Secure Integer Comparisons Using the Homomorphic Properties of Prime Power Subgroups

Secure multi party computation allows two or more parties to jointly compute a function under encryption without leaking information about their private inputs. These secure computations are vital in many fields including law enforcement, secure voting and bioinformatics because the privacy of the information is of paramount importance. One common reference problem for secure multi party computation is the Millionaires\u27 problem which was first introduced by Turing Award winner Yao in his paper Protocols for secure computation . The Millionaires\u27 problem considers two millionaires who want to know who is richer without disclosing their actual worth. There are public-key cryptosystems that currently solve this problem, however they use bitwise decomposition and Boolean algebra on encrypted bits. This type of solution is costly as it requires each bit requires its own encryption and decryption. Our solution to the Millionaires\u27 problem and secure integer comparison looks at a new approach which doesn\u27t use the decomposition method and instead encrypts the full length of the message in one encryption (within scope). This method also extends in a linear fashion, so larger integers remain efficient to compare. In this thesis, we present a new cryptosystem with a novel homomorphic property used for secure integer comparison, as well as a protocol implementing the cryptosystem and a simulation security proof for the protocol. Finally, we implemented the system and compared it to systems that are being used today

Viral CpG Deficiency Provides No Evidence That Dogs Were Intermediate Hosts for SARS-CoV-2.

Due to the scope and impact of the COVID-19 pandemic there exists a strong desire to understand where the SARS-CoV-2 virus came from and how it jumped species boundaries to humans. Molecular evolutionary analyses can trace viral origins by establishing relatedness and divergence times of viruses and identifying past selective pressures. However, we must uphold rigorous standards of inference and interpretation on this topic because of the ramifications of being wrong. Here, we dispute the conclusions of Xia (2020. Extreme genomic CpG deficiency in SARS-CoV-2 and evasion of host antiviral defense. Mol Biol Evol. doi:10.1093/molbev/masa095) that dogs are a likely intermediate host of a SARS-CoV-2 ancestor. We highlight major flaws in Xia's inference process and his analysis of CpG deficiencies, and conclude that there is no direct evidence for the role of dogs as intermediate hosts. Bats and pangolins currently have the greatest support as ancestral hosts of SARS-CoV-2, with the strong caveat that sampling of wildlife species for coronaviruses has been limited

Viral CpG deficiency provides no evidence that dogs were intermediate hosts for SARS-CoV-2

Due to the scope and impact of the COVID-19 pandemic there exists a strong desire to understand where the SARS-CoV-2 virus came from and how it jumped species boundaries to humans. Molecular evolutionary analyses can trace viral origins by establishing relatedness and divergence times of viruses and identifying past selective pressures. However, we must uphold rigorous standards of inference and interpretation on this topic because of the ramifications of being wrong. Here, we dispute the conclusions of Xia (2020) that dogs are a likely intermediate host of a SARS-CoV-2 ancestor. We highlight major flaws in Xia's inference process and his analysis of CpG deficiencies, and conclude that there is no direct evidence for the role of dogs as intermediate hosts. Bats and pangolins currently have the greatest support as ancestral hosts of SARS-CoV-2, with the strong caveat that sampling of wildlife species for coronaviruses has been limited

Cytokinesis defects and cancer

Whole-genome and centrosome duplication as a consequence of cytokinesis failure can drive tumorigenesis in experimental model systems. However, whether cytokinesis failure is in fact an important cause of human cancers has remained unclear. In this Review, we summarize evidence that whole-genome-doubling events are frequently observed in human cancers and discuss the contribution that cytokinesis defects can make to tumorigenesis. We provide an overview of the potential causes of cytokinesis failure and discuss how tetraploid cells that are generated through cytokinesis defects are used in cancer as a transitory state on the route to aneuploidy. Finally, we discuss how cytokinesis defects can facilitate genetic diversification within the tumour to promote cancer development and could constitute the path of least resistance in tumour evolution