Fast authentication in wireless sensor networks

Broadcast authentication is a fundamental security service in wireless sen- sor networks (WSNs). Although symmetric-key-based μTESLA-like schemes were employed due to their energy efficiency, they all suffer from DoS attacks resulting from the nature of delayed message authentication. Recently, sev- eral public-key-based schemes were proposed to achieve immediate broadcast authentication that may significantly improved security strength. However, while the public-key-based schemes obviate the security vulnerability inher- ent to symmetric-key-based μTESLA-like schemes, their signature verifica- tion is time-consuming. Thus, speeding up signature verification is a problem of considerable practical importance, especially in resource-constrained en- vironments. This paper exploits the cooperation among sensor nodes to ac- celerate the signature verification of vBNN-IBS, a pairing-free identity-based signature with reduced signature size. We demonstrate through on exten- sive performance evaluation study that the accelerated vBNN-IBS achieves the longest network lifetime compared to both the traditional vBNN-IBS and the accelerated ECDSA schemes. The accelerated vBNN-IBS runs 66% faster than the traditional signature verification method. Results from theoretical analysis, simulation, and real-world experimentation on a MICAz platform are provided to validate our claims

Septin 9_i2 is downregulated in tumors, impairs cancer cell migration and alters subnuclear actin filaments

International audienceFunctions of septin cytoskeletal polymers in tumorigenesis are still poorly defined. Their role in the regulation of cytokinesis and cell migration were proposed to contribute to cancer associated aneuploidy and metastasis. Overexpression of Septin 9 (Sept9) promotes migration of cancer cell lines. SEPT9 mRNA and protein expression is increased in breast tumors compared to normal and peritumoral tissues and amplification of SEPT9 gene was positively correlated with breast tumor progression. However, the existence of multiple isoforms of Sept9 is a confounding factor in the analysis of Sept9 functions. In the present study, we analyze the protein expression of Sept9_i2, an uncharacterized isoform, in breast cancer cell lines and tumors and describe its specific impact on cancer cell migration and Sept9 cytoskeletal distribution. Collectively, our results showed that, contrary to Sept9_i1, Sept9_ i2 did not support cancer cell migration, and induced a loss of subnuclear actin filaments. These effects were dependent on Sept9_i2 specific N-terminal sequence. Sept9_i2 was strongly down-regulated in breast tumors compared to normal mammary tissues. Thus our data indicate that Sept9_i2 is a negative regulator of breast tumorigenesis. We propose that Sept9 tumorigenic properties depend on the balance between Sept9_i1 and Sept9_i2 expression levels

Stellar jitter from variable gravitational redshift: implications for RV confirmation of habitable exoplanets

A variation of gravitational redshift, arising from stellar radius fluctuations, will introduce astrophysical noise into radial velocity measurements by shifting the centroid of the observed spectral lines. Shifting the centroid does not necessarily introduce line asymmetries. This is fundamentally different from other types of stellar jitter so far identified, which do result from line asymmetries. Furthermore, only a very small change in stellar radius, ~0.01%, is necessary to generate a gravitational redshift variation large enough to mask or mimic an Earth-twin. We explore possible mechanisms for stellar radius fluctuations in low-mass stars. Convective inhibition due to varying magnetic field strengths and the Wilson depression of starspots are both found to induce substantial gravitational redshift variations. Finally, we investigate a possible method for monitoring/correcting this newly identified potential source of jitter and comment on its impact for future exoplanet searches.Comment: 6 pages, 1 figure, 1 tabl

Game theory framework for MAC parameter optimization in energy-delay constrained sensor networks

Optimizing energy consumption and end-to-end (e2e) packet delay in energy-constrained, delay-sensitive wireless sensor networks is a conflicting multiobjective optimization problem. We investigate the problem from a game theory perspective, where the two optimization objectives are considered as game players. The cost model of each player is mapped through a generalized optimization framework onto protocol-specific MAC parameters. From the optimization framework, a game is first defined by the Nash bargaining solution (NBS) to assure energy consumption and e2e delay balancing. Secondy, the Kalai-Smorodinsky bargaining solution (KSBS) is used to find an equal proportion of gain between players. Both methods offer a bargaining solution to the duty-cycle MAC protocol under different axioms. As a result, given the two performance requirements (i.e., the maximum latency tolerated by the application and the initial energy budget of nodes), the proposed framework allows to set tunable system parameters to reach a fair equilibrium point that dually minimizes the system latency and energy consumption. For illustration, this formulation is applied to six state-of-the-art wireless sensor network (WSN) MAC protocols: B-MAC, X-MAC, RI-MAC, SMAC, DMAC, and LMAC. The article shows the effectiveness and scalability of such a framework in optimizing protocol parameters that achieve a fair energy-delay performance trade-off under the application requirements

Ret inhibition decreases growth and metastatic potential of estrogen receptor positive breast cancer cells

We show that elevated levels of Ret receptor are found in different sub-types of human breast cancers and that high Ret correlates with decreased metastasis-free survival. The role of Ret in ER+ breast cancer models was explored combining in vitro and in vivo approaches. Our analyses revealed that ligand-induced Ret activation: (i) stimulates migration of breast cancer cells; (ii) rescues cells from anti-proliferative effects of endocrine treatment and (iii) stimulates expression of cytokines in the presence of endocrine agents. Indeed, we uncovered a positive feed-forward loop between the inflammatory cytokine IL6 and Ret that links them at the expression and the functional level. In vivo inhibition of Ret in a metastatic breast cancer model inhibits tumour outgrowth and metastatic potential. Ret inhibition blocks the feed-forward loop by down-regulating Ret levels, as well as decreasing activity of Fak, an integrator of IL6-Ret signalling. Our results suggest that Ret kinase should be considered as a novel therapeutic target in subsets of breast cancer

Subnational inequalities in years of life lost and associations with socioeconomic factors in pre-pandemic Europe, 2009–19: an ecological study

Background: Health inequalities have been associated with shorter lifespans. We aimed to investigate subnational geographical inequalities in all-cause years of life lost (YLLs) and the association between YLLs and socioeconomic factors, such as household income, risk of poverty, and educational attainment, in countries within the European Economic Area (EEA) before the COVID-19 pandemic. Methods: In this ecological study, we extracted demographic and socioeconomic data from Eurostat for 1390 small regions and 285 basic regions for 32 countries in the EEA, which was complemented by a time-trend analysis of subnational regions within the EEA. Age-standardised YLL rates per 100 000 population were estimated from 2009 to 2019 based on methods from the Global Burden of Disease study. Geographical inequalities were assessed using the Gini coefficient and slope index of inequality. Socioeconomic inequalities were assessed by investigating the association between socioeconomic factors (educational attainment, household income, and risk of poverty) and YLLs in 2019 using negative binomial mixed models. Findings: Between Jan 1, 2009, and Dec 31, 2019, YLLs lowered in almost all subnational regions. The Gini coefficient of YLLs across all EEA regions was 14·2% (95% CI 13·6–14·8) for females and 17·0% (16·3 to 17·7) for males. Relative geographical inequalities in YLLs among women were highest in the UK (Gini coefficient 11·2% [95% CI 10·1–12·3]) and among men were highest in Belgium (10·8% [9·3–12·2]). The highest YLLs were observed in subnational regions with the lowest levels of educational attainment (incident rate ratio [IRR] 1·19 [1·13–1·26] for females; 1·22 [1·16–1·28] for males), household income (1·35 [95% CI 1·19–1·53]), and the highest poverty risk (1·25 [1·18–1·34]). Interpretation: Differences in YLLs remain within, and between, EEA countries and are associated with socioeconomic factors. This evidence can assist stakeholders in addressing health inequities to improve overall disease burden within the EEA. Funding: Research Council of Norway; Development, and Innovation Fund of Hungary; Norwegian Institute of Public Medicine; and COST Action 18218 European Burden of Disease Network

Cross talk of signals between EGFR and IL-6R through JAK2/STAT3 mediate epithelial–mesenchymal transition in ovarian carcinomas

Epidermal growth factor receptor (EGFR) is overexpressed in ovarian carcinomas, with direct or indirect activation of EGFR able to trigger tumour growth. We demonstrate significant activation of both signal transducer and activator of transcription (STAT)3 and its upstream activator Janus kinase (JAK)2, in high-grade ovarian carcinomas compared with normal ovaries and benign tumours. The association between STAT3 activation and migratory phenotype of ovarian cancer cells was investigated by EGF-induced epithelial–mesenchymal transition (EMT) in OVCA 433 and SKOV3 ovarian cancer cell lines. Ligand activation of EGFR induced a fibroblast-like morphology and migratory phenotype, consistent with the upregulation of mesenchyme-associated N-cadherin, vimentin and nuclear translocation of β-catenin. This occurred concomitantly with activation of the downstream JAK2/STAT3 pathway. Both cell lines expressed interleukin-6 receptor (IL-6R), and treatment with EGF within 1 h resulted in a several-fold enhancement of mRNA expression of IL-6. Consistent with that, EGF treatment of both OVCA 433 and SKOV3 cell lines resulted in enhanced IL-6 production in the serum-free medium. Exogenous addition of IL-6 to OVCA 433 cells stimulated STAT3 activation and enhanced migration. Blocking antibodies against IL-6R inhibited IL-6 production and EGF- and IL-6-induced migration. Specific inhibition of STAT3 activation by JAK2-specific inhibitor AG490 blocked STAT3 phosphorylation, cell motility, induction of N-cadherin and vimentin expression and IL6 production. These data suggest that the activated status of STAT3 in high-grade ovarian carcinomas may occur directly through activation of EGFR or IL-6R or indirectly through induction of IL-6R signalling. Such activation of STAT3 suggests a rationale for a combination of anti-STAT3 and EGFR/IL-6R therapy to suppress the peritoneal spread of ovarian cancer

LAP2 Is Widely Overexpressed in Diverse Digestive Tract Cancers and Regulates Motility of Cancer Cells

BACKGROUND: Lamina-associated polypeptides 2 (LAP2) is a nuclear protein that connects the nuclear lamina with chromatin. Although its critical roles in genetic disorders and hematopoietic malignancies have been described, its expression and roles in digestive tract cancers have been poorly characterized. METHODS: To examine the expression of LAP2 in patient tissues, we performed immunohistochemistry and real-time PCR. To examine motility of cancer cells, we employed Boyden chamber, wound healing and Matrigel invasion assays. To reveal its roles in metastasis in vivo, we used a liver metastasis xenograft model. To investigate the underlying mechanism, a cDNA microarray was conducted. RESULTS: Immunohistochemistry in patient tissues showed widespread expression of LAP2 in diverse digestive tract cancers including stomach, pancreas, liver, and bile duct cancers. Real-time PCR confirmed that LAP2β is over-expressed in gastric cancer tissues. Knockdown of LAP2β did not affect proliferation of most digestive tract cancer cells except pancreatic cancer cells. However, knockdown of LAP2β decreased motility of all tested cancer cells. Moreover, overexpression of LAP2β increased motility of gastric and pancreatic cancer cells. In the liver metastasis xenograft model, LAP2β increased metastatic efficacy of gastric cancer cells and mortality in tested mice. cDNA microarrays showed the possibility that myristoylated alanine-rich C kinase substrate (MARCKS) and interleukin6 (IL6) may mediate LAP2β-regulated motility of cancer cells. CONCLUSIONS: From the above results, we conclude that LAP2 is widely overexpressed in diverse digestive tract cancers and LAP2β regulates motility of cancer cells and suggest that LAP2β may have utility for diagnostics and therapeutics in digestive tract cancers

Knockdown of STAT3 expression by RNAi induces apoptosis in astrocytoma cells

BACKGROUND: Astrocytomas are the most common type of primary central nervous system tumors. They are frequently associated with genetic mutations that deregulate cell cycle and render these tumors resistant to apoptosis. STAT3, signal transducer and activator of transcription 3, participates in several human cancers by inducing cell proliferation and inhibiting apoptosis and is frequently activated in astrocytomas. METHODS: RNA interference was used to knockdown STAT3 expression in human astrocytes and astrocytoma cell lines. The effect of STAT3 knockdown on apoptosis, cell proliferation, and gene expression was then assessed by standard methods. RESULTS: We have found that STAT3 is constitutively activated in several human astrocytoma cell lines. Knockdown of STAT3 expression by siRNA induces morphologic and biochemical changes consistent with apoptosis in several astrocytoma cell lines, but not in primary human astrocytes. Moreover, STAT3 is required for the expression of the antiapoptotic genes survivin and Bcl-xL in the A172 glioblastoma cell line. CONCLUSION: These results show that STAT3 is required for the survival of some astrocytomas. These studies suggest STAT3 siRNA could be a useful therapeutic agent for the treatment of astrocytomas