Bis[2-(2-pyridyl­sulfan­yl)eth­yl]ammonium perchlorate

The cation and anion of the title salt, C14H18N3S2 +·ClO4 −, lie on a twofold rotation axis. The cation is a W-shaped entity with the aromatic rings at the ends; the ammonium NH2 + group is a hydrogen-bond donor to the pyridyl N atoms. The perchlorate ion has one O atom disordered over two sites in a 0.50:0.50 ratio

Time-Reversal-Even Nonlinear Current Induced Spin Polarization

We propose a time-reversal-even spin generation in second order of electric fields, which dominates the current induced spin polarization in a wide class of centrosymmetric nonmagnetic materials, and leads to a novel nonlinear spin-orbit torque in magnets. We reveal a quantum origin of this effect from the momentum space dipole of the anomalous spin polarizability. First-principles calculations predict sizable spin generations in several nonmagnetic hcp metals, in monolayer TiTe$_{2}$, and in ferromagnetic monolayer MnSe$_{2}$, which can be detected in experiment. Our work opens up the broad vista of nonlinear spintronics in both nonmagnetic and magnetic systems.Comment: 4 pages, 2 figure

Bis[2-((4,6-dimethyl­pyrimidin-2-yl){2-[(4,6-dimethyl­pyrimidin-2-yl)sulfan­yl]eth­yl}amino)­eth­yl] disulfide

Bis[2-(4,6-dimethyl­pyrimidin-2-ylsulfan­yl)eth­yl]amine under hydro­thermal conditions has unexpectedly been transformed into the title compound, C32H44N10S4. In the title mol­ecule, the zigzag 3,10-diaza-6,7-disulfanyldodecyl skeleton has two dimethyl­pyrimidinylsulfanyl groups at both ends, and the aza atoms each carry a dimethyl­pyrimidinyl unit. The N atoms in the skeleton show a planar coordination

An inverted J-shaped association of serum uric acid with muscle strength among Japanese adult men: a cross-sectional study

BACKGROUND: Uric acid (UA) may protect muscle function from oxidative damage due to reactive oxygen species through its powerful antioxidant capacity. However, several studies have demonstrated that hyperuricemia is closely related to systemic inflammation and has oxidant properties effects, both of which may increase the risk of muscle strength loss. The purpose of this study was to examine the association of serum UA concentration with grip strength and leg extension power in adult men. METHODS: This study is a cross-sectional survey in which 630 Japanese male employees aged 30 years and older participated. Five hundred and eighty-six subjects participated in the measurement of grip strength, and 355 subjects participated in the measurement of leg extension power. Blood samples were obtained for serum UA analysis. RESULTS: After adjustment for potential confounders, grip strength differed significantly between participants with and those without hyperuricemia (geometric mean and 95% confidence interval [CI]: 40.3 [39.2–41.3] kg vs. 41.9 [41.3–42.5] kg; P = 0.01). In addition, serum UA levels (quartiles) showed an inverted J-shaped curve with grip strength (mean and 95% CI: Q1, 41.6 [40.6–42.6] kg; Q2, 42.2 [41.2–43.2] kg; Q3, 41.8 [40.8–42.8] kg; Q4, 40.4 [39.3–41.4] kg; P for quadratic trend = 0.05). The results in the leg extension power group were similar to those observed in the grip strength group. CONCLUSION: This population-based cross-sectional study shows for the first time that hyperuricemia is associated with poor muscle strength. Moreover, the results indicate an inverted J-shaped association between serum UA quartiles and muscle strength

Role of NRP1 in Bladder Cancer Pathogenesis and Progression

Bladder urothelial carcinoma (BC) is a fatal invasive malignancy and the most common malignancy of the urinary system. In the current study, we investigated the function and mechanisms of Neuropilin-1 (NRP1), the co-receptor for vascular endothelial growth factor, in BC pathogenesis and progression. The expression of NRP1 was evaluated using data extracted from GEO and HPA databases and examined in BC cell lines. The effect on proliferation, apoptosis, angiogenesis, migration, and invasion of BC cells were validated after NRP1 knockdown. After identifying differentially expressed genes (DEGs) induced by NRP1 silencing, GO/KEGG and IPA® bioinformatics analyses were performed and specific predicted pathways and targets were confirmed in vitro. Additionally, the co-expressed genes and ceRNA network were predicted using data downloaded from CCLE and TCGA databases, respectively. High expression of NRP1 was observed in BC tissues and cells. NRP1 knockdown promoted apoptosis and suppressed proliferation, angiogenesis, migration, and invasion of BC cells. Additionally, after NRP1 silencing the activity of MAPK signaling and molecular mechanisms of cancer pathways were predicted by KEGG and IPA® pathway analysis and validated using western blot in BC cells. NRP1 knockdown also affected various biological functions, including antiviral response, immune response, cell cycle, proliferation and migration of cells, and neovascularisation. Furthermore, the main upstream molecule of the DEGs induced by NRP1 knockdown may be NUPR1, and NRP1 was also the downstream target of NUPR1 and essential for regulation of FOXP3 expression to activate neovascularisation. DCBLD2 was positively regulated by NRP1, and PPAR signaling was significantly associated with low NRP1 expression. We also found that NRP1 was a predicted target of miR-204, miR-143, miR-145, and miR-195 in BC development. Our data provide evidence for the biological function and molecular aetiology of NRP1 in BC and for the first time demonstrated an association between NRP1 and NUPR1, FOXP3, and DCBLD2. Specifically, downregulation of NRP1 contributes to BC progression, which is associated with activation of MAPK signaling and molecular mechanisms involved in cancer pathways. Therefore, NRP1 may serve as a target for new therapeutic strategies to treat BC and other cancers