Researching trust in the police and trust in justice: a UK perspective

This paper describes the immediate and more distant origins of a programme of comparative research that is examining cross-national variations in public trust in justice and in the police. The programme is built around a module of the fifth European Social Survey, and evolved from a study funded by the European Commission. The paper describes the conceptual framework within which we are operating – developed in large measure from theories of procedural justice. It reviews some of the methodological issues raised by the use of sample surveys to research issues of public trust in the police, public perceptions of institutional legitimacy and compliance with the law. Finally it gives a flavour of some of the early findings emerging from the programme

Transport properties of strongly correlated metals:a dynamical mean-field approach

The temperature dependence of the transport properties of the metallic phase of a frustrated Hubbard model on the hypercubic lattice at half-filling are calculated. Dynamical mean-field theory, which maps the Hubbard model onto a single impurity Anderson model that is solved self-consistently, and becomes exact in the limit of large dimensionality, is used. As the temperature increases there is a smooth crossover from coherent Fermi liquid excitations at low temperatures to incoherent excitations at high temperatures. This crossover leads to a non-monotonic temperature dependence for the resistance, thermopower, and Hall coefficient, unlike in conventional metals. The resistance smoothly increases from a quadratic temperature dependence at low temperatures to large values which can exceed the Mott-Ioffe-Regel value, hbar a/e^2 (where "a" is a lattice constant) associated with mean-free paths less than a lattice constant. Further signatures of the thermal destruction of quasiparticle excitations are a peak in the thermopower and the absence of a Drude peak in the optical conductivity. The results presented here are relevant to a wide range of strongly correlated metals, including transition metal oxides, strontium ruthenates, and organic metals.Comment: 19 pages, 9 eps figure

Petrogenesis and Ni-Cu sulphide potential of mafic-ultramafic rocks in the Mesoproterozoic Fraser Zone within the Albany-Fraser Orogen, Western Australia

The Albany Fraser Orogen is located along the southern and southeastern margins of the Archean Yilgarn Craton. The orogen formed during reworking of the Yilgarn Craton, along with variable additions of juvenile mantle material, from at least 1810 Ma to 1140 Ma. The Fraser Zone is a 425 km long and 50 km wide geophysically distinct belt near the northwestern edge of the orogen, hosting abundant sills of predominantly metagabbroic non-cumulate rocks, but including larger cumulate bodies, all emplaced at c. 1300 Ma. The gabbroic rocks are interpreted to have crystallised from a basaltic magma that had ∼8.8% MgO, 185 ppm Ni, 51 ppm Cu, and extremely low contents of platinum-group elements (PGE, <1 ppb). Levels of high field-strength elements (HFSE) in the least enriched rocks indicate that the magma was derived from a mantle source more depleted than a MORB source. Isotope and trace element systematics suggest that the magma was contaminated (εNd 0 to −2 throughout, La/Nb around 3) with small (<10%) amounts of crust before and during ascent and emplacement. Larger bodies of cumulate rocks show evidence for additional contamination, at the emplacement level, with country-rock metasedimentary rocks or their anatectic melts. The area has been the focus of considerable exploration for Ni–Cu sulphides following the discovery of the Nova deposit in 2012 in an intrusion consisting of olivine gabbronoritic, noritic and peridotitic cumulates, interlayered with metasedimentary rocks belonging to the Snowys Dam Formation of the Arid Basin. Disseminated sulphides from a drillcore intersecting the structurally upper portion of the intrusion, above the main ore zone, have tenors of ∼3–6.3% Ni, 1.8–6% Cu and mostly <500 ppb PGE, suggesting derivation from magma with the same composition as the regional Fraser Zone metagabbroic sills, at R factors of ∼1500. However, the Nova rocks tend to have higher εSr (38–52) and more variable δ34S (−2 to +4) than the regional metagabbros (εSr 17–32, δ34S around 0), consistent with the geochemical evidence for enhanced crustal assimilation of the metasedimentary country-rock in a relatively large magma staging chamber from which pulses of sulphide bearing, crystal-charged magmas were emplaced at slightly different crustal levels. Preliminary investigations suggest that the critical factors determining whether or not Fraser Zone mafic magmas are mineralised probably relate to local geodynamic conditions that allow large magma chambers to endure long enough to sequester country-rock sulphur

Loss-of-function mutations in UDP-Glucose 6-Dehydrogenase cause recessive developmental epileptic encephalopathy

Developmental epileptic encephalopathies are devastating disorders characterized by intractable epileptic seizures and developmental delay. Here, we report an allelic series of germline recessive mutations in UGDH in 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia. UGDH encodes an oxidoreductase that converts UDP-glucose to UDP-glucuronic acid, a key component of specific proteoglycans and glycolipids. Consistent with being loss-of-function alleles, we show using patients’ primary fibroblasts and biochemical assays, that these mutations either impair UGDH stability, oligomerization, or enzymatic activity. In vitro, patient-derived cerebral organoids are smaller with a reduced number of proliferating neuronal progenitors while mutant ugdh zebrafish do not phenocopy the human disease. Our study defines UGDH as a key player for the production of extracellular matrix components that are essential for human brain development. Based on the incidence of variants observed, UGDH mutations are likely to be a frequent cause of recessive epileptic encephalopathy

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