Perspective of understanding for Children’s Privacy and Security

The thirteen years of age requirement to open any social network account does not guarantee that children under this age would not have access to social networks such as Facebook, Snapchat, Instagram, or YouTube just to mention some. The reason for this is that children want to be a part of this technological revolution, and create these accounts by lying about their age, or are aid by their parents without realizing the consequences this action might bring. While these social networks disclose that they delete information belonging to children under 13 from their databases as soon as they are aware of it, it is questionable if they are doing enough to protect children’s privacy , and if they should be liable for any incident related to this issue since such is widely known, but apparently neglected. Unfortunately, by social network administrators not reinforcing the age requirement policy, and launching features that makes its user’s personal information available to third parties, are indirectly exposing children with fraudulent accounts at risk of being victims of more serious ethical and social issues such as cyber bulling, and sex crimes. While it is determined that social network has little control over this issue, all which is left to do, is to provide parents with education and control of their children’s social network activity interaction to protect their privacy and keep them safe

Dissipative Dark Matter on FIRE: I. Structural and kinematic properties of dwarf galaxies

We present the first set of cosmological baryonic zoom-in simulations of galaxies including dissipative self-interacting dark matter (dSIDM). These simulations utilize the Feedback In Realistic Environments (FIRE-2) galaxy formation physics, but allow the dark matter to have dissipative self-interactions analogous to Standard Model forces, parameterized by the self-interaction cross-section per unit mass, $(\sigma/m)$, and the dimensionless degree of dissipation, $0<f_{\rm diss}<1$. We survey this parameter space, including constant and velocity-dependent cross-sections, and focus on structural and kinematic properties of dwarf galaxies with $M_{\rm halo} \simeq 10^{10-11} {\rm M}_{\odot}$. Central density profiles of simulated dwarfs become cuspy when $(\sigma/m)_{\rm eff} \gtrsim 0.1\,{\rm cm^{2}\,g^{-1}}$ (and $f_{\rm diss}=0.5$ as fiducial). The power-law slopes asymptote to $\alpha \approx -1.5$ in low-mass dwarfs independent of cross-section, which arises from a dark matter "cooling flow". Through comparisons with dark matter only simulations, we find the profile in this regime is insensitive to the inclusion of baryons. However, when $(\sigma/m)_{\rm eff} \ll 0.1\,{\rm cm^{2}\,g^{-1}}$, baryonic effects can produce cored density profiles comparable to non-dissipative cold dark matter (CDM) runs but at smaller radii. Simulated galaxies with $(\sigma/m) \gtrsim 10\,{\rm cm^{2}\,g^{-1}}$ develop significant coherent rotation of dark matter, accompanied by halo deformation, but this is unlike the well-defined thin "dark disks" often attributed to baryon-like dSIDM. The density profiles in this high cross-section model exhibit lower normalizations given the onset of halo deformation. For our surveyed dSIDM parameters, halo masses and galaxy stellar masses do not show appreciable difference from CDM, but dark matter kinematics and halo concentrations/shapes can differ.Comment: Accepted by MNRAS. 23 pages, 19 figure

Expression of the mismatch repair gene hMLH1 is enhanced in non-small cell lung cancer with EGFR mutations

Mismatch repair (MMR) plays a pivotal role in keeping the genome stable. MMR dysfunction can lead to carcinogenesis by gene mutation accumulation. HMSH2 and hMLH1 are two key components of MMR. High or low expression of them often mark the status of MMR function. Mutations (EGFR, KRAS, etc) are common in non-small cell lung cancer (NSCLC). However, it is not clear what role MMR plays in NSCLC gene mutations. The expression of MMR proteins hMSH2 and hMLH1, and the proliferation markers PCNA and Ki67 were measured by immunohistochemistry in 181 NSCLCs. EGFR and KRAS mutations were identified by high resolution melting analysis. Stronger hMLH1 expression correlated to a higher frequency of EGFR mutations in exon 19 and 21 (p<0.0005). Overexpression of hMLH1 and the adenocarcinoma subtype were both independent factors that related to EGFR mutations in NSCLCs (p=0.013 and p<0.0005). The expression of hMLH1, hMSH2 and PCNA increased, while Ki67 expression significantly decreased (p=0.030) in NSCLCs with EGFR mutations. Overexpression of hMLH1 could be a new molecular marker to predict the response to EGFR-TKIs in NSCLCs. Furthermore, EGFR mutations might be an early event of NSCLC that occur before MMR dysfunction.This work was supported by the National Nature Science Funds in China (Fund No. 81071805; URL: http://isisn.nsfc.gov.cn/egrantweb/), and Dalian Merricon Gene Diagnosis Technology Co., Ltd. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript