Quantum mechanics puts a restriction on the number of observers who can simultaneously steer another observer's system, known as the monogamy of steering. In this work we find the limit of the number of observers (Bobs) who can steer another party's (Alice's) system invoking a scenario where half of an entangled pair is shared between a single Alice in one wing and several Bobs on the other wing, who act sequentially and independently of each other. When all the observers measure two dichotomic observables, we find that two Bobs can steer Alice's system going beyond the monogamy restriction. We further show that three Bobs can steer Alice's system considering a three-settings linear steering inequality, and then conjecture that at most n Bobs can demonstrate steering of Alice's system when steering is probed through an n-settings linear steering inequality.

We derive an exact computable formula for fidelity deviation in quantum teleportation with an arbitrary state of two qubits. As an application, we obtain the condition for universality: the condition that all input states are teleported equally well and provide a necessary and sufficient condition for a state to be both useful and universal for quantum teleportation. We illustrate these results with examples from well-known classes of two-qubit states. * Electronic address: a.

Recently, it has been shown that at most two observers (Bobs) can sequentially demonstrate bipartite nonlocality with a spatially separated single observer (Alice) invoking a scenario where an entangled system of two spin-1 2 particles are shared between a single Alice in one wing and several Bobs on the other wing, who act sequentially and independently of each other [Phys. Rev. Lett. 114, 250401 (2015)]. This has been probed through the quantum violations of CHSH inequality, i. e., when each observer performs two dichotomic measurements.In the present study we investigate how many Bobs can sequentially demonstrate bipartite nonlocality with a single Alice in the above scenario when the number of measurement settings per observer is increased. It is shown that at most two Bobs can exhibit bipartite nonlocality with a single Alice using local realist inequalities with three as well as four dichotomic measurements per observer. We then conjecture that the above feature remains unchanged contingent upon using local realist inequalities with n dichotomic measurements per observer, where n is arbitrary. We further present the robustness of bipartite nonlocality sharing in the above scenario against the entanglement and mixedness of the shared state. arXiv:1811.04813v2 [quant-ph]

Background and Aims Alcoholic liver disease is associated with inflammation and cell death. Heme oxygenase-1 (HO-1) is a stress-inducible enzyme with anti-apoptotic and anti-inflammatory properties. Here we tested the hypothesis that induction of HO-1 or treatment with a carbon monoxide releasing molecule (CORM) during chronic ethanol exposure protects and/or reverses ethanol-induced liver injury. Methods Female C57BL/6J mice were allowed free access to a complete liquid diet containing ethanol or pair-fed control diets for 25 days. Mice were treated with cobalt protoporphyrin (CoPP) to induce HO-1 expression during ethanol feeding or once injury had been established. Mice were also treated with CORM-A1, a CO-releasing molecule (CORM), after ethanol-induced liver injury was established. The impact of HO-1 induction on ethanol-induced cell death was investigated in primary cultures of hepatocytes. Results Induction of HO-1 during or after ethanol feeding, as well as treatment with CORM-A1, ameliorated ethanol-induced increases in AST and expression of mRNA for inflammatory cytokines. Treatment with CoPP or CORM-A1 also reduced hepatocyte cell death, indicated by decreased accumulation of CK18 cleavage products and reduced RIP3 expression in hepatocytes. Exposure of primary hepatocyte cultures to ethanol increased their sensitivity to TNFα-induced cell death; this response was attenuated by necrostatin-1, an inhibitor of necroptosis, but not by caspase inhibitors. Induction of HO-1 with CoPP or CORM-3 treatment normalized the sensitivity of hepatocytes to TNFα-induced cell death after ethanol exposure. Conclusions Therapeutic strategies to increase HO-1 and/or modulate CO availability ameliorated chronic ethanol-induced liver injury in mice, at least in part by decreasing hepatocellular death.

Imbalance of brain metal homeostasis and associated oxidative stress by redox-active metals like iron and copper is an important trigger of neurotoxicity in several neurodegenerative conditions, including prion disorders. Whereas some reports attribute this to end-stage disease, others provide evidence for specific mechanisms leading to brain metal dyshomeostasis during disease progression. In prion disorders, imbalance of brain-iron homeostasis is observed before end-stage disease and worsens with disease progression, implicating ironinduced oxidative stress in disease pathogenesis. This is an unexpected observation, because the underlying cause of brain pathology in all prion disorders is PrP-scrapie (PrP Sc ), a b-sheet-rich conformation of a normal glycoprotein, the prion protein (PrP C ). Whether brain-iron dyshomeostasis occurs because of gain of toxic function by PrP Sc or loss of normal function of PrP C remains unclear. In this review, we summarize available evidence suggesting the involvement of oxidative stress in prion-disease pathogenesis. Subsequently, we review the biology of PrP C to highlight its possible role in maintaining brain metal homeostasis during health and the contribution of PrP Sc in inducing brain metal imbalance with disease progression. Finally, we discuss possible therapeutic avenues directed at restoring brain metal homeostasis and alleviating metal-induced oxidative stress in prion disorders. Antioxid. Redox Signal. 12, 1271-1294.