CloudMe forensics : a case of big-data investigation

The significant increase in the volume, variety and velocity of data complicates cloud forensic efforts, as such big data will, at some point, become computationally expensive to be fully extracted and analyzed in a timely manner. Thus, it is important for a digital forensic practitioner to have a well-rounded knowledge about the most relevant data artefacts that could be forensically recovered from the cloud product under investigation. In this paper, CloudMe, a popular cloud storage service, is studied. The types and locations of the artefacts relating to the installation and uninstallation of the client application, logging in and out, and file synchronization events from the computer desktop and mobile clients are described. Findings from this research will pave the way towards the development of tools and techniques (e.g. data mining techniques) for cloud-enabled big data endpoint forensics investigation

Greening cloud-enabled big data storage forensics : Syncany as a case study

The pervasive nature of cloud-enabled big data storage solutions introduces new challenges in the identification, collection, analysis, preservation and archiving of digital evidences. Investigation of such complex platforms to locate and recover traces of criminal activities is a time-consuming process. Hence, cyber forensics researchers are moving towards streamlining the investigation process by locating and documenting residual artefacts (evidences) of forensic value of users’ activities on cloud-enabled big data platforms in order to reduce the investigation time and resources involved in a real-world investigation. In this paper, we seek to determine the data remnants of forensic value from Syncany private cloud storage service, a popular storage engine for big data platforms. We demonstrate the types and the locations of the artefacts that can be forensically recovered. Findings from this research contribute to an in-depth understanding of cloud-enabled big data storage forensics, which can result in reduced time and resources spent in real-world investigations involving Syncany-based cloud platforms

Forensic investigation of cooperative storage cloud service: Symform as a case study

Researchers envisioned Storage as a Service (StaaS) as an effective solution to the distributed management of digital data. Cooperative storage cloud forensic is relatively new and is an under-explored area of research. Using Symform as a case study, we seek to determine the data remnants from the use of cooperative cloud storage services. In particular, we consider both mobile devices and personal computers running various popular operating systems, namely Windows 8.1, Mac OS X Mavericks 10.9.5, Ubuntu 14.04.1 LTS, iOS 7.1.2, and Android KitKat 4.4.4. Potential artefacts recovered during the research include data relating to the installation and uninstallation of the cloud applications, log-in to and log-out from Symform account using the client application, file synchronization as well as their time stamp information. This research contributes to an in-depth understanding of the types of terrestrial artifacts that are likely to remain after the use of cooperative storage cloud on client devices

IL-11 is a crucial determinant of cardiovascular fibrosis

Fibrosis is a common pathology in cardiovascular disease1. In the heart, fibrosis causes mechanical and electrical dysfunction1,2 and in the kidney, it predicts the onset of renal failure3. Transforming growth factor β1 (TGFβ1) is the principal pro-fibrotic factor4,5, but its inhibition is associated with side effects due to its pleiotropic roles6,7. We hypothesized that downstream effectors of TGFβ1 in fibroblasts could be attractive therapeutic targets and lack upstream toxicity. Here we show, using integrated imaging–genomics analyses of primary human fibroblasts, that upregulation of interleukin-11 (IL-11) is the dominant transcriptional response to TGFβ1 exposure and required for its pro-fibrotic effect. IL-11 and its receptor (IL11RA) are expressed specifically in fibroblasts, in which they drive non-canonical, ERK-dependent autocrine signalling that is required for fibrogenic protein synthesis. In mice, fibroblast-specific Il11 transgene expression or Il-11 injection causes heart and kidney fibrosis and organ failure, whereas genetic deletion of Il11ra1 protects against disease. Therefore, inhibition of IL-11 prevents fibroblast activation across organs and species in response to a range of important pro-fibrotic stimuli. These results reveal a central role of IL-11 in fibrosis and we propose that inhibition of IL-11 is a potential therapeutic strategy to treat fibrotic diseases

IL-11 is a crucial determinant of cardiovascular fibrosis

Fibrosis is a common pathology in cardiovascular disease1. In the heart, fibrosis causes mechanical and electrical dysfunction1,2 and in the kidney, it predicts the onset of renal failure3. Transforming growth factor β1 (TGFβ1) is the principal pro-fibrotic factor4,5, but its inhibition is associated with side effects due to its pleiotropic roles6,7. We hypothesized that downstream effectors of TGFβ1 in fibroblasts could be attractive therapeutic targets and lack upstream toxicity. Here we show, using integrated imaging–genomics analyses of primary human fibroblasts, that upregulation of interleukin-11 (IL-11) is the dominant transcriptional response to TGFβ1 exposure and required for its pro-fibrotic effect. IL-11 and its receptor (IL11RA) are expressed specifically in fibroblasts, in which they drive non-canonical, ERK-dependent autocrine signalling that is required for fibrogenic protein synthesis. In mice, fibroblast-specific Il11 transgene expression or Il-11 injection causes heart and kidney fibrosis and organ failure, whereas genetic deletion of Il11ra1 protects against disease. Therefore, inhibition of IL-11 prevents fibroblast activation across organs and species in response to a range of important pro-fibrotic stimuli. These results reveal a central role of IL-11 in fibrosis and we propose that inhibition of IL-11 is a potential therapeutic strategy to treat fibrotic diseases