We investigate how the fixed-node diffusion Monte Carlo energy of solids depends on singleparticle orbitals used in Slater-Jastrow wave functions. We demonstrate that the dependence can be significant, in particular in the case of 3d transition-metal compounds, which we adopt as examples. We illustrate how exchange-correlation functionals with variable exact-exchange component can be exploited to reduce the fixed-node errors. On the basis of these results we argue that the fixed-node quantum Monte Carlo provides a variational approach for optimization of effective hamiltonians with parameters.

Perspective: Explicitly correlated electronic structure theory for complex systems

No abstract

We outline the basic notions of nodal hypersurface and domain averages for antisymmetric wave functions. We illustrate their properties and analyze the results for a few electron explicitly solvable cases and discuss possible further developments.PACS numbers: 61.46.+w, 36.40.Cg Quantum Monte Carlo is one of the most effective many-body methodologies for the study of quantum systems. It is based on a combination of analytical insights, robustness of stochastic approaches, and performance of parallel architectures [1][2][3][4][5][6][7][8][9][10]. The approach has been applied to a variety of challenging problems in electronic structure of atoms, small molecules, clusters, solids, ultracold condensates, and beyond [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15]. The two most commonly used QMC methods are variational Monte Carlo and diffusion Monte Carlo (DMC). Let us briefly recapitulate the basics of the DMC method.It is straightforward to show that for τ → ∞, the operator exp(−τ H) projects out the ground state of a given symmetry from any trial function with nonzero overlap. We assume that the Hamiltonian H is time-reversal symmetric so that the eigenstates can be chosen to be real. This projection is most conveniently carried out by solving the Schrödinger equation in an imaginary time integral form so that the product f (R, t) = Φ(R, t)Ψ T (R) obeysThe Green's function is given bywhere R = (r 1 , ..., r N ) denotes positions of N particles and E T is an energy offset. In the DMC method, the function f (R, t) is represented by a set of 10 2 -10 4 random walkers (sampling points) in the 3N -dimensional space of electron configurations. The walkers are propagated for a time slice τ by interpreting the Green's function as a transition probability from R ′ → R. The kernel is known for small τ , and the large time t limit is obtained by iterating the propagation. The method is formally exact provided that the boundary conditions, i.e., the fermion nodes of the antisymmetric solution defined as Φ(R, ∞) = 0, are known [1,5,14]. Unfortunately the antisymmetry does not specify the nodes completely, and currently we have to use approximations. The commonly used fixed-node approximation [14] enforces the nodes of f (R, t) to be identical to the nodes of Ψ T (R) which then implies that f (R, t) ≥ 0 everywhere. It is therefore clear that the accuracy of the fixed-node DMC is determined by the quality of the trial wave function nodes. The commonly used form for Ψ T is the Slater-Jastrow wave function given aswhere U corr is the correlation factor explicitly depending on interparticle distances thus describing pair or higher order correlations explicitly. The typical number of Slater determinants is between 1 and 10 3 , and the corresponding weights {d n } are usually estimated in multi-reference Hartree-Fock (HF) or Configuration Interaction (CI) calculations and then re-optimized in the variational framework.It is quite remarkable that the nodes of such SlaterJastrow wave functions (often with a single-determinant p...

Antioxidant transcription factor NRF2 plays a pivotal role in cell ferroptosis. KLK lung adenocarcinoma (LUAD) is a specific molecular subtype of Kras-mutant LUAD. The activation of mutant Kras in combination with the inactivation of Lkb1 and Keap1 abnormally increases NRF2 expression, while high NRF2 confers KLK LUAD cell resistance to ferroptosis. This study assessed the inhibition of NRF2-GSH axis to sensitize a small molecule RSL3 to induce KLK LUAD cell ferroptosis and then explored the underlying molecular mechanisms. The data showed that the NRF2-GSH inhibition sensitized RSL3 induction of KLK LUAD cell ferroptosis in vitro, while RSL3 treatment reduced level of NRF2 protein in KLK LUAD during ferroptosis. Moreover, RSL3 treatment inhibited activity of the NRF2-GSH signaling during in KLK LUAD cell ferroptosis in vitro and in vivo. Mechanistically, the RSL3 reduction of NRF2 expression was through the promotion of NRF2 ubiquitination in KLK LUAD cells. In addition, RSL3 was able to directly bind to USP11, a recently identified de-ubiquitinase of NRF2, and inactivate USP11 protein to induce NRF2 protein ubiquitination and degradation in KLK LUAD cells. These data revealed a novel mechanism of RSL3 induction in KLK LUAD cell ferroptosis by suppression of the USP11-NRF2-GSH signaling. Future study will confirm RSL3 as a novel therapeutic approach in control of KLK lung adenocarcinoma.