Privacy Law Disparities between the United States and the European Union

Data is the world’s most valuable resource today. In the 21st century, big data has overtaken the world’s commonly known large industries to become one of the most sought after markets, and companies pay to own this data (The Economist, 2017). Advertisements may have been targeted towards demographics such as race or sex in past years. However, in the digital age, the capability exists to push advertisements to the screens of specific users with known interests. This has been made possible, in part, by unregulated data collection practices across the globe, including in the United States and the European Union. Data collection practices, from the conception of the Internet until the present day, have been disregarding the consent of the user the data represents. This unregulated data collection practice was halted recently in the European Union with the passing of the General Data and Privacy Regulation. However, the practice remains of concern in the United States. This research aims to conduct a classic comparative analysis of the omnibus privacy laws of the United States and the European Union. The existing laws will be compared across the following variables: the right to be informed, right of access, right to rectification, right to erasure, right to restrict processing, right to data portability, and the right to object. Recommendations for improving the United States privacy legislation will be highlighted based on this comparative analysis

ASB9 interacts with ubiquitous mitochondrial creatine kinase and inhibits mitochondrial function

<p>Abstract</p> <p>Background</p> <p>The ankyrin repeat and suppressor of cytokine signalling (SOCS) box proteins (Asbs) are a large protein family implicated in diverse biological processes including regulation of proliferation and differentiation. The SOCS box of Asb proteins is important in a ubiquitination-mediated proteolysis pathway. Here, we aimed to evaluate expression and function of human Asb-9 (ASB9).</p> <p>Results</p> <p>We found that a variant of ASB9 that lacks the SOCS box (ASB9ΔSOCS) was naturally detected in human cell lines but not in peripheral blood mononuclear cells or normal hepatocytes. We also identified ubiquitous mitochondrial creatine kinase (uMtCK) as a new target of ASB9 in human embryonic kidney 293 (HEK293) cells. The ankyrin repeat domains of ASB9 can associate with the substrate binding site of uMtCK in a SOCS box-independent manner. The overexpression of ASB9, but not ASB9ΔSOCS, induces ubiquitination of uMtCK. ASB9 and ASB9ΔSOCS can interact and colocalise with uMtCK in the mitochondria. However, only expression of ASB9 induced abnormal mitochondrial structure and a decrease of mitochondrial membrane potential. Furthermore, the creatine kinase activities and cell growth were significantly reduced by ASB9 but not by ASB9ΔSOCS.</p> <p>Conclusions</p> <p>ASB9 interacts with the creatine kinase system and negatively regulates cell growth. The differential expression and function of ASB9 and ASB9ΔSOCS may be a key factor in the growth of human cell lines and primary cells.</p

The dystrobrevin binding protein 1 (DTNBP1) gene is associated with schizophrenia in the Irish Case Control Study of Schizophrenia (ICCSS) sample

BACKGROUND: DTNBP1 is associated with schizophrenia in many studies, but the associated alleles and haplotypes vary between samples. METHOD: We assessed nine single nucleotide polymorphisms (SNPs) in this gene for association with schizophrenia in a new sample of 1021 cases and 626 controls from Ireland. RESULTS: Four SNPs give evidence of association (0.000018<p<0.045), most strongly with the common allele at rs760761. A haplotype of the common alleles of five markers (including rs760761) and the minor allele of rs2619538 overlapping the 5′ end of the DTNBP1 gene also gives evidence for association (p=0.0002). Secondary analyses showed no difference in the association signal based on sex or family history. These results are in agreement with the most consistently observed association with common alleles and common-allele haplotypes, reported in a previous study of Irish cases and controls but not in an Irish high-density family sample. Our results do not support the prior report from a Swedish sample of increased association in cases with a family history of psychotic illness. Comparison of human, chimpanzee and rhesus sequence suggest that rs760761 is a particularly variable position in the primate lineage. CONCLUSION: This study provides further evidence from a large case/control sample for association of common DTNBP1 alleles and haplotypes with schizophrenia