Reducing DRIFT backgrounds with a submicron aluminized-mylar cathode

Background events in the DRIFT-IId dark matter detector, mimicking potential WIMP signals, are predominantly caused by alpha decays on the central cathode in which the alpha particle is completely or partially absorbed by the cathode material. We installed a View the MathML source thick aluminized-mylar cathode as a way to reduce the probability of producing these backgrounds. We study three generations of cathode (wire, thin-film, and radiologically clean thin-film) with a focus on the ratio of background events to alpha decays. Two independent methods of measuring the absolute alpha decay rate are used to ensure an accurate result, and agree to within 10%. Using alpha range spectroscopy, we measure the radiologically cleanest cathode version to have a contamination of 3.3±0.1 ppt 234U and 73±2 ppb 238U. This cathode reduces the probability of producing an RPR from an alpha decay by a factor of 70±20 compared to the original stainless steel wire cathode. First results are presented from a texturized version of the cathode, intended to be even more transparent to alpha particles. These efforts, along with other background reduction measures, have resulted in a drop in the observed background rate from 500/day to 1/day. With the recent implementation of full-volume fiducialization, these remaining background events are identified, allowing for background-free operation

Radon in the DRIFT-II directional dark matter TPC: emanation, detection and mitigation

Radon gas emanating from materials is of interest in environmental science and also a major concern in rare event non-accelerator particle physics experiments such as dark matter and double beta decay searches, where it is a major source of background. Notable for dark matter experiments is the production of radon progeny recoils (RPRs), the low energy (~ 100 keV) recoils of radon daughter isotopes, which can mimic the signal expected from WIMP interactions. Presented here are results of measurements of radon emanation from detector materials in the 1 m3 DRIFT-II directional dark matter gas time projection chamber experiment. Construction and operation of a radon emanation facility for this work is described, along with an analysis to continuously monitor DRIFT data for the presence of internal 222Rn and 218Po. Applying this analysis to historical DRIFT data, we show how systematic substitution of detector materials for alternatives, selected by this device for low radon emanation, has resulted in a factor of ~ 10 reduction in internal radon rates. Levels are found to be consistent with the sum from separate radon emanation measurements of the internal materials and also with direct measurement using an attached alpha spectrometer. The current DRIFT detector, DRIFT-IId, is found to have sensitivity to 222Rn of 2.5 μBql−1 with current analysis efficiency, potentially opening up DRIFT technology as a new tool for sensitive radon assay of materials

Placental CD4(+) T cells from preeclamptic patients cause autoantibodies to the angiotensin II type I receptor and hypertension in a pregnant rat model of preeclampsia

AIM: Preeclampsia (PE) is a hypertensive disorder of pregnancy associated with activated CD4(+) T cells and autoantibodies to angiotensin II type 1 receptor (AT1-AA). We have previously shown that CD4(+) T cells isolated from women with PE cause hypertension, increased tumor necrosis factor alpha (TNF-α), endothelin-1, and soluble fms-like tyrosine kinase-1 (sFlt-1) when injected into pregnant nude-athymic rats compared to CD4(+) T cells from normal pregnant (NP) women. However, the role of PE CD4(+) T cells to cause AT1-AA as a mechanism of hypertension is not known. Our goal was to determine if PE CD4(+) T cells stimulate AT1-AA in pregnant nude-athymic rats. METHODS: CD4(+) T cells were isolated from human NP and PE placentasand injected into nude-athymic rats on gestational day (GD) 12. In order to examine the role of the PE CD4(+) T cells to stimulate B cell secretion of AT1-AA, a subset of the rats receiving PE CD4(+) T cells were treated with rituximab on GD 14 or anti-CD40 ligand (anti-CD40L) on GD 12. On GD 19, mean arterial pressure (MAP) and tissues were obtained. RESULTS: MAP [114 ± 1 mmHg (n = 9)] and AT1-AA [19.8 ± 0.9 beats per minute (bpm, n = 4)] were increased in NP nude + PE CD4(+) T cells compared to NP nude + NP CD4(+) T cells [98 ± 2 mmHg (n = 7, P < 0.05) and 1.3 ± 0.9 bpm (n = 5, P < 0.05)]. Rituximab (103 ± 2 mmHg, n = 3, P < 0.05) and anti-CD40L (102 ± 1 mmHg, n = 3, P < 0.05) lowered MAP compared to NP nude + PE CD4(+) T cells. Circulating a proliferation-inducing ligand (APRIL) and placental angiotensin-converting enzyme 2 (ACE-2) activity was increased in response to PE CD4(+) T cells. CONCLUSIONS: These results show that placental CD4(+) T cells play an important role in the pathophysiology of PE, by activating B cells secreting AT1-AA to cause hypertension during pregnancy

Track D Social Science, Human Rights and Political Science

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138414/1/jia218442.pd