14 research outputs found
Observation of Coherent Elastic Neutrino-Nucleus Scattering
The coherent elastic scattering of neutrinos off nuclei has eluded detection
for four decades, even though its predicted cross-section is the largest by far
of all low-energy neutrino couplings. This mode of interaction provides new
opportunities to study neutrino properties, and leads to a miniaturization of
detector size, with potential technological applications. We observe this
process at a 6.7-sigma confidence level, using a low-background, 14.6-kg
CsI[Na] scintillator exposed to the neutrino emissions from the Spallation
Neutron Source (SNS) at Oak Ridge National Laboratory. Characteristic
signatures in energy and time, predicted by the Standard Model for this
process, are observed in high signal-to-background conditions. Improved
constraints on non-standard neutrino interactions with quarks are derived from
this initial dataset
Signal transduction underlying the control of urinary bladder smooth muscle tone by muscarinic receptors and β-adrenoceptors
The normal physiological contraction of the urinary bladder, which is required for voiding, is predominantly mediated by muscarinic receptors, primarily the M3 subtype, with the M2 subtype providing a secondary backup role. Bladder relaxation, which is required for urine storage, is mediated by β-adrenoceptors, in most species involving a strong β3-component. An excessive stimulation of contraction or a reduced relaxation of the detrusor smooth muscle during the storage phase of the micturition cycle may contribute to bladder dysfunction known as the overactive bladder. Therefore, interference with the signal transduction of these receptors may be a viable approach to develop drugs for the treatment of overactive bladder. The prototypical signaling pathway of M3 receptors is activation of phospholipase C (PLC), and this pathway is also activated in the bladder. Nevertheless, PLC apparently contributes only in a very minor way to bladder contraction. Rather, muscarinic-receptor-mediated bladder contraction involves voltage-operated Ca2+ channels and Rho kinase. The prototypical signaling pathway of β-adrenoceptors is an activation of adenylyl cyclase with the subsequent formation of cAMP. Nevertheless, cAMP apparently contributes in a minor way only to β-adrenoceptor-mediated bladder relaxation. BKCa channels may play a greater role in β-adrenoceptor-mediated bladder relaxation. We conclude that apart from muscarinic receptor antagonists and β-adrenoceptor agonists, inhibitors of Rho kinase and activators of BKCa channels may have potential to treat an overactive bladder