Toward Understanding Personalities Working on Computer: A Preliminary Study Focusing on Collusion/Plagiarism

Ample research has been carried out in the area of collusion, plagiarism and e-learning. Collusion is a form of active cheating where two or more parties secretly or illegally corporate. Collusion is at the root of common knowledge plagiarism. While plagiarism requires two or more entities to compare, collusion can be determined in isolation. It is also possible that collusion do not lead to positive plagiarism checks. It is therefore the aims of this preliminary study to: (i) identify the factors responsible for collusion in e-learning (ii) determine the prominent factor that is representative of collusion and (iii) through user behaviour including, but not limited to, application switching time, determine collusion. We claim that user computer activities and application processes can help understand user behaviour during assessment task. It is on this premise that we develop a machine learning model to predict collusion through user behaviour during assessment tas

Absence of ERK5/MAPK7 delays tumorigenesis in Atm-/- mice

Ataxia-telangiectasia mutated (ATM) is a cell cycle checkpoint kinase that upon activation by DNA damage leads to cell cycle arrest and DNA repair or apoptosis. The absence of Atm or the occurrence of loss-of-function mutations in Atm predisposes to tumorigenesis. MAPK7 has been implicated in numerous types of cancer with pro-survival and pro-growth roles in tumor cells, but its functional relation with tumor suppressors is not clear. In this study, we show that absence of MAPK7 delays death due to spontaneous tumor development in Atm-/- mice. Compared with Atm-/- thymocytes, Mapk7-/-Atm-/- thymocytes exhibited an improved response to DNA damage (increased phosphorylation of H2AX) and a restored apoptotic response after treatment of mice with ionizing radiation. These findings define an antagonistic function of ATM and MAPK7 in the thymocyte response to DNA damage, and suggest that the lack of MAPK7 inhibits thymic lymphoma growth in Atm-/- mice by partially restoring the DNA damage response in thymocytes

Modifying the surface electronic properties of YBa2Cu3O7-delta with cryogenic scanning probe microscopy

We report the results of a cryogenic study of the modification of YBa2Cu3O7-delta surface electronic properties with the probe of a scanning tunneling microscope (STM). A negative voltage applied to the sample during STM tunneling is found to modify locally the conductance of the native degraded surface layer. When the degraded layer is removed by etching, the effect disappears. An additional surface effect is identified using Scanning Kelvin Probe Microscopy in combination with STM. We observe reversible surface charging for both etched and unetched samples, indicating the presence of a defect layer even on a surface never exposed to air.Comment: 6 pages, 4 figures. To appear in Superconductor Science and Technolog

Evidence of Doping-Dependent Pairing Symmetry in Cuprate Superconductors

Scanning tunneling spectroscopy (STS) studies reveal long-range spatial homogeneity and predominantly $d_{x^2-y^2}$-pairing spectral characteristics in under- and optimally doped $\rm YBa_2Cu_3O_{7-\delta}$ superconductors, whereas STS on $\rm YBa_2(Cu_{0.9934}Zn_{0.0026}Mg_{0.004})_3O_{6.9}$ exhibits {\it microscopic} spatial modulations and strong scattering near the Zn or Mg impurity sites, together with global suppression of the pairing potential. In contrast, in overdoped $\rm (Y_{0.7}Ca_{0.3})Ba_2Cu_3O_{7-\delta}$, $(d_{x^2-y^2}+s)$-pairing symmetry is found, suggesting significant changes in the superconducting ground-state at a critical doping value.Comment: 4 pages, 4 figures. Published in Physical Review Letters. Corresponding author: Nai-Chang Yeh (e-mail address: [email protected]

Local DNA dynamics shape mutational patterns of mononucleotide repeats in human genomes

Single base substitutions (SBSs) and insertions/deletions are critical for generating population diversity and can lead both to inherited disease and cancer. Whereas on a genome-wide scale SBSs are influenced by cellular factors, on a fine scale SBSs are influenced by the local DNA sequence-context, although the role of flanking sequence is often unclear. Herein, we used bioinformatics, molecular dynamics and hybrid quantum mechanics/molecular mechanics to analyze sequence context-dependent mutagenesis at mononucleotide repeats (A-tracts and G-tracts) in human population variation and in cancer genomes. SBSs and insertions/deletions occur predominantly at the first and last base-pairs of A-tracts, whereas they are concentrated at the second and third base-pairs in G-tracts. These positions correspond to the most flexible sites along A-tracts, and to sites where a ‘hole’, generated by the loss of an electron through oxidation, is most likely to be localized in G-tracts. For A-tracts, most SBSs occur in the direction of the base-pair flanking the tracts. We conclude that intrinsic features of local DNA structure, i.e. base-pair flexibility and charge transfer, render specific nucleotides along mononucleotide runs susceptible to base modification, which then yields mutations. Thus, local DNA dynamics contributes to phenotypic variation and disease in the human population

Human MLH1 Protein Participates in Genomic Damage Checkpoint Signaling in Response to DNA Interstrand Crosslinks, while MSH2 Functions in DNA Repair

DNA interstrand crosslinks (ICLs) are among the most toxic types of damage to a cell. For this reason, many ICL-inducing agents are effective therapeutic agents. For example, cisplatin and nitrogen mustards are used for treating cancer and psoralen plus UVA (PUVA) is useful for treating psoriasis. However, repair mechanisms for ICLs in the human genome are not clearly defined. Previously, we have shown that MSH2, the common subunit of the human MutSα and MutSβ mismatch recognition complexes, plays a role in the error-free repair of psoralen ICLs. We hypothesized that MLH1, the common subunit of human MutL complexes, is also involved in the cellular response to psoralen ICLs. Surprisingly, we instead found that MLH1-deficient human cells are more resistant to psoralen ICLs, in contrast to the sensitivity to these lesions displayed by MSH2-deficient cells. Apoptosis was not as efficiently induced by psoralen ICLs in MLH1-deficient cells as in MLH1-proficient cells as determined by caspase-3/7 activity and binding of annexin V. Strikingly, CHK2 phosphorylation was undetectable in MLH1-deficient cells, and phosphorylation of CHK1 was reduced after PUVA treatment, indicating that MLH1 is involved in signaling psoralen ICL-induced checkpoint activation. Psoralen ICLs can result in mutations near the crosslinked sites; however, MLH1 function was not required for the mutagenic repair of these lesions, and so its signaling function appears to have a role in maintaining genomic stability following exposure to ICL-induced DNA damage. Distinguishing the genetic status of MMR-deficient tumors as MSH2-deficient or MLH1-deficient is thus potentially important in predicting the efficacy of treatment with psoralen and perhaps with other ICL-inducing agents

Gravity duals for logarithmic conformal field theories

Logarithmic conformal field theories with vanishing central charge describe systems with quenched disorder, percolation or dilute self-avoiding polymers. In these theories the energy momentum tensor acquires a logarithmic partner. In this talk we address the construction of possible gravity duals for these logarithmic conformal field theories and present two viable candidates for such duals, namely theories of massive gravity in three dimensions at a chiral point.Comment: 15 pages, 1 figure, invited plenary talk at the First Mediterranean Conference on Classical and Quantum Gravity, v2: published version, corrected typo in left eq. (5

Probing natural SUSY from stop pair production at the LHC

We consider the natural supersymmetry scenario in the framework of the R-parity conserving minimal supersymmetric standard model (called natural MSSM) and examine the observability of stop pair production at the LHC. We first scan the parameters of this scenario under various experimental constraints, including the SM-like Higgs boson mass, the indirect limits from precision electroweak data and B-decays. Then in the allowed parameter space we study the stop pair production at the LHC followed by the stop decay into a top quark plus a lightest neutralino or into a bottom quark plus a chargino. From detailed Monte Carlo simulations of the signals and backgrounds, we find the two decay modes are complementary to each other in probing the stop pair production, and the LHC with $\sqrt{s}= 14$ TeV and 100 $fb^{-1}$ luminosity is capable of discovering the stop predicted in natural MSSM up to 450 GeV. If no excess events were observed at the LHC, the 95% C.L. exclusion limits of the stop masses can reach around 537 GeV.Comment: 19 pages, 10 figures, version accepted by JHE