The AMoRE (Advanced Mo-based Rare process Experiment) project is a series of experiments that use advanced cryogenic techniques to search for the neutrinoless double-beta decay of 100 Mo. The work is being carried out by an international collaboration of researchers from eight countries. These searches involve high precision measurements of radiation-induced temperature changes and scintillation light produced in ultra-pure 100 Mo-enriched and 48 Ca-depleted calcium molybdate ( 48depl Ca 100 MoO 4 ) crystals that are located in a deep underground laboratory in Korea. The 100 Mo nuclide was chosen for this 0νββ decay search because of its high Q-value and favorable nuclear matrix element. Tests have demonstrated that CaMoO 4 crystals produce the brightest scintillation light among all of the molybdate crystals, both at room and at cryogenic temperatures. 48depl Ca 100 MoO 4 crystals are being operated at milli-Kelvin temperatures and read out via specially developed metallic-magnetic-calorimeter (MMC) temperature sensors that have excellent energy resolution and relatively fast response times. The excellent energy resolution provides good discrimination of signal from backgrounds, and the fast response time is important for minimizing the irreducible background caused by random coincidence of two-neutrino double-beta decay events of 100 Mo nuclei. Comparisons of the scintillating-light and phonon yields and pulse shape discrimination of the phonon signals will be used to provide redundant rejection of alpha-ray-induced backgrounds. An effective Majorana neutrino mass sensitivity that reaches the expected range of the inverted neutrino mass hierarchy, i.e., 20-50 meV, could be achieved with a 200 kg array of 48depl Ca 100 MoO 4 crystals operating for three years.
1 Cirrhosis is associated with cardiovascular and renal dysfunction including sodium retention. Many vasoactive peptides such as atrial natriuretic peptide (ANP) and endothelin-1 (ET-1) are degraded by neutral endopeptidase 24.11 (NEP). We investigated the hemodynamic and renal effects of thiorphan, a NEP inhibitor, in a rat cirrhosis model. 2 Cirrhosis was induced by chronic bile duct ligation, and controls had sham operation. Systemic and renal hemodynamics in conscious, restrained animals were determined using radiolabeled microspheres, and glomerular filtration rate (GFR) was measured by 3 H-inulin clearance. Plasma ANP and ET-1, and renal cGMP and Na + -K + ATPase activity were assayed. These variables were measured at baseline and after intravenous infusion of thiorphan (0.5 mg kg À1 loading dose followed by 0.1 mg kg À1 min À1 Â 30 min). 3 Thiorphan significantly decreased cardiac output, and increased systemic vascular resistance in controls, whereas in cirrhotic rats these variables were unchanged. 4 Compared to the controls, cirrhotic rats showed a decreased baseline GFR and urine sodium excretion, and the latter was significantly increased by thiorphan. 5 Thiorphan increased plasma ET-1 levels in controls, but not cirrhotic rats. ANP levels were not significantly increased in either group by thiorphan. 6 Thiorphan significantly increased cGMP concentrations and decreased Na + -K + ATPase activity of renal medulla but not cortex in cirrhotic rats; no effect was observed in the control rats. 7 We conclude that thiorphan induces natriuresis in cirrhotic rats by a direct renal medullary mechanism via cGMP and Na + -K + ATPase, without affecting systemic hemodynamics. This may potentially be useful in patients with ascites.
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