Control energy of complex networks towards distinct mixture states

Controlling complex networked systems is a real-world puzzle that remains largely unsolved. Despite recent progress in understanding the structural characteristics of network control energy, target state and system dynamics have not been explored. We examine how varying the final state mixture affects the control energy of canonical and conformity-incorporated dynamical systems. We find that the control energy required to drive a network to an identical final state is lower than that required to arrive a non-identical final state. We also demonstrate that it is easier to achieve full control in a conformity-based dynamical network. Finally we determine the optimal control strategy in terms of the network hierarchical structure. Our work offers a realistic understanding of the control energy within the final state mixture and sheds light on controlling complex systems.This work was funded by The National Natural Science Foundation of China (Grant Nos. 61763013, 61703159, 61403421), The Natural Science Foundation of Jiangxi Province (No. 20171BAB212017), The Measurement and Control of Aircraft at Sea Laboratory (No. FOM2016OF010), and China Scholarship Council (201708360048). The Boston University Center for Polymer Studies is supported by NSF Grants PHY-1505000, CMMI-1125290, and CHE-1213217, and by DTRA Grant HDTRA1-14-1-0017. (61763013 - National Natural Science Foundation of China; 61703159 - National Natural Science Foundation of China; 61403421 - National Natural Science Foundation of China; 20171BAB212017 - Natural Science Foundation of Jiangxi Province; FOM2016OF010 - Measurement and Control of Aircraft at Sea Laboratory; 201708360048 - China Scholarship Council; PHY-1505000 - NSF; CMMI-1125290 - NSF; CHE-1213217 - NSF; HDTRA1-14-1-0017 - DTRA)Published versio

Abnormal magnetoresistance behavior in Nb thin film with rectangular antidot lattice

Abnormal magnetoresistance behavior is found in superconducting Nb films perforated with rectangular arrays of antidots (holes). Generally magnetoresistance were always found to increase with increasing magnetic field. Here we observed a reversal of this behavior for particular in low temperature or current density. This phenomenon is due to a strong 'caging effect' which interstitial vortices are strongly trapped among pinned multivortices.Comment: 4 pages, 2 figure

miR-638 is a new biomarker for outcome prediction of non-small cell lung cancer patients receiving chemotherapy.

MicroRNAs (miRNAs), a class of small non-coding RNAs, mediate gene expression by either cleaving target mRNAs or inhibiting their translation. They have key roles in the tumorigenesis of several cancers, including non-small cell lung cancer (NSCLC). The aim of this study was to investigate the clinical significance of miR-638 in the evaluation of NSCLC patient prognosis in response to chemotherapy. First, we detected miR-638 expression levels in vitro in the culture supernatants of the NSCLC cell line SPC-A1 treated with cisplatin, as well as the apoptosis rates of SPC-A1. Second, serum miR-638 expression levels were detected in vivo by using nude mice xenograft models bearing SPC-A1 with and without cisplatin treatment. In the clinic, the serum miR-638 levels of 200 cases of NSCLC patients before and after chemotherapy were determined by quantitative real-time PCR, and the associations of clinicopathological features with miR-638 expression patterns after chemotherapy were analyzed. Our data helped in demonstrating that cisplatin induced apoptosis of the SPC-A1 cells in a dose- and time-dependent manner accompanied by increased miR-638 expression levels in the culture supernatants. In vivo data further revealed that cisplatin induced miR-638 upregulation in the serum derived from mice xenograft models, and in NSCLC patient sera, miR-638 expression patterns after chemotherapy significantly correlated with lymph node metastasis. Moreover, survival analyses revealed that patients who had increased miR-638 levels after chemotherapy showed significantly longer survival time than those who had decreased miR-638 levels. Our findings suggest that serum miR-638 levels are associated with the survival of NSCLC patients and may be considered a potential independent predictor for NSCLC prognosis

Targeted antimicrobial therapy against Streptococcus mutans establishes protective non-cariogenic oral biofilms and reduces subsequent infection.

AimDental biofilms are complex communities composed largely of harmless bacteria. Certain pathogenic species including Streptococcus mutans (S. mutans) can become predominant when host factors such as dietary sucrose intake imbalance the biofilm ecology. Current approaches to control S. mutans infection are not pathogen-specific and eliminate the entire oral community along with any protective benefits provided. Here, we tested the hypothesis that removal of S. mutans from the oral community through targeted antimicrobial therapy achieves protection against subsequent S. mutans colonization.MethodologyControlled amounts of S. mutans were mixed with S. mutans-free saliva, grown into biofilms and visualized by antibody staining and cfu quantization. Two specifically-targeted antimicrobial peptides (STAMPs) against S. mutans were tested for their ability to reduce S. mutans biofilm incorporation upon treatment of the inocula. The resulting biofilms were also evaluated for their ability to resist subsequent exogenous S. mutans colonization.ResultsS. mutans colonization was considerably reduced ( +/- 0.4 fold reduction, P=0.01) when the surface was preoccupied with saliva-derived biofilms. Furthermore, treatment with S. mutans-specific STAMPs yielded S. mutans-deficient biofilms with significant protection against further S. mutans colonization (5 minutes treatment: 38 +/- 13 fold reduction P=0.01; 16 hours treatment: 96 +/- 28 fold reduction P=0.07).ConclusionS. mutans infection is reduced by the presence of existing biofilms. Thus maintaining a healthy or "normal" biofilm through targeted antimicrobial therapy (such as the STAMPs) could represent an effective strategy for the treatment and prevention of S. mutans colonization in the oral cavity and caries progression

Human Gingiva-Derived Mesenchymal Stromal Cells Attenuate Contact Hypersensitivity via Prostaglandin E2- Dependent Mechanisms

The immunomodulatory and anti-inflammatory functions of mesenchymal stromal cells (MSCs) have been demonstrated in several autoimmune/inflammatory disease models, but their contribution to the mitigation of contact hypersensitivity (CHS) remains unclear. Here, we report a new immunological approach using human gingiva-derived MSCs (GMSCs) to desensitize and suppress CHS and the underlying mechanisms. Our results showed that systemic infusion of GMSCs before the sensitization and challenge phase dramatically suppress CHS, manifested as a decreased infiltration of dendritic cells (DCs), CD8 + T cells, T H-17 and mast cells (MCs), a suppression of a variety of inflammatory cytokines, and a reciprocal increased infiltration of regulatory T cells and expression of IL-10 at the regional lymph nodes and the allergic contact areas. The GMSC-mediated immunosuppressive effects and mitigation of CHS were significantly abrogated on pretreatment with indomethacin, an inhibitor of cyclooxygenases. Under coculture condition of direct cell-cell contact or via transwell system, GMSCs were capable of direct suppression of differentiation of DCs and phorbol 12-myristate 13-acetate-stimulated activation of MCs, whereas the inhibitory effects were attenuated by indomethacin. Mechanistically, GMSC-induced blockage of de novo synthesis of proinflammatory cytokines by MCs is mediated partly by the tumor necrosis factor-alpha/prostaglandin E 2 (PGE 2) feedback axis. These results demonstrate that GMSCs are capable of desensitizing allergic contact dermatitis via PGE 2-dependent mechanisms. © AlphaMed Press