catena-Poly[[[diaqua­nickel(II)]-μ-pyrazine-2-carboxyl­ato-silver(I)-μ-pyrazine-2-carboxyl­ato] nitrate dihydrate]

In the polymeric complex of the title compound, {[AgNi(C5H3N2O2)2(H2O)2]NO3·2H2O}n, the AgI ion displays an angular coordination geometry with two N atoms from pyrazine-2-carboxyl­ate ligands, and the NiII ion is hexa­coordinated by two O atoms from two water mol­ecules, two O and two N atoms from pyrazine-2-carboxyl­ate ligands in a distorted octa­hedral geometry. In the crystal, the AgI and NiII ions lie on a mirror plane and an inversion centre, respectively. The complex chains, the nitrate ions and the uncoordinated water mol­ecules are linked together through O—H⋯O hydrogen bonds and weak Ag⋯O inter­actions [2.619 (17)–2.749 (17) Å] into a three-dimensional network

Quantum Simulation of Dissipative Energy Transfer via Noisy Quantum Computer

In recent years, due to its formidable potential in computational theory, quantum computing has become a very popular research topic. However, the implementation of practical quantum algorithms, which hold the potential to solve real-world problems, is often hindered by the significant error rates associated with quantum gates and the limited availability of qubits. In this study, we propose a practical approach to simulate the dynamics of an open quantum system on a noisy computer, which encompasses general and valuable characteristics. Notably, our method leverages gate noises on the IBM-Q real device, enabling us to perform calculations using only two qubits. The results generated by our method performed on IBM-Q Jakarta aligned with the those calculated by hierarchical equations of motion (HEOM), which is a classical numerically-exact method, while our simulation method runs with a much better computing complexity. In the last, to deal with the increasing depth of quantum circuits when doing Trotter expansion, we introduced the transfer tensor method(TTM) to extend our short-term dynamics simulation. Based on quantum simulator, we show the extending ability of TTM, which allows us to get a longer simulation using a relatively short quantum circuits

Aerodynamic response of micro rotary wings in wind perturbation

One high fidelity numerical method is extended to compute the unsteady aerodynamic loads when micro rotary wings suffer wind. The unsteady solutions are obtained by solving Navier-Stokes equations, where field velocity method is proposed to carry out the atmospheric perturbation. The convective terms are approximated by a high order WENO-Roe scheme, and time advance is performed by an implicit scheme of dual time stepping which can guarantee a degree of efficiency. Moving overset grids are used to facilitate the implement of rotational motion of rotary wings and relative movements between rotary wings, as well as the atmospheric perturbation. The results reveal that small atmospheric perturbation has an important impact on the flows of micro rotary wings under low Reynolds number. The response of thrust coefficient presents periodic fluctuation and its amplitude is proportional to that of wind disturbance, which provides the clue for active control research of rotary wing aircraft

FSD-C10, a Fasudil derivative, promotes neuroregeneration through indirect and direct mechanisms.

FSD-C10, a Fasudil derivative, was shown to reduce severity of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), through the modulation of the immune response and induction of neuroprotective molecules in the central nervous system (CNS). However, whether FSD-C10 can promote neuroregeneration remains unknown. In this study, we further analyzed the effect of FSD-C10 on neuroprotection and remyelination. FSD-C10-treated mice showed a longer, thicker and more intense MAP2 and synaptophysin positive signal in the CNS, with significantly fewer CD4(+) T cells, macrophages and microglia. Importantly, the CNS of FSD-C10-treated mice showed a shift of activated macrophages/microglia from the type 1 to type 2 status, elevated numbers of oligodendrocyte precursor cells (OPCs) and oligodendrocytes, and increased levels of neurotrophic factors NT-3, GDNF and BDNF. FSD-C10-treated microglia significantly inhibited Th1/Th17 cell differentiation and increased the number of IL-10(+) CD4(+) T cells, and the conditioned medium from FSD-C10-treated microglia promoted OPC survival and oligodendrocyte maturation. Addition of FSD-C10 directly promoted remyelination in a chemical-induced demyelination model on organotypic slice culture, in a BDNF-dependent manner. Together, these findings demonstrate that FSD-C10 promotes neural repair through mechanisms that involved both immunomodulation and induction of neurotrophic factors

Asymptotic behavior of solutions of a Fisher equation with free boundaries and nonlocal term

We study the asymptotic behavior of solutions of a Fisher equation with free boundaries and the nonlocal term (an integral convolution in space). This problem can model the spreading of a biological or chemical species, where free boundaries represent the spreading fronts of the species. We give a dichotomy result, that is, the solution either converges to $1$ locally uniformly in $\mathbb{R}$, or to $0$ uniformly in the occupying domain. Moreover, we give the sharp threshold when the initial data $u_0=\sigma \phi$, that is, there exists $\sigma^*>0$ such that spreading happens when $\sigma>\sigma^*$, and vanishing happens when $\sigma\leq \sigma^*$

Asymptotic behavior of solutions of a Fisher equation with free boundaries and nonlocal term

We study the asymptotic behavior of solutions of a Fisher equation with free boundaries and the nonlocal term (an integral convolution in space). This problem can model the spreading of a biological or chemical species, where free boundaries represent the spreading fronts of the species. We give a dichotomy result, that is, the solution either converges to 1 locally uniformly in R, or to 0 uniformly in the occupying domain. Moreover, we give the sharp threshold when the initial data u0 = σφ, that is, there exists σ ∗ > 0 such that spreading happens when σ > σ , and vanishing happens when σ ≤

Dexamethasone disrupts intercellular junction formation and cytoskeleton organization in human trabecular meshwork cells

Purpose: Patients reproduce symptoms of primary open-angle glaucoma (POAG) when treated with glucocorticoids (GCs) topically on the eyes. Here we investigated the effects of GCs on junctional protein expression and cytoskeleton organization in primary human trabecular meshwork (TM) cultures to understand the molecular pathologies of POAG. Methods: Human TM cells from POAG (GTM) and age-matched nondiseased (NTM) individuals were obtained by standard surgical trabeculectomy. Some of the cultures were treated with dexamethasone (DEX), a synthetic GC, at 1-5x10(-7) mol/l for 1-7 days. The expression levels of zonula occluden-1 (ZO-1) and connexin43 (Cx43) in TM cells with or without DEX treatment were measured using reverse transcription (RT)-PCR, immunocytochemistry, and western blot analysis. Results: mRNA and proteins of ZO-1 and Cx43 were found in both NTM and GTM cells. ZO-1 and Cx43 were located on the plasma membrane, especially along the border of adjacent cells. ZO-1 had no marked changes in localization in NTM and GTM cells after treatment with 10(-7) mol/l DEX for 48 h, whereas Cx43 appeared to increase in the cytoplasm. mRNA of two ZO-1 isoforms, alpha+ and alpha-, were present in TM cells, and the former was expressed less than the latter. Only ZO-1 alpha-isoform protein was expressed in NTM cells, whereas proteins of both isoforms were found in GTM cells. DEX increased the protein levels of ZO-1 and Cx43 in both NTM and GTM cells. DEX also altered the F-actin architecture and promoted cross-linked actin network formation, the effects of which were more pronounced in GTM cells. Conclusions: Our findings not only provide molecular insights to the pathogenesis of GC-induced glaucoma but also suggest that junctional proteins ZO-1 and Cx43 as well as F-actin are targets for developing new modalities in glaucoma therapy