On the fairness of the main galaxy sample of SDSS

Flux-limited and volume-limited galaxy samples are constructed from SDSS data releases DR4, DR6 and DR7 for statistical analysis. The two-point correlation functions $\xi(s)$, monopole of three-point correlation functions $\zeta_0$, projected two-point correlation function $w_p$ and pairwise velocity dispersion $\sigma_{12}$ are measured to test if galaxy samples are fair for these statistics. We find that with increment of sky coverage of SDSS, $\xi(s)$ of flux-limited sample is extremely robust and insensitive to local structures at low redshift. But for volume-limited samples fainter than $L^*$ at large scales s>\sim 10\hmpc, deviation of $\xi(s)$ and $\zeta_0$ of DR7 to those of DR4 and DR6 increases with larger absolute magnitude. In the weakly nonlinear regime, there is no agreement between $\zeta_0$ of different data releases in all luminosity bins. Furthermore, $w_p$ of volume-limited samples of DR7 in luminosity bins fainter than $-M_{r,0.1}=[18.5,19.5]$ are significantly larger, and $\sigma_{12}$ of the two faintest volume-limited samples of DR7 display very different scale dependence than results of DR4 and DR6. Our findings call for cautions in understanding clustering analysis results of SDSS faint galaxy samples, and higher order statistics of SDSS volume-limited samples in the weakly nonlinear regime. The first zero-crossing points of $\xi(s)$ of volume-limited samples are also investigated and discussed.Comment: 16 pages, 12 figures, accepte

The Effect of the Curvature-Rate on the Response of Local Sharp-Notched SUS304 Stainless Steel Tubes under Cyclic Bending

In this study, the response of local sharp-notched SUS304 stainless steel tubes with different notch depths of 0.2, 0.4, 0.6, 0.8 and 1.0 mm subjected to cyclic bending at different curvature-rates of 0.0035, 0.035 and 0.35 m-1s-1 were experimentally investigated. The tube bending machine and curvature-ovalization measurement apparatus, which was designed by Pan et al. [1], were used for conducting the curvature-controlled cyclic bending. For a constant curvature-rate, the moment-curvature curve revealed that the cyclic hardening and became a steady loop after a few bending cycles; the notch depth had almost no influence on the curves. Moreover, the ovalization-curvature curve increased in an increasing and ratcheting manner with the number of bending cycles. Large notch depths resulted in larger ovalization of the tube cross-section. In addition, for a constant notch depth, higher curvature-rates led to larger cyclic hardening and faster increasing of ovalization

Extracellular ATP enhances radiation-induced brain injury through microglial activation and paracrine signaling via P2X7 receptor

AbstractActivation of purinergic receptors by extracellular ATP (eATP) released from injured cells has been implicated in the pathogenesis of many neuronal disorders. The P2X7 receptor (P2X7R), an ion-selective purinergic receptor, is associated with microglial activation and paracrine signaling. However, whether ATP and P2X7R are involved in radiation-induced brain injury (RBI) remains to be determined. Here, we found that the eATP level was elevated in the cerebrospinal fluid (CSF) of RBI patients and was associated with the clinical severity of the disorder. In our experimental model, radiation treatment increased the level of eATP in the supernatant of primary cultures of neurons and glial cells and in the CSF of irradiated mice. In addition, ATP administration activated microglia, induced the release of the inflammatory mediators such as cyclooxygenase-2, tumor necrosis factor α and interleukin 6, and promoted neuronal apoptosis. Furthermore, blockade of ATP–P2X7R interaction using P2X7 antagonist Brilliant Blue G or P2X7 knockdown suppressed radiation-induced microglial activation and proliferation in the hippocampus, and restored the spatial memory of irradiated mice. Finally, we found that the PI3K/AKT and nuclear factor κB mediated pathways were downstream of ATP–P2X7R signaling in RBI. Taken together, our results unveiled the critical role of ATP–P2X7R in brain damage in RBI, suggesting that inhibition of ATP–P2X7R axis might be a potential strategy for the treatment of patients with RBI

LAYN Is a Prognostic Biomarker and Correlated With Immune Infiltrates in Gastric and Colon Cancers

Background: Layilin (LAYN) is a critical gene that regulates T cell function. However, the correlations of LAYN to prognosis and tumor-infiltrating lymphocytes in different cancers remain unclear.Methods: LAYN expression was analyzed via the Oncomine database and Tumor Immune Estimation Resource (TIMER) site. We evaluated the influence of LAYN on clinical prognosis using Kaplan-Meier plotter, the PrognoScan database and Gene Expression Profiling Interactive Analysis (GEPIA). The correlations between LAYN and cancer immune infiltrates was investigated via TIMER. In addition, correlations between LAYN expression and gene marker sets of immune infiltrates were analyzed by TIMER and GEPIA.Results: A cohort (GSE17536) of colorectal cancer patients showed that high LAYN expression was associated with poorer overall survival (OS), disease-specific survival (DSS), and disease-free survival (DFS). In addition, high LAYN expression was significantly correlated with poor OS and progression-free survival (PFS) in gastric cancers (OS HR = 1.97, P = 3.6e-10; PFS HR = 2.12, P = 2.3e-10). Moreover, LAYN significantly impacts the prognosis of diverse cancers via The Cancer Genome Atlas (TCGA). Specifically, high LAYN expression was correlated with worse OS and PFS in stage 2 to 4 but not stage 1 and stage N0 gastric cancer patients (P = 0.28, 0.34; P = 0.073, 0.092). LAYN expression was positively correlated with infiltrating levels of CD4+ T and CD8+ T cells, macrophages, neutrophils, and dendritic cells (DCs) in colon adenocarcinoma (COAD) and stomach adenocarcinoma (STAD). LAYN expression showed strong correlations with diverse immune marker sets in COAD and STAD.Conclusions: These findings suggest that LAYN is correlated with prognosis and immune infiltrating levels of, including those of CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and DCs in multiple cancers, especially in colon and gastric cancer patients. In addition, LAYN expression potentially contributes to regulation of tumor-associated macrophages (TAMs), DCs, T cell exhaustion and Tregs in colon and gastric cancer. These findings suggest that LAYN can be used as a prognostic biomarker for determining prognosis and immune infiltration in gastric and colon cancers

Experimental Side-Channel-Free Quantum Key Distribution

Quantum key distribution can provide unconditionally secure key exchange for remote users in theory. In practice, however, in most quantum key distribution systems, quantum hackers might steal the secure keys by listening to the side channels in the source, such as the photon frequency spectrum, emission time, propagation direction, spatial angular momentum, and so on. It is hard to prevent such kinds of attacks because side channels may exist in any of the encoding space whether the designers take care of or not. Here we report an experimental realization of a side-channel-free quantum key distribution protocol which is not only measurement-device-independent, but also immune to all side-channel attacks in the source. We achieve a secure key rate of 4.80e-7 per pulse through 50 km fiber spools.Comment: 23 pages, 5 figure

Aurora-A down-regulates IkappaBα via Akt activation and interacts with insulin-like growth factor-1 induced phosphatidylinositol 3-kinase pathway for cancer cell survival

<p>Abstract</p> <p>Background</p> <p>The mitotic Aurora-A kinase exerts crucial functions in maintaining mitotic fidelity. As a bona fide oncoprotein, Aurora-A aberrant overexpression leads to oncogenic transformation. Yet, the mechanisms by which Aurora-A enhances cancer cell survival remain to be elucidated.</p> <p>Results</p> <p>Here, we found that Aurora-A overexpression was closely correlated with clinic stage and lymph node metastasis in tongue carcinoma. Aurora-A inhibitory VX-680 suppressed proliferation, induced apoptosis and markedly reduced migration in cancer cells. We further showed that insulin-like growth factor-1, a PI3K physiological activator, reversed VX-680-decreased cell survival and motility. Conversely, wortmannin, a PI3K inhibitor, combined with VX-680 showed a synergistic effect on inducing apoptosis and suppressing migration. In addition, Aurora-A inhibition suppressed Akt activation, and VX-680-induced apoptosis was attenuated by Myr-Akt overexpression, revealing a cross-talk between Aurora-A and PI3K pathway interacting at Akt activation. Significantly, we showed that suppression of Aurora-A decreased phosphorylated Akt and was associated with increased IkappaBα expression. By contrast, Aurora-A overexpression upregulated Akt activity and downregulated IkappaBα, these changes were accompanied by nuclear translocation of nuclear factor-κB and increased expression of its target gene Bcl-xL. Lastly, Aurora-A overexpression induced IkappaBα reduction was abrogated by suppression of Akt either chemically or genetically.</p> <p>Conclusion</p> <p>Taken together, our data established that Aurora-A, via activating Akt, stimulated nuclear factor-κB signaling pathway to promote cancer cell survival, and promised a novel combined chemotherapy targeting both Aurora-A and PI3K in cancer treatment.</p