Side-channel based intrusion detection for industrial control systems

Industrial Control Systems are under increased scrutiny. Their security is historically sub-par, and although measures are being taken by the manufacturers to remedy this, the large installed base of legacy systems cannot easily be updated with state-of-the-art security measures. We propose a system that uses electromagnetic side-channel measurements to detect behavioural changes of the software running on industrial control systems. To demonstrate the feasibility of this method, we show it is possible to profile and distinguish between even small changes in programs on Siemens S7-317 PLCs, using methods from cryptographic side-channel analysis.Comment: 12 pages, 7 figures. For associated code, see https://polvanaubel.com/research/em-ics/code

Prolactin

During an oral glucose tolerance test (OGTT) glucose and insulin levels were measured in 26 patients with prolactin-producing pituitary tumours without growth hormone excess. Basal glucose and insulin levels did not differ from the values of an age-matched control group. After glucose load the hyperprolactinaemic patients showed a decrease in glucose tolerance and a hyperinsulinaemia. Bromocriptine (CB 154), which suppressed PRL, improved glucose tolerance and decreased insulin towards normal in a second OGTT. — Human PRL or CB 154 had no significant influence on insulin release due to glucose in the perfused rat pancreas. — These findings suggest a diabetogenic effect of PRL. CB 154 might be a useful drug in improving glucose utilization in hormone-active pituitary tumours

Alpha and lambda interferon together mediate suppression of CD4 T cells induced by respiratory syncytial virus

The mechanism by which respiratory syncytial virus (RSV) suppresses T-cell proliferation to itself and other antigens is poorly understood. We used monocyte-derived dendritic cells (MDDC) and CD4 T cells and measured [(3)H]thymidine incorporation to determine the factors responsible for RSV-induced T-cell suppression. These two cell types were sufficient for RSV-induced suppression of T-cell proliferation in response to cytomegalovirus or Staphylococcus enterotoxin B. Suppressive activity was transferable with supernatants from RSV-infected MDDC and was not due to transfer of live virus or RSV F (fusion) protein. Supernatants from RSV-infected MDDC, but not MDDC exposed to UV-killed RSV or mock conditions, contained alpha interferon (IFN-alpha; median, 43 pg/ml) and IFN-lambda (approximately 1 to 20 ng/ml). Neutralization of IFN-alpha with monoclonal antibody (MAb) against one of its receptor chains, IFNAR2, or of IFN-lambda with MAb against either of its receptor chains, IFN-lambdaR1 (interleukin 28R [IL-28R]) or IL-10R2, had a modest effect. In contrast, blocking the two receptors together markedly reduced or completely blocked the RSV-induced suppression of CD4 T-cell proliferation. Defining the mechanism of RSV-induced suppression may guide vaccine design and provide insight into previously uncharacterized human T-cell responses and activities of interferons

The role of multiple marks in epigenetic silencing and the emergence of a stable bivalent chromatin state

We introduce and analyze a minimal model of epigenetic silencing in budding yeast, built upon known biomolecular interactions in the system. Doing so, we identify the epigenetic marks essential for the bistability of epigenetic states. The model explicitly incorporates two key chromatin marks, namely H4K16 acetylation and H3K79 methylation, and explores whether the presence of multiple marks lead to a qualitatively different systems behavior. We find that having both modifications is important for the robustness of epigenetic silencing. Besides the silenced and transcriptionally active fate of chromatin, our model leads to a novel state with bivalent (i.e., both active and silencing) marks under certain perturbations (knock-out mutations, inhibition or enhancement of enzymatic activity). The bivalent state appears under several perturbations and is shown to result in patchy silencing. We also show that the titration effect, owing to a limited supply of silencing proteins, can result in counter-intuitive responses. The design principles of the silencing system is systematically investigated and disparate experimental observations are assessed within a single theoretical framework. Specifically, we discuss the behavior of Sir protein recruitment, spreading and stability of silenced regions in commonly-studied mutants (e.g., sas2, dot1) illuminating the controversial role of Dot1 in the systems biology of yeast silencing.Comment: Supplementary Material, 14 page

Error-Tolerant Algebraic Side-Channel Attacks Using BEE

Algebraic side-channel attacks are a type of side-channel analysis which can recover the secret information with a small number of samples (e.g., power traces). However, this type of side-channel analysis is sensitive to measurement errors which may make the attacks fail. In this paper, we propose a new method of algebraic side-channel attacks which considers noisy leakages as integers restricted to intervls and finds out the secret information with a constraint programming solver named BEE. To demonstrate the efficiency of this new method in algebraic side-channel attacks, we analyze some popular implementations of block ciphers---PRESENT, AES, and SIMON under the Hamming weight or Hamming distance leakage model. For AES, our method requires the least leakages compared with existing works under the same error model. For both PRESENT and SIMON, we provide the first analytical results of them under algebraic side-channel attacks in the presence of errors. To further demonstrate the wide applicability of this new method, we also extend it to cold boot attacks. In the cold boot attacks against AES, our method increases the success rate by over $25\%$ than previous works

Characterization of STAT6 Target Genes in Human B Cells and Lung Epithelial Cells

Using ChIP Seq, we identified 556 and 467 putative STAT6 target sites in the Burkitt's lymphoma cell line Ramos and in the normal lung epithelial cell line BEAS2B, respectively. We also examined the positions and expression of transcriptional start sites (TSSs) in these cells using our TSS Seq method. We observed that 44 and 132 genes in Ramos and BEAS2B, respectively, had STAT6 binding sites in proximal regions of their previously reported TSSs that were up-regulated at the transcriptional level. In addition, 406 and 109 of the STAT6 target sites in Ramos and BEAS2B, respectively, were located in proximal regions of previously uncharacterized TSSs. The target genes identified in Ramos and BEAS2B cells in this study and in Th2 cells in previous studies rarely overlapped and differed in their identity. Interestingly, ChIP Seq analyses of histone modifications and RNA polymerase II revealed that chromatin formed an active structure in regions surrounding the STAT6 binding sites; this event also frequently occurred in different cell types, although neither STAT6 binding nor TSS induction was observed. The rough landscape of STAT6-responsive sites was found to be shaped by chromatin structure, but distinct cellular responses were mainly mediated by distinct sets of transcription factors

On gene dosage balance in protein complexes: a comment on Semple JI, Vavouri T, Lehner B. A simple principle concerning the robustness of protein complex activity to changes in gene expression.

A comment on Semple JI, Vavouri T, Lehner B. A simple principle concerning the robustness of protein complex activity to changes in gene expression. BMC Syst Biol. 2008;2: