Enhanced end-to-end security through symmetric-key cryptography in wearable medical sensor networks

Computer Science

Towards real-time deep learning-based network intrusion detection on FPGA

Computer Science

Machine learning for misuse-based network intrusion detection: overview, unified evaluation and feature choice comparison framework

Computer Science

Communication and security trade-offs for battery-powered devices: a case study on wearable medical sensor systems

Computer Science

In-depth energy analysis of security algorithms and protocols for the Internet of Things

Computer Science

Efficient utilization of DSPs and BRAMs revisited : new AES-GCM recipes on FPGAs

In 2008, Drimer et al. proposed different AES implementations on a Xilinx Virtex-5 FPGA, making efficient use of the DSP slices and BRAM tiles available on the device. Inspired by their work, we evaluate the feasibility of extending AES with the popular GCM mode of operation, still concentrating on the optimal use of DSP slices and BRAM tiles. We make use of a Xilinx Zynq UltraScale+ MPSoC FPGA with improved DSP features. For the AES part, we implement Drimer's round-based and unrolled pipelined architectures differently, still using DSPs and BRAMs efficiently based on the AES Tbox approach. On top of AES, we append the GCM mode of operation, where we use DSP slices to support the GCM finite field multiplication. This allows us to implement AES-GCM with a small amount of FFs and LUTs. We propose two implementations: A relatively compact round-based design and a faster unrolled design

Evidence for position effects as a variant ETV6-mediated leukemogenic mechanism in myeloid leukemias with a t(4;12)(q11-q12;p13) or t(5;12)(q31;p13)

The ETV6 gene (first identified as TEL) is a frequent target of chromosomal translocations in both myeloid and lymphoid leukemias. At present, more than 40 distinct translocations have been cytogenetically described, of which 13 have now also been characterized at the molecular level. These studies revealed the generation of in-frame fusion genes between different domains of ETV6 and partner genes encoding either kinases or transcription factors. However, in a number of cases-including a t(6;12)(q23;p13), the recurrent t(5;12)(q31;p13), and some cases of the t(4;12)(q11-q12;p13) described in this work-functionally significant fusions could not be identified, raising the question as to what leukemogenic mechanism is implicated in these cases. To investigate this, we have evaluated the genomic regions at 4q11-q12 and 5q31, telomeric to the breakpoints of the t(4;12)(q11-q12;p13) and t(5;12)(q31;p13). The homeobox gene GSH2 at 4q11-q12 and the IL-3/CSF2 locus at 5q31 were found to be located close to the respective breakpoints. In addition, GSH2 and IL-3 were found to be ectopically expressed in the leukemic cells, suggesting that expression of GSH2 and IL-3 was deregulated by the translocation. Our results indicate that, besides the generation of fusion transcripts, deregulation of the expression of oncogenes could be a variant leukemogenic mechanism for translocations involving the 5' end of ETV6, especially for those translocations lacking functionally significant fusion transcripts

Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32)

The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL). We recently identified NUP214-ABL1 as a variant ABL1 fusion gene in 6% of T-ALL patients. Here we describe the identification of another ABL1 fusion, EML1-ABL1, in a T-ALL patient with a cryptic t(9;14)(q34;q32) associated with deletion of CDKN2A (p16) and expression of TLX1 (HOX11). Echinoderm microtubule-associated protein-like 1-Abelson 1 (EML1-ABL1) is a constitutively phosphorylated tyrosine kinase that transforms Ba/F3 cells to growth factor-independent growth through activation of survival and proliferation pathways, including extracellular signal-related kinase 1/2 (Erk1/2), signal transducers and activators of transcription 5 (Stat5), and Lyn kinase. Deletion of the coiled-coil domain of EML1 abrogated the transforming properties of the fusion kinase. EML1-ABL1 and breakpoint cluster region (BCR)-ABL1 were equally sensitive to the tyrosine kinase inhibitor imatinib. These data further demonstrate the involvement of ABL1 fusions in the pathogenesis of T-ALL and identify EML1-ABL1 as a novel therapeutic target of imatinib