Dynamically-Induced Frustration as a Route to a Quantum Spin Ice State in Tb2Ti2O7 via Virtual Crystal Field Excitations and Quantum Many-Body Effects

The Tb$_2$Ti$_2$O$_7$ pyrochlore magnetic material is attracting much attention for its {\em spin liquid} state, failing to develop long range order down to 50 mK despite a Curie-Weiss temperature $\theta_{\rm CW} \sim -14$ K. In this paper we reinvestigate the theoretical description of this material by considering a quantum model of independent tetrahedra to describe its low temperature properties. The naturally-tuned proximity of this system near a N\'eel to spin ice phase boundary allows for a resurgence of quantum fluctuation effects that lead to an important renormalization of its effective low energy spin Hamiltonian. As a result, Tb$_2$Ti$_2$O$_7$ is argued to be a {\em quantum spin ice}. We put forward an experimental test of this proposal using neutron scattering on a single crystal.Comment: 5 pages, 3 figures. Version 2 has a modified introduction. Figure 2b of version 1 (experimental neutron scattering has been removed. A proposal for an experimental test is now included accompanied by a new Figure (Fig. 3

Understanding Paramagnetic Spin Correlations in the Spin-Liquid Pyrochlore Tb2Ti2O7

Recent elastic and inelastic neutron scattering studies of the highly frustrated pyrochlore antiferromagnet Tb2Ti2O7 have shown some very intriguing features that cannot be modeled by the local classical Ising model, naively expected to describe this system at low temperatures. Using the random phase approximation to take into account fluctuations between the ground state doublet and the first excited doublet, we successfully describe the elastic neutron scattering pattern and dispersion relations in Tb2Ti2O7, semi-quantitatively consistent with experimental observations.Comment: revtex4, 4 pages, 1 Color+ 2 BW figure

Drug-induced reactive oxygen species (ROS) rely on cell membrane properties to exert anticancer effects

Pharmacological concentrations of small molecule natural products, such as ascorbic acid, have exhibited distinct cell killing outcomes between cancer and normal cells whereby cancer cells undergo apoptosis or necrosis while normal cells are not adversely affected. Here, we develop a mathematical model for ascorbic acid that can be utilized as a tool to understand the dynamics of reactive oxygen species (ROS) induced cell death. We determine that not only do endogenous antioxidants such as catalase contribute to ROS-induced cell death, but also cell membrane properties play a critical role in the efficacy of ROS as a cytotoxic mechanism against cancer cells vs. normal cells. Using in vitro assays with breast cancer cells, we have confirmed that cell membrane properties are essential for ROS, in the form of hydrogen peroxide (H[subscript 2]O[subscript 2]), to induce cell death. Interestingly, we did not observe any correlation between intracellular H[subscript 2]O[subscript 2] and cell survival, suggesting that cell death by H[subscript 2]O[subscript 2] is triggered by interaction with the cell membrane and not necessarily due to intracellular levels of H[subscript 2]O[subscript 2]. These findings provide a putative mechanistic explanation for the efficacy and selectivity of therapies such as ascorbic acid that rely on ROS-induced cell death for their anti-tumor properties.Natural Sciences and Engineering Research Council of Canada (NSERC discovery grant)Natural Sciences and Engineering Research Council of Canada (NSERC/CIHR Collaborative Health Research grant

Drug-induced reactive oxygen species (ROS) rely on cell membrane properties to exert anticancer effects

Pharmacological concentrations of small molecule natural products, such as ascorbic acid, have exhibited distinct cell killing outcomes between cancer and normal cells whereby cancer cells undergo apoptosis or necrosis while normal cells are not adversely affected. Here, we develop a mathematical model for ascorbic acid that can be utilized as a tool to understand the dynamics of reactive oxygen species (ROS) induced cell death. We determine that not only do endogenous antioxidants such as catalase contribute to ROS-induced cell death, but also cell membrane properties play a critical role in the efficacy of ROS as a cytotoxic mechanism against cancer cells vs. normal cells. Using in vitro assays with breast cancer cells, we have confirmed that cell membrane properties are essential for ROS, in the form of hydrogen peroxide (H2O2), to induce cell death. Interestingly, we did not observe any correlation between intracellular H2O2 and cell survival, suggesting that cell death by H2O2 is triggered by interaction with the cell membrane and not necessarily due to intracellular levels of H2O2. These findings provide a putative mechanistic explanation for the efficacy and selectivity of therapies such as ascorbic acid that rely on ROS-induced cell death for their anti-tumor properties