Memory acquisition: A 2-Take approach

When more and more people recognize the value of volatile data, live forensics gains more weight in digital forensics. It is often used in parallel with traditional pull-the-plug forensics to provide a more reliable result in forensic examination. One of the core components in live forensics is the collection and analysis of memory volatile data, during which the memory content is acquired for searching of relevant evidential data or investigating various computer processes to unveil the activities being performed by a user. However, this conventional method may have weaknesses because of the volatile nature of memory data and the absence of original data for validation. This may cause implication to the admissibility of memory data at the court of law which requires strict authenticity and reliability of evidence. In this paper, we discuss the impact of various memory acquisition methods and suggest a 2-Take approach which aims to enhance the confidence level of the acquired memory data for legal proceedings. © 2009 IEEE.published_or_final_versionThe 2009 International Workshop on Forensics for Future Generation Communication Environments (F2GC-09) in conjunction with CSA 2009, Jeju Island, Korea, 10-12 December 2009. In Proceedings of CSA, 2009, p. 1-

Analyzing storage media of digital camera

Digital photography has become popular in recent years. Photographs have become common tools for people to record every tiny parts of their daily life. By analyzing the storage media of a digital camera, crime investigators may extract a lot of useful information to reconstruct the events. In this work, we will discuss a few approaches in analyzing these kinds of storage media of digital cameras. A hypothetical crime case will be used as case study for demonstration of concepts. © 2009 IEEE.published_or_final_versionThe 2009 International Workshop on Forensics for Future Generation Communication Environments (F2GC-09) in conjunction with CSA 2009, Jeju Island, Korea, 10-12 December 2009. In Proceedings of CSA, 2009, p. 1-

Attenuation of Hind-limb Ischemia in Mice with Endothelial-like Cells Derived from Different Sources of Human Stem Cells

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Improvement of Myocardial Function Following Catheter-Based Renal Denervation in Heart Failure

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Recent Advances in Animal and Human Pluripotent Stem Cell Modeling of Cardiac Laminopathy

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Efficient attenuation of Friedreich's ataxia (FRDA) cardiomyopathy by modulation of iron homeostasis-human induced pluripotent stem cell (hiPSC) as a drug screening platform for FRDA

Friedreich’s ataxia (FRDA), a recessive neurodegenerative disorder commonly associated with hypertrophic cardiomyopathy, is caused by silencing of the frataxin (FXN) gene encoding the mitochondrial protein involved in iron-sulfur cluster biosynthesis. We aimed to utilize our previously established FRDA human induced pluripotent stem cell (hiPSC) derived cardiomyocytes model as a platform to assess the efficacy of treatment with either the antioxidant coenzyme Q10 analog, idebenone (IDE) or the iron chelator, deferiprone (DFP), which are both under clinical trial. In fact, DFP was able to more significantly suppress synthesis of reactive oxygen species (ROS) than IDE at the dosages of 10 nM and 25 μM respectively which agreed with the reduced rate of intracellular accumulation of iron by DFP treatment from 25 to 50 µM. With regard to cardiac electrical-contraction (EC) coupling function, decay velocity of calcium handling kinetics in FRDA-hiPSC-cardiomyocytes was significantly improved by DFP treatment but not by IDE. Further mechanistic studies revealed DFP also modulated iron induced mitochondrial stress as reflected by mitochondria network disorganization and decline in level of respiratory chain protein. In addition, iron-response protein (IRP-1) regulatory loop was overridden by DFP as reflected by the attenuated transferrin receptor (TSFR) suppression thereby reducing further iron uptake.published_or_final_versio

Modeling Treatment Response for Lamin A/C Related Dilated Cardiomyopathy in Human Induced Pluripotent Stem Cells.

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Lysosomal membrane permeabilization is involved in oxidative stress-induced apoptotic cell death in LAMP2-deficient iPSCs-derived cerebral cortical neurons

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Correction of Hirschsprung-Associated Mutations in Human Induced Pluripotent Stem Cells Via Clustered Regularly Interspaced Short Palindromic Repeats/Cas9, Restores Neural Crest Cell Function

ACKGROUND & AIMS: Hirschsprung disease is caused by failure of enteric neural crest cells (ENCCs) to fully colonize the bowel, leading to bowel obstruction and megacolon. Heterozygous mutations in the coding region of the RET gene cause a severe form of Hirschsprung disease (total colonic aganglionosis). However, 80% of HSCR patients have short-segment Hirschsprung disease (S-HSCR), which has not been associated with genetic factors. We sought to identify mutations associated with S-HSCR, and used the clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 gene editing system to determine how mutations affect ENCC function. METHODS: We created induced pluripotent stem cell (iPSC) lines from 1 patient with total colonic aganglionosis (with the G731del mutation in RET) and from 2 patients with S-HSCR (without a RET mutation), as well as RET+/- and RET-/- iPSCs. IMR90-iPSC cells were used as the control cell line. Migration and differentiation capacities of iPSC-derived ENCCs were analyzed in differentiation and migration assays. We searched for mutation(s) associated with S-HSCR by combining genetic and transcriptome data from patient blood- and iPSC-derived ENCCs, respectively. Mutations in the iPSCs were corrected using the CRISPR/Cas9 system. RESULTS: ENCCs derived from all iPSC lines, but not control iPSCs, had defects in migration and neuronal lineage differentiation. RET mutations were associated with differentiation and migration defects of ENCCs in vitro. Genetic and transcriptome analyses associated a mutation in the vinculin gene (VCL M209L) with S-HSCR. CRISPR/Cas9 correction of the RET G731del and VCL M209L mutations in iPSCs restored the differentiation and migration capacities of ENCCs. CONCLUSIONS: We identified mutations in VCL associated with S-HSCR. Correction of this mutation in iPSC using CRISPR/Cas9 editing, as well as the RET G731del mutation that causes Hirschsprung disease with total colonic aganglionosis, restored ENCC function. Our study demonstrates how human iPSCs can be used to identify disease-associated mutations and determine how they affect cell functions and contribute to pathogenesis.postprin

Generation of Human Liver Chimeric Mice with Hepatocytes from Familial Hypercholesterolemia Induced Pluripotent Stem Cells

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