First Results from the AMoRE-Pilot neutrinoless double beta decay experiment

The Advanced Molybdenum-based Rare process Experiment (AMoRE) aims to search for neutrinoless double beta decay (0$\nu\beta\beta$) of $^{100}$Mo with $\sim$100 kg of $^{100}$Mo-enriched molybdenum embedded in cryogenic detectors with a dual heat and light readout. At the current, pilot stage of the AMoRE project we employ six calcium molybdate crystals with a total mass of 1.9 kg, produced from $^{48}$Ca-depleted calcium and $^{100}$Mo-enriched molybdenum ($^{48\textrm{depl}}$Ca$^{100}$MoO$_4$). The simultaneous detection of heat(phonon) and scintillation (photon) signals is realized with high resolution metallic magnetic calorimeter sensors that operate at milli-Kelvin temperatures. This stage of the project is carried out in the Yangyang underground laboratory at a depth of 700 m. We report first results from the AMoRE-Pilot $0\nu\beta\beta$ search with a 111 kg$\cdot$d live exposure of $^{48\textrm{depl}}$Ca$^{100}$MoO$_4$ crystals. No evidence for $0\nu\beta\beta$ decay of $^{100}$Mo is found, and a upper limit is set for the half-life of 0$\nu\beta\beta$ of $^{100}$Mo of $T^{0\nu}_{1/2} > 9.5\times10^{22}$ y at 90% C.L.. This limit corresponds to an effective Majorana neutrino mass limit in the range $\langle m_{\beta\beta}\rangle\le(1.2-2.1)$ eV

Background study of the AMoRE-pilot experiment

We report a study on the background of the Advanced Molybdenum-Based Rare process Experiment (AMoRE), a search for neutrinoless double beta decay (\znbb) of $^{100}$Mo. The pilot stage of the experiment was conducted using $\sim$1.9 kg of \CAMOO~ crystals at the Yangyang Underground Laboratory, South Korea, from 2015 to 2018. We compared the measured $\beta/\gamma$ energy spectra in three experimental configurations with the results of Monte Carlo simulations and identified the background sources in each configuration. We replaced several detector components and enhanced the neutron shielding to lower the background level between configurations. A limit on the half-life of $0\nu\beta\beta$ decay of $^{100}$Mo was found at $T_{1/2}^{0\nu} \ge 3.0\times 10^{23}$ years at 90\% confidence level, based on the measured background and its modeling. Further reduction of the background rate in the AMoRE-I and AMoRE-II are discussed

Radioassay of the materials for AMoRE-II experiment

The AMoRE-II experiment will search for the 0νββ decay of 100Mo nuclei using molybdate crystal scintillators, operating at milli-Kelvin (mK) temperatures, with a total of 80 kg of 100Mo. The background goal for the experiment is 10–4 counts/keV/kg/year in the region of interest around the 0νββ decay Q-value of 3,034 keV. To achieve this level, the rate of background signals arising from emissions produced by decays of radioactive impurities in the detector and shielding materials must be strictly controlled. To do this, concentrations of such impurities are measured and are controlled through materials selection and purification. In this paper, we describe the design and the construction materials used to build the AMoRE-II detector and shielding system, including active and passive shielding, the cryostat, and the detector holders and instrumentation, and we report on measurements of radioactive impurities within candidate and selected materials

Serum amyloid A inhibits RANKL-induced osteoclast formation

When mouse bone marrow-derived macrophages were stimulated with serum amyloid A (SAA), which is a major acute-phase protein, there was strong inhibition of osteoclast formation induced by the receptor activator of nuclear factor kappaB ligand. SAA not only markedly blocked the expression of several osteoclast-associated genes (TNF receptor-associated factor 6 and osteoclast-associated receptor) but also strongly induced the expression of negative regulators (MafB and interferon regulatory factor 8). Moreover, SAA decreased c-fms expression on the cell surface via shedding of the c-fms extracellular domain. SAA also restrained the fusion of osteoclast precursors by blocking intracellular ATP release. This inhibitory response of SAA is not mediated by the well-known SAA receptors (formyl peptide receptor 2, Toll-like receptor 2 (TLR2) or TLR4). These findings provide insight into a novel inhibitory role of SAA in osteoclastogenesis and suggest that SAA is an important endogenous modulator that regulates bone homeostasis.open

Direct Inhibition of GSK3β by the Phosphorylated Cytoplasmic Domain of LRP6 in Wnt/β-Catenin Signaling

Wnt/β-catenin signaling plays a central role in development and is also involved in a diverse array of diseases. Binding of Wnts to the coreceptors Frizzled and LRP6/5 leads to phosphorylation of PPPSPxS motifs in the LRP6/5 intracellular region and the inhibition of GSK3β bound to the scaffold protein Axin. However, it remains unknown how GSK3β is specifically inhibited upon Wnt stimulation. Here, we show that overexpression of the intracellular region of LRP6 containing a Ser/Thr rich cluster and a PPPSPxS motif impairs the activity of GSK3β in cells. Synthetic peptides containing the PPPSPxS motif strongly inhibit GSK3β in vitro only when they are phosphorylated. Microinjection of these peptides into Xenopus embryos confirms that the phosphorylated PPPSPxS motif potentiates Wnt-induced second body axis formation. In addition, we show that the Ser/Thr rich cluster of LRP6 plays an important role in LRP6 binding to GSK3β. These observations demonstrate that phosphorylated LRP6/5 both recruits and directly inhibits GSK3β using two distinct portions of its cytoplasmic sequence, and suggest a novel mechanism of activation in this signaling pathway