Shame: In Defence of an Essential Moral Emotion

I argue that shame is an essential moral emotion, and that the capacity to feel shame is vital to allow us to pick out certain types of moral value. I do this by sketching out a general role for moral emotions, distinguishing shame from other moral emotions, notably guilt, and then arguing that shame has a distinctive role to play as a moral emotion that cannot be played by guilt. By marking out a key role for the emotions in moral life, I am able to address two key concerns about moral judgement. First, I am able to explain how we overcome frame problems, allowing us to notice and appropriately conceptualise moral concerns, against a backdrop of everyday life. Second, I can give an account of the apparent intrinsically-motivating nature of moral judgements. Shame, in central cases, is based on self-assessments of inadequacy; we judge ourselves to be less than we should be. This is contrasted with guilt, which centres on judgements of transgression against moral norms. It is also contrasted with embarrassment and humiliation, neither of which are primarily moral emotions. Shame has a distinctive role to play as a moral emotion. It is capable of picking out cases of moral value that guilt cannot; in particular, supererogatory value and cases of wrongdoing by collectives, in the absence of individual culpability. Pace the claims of numerous psychologists and philosophers, shame is not necessarily a dangerous emotion; rather, only certain types of shame have the potential to do damage to those experiencing them. Situationist arguments threaten the role of shame as a moral emotion, by suggesting that there are no robust character traits; these claims are mistaken. Therefore, I am able to sustain the conclusion that shame has a vital role to play in moral life

Shame: In Defence of an Essential Moral Emotion

I argue that shame is an essential moral emotion, and that the capacity to feel shame is vital to allow us to pick out certain types of moral value. I do this by sketching out a general role for moral emotions, distinguishing shame from other moral emotions, notably guilt, and then arguing that shame has a distinctive role to play as a moral emotion that cannot be played by guilt. By marking out a key role for the emotions in moral life, I am able to address two key concerns about moral judgement. First, I am able to explain how we overcome frame problems, allowing us to notice and appropriately conceptualise moral concerns, against a backdrop of everyday life. Second, I can give an account of the apparent intrinsically-motivating nature of moral judgements. Shame, in central cases, is based on self-assessments of inadequacy; we judge ourselves to be less than we should be. This is contrasted with guilt, which centres on judgements of transgression against moral norms. It is also contrasted with embarrassment and humiliation, neither of which are primarily moral emotions. Shame has a distinctive role to play as a moral emotion. It is capable of picking out cases of moral value that guilt cannot; in particular, supererogatory value and cases of wrongdoing by collectives, in the absence of individual culpability. Pace the claims of numerous psychologists and philosophers, shame is not necessarily a dangerous emotion; rather, only certain types of shame have the potential to do damage to those experiencing them. Situationist arguments threaten the role of shame as a moral emotion, by suggesting that there are no robust character traits; these claims are mistaken. Therefore, I am able to sustain the conclusion that shame has a vital role to play in moral life

Mapping Glacier Dynamics: A Flux-Gate Approach to Analysing Ice Discharge Variability and Sea Level Contributions in the Patagonian Icefields

This study used a flux-gate methodology coupled with ice thickness and ice velocity grids equivalent to 2004 and 2017 to ascertain ice discharge (Gt yr-1) and associated sea level equivalents (mm yr-1) through 124 outlet glaciers spanning the different termini environments of the Patagonian Icefields. In addition, glaciers that experienced a terminus environment transition (i.e., from land-terminating to lake-terminating or vice versa) were identified and any associated changes in ice discharge were quantified. Overall, total ice discharge equalled 24.59 Gt yr-1 (0.068 mm yr-1) in 2004 (Northern Patagonian Icefield = 7.07 Gt yr-1 or 0.019 mm yr-1, Southern Patagonian Icefield = 17.52 Gt yr-1 or 0.049 mm yr-1) and 23.94 ± 7.18 Gt yr-1 (0.066 mm yr-1) in 2017 (Northern Patagonian Icefield = 5.02 ± 1.57 Gt yr-1 or 0.014 mm yr-1, Southern Patagonian Icefield = 18.92 ± 5.98 Gt yr-1 or 0.052 mm yr-1). In 2004 most of the ice was discharged through marine-terminating environments in the Western regions of the icefields. But, in 2017 there was a shift towards equilibrium whereby lake-terminating environments in the eastern regions matched the ice discharge of marine-terminating environments. This is attributed to the expansion of lake-terminating environments and an apparent acceleration of surface velocity. Although these trends do exist there were heterogeneous changes in ice discharge for all termini environments resulting from a complex array of dynamics at the calving front. A strong agreement was found between the ice discharge estimates in this study and geodetic mass loss estimates found in the literature, reinforcing the current knowledge around mass loss on the Patagonian Icefields. Future work should focus on the accuracy of ice thickness and ice velocity grids at the margins of icefields and using accurate frontal ablation estimates to constrain future sea level rise projections

Body condition changes at sea: onboard calculation and telemetry of body density in diving animals

This study was supported by grants from the Office of Naval Research N00014-18-1-2822, DoD SERDP contract W912HQ20C0056, IPEV (Institut Paul Emile Victor) under the Antarctic research program 109 (C. Barbraud) and 1201 (C. Gilbert & C. Guinet), and CNES-TOSCA as part of the SNO-MEMO.The ability of marine mammals to accumulate sufficient lipid energy reserves is vital for mammals' survival and successful reproduction. However, long-term monitoring of at-sea changes in body condition, specifically lipid stores, has only been possible in elephant seals performing prolonged drift dives (low-density lipids alter the rates of depth change while drifting). This approach has limited applicability to other species. Using hydrodynamic performance analysis during transit glides, we developed and validated a novel satellite-linked data logger that calculates real-time changes in body density (∝lipid stores). As gliding is ubiquitous amongst divers, the system can assess body condition in a broad array of diving animals. The tag processes high sampling rate depth and three-axis acceleration data to identify 5 s high pitch angle glide segments at depths >100 m. Body density is estimated for each glide using gliding speed and pitch to quantify drag versus buoyancy forces acting on the gliding animal. We used tag data from 24 elephant seals (Mirounga spp.) to validate the onboard calculation of body density relative to drift rate. The new tags relayed body density estimates over 200 days and documented lipid store accumulation during migration with good correspondence between changes in body density and drift rate. Our study provided updated drag coefficient values for gliding (Cd,f = 0.03) and drifting (Cd,s = 0.12) elephant seals, both substantially lower than previous estimates. We also demonstrated post-hoc estimation of the gliding drag coefficient and body density using transmitted data, which is especially useful when drag parameters cannot be estimated with sufficient accuracy before tag deployment. Our method has the potential to advance the field of marine biology by switching the research paradigm from indirectly inferring animal body condition from foraging effort to directly measuring changes in body condition relative to foraging effort, habitat, ecological factors and anthropogenic stressors in the changing oceans. Expanding the method to account for diving air volumes will expand the system's applicability to shallower-diving (<100 m) species, facilitating real-time monitoring of body condition in a broad range of breath-hold divers.Publisher PDFPeer reviewe

The Indianapolis Flux Experiment (INFLUX): A test-bed for developing urban greenhouse gas emission measurements

The objective of the Indianapolis Flux Experiment (INFLUX) is to develop, evaluate and improve methods for measuring greenhouse gas (GHG) emissions from cities. INFLUX’s scientific objectives are to quantify CO2 and CH4 emission rates at 1 km2 resolution with a 10% or better accuracy and precision, to determine whole-city emissions with similar skill, and to achieve high (weekly or finer) temporal resolution at both spatial resolutions. The experiment employs atmospheric GHG measurements from both towers and aircraft, atmospheric transport observations and models, and activity-based inventory products to quantify urban GHG emissions. Multiple, independent methods for estimating urban emissions are a central facet of our experimental design. INFLUX was initiated in 2010 and measurements and analyses are ongoing. To date we have quantified urban atmospheric GHG enhancements using aircraft and towers with measurements collected over multiple years, and have estimated whole-city CO2 and CH4 emissions using aircraft and tower GHG measurements, and inventory methods. Significant differences exist across methods; these differences have not yet been resolved; research to reduce uncertainties and reconcile these differences is underway. Sectorally- and spatially-resolved flux estimates, and detection of changes of fluxes over time, are also active research topics. Major challenges include developing methods for distinguishing anthropogenic from biogenic CO2 fluxes, improving our ability to interpret atmospheric GHG measurements close to urban GHG sources and across a broader range of atmospheric stability conditions, and quantifying uncertainties in inventory data products. INFLUX data and tools are intended to serve as an open resource and test bed for future investigations. Well-documented, public archival of data and methods is under development in support of this objective

TESS asteroseismology of the known red-giant host stars HD 212771 and HD 203949

International audienc

Sortase-Modified Cholera Toxoids Show Specific Golgi Localization

Cholera toxoid is an established tool for use in cellular tracing in neuroscience and cell biology. We use a sortase labeling approach to generate site-specific N-terminally modified variants of both the A2-B5 heterohexamer and B5 pentamer forms of the toxoid. Both forms of the toxoid are endocytosed by GM1-positive mammalian cells, and while the heterohexameric toxoid was principally localized in the ER, the B5 pentamer showed an unexpectedly specific localization in the medial/trans-Golgi. This study suggests a future role for specifically labeled cholera toxoids in live-cell imaging beyond their current applications in neuronal tracing and labeling of lipid rafts in fixed cells

TLR7 gain-of-function genetic variation causes human lupus

Although circumstantial evidence supports enhanced Toll-like receptor 7 (TLR7) signalling as a mechanism of human systemic autoimmune disease evidence of lupus-causing TLR7 gene variants is lacking. Here we describe human systemic lupus erythematosus caused by a TLR7 gain-of-function variant. TLR7 is a sensor of viral RNA and binds to guanosine. We identified a de novo, previously undescribed missense TLR7Y264H variant in a child with severe lupus and additional variants in other patients with lupus. The TLR7Y264H variant selectively increased sensing of guanosine and 2',3'-cGMP1 and was sufficient to cause lupus when introduced into mice. We show that enhanced TLR7 signalling drives aberrant survival of B cell receptor (BCR)-activated B cells, and in a cell-intrinsic manner, accumulation of CD11c+ age-associated B cells and germinal centre B cells. Follicular and extrafollicular helper T cells were also increased but these phenotypes were cell-extrinsic. Deficiency of MyD88 (an adaptor protein downstream of TLR7) rescued autoimmunity, aberrant B cell survival, and all cellular and serological phenotypes. Despite prominent spontaneous germinal-centre formation in Tlr7Y264H mice, autoimmunity was not ameliorated by germinal-centre deficiency, suggesting an extrafollicular origin of pathogenic B cells. We establish the importance of TLR7 and guanosine-containing self-ligands for human lupus pathogenesis, which paves the way for therapeutic TLR7 or MyD88 inhibition