Optimal Placement of Intrusion Detection Systems to Identify Multi-Stage Attacks in Software Defined Networks

A major threat to network security is the multi-stage attack, where an attacker compromises an outer edge server from which he penetrates an inner server, and so on, until he gains access to protected information deep in the network. Intrusion detection systems (IDS) can detect such attacks, but limited resources constrain the number of IDS deployed. Software defined networking (SDN) provides network flexibility, and combined with network function virtualization (NFV), it enables IDS placement optimizations that can relieve cost constraint pressures. In this work, we develop a novel algorithm for placing IDS to maximize network protection benefits and minimize costs. The benefit of an IDS configuration is given by the probability of reducing an attacker’s chance of success, and the corresponding cost includes IDS installation and operational costs. We find the configuration which yields the highest benefit given a cost constraint by using the genetic algorithm for optimization, and we compare its results to exhaustive techniques. For networks with more than 5 servers, the algorithm consistently maintains over 85% of the maximum benefit with its placement of IDS, while keeping costs as low as 30% of the naive complete-coverage cost. The genetic algorithm error is less than 5% when compared to exhaustive techniques; and for networks larger than 10 servers, the genetic algorithm runtime is less than a third of the exhaustive search runtime. Using our solution, network administrators can reduce the costs of protecting their systems from multi-stage attacks

Biomass-derived carbon–silicon composites (C@Si) as anodes for lithium-ion and sodium-ion batteries: A promising strategy towards long-term cycling stability: A mini review

The global need for high energy density and performing rechargeable batteries has led to the development of high-capacity silicon-based anode materials to meet the energy demands imposed to electrify plug-in vehicles to curtail carbon emissions by 2035. Unfortunately, the high theoretical capacity (4200 mA h g−1) of silicon by (de-)alloy mechanism is limited by its severe volume changes (ΔV ∼ 200% − 400%) during cycling for lithium-ion batteries (LIBs), while for sodium-ion batteries (NIBs) remain uncertain, and hence, compositing with carbons (C@Si) represent a promising strategy to enable the aforementioned practical application. The present review outlines the recent progress of biomass-derived Si-carbon composite (C@Si) anodes for LIBs and NIBs. In this perspective, we present different types of biomass precursors, silicon sources, and compositing strategies, and how these impact on the C@Si physicochemical properties and their electrochemical performance are discussed

Immunotherapy with CD25/CD71-allodepleted T cells to improve T-cell reconstitution after matched unrelated donor hematopoietic stem cell transplant: a randomized trial

BACKGROUND AND AIMS: Delayed immune reconstitution is a major challenge after matched unrelated donor (MUD) stem cell transplant (SCT). In this randomized phase 2 multi-center trial, Adoptive Immunotherapy with CD25/71 allodepleted donor T cells to improve immunity after unrelated donor stem cell transplant (NCT01827579), the authors tested whether allodepleted donor T cells (ADTs) can safely be used to improve immune reconstitution after alemtuzumab-based MUD SCT for hematological malignancies. METHODS: Patients received standard of care or up to three escalating doses of ADTs generated through CD25+/CD71+ immunomagnetic depletion. The primary endpoint of the study was circulating CD3+ T-cell count at 4 months post-SCT. Twenty-one patients were treated, 13 in the ADT arm and eight in the control arm. RESULTS: The authors observed a trend toward improved CD3+ T-cell count at 4 months in the ADT arm versus the control arm (230/µL versus 145/µL, P = 0.18), and three ADT patients achieved normal CD3+ T-cell count at 4 months (>700/µL). The rates of significant graft-versus-host disease (GVHD) were comparable in both cohorts, with grade ≥2 acute GVHD in seven of 13 and four of eight patients and chronic GVHD in three of 13 and three of eight patients in the ADT and control arms, respectively. CONCLUSIONS: These data suggest that adoptive transfer of ADTs is safe, but that in the MUD setting the benefit in terms of T-cell reconstitution is limited. This approach may be of more use in the context of more rigorous T-cell depletion

Is the rise in childhood obesity rates leading to an increase in hospitalizations due to dengue?

Background: Obesity and diabetes are known risk factors for severe dengue. Therefore, we sought to investigate the association of obesity with increased risk of hospitalization, as there is limited information. Methods and findings: Children aged 10 to 18 years (n = 4782), were recruited from 9 districts in Sri Lanka using a stratified multi-stage cluster sampling method. Details of previous admissions to hospital due to dengue and anthropometric measurements were recorded and seropositivity rates for dengue were assessed. The body mass index (BMI) centile in children aged 10 to 18, was derived by plotting the values on the WHO BMI-for-age growth charts, to acquire the percentile ranking. Results: Although the dengue seropositivity rates were similar in children of the different BMI centiles, 12/66 (18.2%) seropositive children with a BMI centile >97th, had been hospitalized for dengue, compared to 103/1086 (9.48%) of children with a BMI centile of 97th (OR 2.33, 95% CI, 1.47 to 3.67, p = 0.0003) was significantly associated with hospitalization when compared to children in other BMI categories. Conclusions: Obesity appears to be associated with an increased risk of hospitalization in dengue, which should be further investigated in longitudinal prospective studies. With the increase in obesity in many countries, it would be important to create awareness regarding obesity and risk of severe disease and hospitalization in dengue

Increased ERK signalling promotes inflammatory signalling in primary airway epithelial cells expressing Z α1-antitrypsin.

Overexpression of Z α1-antitrypsin is known to induce polymer formation, prime the cells for endoplasmic reticulum stress and initiate nuclear factor kappa B (NF-κB) signalling. However, whether endogenous expression in primary bronchial epithelial cells has similar consequences remains unclear. Moreover, the mechanism of NF-κB activation has not yet been elucidated. Here, we report excessive NF-κB signalling in resting primary bronchial epithelial cells from ZZ patients compared with wild-type (MM) controls, and this appears to be mediated by mitogen-activated protein/extracellular signal-regulated kinase, EGF receptor and ADAM17 activity. Moreover, we show that rather than being a response to protein polymers, NF-κB signalling in airway-derived cells represents a loss of anti-inflammatory signalling by M α1-antitrypsin. Treatment of ZZ primary bronchial epithelial cells with purified plasma M α1-antitrypsin attenuates this inflammatory response, opening up new therapeutic options to modulate airway inflammation in the lung

Recurrent gross mutations of the PTEN tumor suppressor gene in breast cancers with deficient DSB repair

Basal-like breast cancer (BBC) is a subtype of breast cancer with poor prognosis. Inherited mutations of BRCA1, a cancer susceptibility gene involved in double-strand DNA break (DSB) repair, lead to breast cancers that are nearly always of the BBC subtype; however, the precise molecular lesions and oncogenic consequences of BRCA1 dysfunction are poorly understood. Here we show that heterozygous inactivation of the tumor suppressor gene Pten leads to the formation of basal-like mammary tumors in mice, and that loss of PTEN expression is significantly associated with the BBC subtype in human sporadic and BRCA1-associated hereditary breast cancers. In addition, we identify frequent gross PTEN mutations, involving intragenic chromosome breaks, inversions, deletions and micro copy number aberrations, specifically in BRCA1-deficient tumors. These data provide an example of a specific and recurrent oncogenic consequence of BRCA1-dependent dysfunction in DNA repair and provide insight into the pathogenesis of BBC with therapeutic implications. These findings also argue that obtaining an accurate census of genes mutated in cancer will require a systematic examination for gross gene rearrangements, particularly in tumors with deficient DSB repair