Complex visual processes such as visual attention are often computationally too expensive to allow real-time implementation on a single computer. To solve this problem we study distributed computer architectures that enable us to divide complex tasks into several smaller problems. In this paper we demonstrate how to implement distributed visual attention system on a humanoid robot to achieve real-time operation at relatively high resolutions and frame rates. We start from a popular theory of bottom-up visual attention that assumes that information across various modalities is used for the early encoding of visual information. Our system uses five different modalities including color, intensity, edges, stereo, and motion. We show how to distribute the attention processing on a computer cluster and study the issues arising on such systems. The system was fully implemented on a workstation cluster comprised of eight PCs. It was used to drive the gaze of a humanoid head towards potential regions of interest.

No abstract

The rapid and ultralow detection of toxic organophosphate chemicals is a well-known, important step to reduce adverse health issues and yet also remains challenging. Here, we show electrochemical detection of methyl parathion (MP) using SnS 2 nanosheets supported in a N, S-codoped reduced graphene oxide nanocomposite (SnS 2 /NS−RGO) in a neutral medium. The SnS 2 /NS−RGO is obtained by one-pot hydrothermal synthesis and modified onto a glassy carbon electrode (GCE) for electrochemical MP detection ability. The effects of SnS 2 in NS−RGO showed a substantial reduction in the electron resistivity and increase in the acceleration of electron mobility. The cyclic voltammetry investigation of SnS 2 /NS−RGO to the MP detection showed a superior electrochemical detection property, while unmodified GCE, SnS 2 , and NS−RGO yielded unsatisfactory results. Thus, the SnS 2 /NS−RGO showed the best performance in terms of the sensitivity (4.033 μA μM −1 cm −2 ), limit of detection (0.17 nM), accuracy, and stability. In practical detection, the SnS 2 /NS−RGO sensing retained satisfactory recovery of MP added in river water and black grape samples.

Background: MiRNAs play important roles in the development of ovarian cancer, activation of primitive follicles, follicular development, oocyte maturation and ovulation. In the present study, we investigated the specific role of miR-23a in cov434 cells. Results: Downregulation of miR-23a was observed in serum of PCOS patients compared with the healthy control, suggesting the inhibitory effect of miR-23a in PCOS. MiR-23a was positively correlated with Body Mass Index (BMI) and negatively correlated with Luteinizing hormone (LH), Testostrone (T), Glucose (Glu) and Insulin (INS) of PCOS patients. MiR-23a mimic inhibited the proliferation and promoted apoptosis of human cov434 cells. In addition, flow cytometry assay confirmed that miR-23a blocked cell cycle on G0/G1 phase. MiR-23a inhibitor showed opposite results. Furthermore, double luciferase reporter assay proved that miR-23a could bind to the 3'UTR of FGD4 directly through sites predicted on Target Scan. FGD4 level was significantly suppressed by miR-23a mimic, but was significantly enhanced by miR-23a inhibitor. We further proved that miR-23a increased the expression of activated CDC42 (GTP bround) and p-PAK-1, suggesting that miR-23a induced cell cycle arrest through CDC42/PAK1 pathway. Conclusions: In conclusion, our study reveals that miR-23a participates in the regulation of proliferation and apoptosis of cov434 cells through target FGD4, and may play a role in the pathophysiology of PCOS.

No abstract

PurposeIn prostate cancer, castration resistance is a factor that frequently leads to death in individuals with this disease. Recent studies have suggested that prostate cancer stem cells (PCSCs) are pivotal regulators in the establishment of castration resistance. The nanog homeobox (NANOG) and the transforming growth factor (TGF)-β1/drosophila mothers against decapentaplegic protein (SMAD) signaling pathways are involved in several cancer stem cells but are not involved in PCSCs. The purpose of this study is to investigate the effect of NANOG on the proliferation of PCSCs regulated by the TGF-β1/SMAD signaling pathway.MethodsIn this study, we used flow cytometry to isolate CD44+/CD133+/NANOG+ PCSCs from DU145 prostate cancer cells. Then we used short hairpin RNA to silence NANOG and observed the biological behavior and the TGF-β1/SMAD signal of PCSCs.ResultsNANOG decreased PCSC proliferation, increased apoptosis, and blocked cell cycling at G0/G1. Furthermore, reduction in the TGF-β1, p15, and p-SMAD2 expression was observed.ConclusionThese findings suggest that NANOG positively regulates the growth of PCSCs through the TGF-β1/SMAD signaling pathway.

No abstract

No abstract