The ν\nu-cleus experiment: A gram-scale fiducial-volume cryogenic detector for the first detection of coherent neutrino-nucleus scattering

We discuss a small-scale experiment, called $\nu$-cleus, for the first detection of coherent neutrino-nucleus scattering by probing nuclear-recoil energies down to the 10 eV-regime. The detector consists of low-threshold CaWO$_4$ and Al$_2$O$_3$ calorimeter arrays with a total mass of about 10 g and several cryogenic veto detectors operated at millikelvin temperatures. Realizing a fiducial volume and a multi-element target, the detector enables active discrimination of $\gamma$, neutron and surface backgrounds. A first prototype Al$_2$O$_3$ device, operated above ground in a setup without shielding, has achieved an energy threshold of ${\sim20}$ eV and further improvements are in reach. A sensitivity study for the detection of coherent neutrino scattering at nuclear power plants shows a unique discovery potential (5$\sigma$) within a measuring time of ${\lesssim2}$ weeks. Furthermore, a site at a thermal research reactor and the use of a radioactive neutrino source are investigated. With this technology, real-time monitoring of nuclear power plants is feasible.Comment: 14 pages, 19 figure

Cardiac myocyte-specific knock-out of calcium-independent phospholipase A2γ (iPLA2γ) decreases oxidized fatty acids during ischemia/reperfusion and reduces infarct size

Calcium-independent phospholipase A(2)γ (iPLA(2)γ) is a mitochondrial enzyme that produces lipid second messengers that facilitate opening of the mitochondrial permeability transition pore (mPTP) and contribute to the production of oxidized fatty acids in myocardium. To specifically identify the roles of iPLA(2)γ in cardiac myocytes, we generated cardiac myocyte-specific iPLA(2)γ knock-out (CMiPLA(2)γKO) mice by removing the exon encoding the active site serine (Ser-477). Hearts of CMiPLA(2)γKO mice exhibited normal hemodynamic function, glycerophospholipid molecular species composition, and normal rates of mitochondrial respiration and ATP production. In contrast, CMiPLA(2)γKO mice demonstrated attenuated Ca(2+)-induced mPTP opening that could be rapidly restored by the addition of palmitate and substantially reduced production of oxidized polyunsaturated fatty acids (PUFAs). Furthermore, myocardial ischemia/reperfusion (I/R) in CMiPLA(2)γKO mice (30 min of ischemia followed by 30 min of reperfusion in vivo) dramatically decreased oxidized fatty acid production in the ischemic border zones. Moreover, CMiPLA(2)γKO mice subjected to 30 min of ischemia followed by 24 h of reperfusion in vivo developed substantially less cardiac necrosis in the area-at-risk in comparison with their WT littermates. Furthermore, we found that membrane depolarization in murine heart mitochondria was sensitized to Ca(2+) by the presence of oxidized PUFAs. Because mitochondrial membrane depolarization and calcium are known to activate iPLA(2)γ, these results are consistent with salvage of myocardium after I/R by iPLA(2)γ loss of function through decreasing mPTP opening, diminishing production of proinflammatory oxidized fatty acids, and attenuating the deleterious effects of abrupt increases in calcium ion on membrane potential during reperfusion

Exploring the selective gray matter profile of autism spectrum disorder through Bayes Factor Modeling

INTRODUCTION: Despite decades of brain MRI research demonstrating atypical neuroanatomical substrate in patients with autism spectrum disorder (ASD), it remains unclear whether and to what extent disorder-selective neuroanatomical abnormalities occur in this spectrum. This, and the fact that multiple brain disorders report a common neuroanatomical substrate, makes transference and the application of neuroimaging findings into the clinical setting an open challenge. OBJECTIVES: To investigate the selective neuroanatomical alteration profile of the ASD brain, we employed a meta-analytic, data-driven, and reverse inference-based approach (i.e.; Bayes fACtor mOdeliNg). METHODS: Eligible voxel-based morphometry data were extracted by a standardized search on BrainMap and MEDLINE databases (849 published experiments, 131 brain disorders, 22747 clinical subjects, 16572 x-y-z coordinates). Two distinct datasets were generated: the ASD dataset, composed of ASD-related data; and the non-ASD dataset, composed of all other clinical conditions data. Starting from the two unthresholded activation likelihood estimation (ALE) maps, the calculus of the Bayes fACtor mOdeliNg was performed. This allowed us to obtain posterior probability distributions on the evidence of brain alteration specificity in ASD. RESULTS: We revealed both cortical and cerebellar areas of neuroanatomical alteration selectivity in ASD. Eight clusters showed a selectivity value ≥ 90%, namely the bilateral precuneus, the right inferior occipital gyrus, left lobule IX, left Crus II, right Crus I, and the right lobule VIIIA (Fig. 1). CONCLUSIONS: The identification of this neuroanatomical pattern provides new insights into the complex pathophysiology of ASD, opening attractive prospects for future neuroimaging-based interventions. DISCLOSURE: No significant relationships