g-factor symmetry and topology in semiconductor band states.

The [Formula: see text] tensor, which determines the reaction of Kramers-degenerate states to an applied magnetic field, is of increasing importance in the current design of spin qubits. It is affected by details of heterostructure composition, disorder, and electric fields, but it inherits much of its structure from the effect of the spin-orbit interaction working at the crystal-lattice level. Here, we uncover interesting symmetry and topological features of [Formula: see text] for important valence and conduction bands in silicon, germanium, and gallium arsenide. For all crystals with high (cubic) symmetry, we show that large departures from the nonrelativistic value [Formula: see text] are guaranteed by symmetry. In particular, considering the spin part [Formula: see text], we prove that the scalar function [Formula: see text] must go to zero on closed surfaces in the Brillouin zone, no matter how weak the spin-orbit coupling is. We also prove that for wave vectors [Formula: see text] on these surfaces, the Bloch states [Formula: see text] have maximal spin-orbital entanglement. Using tight-binding calculations, we observe that the surfaces [Formula: see text] exhibit many interesting topological features, exhibiting Lifshitz critical points as understood in Fermi-surface theory.

Aldose Reductase: An Emerging Target for Development of Interventions for Diabetic Cardiovascular Complications.

Diabetes is a leading cause of cardiovascular morbidity and mortality. Despite numerous treatments for cardiovascular disease (CVD), for patients with diabetes, these therapies provide less benefit for protection from CVD. These considerations spur the concept that diabetes-specific, disease-modifying therapies are essential to identify especially as the diabetes epidemic continues to expand. In this context, high levels of blood glucose stimulate the flux via aldose reductase (AR) pathway leading to metabolic and signaling changes in cells of the cardiovascular system. In animal models flux via AR in hearts is increased by diabetes and ischemia and its inhibition protects diabetic and non-diabetic hearts from ischemia-reperfusion injury. In mouse models of diabetic atherosclerosis, human AR expression accelerates progression and impairs regression of atherosclerotic plaques. Genetic studies have revealed that single nucleotide polymorphisms (SNPs) of the ALD2 (human AR gene) is associated with diabetic complications, including cardiorenal complications. This Review presents current knowledge regarding the roles for AR in the causes and consequences of diabetic cardiovascular disease and the status of AR inhibitors in clinical trials. Studies from both human subjects and animal models are presented to highlight the breadth of evidence linking AR to the cardiovascular consequences of diabetes.