Di-μ-nitrito-κ3 O:O,O′;κ3 O,O′:O-bis­{[2,6-bis­(pyrazol-1-yl-κN 2)pyridine-κN](nitrito-κ2 O,O′)cadmium(II)}

In the title centrosymmetric binuclear complex, [Cd2(NO2)4(C11H9N5)2], the unique CdII ion is in a distorted dodeca­hedral CdN3O5 coordination environment. The two inversion-related CdII ions are separated by 3.9920 (6) Å and are bridged by two O atoms from two nitrite ligands. There are two types of π–π stacking inter­actions involving symmetry-related pyrazole rings, with centroid–centroid distances of 3.445 (2) and 3.431 (2) Å

Geometrically Local Quantum and Classical Codes from Subdivision

A geometrically local quantum code is an error correcting code situated within $\mathbb{R}^D$, where the checks only act on qubits within a fixed spatial distance. The main question is: What is the optimal dimension and distance for a geometrically local code? This question was recently answered by Portnoy which constructed codes with optimal dimension and distance up to polylogs. This paper extends Portnoy's work by constructing a code which additionally has an optimal energy barrier up to polylogs. The key ingredient is a simpler code construction obtained by subdividing the balanced product codes. We also discuss applications to classical codes

An operator extension of weak monotonicity

Let $S(\rho)$ be the von Neumann entropy of a density matrix $\rho$. Weak monotonicity asserts that $S(\rho_{AB}) - S(\rho_A) + S(\rho_{BC}) - S(\rho_C)\geq 0$ for any tripartite density matrix $\rho_{ABC}$, a fact that is equivalent to the strong subadditivity of entropy. We prove an operator inequality, which, upon taking an expectation value with respect to the state $\rho_{ABC}$, reduces to the weak monotonicity inequality. Generalizations of this inequality to the one involving two independent density matrices, as well as their R\'enyi-generalizations, are also presented

Glucagon-like peptide-1 receptor agonist versus basal insulin in type-2 diabetic patients: An efficacy and safety analysis

Purpose: To compare the effectiveness of glucagon-like peptide 1 receptor agonist with that of basal insulin in type 2 diabetes patients. Methods: Type-2 diabetes patients who were insensitive to metformin were treated with glucagon-like peptide 1 receptor agonist (GP cohort, n = 115) or basal insulin (BI cohort, n = 152) with metformin. Hemoglobin A1c (HbA1c) level and body weight were determined, and adverse effects also recorded. Results: After 16 weeks of treatment, glucagon-like peptide 1 receptor agonist did not significantly reduce HbA1c levels (7.45 ± 2.11 % vs. 7.01 ± 2.01, p = 0.107). In contrast, basal insulin significantly reduced the levels of HbA1c (7.91 ± 2.98 % vs. 7.13 ± 2.22 %, p = 0.010, q = 3.852). Glucagon-likepeptide 1 receptor agonist reduced the body weight of patients (65.25 ± 7.55 kg vs. 62.16 ± 6.15 kg, p = 0.0008, q = 5.121), unlike basal insulin (63.71 ± 6.15 vs. 62.65 ± 6.76 kg, p = 0.154). Conclusion: Glucagon-like peptide 1 receptor agonist and basal insulin + metformin produce identical effectiveness in the treatment of type-2 diabetic patients. Keywords: Glucagon-like peptide-1 receptor agonist, Glycemic control, Insulin, Metformin, Type-2 diabete

Paxillin facilitates timely neurite initiation on soft-substrate environments by interacting with the endocytic machinery.

Neurite initiation is the first step in neuronal development and occurs spontaneously in soft tissue environments. Although the mechanisms regulating the morphology of migratory cells on rigid substrates in cell culture are widely known, how soft environments modulate neurite initiation remains elusive. Using hydrogel cultures, pharmacologic inhibition, and genetic approaches, we reveal that paxillin-linked endocytosis and adhesion are components of a bistable switch controlling neurite initiation in a substrate modulus-dependent manner. On soft substrates, most paxillin binds to endocytic factors and facilitates vesicle invagination, elevating neuritogenic Rac1 activity and expression of genes encoding the endocytic machinery. By contrast, on rigid substrates, cells develop extensive adhesions, increase RhoA activity and sequester paxillin from the endocytic machinery, thereby delaying neurite initiation. Our results highlight paxillin as a core molecule in substrate modulus-controlled morphogenesis and define a mechanism whereby neuronal cells respond to environments exhibiting varying mechanical properties