Status of the CRESST Dark Matter Search

The CRESST experiment aims for a detection of dark matter in the form of WIMPs. These particles are expected to scatter elastically off the nuclei of a target material, thereby depositing energy on the recoiling nucleus. CRESST uses scintillating CaWO4 crystals as such a target. The energy deposited by an interacting particle is primarily converted to phonons which are detected by transition edge sensors. In addition, a small fraction of the interaction energy is emitted from the crystals in the form of scintillation light which is measured in coincidence with the phonon signal by a separate cryogenic light detector for each target crystal. The ratio of light to phonon energy permits the discrimination between the nuclear recoils expected from WIMPs and events from radioactive backgrounds which primarily lead to electron recoils. CRESST has shown the success of this method in a commissioning run in 2007 and, since then, further investigated possibilities for an even better suppression of backgrounds. Here, we report on a new class of background events observed in the course of this work. The consequences of this observation are discussed and we present the current status of the experiment.Comment: Proceedings of the 13th International Workshop on Low Temperature Detectors, 4 pages, 3 figure

Composite CaWO4 Detectors for the CRESST-II Experiment

CRESST-II, standing for Cryogenic Rare Events Search with Superconducting Thermometers phase II, is an experiment searching for Dark Matter. In the LNGS facility in Gran Sasso, Italy, a cryogenic detector setup is operated in order to detect WIMPs by elastic scattering off nuclei, generating phononic lattice excitations and scintillation light. The thermometers used in the experiment consist of a tungsten thin-film structure evaporated onto the CaWO4 absorber crystal. The process of evaporation causes a decrease in the scintillation light output. This, together with the need of a big-scale detector production for the upcoming EURECA experiment lead to investigations for producing thermometers on smaller crystals which are glued onto the absorber crystal. In our Run 31 we tested composite detectors for the first time in the Gran Sasso setup. They seem to produce higher light yields as hoped and could provide an additional time based discrimination mechanism for low light yield clamp events.Comment: Proceedings of the Thirteenth International Workshop on Low Temperature Detectors 4 pages, 9 figure

Genomic epidemiology of SARS-CoV-2 in a UK university identifies dynamics of transmission

AbstractUnderstanding SARS-CoV-2 transmission in higher education settings is important to limit spread between students, and into at-risk populations. In this study, we sequenced 482 SARS-CoV-2 isolates from the University of Cambridge from 5 October to 6 December 2020. We perform a detailed phylogenetic comparison with 972 isolates from the surrounding community, complemented with epidemiological and contact tracing data, to determine transmission dynamics. We observe limited viral introductions into the university; the majority of student cases were linked to a single genetic cluster, likely following social gatherings at a venue outside the university. We identify considerable onward transmission associated with student accommodation and courses; this was effectively contained using local infection control measures and following a national lockdown. Transmission clusters were largely segregated within the university or the community. Our study highlights key determinants of SARS-CoV-2 transmission and effective interventions in a higher education setting that will inform public health policy during pandemics.</jats:p

Pulse inhibition of histone deacetylases induces complete resistance to oxidative death in cortical neurons without toxicity and reveals a role for cytoplasmic p21(waf1/cip1) in cell cycle-independent neuroprotection

Histone deacetylase (HDAC) inhibitors are currently in human clinical trials as antitumor drugs because of their ability to induce cell dysfunction and death in cancer cells. The toxic effects of HDAC inhibitors are also apparent in cortical neurons in vitro, despite the ability of these agents to induce significant protection in the cells they do not kill. Here we demonstrate that pulse exposure of cortical neurons (2 h) in an in vitro model of oxidative stress results in durable neuroprotection without toxicity. Protection was associated with transcriptional upregulation of the cell cycle inhibitor, p21(waf1/cip1), both in this model and in an in vivo model of permanent ischemia. Transgenic overexpression of p21(waf1/cip1) in neurons can mimic the protective effect of HDAC inhibitors against oxidative stress-induced toxicity, including death induced by glutathione depletion or peroxide addition. The protective effect of p21(waf1/cip1) in the context of oxidative stress appears to be unrelated to its ability to act in the nucleus to inhibit cell cycle progression. However, although p21(waf1/cip1) is sufficient for neuroprotection, it is not necessary for HDAC inhibitor neuroprotection, because these agents can completely protect neurons cultured from p21(waf1/cip1)-null mice. Together these findings demonstrate (1) that pulse inhibition of HDACs in cortical neurons can induce neuroprotection without apparent toxicity; (2) that p21(waf1/cip1) is sufficient but not necessary to mimic the protective effects of HDAC inhibition; and (3) that oxidative stress in this model induces neuronal cell death via cell cycle-independent pathways that can be inhibited by a cytosolic, noncanonical action of p21(waf1/cip1)