and bottom quarks in proton-proton collisions at √s = 13 TeV with the ATLAS detector

A search for dark mesons originating from strongly-coupled, SU(2) dark favor symmetry conserving models and decaying gaugephobically to pure Standard Model final states containing top and bottom quarks is presented. The search targets fully hadronic final states and final states with exactly one electron or muon and multiple jets. The analyzed data sample corresponds to an integrated luminosity of 140 fb−1 of proton-proton collisions collected at √s = 13 TeV with the ATLAS detector at the Large Hadron Collider. No significant excess over the Standard Model background expectation is observed and the results are used to set the first direct constraints on this type of model. The two-dimensional signal space of dark pion masses mπD and dark rho-meson masses mρD is scanned. For mπD /mρD = 0.45, dark pions with masses mπD < 940 GeV are excluded at the 95% CL, while for mπD /mρD = 0.25 masses mπD < 740 GeV are excluded

Combination of searches for Higgs boson decays into a photon and a massless dark photon using pp collisions at √s = 13 TeV with the ATLAS detector

A combination of searches for Higgs boson decays into a visible photon and a massless dark photon (H → γγd) is presented using 139 fb−1 of proton-proton collision data at a centre-of-mass energy of √s = 13 TeV recorded by the ATLAS detector at the Large Hadron Collider. The observed (expected) 95% confidence level upper limit on the Standard Model Higgs boson decay branching ratio is determined to be B(H → γγd) < 1.3% (1.5)%. The search is also sensitive to higher-mass Higgs bosons decaying into the same final state. The observed (expected) 95% confidence level limit on the cross-section times branching ratio ranges from 16 fb (20 fb) for mH = 400 GeV to 1.0 fb (1.5 fb) for mH = 3 TeV. Results are also interpreted in the context of a minimal simplified model

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