Optimal deployments of defense mechanisms for the internet of things

Internet of Things (IoT) devices can be exploited by the attackers as entry points to break into the IoT networks without early detection. Little work has taken hybrid approaches that combine different defense mechanisms in an optimal way to increase the security of the IoT against sophisticated attacks. In this work, we propose a novel approach to generate the strategic deployment of adaptive deception technology and the patch management solution for the IoT under a budget constraint. We use a graphical security model along with three evaluation metrics to measure the effectiveness and efficiency of the proposed defense mechanisms. We apply the multi-objective genetic algorithm (GA) to compute the {\em Pareto optimal} deployments of defense mechanisms to maximize the security and minimize the deployment cost. We present a case study to show the feasibility of the proposed approach and to provide the defenders with various ways to choose optimal deployments of defense mechanisms for the IoT. We compare the GA with the exhaustive search algorithm (ESA) in terms of the runtime complexity and performance accuracy in optimality. Our results show that the GA is much more efficient in computing a good spread of the deployments than the ESA, in proportion to the increase of the IoT devices

Induction of DKK1 by ox-LDL negatively regulates intracellular lipid accumulation in macrophages

AbstractDickkopf1 (DKK1), a canonical Wnt/β-catenin pathway antagonist, is closely associated with cardiovascular disease and adipogenesis. We performed an in vitro study to determine whether oxidized low-density lipoprotein (ox-LDL) increased the expression of DKK1 in macrophages and whether β-catenin and liver X receptor α (LXRα) were involved in this regulation. Induction of DKK1 expression by ox-LDL decreased the level of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) via a Wnt/β-catenin pathway and increased ATP-binding cassette transporter A/G1 (ABCA/G1) levels via a signal transducer and activator of transcription 3 (STAT3) pathway. Lower LOX-1 and higher ABCA/G1 levels inhibited cholesterol loading in macrophages. In conclusion, ox-LDL may induce DKK1 expression in macrophages to inhibit the accumulation of lipids through a mechanism that involves downregulation of LOX-1-mediated lipid uptake and upregulation of ABCA/G1-dependent cholesterol efflux

Up-regulation of MiR-205 under hypoxia promotes epithelial-mesenchymal transition by targeting ASPP2

The epithelial–mesenchymal transition (EMT) is one of the crucial procedures for cancer invasion and distal metastasis. Despite undergoing intensive studies, the mechanisms underlying EMT remain to be completely elucidated. Here, we identified that apoptosis-stimulating protein of p53-2 (ASPP2) is a novel target of MiR-205 in various cancers. Interestingly, the binding site of MiR-205 at the 3′-untranslated region of ASPP2 was highly conserved among different species. An inverse correlation between MiR-205 and ASPP2 was further observed in vivo in cervical cancers, suggesting MiR-205 may be an important physiological inhibitor of ASPP2. Hypoxia is a hallmark of solid tumor microenvironment and one of such conditions to induce EMT. Notably, MiR-205 was remarkably induced by hypoxia in cervical and lung cancer cells. A marked suppression of ASPP2 was observed simultaneously. Further studies confirmed that hypoxia-induced ASPP2 suppression was mainly attributed to the elevated MiR-205. Interestingly, the alteration of MiR-205/ASPP2 under hypoxia was accompanied with the decreased epithelial marker E-cadherin and increased mesenchymal marker Vimentin, as well as a morphological transition from the typical cobblestone-like appearance to the mesenchymal-like structure. More importantly, MiR-205 mimics or ASPP2 silencing similarly promoted EMT process. By contrast, ASPP2 recovery or MiR-205 inhibitor reversed MiR-205-dependent EMT. Further studies demonstrated that the newly revealed MiR-205/ASPP2 axis promoted cell migration and also increased cell proliferation both in vivo and in vitro. These data together implicated a critical impact of MiR-205/ASPP2 on promoting EMT. MiR-205/ASPP2 may be potential diagnostic and therapeutic biomarkers in cervical and lung cancers

The effects of (+)-Gossypol on 11β-HSD and the concentration of corticosterone and dehydrocorticosterone in mice serum and tissues

11β-hydroxysteroid dehydrogenase (11β-HSD) plays an important part in mediating glucocorticoid action, catalyzing the interconversion of corticosterone (B) and dehydrocorticosterone (A) in rodents. The aim of our study is to investigate the effects of (+)-gossypol (G+) on 11β-HSD. Adult ICR mice were given B and B + (G+) by intraperitoneal injection. The activity of 11β-HSD was evaluated by measuring the ratio of A and B, meanwhile the effects of (+)-gossypol on the conversion rate of B to A was determined with HPLC. Serum A/B levels of the B+(G+) group decreased by 2.42, 7.32, 17.85, 31.39, and 40.02 % compared to the B group at each measured time interval. A/B levels at 1 h for the B + (G+) group decreased by 43.78, 21.29 and 34.47% in liver, kidney and adrenal glands, respectively, in comparison to the B group. However, (+)-gossypol had no effect on brain and testis. (+)-Gossypol was an inhibitor of 11β-HSD.Colegio de Farmacéuticos de la Provincia de Buenos Aire

The effects of (+)-Gossypol on 11β-HSD and the concentration of corticosterone and dehydrocorticosterone in mice serum and tissues

11β-hydroxysteroid dehydrogenase (11β-HSD) plays an important part in mediating glucocorticoid action, catalyzing the interconversion of corticosterone (B) and dehydrocorticosterone (A) in rodents. The aim of our study is to investigate the effects of (+)-gossypol (G+) on 11β-HSD. Adult ICR mice were given B and B + (G+) by intraperitoneal injection. The activity of 11β-HSD was evaluated by measuring the ratio of A and B, meanwhile the effects of (+)-gossypol on the conversion rate of B to A was determined with HPLC. Serum A/B levels of the B+(G+) group decreased by 2.42, 7.32, 17.85, 31.39, and 40.02 % compared to the B group at each measured time interval. A/B levels at 1 h for the B + (G+) group decreased by 43.78, 21.29 and 34.47% in liver, kidney and adrenal glands, respectively, in comparison to the B group. However, (+)-gossypol had no effect on brain and testis. (+)-Gossypol was an inhibitor of 11β-HSD.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Deacetylation of HSD17B10 by SIRT3 regulates cell growth and cell resistance under oxidative and starvation stresses.

17-beta-hydroxysteroid dehydrogenase 10 (HSD17B10) plays an important role in mitochondrial fatty acid metabolism and is also involved in mitochondrial tRNA maturation. HSD17B10 missense mutations cause HSD10 mitochondrial disease (HSD10MD). HSD17B10 with mutations identified from cases of HSD10MD show loss of function in dehydrogenase activity and mitochondrial tRNA maturation, resulting in mitochondrial dysfunction. It has also been implicated to play roles in the development of Alzheimer disease (AD) and tumorigenesis. Here, we found that HSD17B10 is a new substrate of NAD-dependent deacetylase Sirtuin 3 (SIRT3). HSD17B10 is acetylated at lysine residues K79, K99 and K105 by the acetyltransferase CBP, and the acetylation is reversed by SIRT3. HSD17B10 acetylation regulates its enzymatic activity and the formation of mitochondrial RNase P. Furthermore, HSD17B10 acetylation regulates the intracellular functions, affecting cell growth and cell resistance in response to stresses. Our results demonstrated that acetylation is an important regulation mechanism for HSD17B10 and may provide insight into interrupting the development of AD