A family of new iteration methods is presented for designing quantum optimal controls to manipulate the transition probability. Theoretical analysis shows that these new methods exhibit quadratic and monotonic convergence. Numerical calculations verify that for these new methods, within very few steps, the optimized objective functional comes close to its convergent limit.

A new iteration method is presented for achieving quantum optimal control over the expectation value of a positive definite operator. Theoretical analysis shows that this new algorithm exhibits quadratic and monotonic convergence. Numerical calculations verify that for this new algorithm, within a few steps, the optimized objective functional comes close to its converged limit.

Articles you may be interested inA smoothing monotonic convergent optimal control algorithm for nuclear magnetic resonance pulse sequence design Generalized monotonically convergent algorithms for solving quantum optimal control problems A rapid monotonically convergent iteration algorithm for quantum optimal control over the expectation value of a positive definite operator This paper extends a monotonically convergent algorithm for quantum optimal control to treat systems with dissipation. The algorithm working with the density matrix is proved to exhibit quadratic and monotonic convergence. Several numerical tests are implemented in three-level model systems. The algorithm is exploited to control various targets, including the expectation value of a Hermitian operator, the modulus square of the expectation value of a non-Hermitian operator, and off-diagonal elements of the density matrix.

Background Inflammatory response has been recognized as a pivotal pathophysiological process during cerebral ischemic stroke. NLRP3 inflammasome, involved in the regulation of inflammatory cascade, can simultaneously lead to GSDMD-executed pyroptosis in cerebral ischemia. Low-density lipoprotein receptor (LDLR), responsible for cholesterol uptake, was noted to exert potential anti-inflammatory bioactivities. Nevertheless, the role of LDLR in neuroinflammation mobilized by cerebral ischemia/reperfusion (I/R) has not been investigated. Methods Ischemic stroke mice model was accomplished by middle cerebral artery occlusion. Oxygen-glucose deprivation was employed after primary cortical neuron was extracted and cultured. A pharmacological inhibitor of NLRP3 (CY-09) was administered to suppress NLPR3 activation. Histological and biochemical analysis were performed to assess the neuronal death both in vitro and in vivo. In addition, neurological deficits and behavioral deterioration were evaluated in mice. Results The expression of LDLR was downregulated following cerebral I/R injury. Genetic knockout of Ldlr enhanced caspase-1-dependent cleavage of GSDMD and resulted in severe neuronal pyroptosis. LDLR deficiency contributed to excessive NLRP3-mediated maturation and release of IL-1β and IL-18 under in vitro and in vivo ischemic conditions. These influences ultimately led to aggravated neurological deficits and long-term cognitive dysfunction. Blockade of NLRP3 substantially retarded neuronal pyroptosis in Ldlr−/− mice and cultured Ldlr−/− neuron after experimental stroke. Conclusions These results demonstrated that LDLR modulates NLRP3-mediated neuronal pyroptosis and neuroinflammation following ischemic stroke. Our findings characterize a novel role for LDLR as a potential therapeutic target in neuroinflammatory responses to acute cerebral ischemic injury.