Risk Rank Analysis Method for Vulnerabilities in a Network System

Prioritizing on most critical weaknesses in a network system at the correct time is a very important role in network security administration. Due to the complexity and high unpredictability of exploitations it is hard to decide which vulnerabilities and which IP s are at the highest risk at a particular time. Present study proposes a new methodology that enables network administrators to rank vulnerabilities based on the probability of being exploited at a given time using the Markovian process. Markovian process allows us to iterate a transition probability matrix for a network system consisting identified or discovered vulnerabilities. This process result in a steady state with probabilities that a vulnerability will be exploited. Similar approach is used here to develop a risk rank model. Well known Google Page Rank Algorithm also uses a similar approach in estimating the probability of a web surfer reaching a particular webpage. Same concept can be used with several modifications to estimate and rank the risk level of each vulnerability in a network system. New methodology is presented with an example of a small network model with three vulnerabilities

Death due to ingestion of nicotine-containing solution: Case report and review of the literature

Nicotine, a lipid-soluble alkaloid obtained from the dried leaves of Nicotiana, is most frequently encountered in tobacco products for smoking, chewing or sniffing as well as in a limited number of pesticides. Though nicotine is one of the most toxic drugs of abuse, it has rarely led to fatalities. Sudden death can be caused by cardiovascular arrest, respiratory muscle paralysis and/or central respiratory failure. A 42-year-old man was found dead by his wife. He was lying on the floor, next to a box containing many empty bottles of beer and vodka. Some labeled chemical bottles found at the scene contained various substances, including nicotine and brucine. Gross examination of the organs at autopsy revealed no specific findings. The toxicological examination failed to disclose any lethal toxic agents other than a high concentration of nicotine and its primary metabolite cotinine in femoral venous blood (2.2 μg/mL). Blood alcohol was determined to be 2.1 g/L in femoral venous blood. Only a paucity of fatal cases of nicotine poisoning has been reported in the literature so far. © 2009 Elsevier Ireland Ltd. All rights reserved

SLE serum deposits C4d on red blood cells, decreases red blood cell membrane deformability, and promotes nitric oxide production

Objective Systemic lupus erythematosus (SLE) is characterized by intravascular activation of the complement system and deposition of complement fragments (C3 and C4) on plasma membranes of circulating cells, including red blood cells (RBC). The aim of this study was to address whether this process affects the biophysical properties of RBC. Methods Serum and red blood cells were isolated from patients with SLE, and healthy controls. RBC from healthy O Rh negative individuals were incubated with SLE or control serum. We used flow cytometry to assess complement fragment deposition on RBC. RBC membrane deformability was measured using 2D microchannel arrays. Protein phosphorylation levels were quantified by western blot. Results Incubation of healthy donor RBC with sera from patients with SLE but not control sera led to deposition of C4 fragments on the RBC. Complement decorated RBC exhibited significant decrease in both membrane deformability and flickering. Sera from SLE patients triggered a transitory Ca++ influx in RBC that was associated with decreased phosphorylation of ?-spectrin, and increased phosphorylation of band 3, two key proteins of RBC cytoskeleton. Finally, SLE but not control sera led to the production of nitric oxide (NO) by RBC. Conclusion Our data suggest that complement activation in patients with SLE leads to calcium dependent cytosketeletal changes in RBC that render them less deformable, likely impairing their flow through capillaries. This phenomenon may negatively impact the delivery of oxygen to the tissues

The Role of Platelet Factor 4 in Local and Remote Tissue Damage in a Mouse Model of Mesenteric Ischemia/Reperfusion Injury

The robust inflammatory response that occurs during ischemia reperfusion (IR) injury recruits factors from both the innate and adaptive immune systems. However the contribution of platelets and their products such as Platelet Factor 4 (PF4; CXCL4), during the pathogenesis of IR injury has not been thoroughly investigated. We show that a deficiency in PF4 protects mice from local and remote tissue damage after 30 minutes of mesenteric ischemia and 3 hours of reperfusion in PF4-/- mice compared to control B6 mice. This protection was independent from Ig or complement deposition in the tissues. However, neutrophil and monocyte infiltration were decreased in the lungs of PF4-/- mice compared with B6 control mice. Platelet-depleted B6 mice transfused with platelets from PF4-/- mice displayed reduced tissue damage compared with controls. In contrast, transfusion of B6 platelets into platelet depleted PF4-/- mice reconstituted damage in both intestine and lung tissues. We also show that PF4 may modulate the release of IgA. Interestingly, we show that PF4 expression on intestinal epithelial cells is increased after IR at both the mRNA and protein levels. In conclusion, these findings demonstrate that may PF4 represent an important mediator of local and remote tissue damage

ICER is requisite for Th17 differentiation.

Inducible cAMP early repressor (ICER) has been described as a transcriptional repressor isoform of the cAMP response element modulator (CREM). Here we report that ICER is predominantly expressed in Th17 cells through the IL-6-STAT3 pathway and binds to the Il17a promoter, where it facilitates the accumulation of the canonical enhancer RORγt. In vitro differentiation from naive ICER/CREM-deficient CD4(+) T cells to Th17 cells is impaired but can be rescued by forced overexpression of ICER. Consistent with a role of Th17 cells in autoimmune and inflammatory diseases, ICER/CREM-deficient B6.lpr mice are protected from developing autoimmunity. Similarly, both anti-glomerular basement membrane-induced glomerulonephritis and experimental encephalomyelitis are attenuated in ICER/CREM-deficient mice compared with their ICER/CREM-sufficient littermates. Importantly, we find ICER overexpressed in CD4(+) T cells from patients with systemic lupus erythematosus. Collectively, our findings identify a unique role for ICER, which affects both organ-specific and systemic autoimmunity in a Th17-dependent manner

Fermion Back-Reaction and the Sphaleron

Using a simple model, a new sphaleron solution which incorporates finite fermionic density effects is obtained. The main result is that the height of the potential barrier (sphaleron energy) decreases as the fermion density increases. This suggests that the rate of sphaleron-induced transitions increases when the fermionic density increases. However the rate increase is not expected to change significantly the predictions from the standard sphaleron-induced baryogenesis scenarios.Comment: 11 pages, Revtex (2 figures available upon request), to appear in Phys. Rev. D (Rapid Communication

Modeling outcomes of soccer matches

We compare various extensions of the Bradley–Terry model and a hierarchical Poisson log-linear model in terms of their performance in predicting the outcome of soccer matches (win, draw, or loss). The parameters of the Bradley–Terry extensions are estimated by maximizing the log-likelihood, or an appropriately penalized version of it, while the posterior densities of the parameters of the hierarchical Poisson log-linear model are approximated using integrated nested Laplace approximations. The prediction performance of the various modeling approaches is assessed using a novel, context-specific framework for temporal validation that is found to deliver accurate estimates of the test error. The direct modeling of outcomes via the various Bradley–Terry extensions and the modeling of match scores using the hierarchical Poisson log-linear model demonstrate similar behavior in terms of predictive performance

Spleen Tyrosine Kinase (Syk) Regulates Systemic Lupus Erythematosus (SLE) T Cell Signaling

Engagement of the CD3/T cell receptor complex in systemic lupus erythematosus (SLE) T cells involves Syk rather than the zeta-associated protein. Because Syk is being considered as a therapeutic target we asked whether Syk is central to the multiple aberrantly modulated molecules in SLE T cells. Using a gene expression array, we demonstrate that forced expression of Syk in normal T cells reproduces most of the aberrantly expressed molecules whereas silencing of Syk in SLE T cells normalizes the expression of most abnormally expressed molecules. Protein along with gene expression modulation for select molecules was confirmed. Specifically, levels of cytokine IL-21, cell surface receptor CD44, and intracellular molecules PP2A and OAS2 increased following Syk overexpression in normal T cells and decreased after Syk silencing in SLE T cells. Our results demonstrate that levels of Syk affect the expression of a number of enzymes, cytokines and receptors that play a key role in the development of disease pathogenesis in SLE and provide support for therapeutic targeting in SLE patients