MAC OS X Forensics: Password Discovery

OS X provides a password-rich environment in which passwords protect OS X resources and perhaps many other resources accessed through OS X. Every password an investigator discovers in an OS X environment has the potential for use in discovering other such passwords, and any discovered passwords may also be useful in other aspects of an investigation, not directly related to the OS X environment. This research advises the use of multiple attack vectors in approaching the password problem in an OS X system, including the more generally applicable non-OS X-specific techniques such as social engineering or well-known password cracking techniques such as John the Ripper or other versions of dictionary attacks and Rainbow table attacks. In some successful approaches the components of the attack vector will use more OS X specific techniques such as those described here: application-provided password revealing functions, a Javascript attack, an “Evil Website” attack, system file scavenging, exploitation of the keychain, and an OS X install disk attack. Keywords: OS X, password, password discovery, social engineering, sleepimage, keychai

A use of whitehead's theory of prehension as an observation-system meta-language

Thèse de doctorat -- Université catholique de Louvain, 197

PIK3C3 Inhibition Promotes Sensitivity to Colon Cancer Therapy by Inhibiting Cancer Stem Cells

Background: Despite recent advances in therapies, resistance to chemotherapy remains a critical problem in the clinical management of colorectal cancer (CRC). Cancer stem cells (CSCs) play a central role in therapy resistance. Thus, elimination of CSCs is crucial for effective CRC therapy; however, such strategies are limited. Autophagy promotes resistance to cancer therapy; however, whether autophagy protects CSCs to promote resistance to CRC-therapy is not well understood. Moreover, specific and potent autophagy inhibitors are warranted as clinical trials with hydroxychloroquine have not been successful. Methods: Colon cancer cells and tumoroids were used. Fluorescent reporter-based analysis of autophagy flux, spheroid and side population (SP) culture, and qPCR were done. We synthesized 36-077, a potent inhibitor of PIK3C3/VPS34 kinase, to inhibit autophagy. Combination treatments were done using 5-fluorouracil (5-FU) and 36-077. Results: The 5-FU treatment induced autophagy only in a subset of the treated colon cancer. These autophagy-enriched cells also showed increased expression of CSC markers. Co-treatment with 36-077 significantly improved efficacy of the 5-FU treatment. Mechanistic studies revealed that combination therapy inhibited GSK-3β/Wnt/β-catenin signaling to inhibit CSC population. Conclusion: Autophagy promotes resistance to CRC-therapy by specifically promoting GSK-3β/Wnt/β-catenin signaling to promote CSC survival, and 36-077, a PIK3C3/VPS34 inhibitor, helps promote efficacy of CRC therapy