Ginzburg-Landau-type theory of non-polarized spin superconductivity

Since the concept of spin superconductor was proposed, all the related studies concentrate on spin-polarized case. Here, we generalize the study to spin-non-polarized case. The free energy of non-polarized spin superconductor is obtained, and the Ginzburg-Landau-type equations are derived by using the variational method. These Ginzburg-Landau-type equations can be reduced to the spin-polarized case when the spin direction is fixed. Moreover, the expressions of super linear and angular spin currents inside the superconductor are derived. We demonstrate that the electric field induced by super spin current is equal to the one induced by equivalent charge obtained from the second Ginzburg-Landau-type equation, which shows self-consistency of our theory. By applying these Ginzburg-Landau-type equations, the effect of electric field on the superconductor is also studied. These results will help us get a better understanding of the spin superconductor and the related topics such as Bose-Einstein condensate of magnons and spin superfluidity.Comment: 9 pages, 5 figure

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

RRM1 single nucleotide polymorphism -37C→A correlates with progression-free survival in NSCLC patients after gemcitabine-based chemotherapy

<p>Abstract</p> <p>Background</p> <p>The ribonucleotide reductase M1 (RRM1) gene encodes the regulatory subunit of ribonucleotide reductase, the molecular target of gemcitabine. The overexpression of RRM1 mRNA in tumor tissues is reported to be associated with gemcitabine resistance. Thus, single nucleotide polymorphisms (SNPs) of the RRM1 gene are potential biomarkers of the response to gemcitabine chemotherapy. We investigated whether RRM1 expression in peripheral blood mononuclear cells (PBMCs) or SNPs were associated with clinical outcome after gemcitabine-based chemotherapy in advanced non-small cell lung cancer (NSCLC) patients.</p> <p>Methods</p> <p>PBMC samples were obtained from 62 stage IIIB and IV patients treated with gemcitabine-based chemotherapy. RRM1 mRNA expression levels were assessed by real-time PCR. Three RRM1 SNPs, -37C→A, 2455A→G and 2464G→A, were assessed by direct sequencing.</p> <p>Results</p> <p>RRM1 expression was detectable in 57 PBMC samples, and SNPs were sequenced in 56 samples. The overall response rate to gemcitabine was 18%; there was no significant association between RRM1 mRNA expression and response rate (<it>P </it>= 0.560). The median progression-free survival (PFS) was 23.3 weeks in the lower expression group and 26.9 weeks in the higher expression group (<it>P </it>= 0.659). For the -37C→A polymorphism, the median PFS was 30.7 weeks in the C(-)37A group, 24.7 weeks in the A(-)37A group, and 23.3 weeks in the C(-)37C group (<it>P </it>= 0.043). No significant difference in PFS was observed for the SNP 2455A→G or 2464G→A.</p> <p>Conclusions</p> <p>The RRM1 polymorphism -37C→A correlated with PFS in NSCLC patients treated with gemcitabine-based chemotherapy. No significant correlation was found between PBMC RRM1 mRNA expression and the efficacy of gemcitabine.</p

[μ-1,1′-(Butane-1,4-di­yl)di-1H-benz­imidazole-κ2 N 3:N 3′]bis­{[N,N′-bis(car­boxy­meth­yl)ethyl­enediamine-N,N′-di­acetato-κ5 O,O′,O′′,N,N′]mercury(II)} methanol disolvate

The binuclear title complex, [Hg2(C10H14N2O8)2(C18H18N4)]·2CH3OH, lies on an inversion center with the unique HgII ion coordinated in a disorted octa­hedral environment with one Hg—N bond significantly shorter than the other two. In the crystal structure, inter­molecular O—H⋯O hydrogen bonds link complex and solvent mol­ecules into a three-dimensional network

Bostrycin inhibits proliferation of human lung carcinoma A549 cells via downregulation of the PI3K/Akt pathway

<p>Abstract</p> <p>Background</p> <p>Bostrycin is a novel compound isolated from marine fungi that inhibits proliferation of many cancer cells. However, the inhibitory effect of bostrycin on lung cancers has not been reported. This study is to investigate the inhibitory effects and mechanism of bostrycin on human lung cancer cells in vitro.</p> <p>Methods</p> <p>We used MTT assay, flow cytometry, microarray, real time PCR, and Western blotting to detect the effect of bostrycin on A549 human pulmonary adenocarcinoma cells.</p> <p>Results</p> <p>We showed a significant inhibition of cell proliferation and induction of apoptosis in bostrycin-treated lung adenocarcinoma cells. Bostrycin treatment caused cell cycle arrest in the G0/G1 phase. We also found the upregulation of microRNA-638 and microRNA-923 in bostrycin-treated cells. further, we found the downregulation of p110α and p-Akt/PKB proteins and increased activity of p27 protein after bostrycin treatment in A549 cells.</p> <p>Conclusions</p> <p>Our study indicated that bostrycin had a significant inhibitory effect on proliferation of A549 cells. It is possible that upregulation of microRNA-638 and microRNA-923 and downregulaton of the PI3K/AKT pathway proteins played a role in induction of cell cycle arrest and apoptosis in bostrycin-treated cells.</p