49 research outputs found

    Restricted three body problems at the nanoscale

    Full text link
    In this paper, we investigate some of the classical restricted three body problems at the nanoscale, such as the circular planar restricted problem for three C60 fullerenes, and a carbon atom and two C60 fullerenes. We model the van der Waals forces between the fullerenes by the Lennard-Jones potential. In particular, the pairwise potential energies between the carbon atoms on the fullerenes are approximated by the continuous approach, so that the total molecular energy between two fullerenes can be determined analytically. Since we assume that such interactions between the molecules occur at sufficiently large distance, the classical three body problems analysis is legitimate to determine the collective angular velocity of the two and three C60 fullerenes at the nanoscale. We find that the maximum angular frequency of the two and three fullerenes systems reach the terahertz range and we determine the stationary points and the points which have maximum velocity for the carbon atom for the carbon atom and the two fullerenes system

    Identification of regulatory variants associated with genetic susceptibility to meningococcal disease

    Get PDF
    Non-coding genetic variants play an important role in driving susceptibility to complex diseases but their characterization remains challenging. Here, we employed a novel approach to interrogate the genetic risk of such polymorphisms in a more systematic way by targeting specific regulatory regions relevant for the phenotype studied. We applied this method to meningococcal disease susceptibility, using the DNA binding pattern of RELA - a NF-kB subunit, master regulator of the response to infection - under bacterial stimuli in nasopharyngeal epithelial cells. We designed a custom panel to cover these RELA binding sites and used it for targeted sequencing in cases and controls. Variant calling and association analysis were performed followed by validation of candidate polymorphisms by genotyping in three independent cohorts. We identified two new polymorphisms, rs4823231 and rs11913168, showing signs of association with meningococcal disease susceptibility. In addition, using our genomic data as well as publicly available resources, we found evidences for these SNPs to have potential regulatory effects on ATXN10 and LIF genes respectively. The variants and related candidate genes are relevant for infectious diseases and may have important contribution for meningococcal disease pathology. Finally, we described a novel genetic association approach that could be applied to other phenotypes

    Plasma lipid profiles discriminate bacterial from viral infection in febrile children

    Get PDF
    Fever is the most common reason that children present to Emergency Departments. Clinical signs and symptoms suggestive of bacterial infection ar

    Dishevelled regulates the metabolism of amyloid precursor protein via protein kinase C/Mitogen-activated protein kinase and c-Jun terminal kinase

    No full text
    Alzheimer’s disease (AD) is a disorder of two pathologies: amyloid plaques, the core of which is a peptide derived from the amyloid precursor protein (APP), and neurofibrillary tangles composed of highly phosphorylated tau. Protein kinase C (PKC)is known to increase non-amyloidogenic a-secretase cleavage of APP, producing secreted APP (sAPPa), and glycogen synthasekinase (GSK)-3b is known to increase tau phosphorylation. Both PKC and GSK-3b are components of the wnt signaling cascade. Here we demonstrate that overexpression of another member of this pathway, dishevelled (dvl-1), increasess APPa production. The dishevelled action on APP is mediated via both c-jun terminal kinase (JNK) and protein kinase C(PKC)/mitogen-activated protein (MAP) kinase but not via p38MAP kinase. These data position dvl-1 upstream of both PKCand JNK, thereby explaining the previously observed dual signaling action of dvl-1. Furthermore, we show that human dvl-1and wnt-1 also reduce the phosphorylation of tau by GSK-3b. Therefore, both APP metabolism and tau phosphorylation are potentially linked through wnt signaling
    corecore