RiskREP: Risk-Based Security Requirements Elicitation and Prioritization (extended version)

Today, companies are required to be in control of the security of their IT assets. This is especially challenging in the presence of limited budgets and conflicting requirements. Here, we present Risk-Based Requirements Elicitation and Prioritization (RiskREP), a method for managing IT security risks by combining the results of a top-down requirements analysis with a bottom-up threat analysis. Top-down, it prioritizes security goals and from there derives verifiable requirements. Bottom-up, it analyzes architectures in order to identify security risks in the form of critical components. Linking these critical components to security requirements helps to analyze the effects of these requirements on business goals, and to prioritize security requirements. The security requirements also are the basis for deriving test cases for security analysis and compliance monitoring

RiskREP: Risk-Based Security Requirements Elicitation and Prioritization

Companies are under pressure to be in control of their assets but at the same time they must operate as efficiently as possible. This means that they aim to implement "good-enough security" but need to be able to justify their security investment plans. In this paper, we present a Risk-Based Requirements Prioritization method (RiskREP) that extends misuse case-based methods with IT architecturebased risk assessment and countermeasure definition and prioritization. Countermeasure prioritization is linked to business goals to achieve and based on cost of countermeasures and their effectiveness in reducing risks. RiskREP offers the potential to elicit complete security countermeasures, but also supports the deliberate decision and documentation of why the security analysis is focused on certain aspects. We illustrate RiskREP by an application to an action case

Induction maintenance concept for HAART as initial treatment in HIV infected infants

<p>Abstract</p> <p>Background</p> <p>Early initiated antiretroviral therapy (ART) in HIV infected infants leads to improved long-term viral suppression and survival. Guidelines recommend initiating therapy with a triple ART consisting of two nucleoside reverse transcriptase inhibitors (NRTIs) and either one additional non-nucleoside reverse transcriptase inhibitor (NNRTI) or a protease inhibitor (PI). Compared to older children and adults, viral relapse is seen more frequently in infants receiving triple ART. We now address the possibility of a more potent ART with a quadruple induction and triple maintenance therapy.</p> <p>Methods</p> <p>We examine the longitudinal course in four HIV infected infants, who were referred from other centers and could not be recruited to multicentre trials. We introduced ART initially consisting of two NRTIs, one NNRTI and one PI and later discontinued the PI at the age of 12 months maintaining a triple regime consisting of two NRTIs and one NNRTI.</p> <p>Results</p> <p>Provided that therapy adherence was maintained we observed an effective sustained decline of viral load and significant CD4 cell reconstitution even after switching to a triple regime. No drug associated toxicity was seen.</p> <p>Conclusion</p> <p>We suggest that a four drug therapy might be a possible initial therapy option in HIV infected infants, at least in those with a high viral load, followed by a maintenance triple regime after 12 months of therapy.</p

Unleashing the piezoelectric potential of PVDF: a study on phase transformation from gamma (γ) to beta (β) phase through thermal contact poling

ABSTRACT: Polyvinylidene fluoride (PVDF) is known for its piezoelectric properties. This material has different crystalline phases, alpha (α), beta (β) and gamma (γ), where the β-phase, in particular, is related to the piezoelectric behavior of PVDF. While the transformation from the α-phase to β-phase in PVDF is well-documented and widely studied, the transformation from γ- to β-phase has not yet been fully explored. However, when PVDF is produced by certain solution-based methods it can adopt its γ-form, which is not as piezoelectric as the β-phase. Hence, this study aims to bridge this gap by investigating the transformation from γ- to β-phase in PVDF nanocomposites films obtained from solution-based techniques. Our PVDF nanocomposite is made by solvent evaporation-assisted 3D printing of PVDF's nanocomposite with barium-titanate nanoparticles (BTO). To achieve the γ- to β-phase transformation, we first highlight the importance of annealing in the successful poling of PVDF samples. We then perform an in-depth analysis of the α-, β- and γ-crystallographic phases of PVDF-BTO using Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD) and differential scanning calorimetry (DSC). We observed that after annealing but before poling, the PVDF-BTO nanocomposite contains 76% of β + γ phases, the majority of which is the γ-phase. Poling of these samples resulted in the combination of the β + γ phases reaching 93% with the appearance of 40% of absolute fraction of the β-phase. We then demonstrated that the fraction of β-phase in the nanocomposite – as indicated by the 1275 cm−1 peak in PVDF's FTIR spectra – is not uniform on the surface area of the film. Additionally, the value of the absolute β-phase content also depends on the poling field's direction. Our work reveals that while considering PVDF's piezoelectric behavior, it is critical to be aware of these nuances and this article offers essential insights on how to address them. Overall, this study provides a step-by-step guideline to enhance the piezoelectricity of PVDF-based nanocomposites for sensing applications

Characteristics and management of congenital esophageal stenosis: findings from a multicenter study.

BACKGROUND: Congenital esophageal stenosis (CES) is a rare condition frequently associated with esophageal atresia (EA). There are limited data from small series about the presentation, treatment, and outcomes of CES. METHODS: Medical records of all patients with CES included in the French Network on Esophageal Malformations and Congenital Diseases were reviewed retrospectively with regard to diagnosis, treatment, and outcome. RESULTS: Over 18 years, 61 patients (30 boys) had CES, and 29 (47%) of these patients also had EA. The mean age at diagnosis was 24 months (1 day to 14 years) and was younger in patients with CES and EA than in those with isolated CES (7 vs. 126 months, p &lt; 0.05). Twenty-one of the 61 patients with CES had no clinical symptoms: in three patients, the findings were incidental, and in 18 of the 29 patients with associated EA, CES was diagnosed at the time of surgical repair of EA or during a postoperative systematic esophageal barium study. In the 40 other patients, at diagnosis, 50% presented with dysphasia, 40% with vomiting, 50% with food impaction, and 42% with respiratory symptoms. Diagnosis of CES was confirmed by esophageal barium study (56/61) and/or esophageal endoscopy (50/61). Sixteen patients had tracheobronchial remnants (TBR), 40 had fibromuscular stenosis (FMS), and five had membrane stenosis (MS). Thirty-four patients (56%) were treated by dilation only (13/34 remained asymptomatic at follow-up); 15 patients were treated by dilation but required later surgery because of failure (4/15 remained asymptomatic at follow-up); and nine patients had a primary surgical intervention (4/9 were asymptomatic at follow-up). Dilation was complicated by esophageal perforation in two patients (3.4%). At follow-up, dysphagia remained in 36% (21/58) of patients, but the incidence did not differ between the EA and the isolated CS groups (10/29 vs. 7/32, p = 0.27). CONCLUSIONS: CS diagnosis can be delayed when associated with EA. Dilation may be effective for treating patients with FMS and MS, but surgical repair is often required for those with TBR. Our results show clearly that, regardless of the therapeutic option, dysphagia occurs frequently, and patients with CES should be followed over the long term

Inhibition of Akt activity induces the mesenchymal-to-epithelial reverting transition with restoring E-cadherin expression in KB and KOSCC-25B oral squamous cell carcinoma cells

<p>Abstract</p> <p>Background</p> <p>The Akt/PKB family of kinases is frequently activated in human cancers, including oral squamous cell carcinoma (OSCC). Akt-induced epithelial-to-mesenchymal transition (EMT) involves downregulation of E-cadherin, which appears to result from upregulation of the transcription repressor Snail. Recently, it was proposed that carcinoma cells, especially in metastatic sites, could acquire the mesenchymal-to-epithelial reverting transition (MErT) in order to adapt the microenvironments and re-expression of E-cadherin be a critical indicator of MErT. However, the precise mechanism and biologic or clinical importance of the MErT in cancers have been little known. This study aimed to investigate whether Akt inhibition would restore the expression of E-cadherin and β-catenin, reduce that of Vimentin, and induce the MErT in OSCC cells with low or negative expression of E-cadherin. We also investigate whether inhibition of Akt activity would affect the E-cadherin repressors and signaling molecules like NF-κB, ERK, and p38.</p> <p>Methods</p> <p>We screened several OSCC cell lines in order to select suitable cell line models for inducing MErT, using immunoblotting and methylation specific-PCR. We examined whether Akt inhibitor phosphatidylinositol ether lipid analogues (PIA) treatment would restore the expression of E-cadherin and β-catenin, reduce that of Vimentin, and induce the MErT in KB and KOSCC-25B cells using RT-PCR, immunoblotting, immunofluorescence analysis, and <it>in vitro </it>migration assay. We also investigated whether inhibition of Akt activity would affect the E-cadherin repressors, including Snail, Twist, and SIP-1/ZEB-2 and signaling molecules like NF-κB, ERK, JNK, and p38 using RT-PCR, immunoblotting, and immunofluorescence analysis.</p> <p>Results</p> <p>Of the 7 OSCC cell lines, KB and KOSCC-25B showed constitutively activated phosphorylated Akt and low or negative expression of E-cadherin. Inhibition of Akt activity by PIA decreased NF-κB signaling, but did not affect phosphorylation of ERK, JNK, and p38 in KB and KOSCC-25B cells. Akt inhibition led to downregulation of Snail and Twist expression. In contrast, inhibition of Akt activity by PIA did not induce any changes in SIP-1/ZEB-2 expression. PIA treatment induced the expression of E-cadherin and β-catenin, reduce that of Vimentin, restored their epithelial morphology of a polygonal shape, and reduced tumor cell migration in KB and KOSCC-25B cells, which was the corresponding feature of MErT.</p> <p>Conclusion</p> <p>All of these findings suggest that Akt inhibition could induce the MErT through decreased NF-κB signaling and downregulation of Snail and Twist in OSCC cells. A strategy involving Akt inhibition might be a useful therapeutic tool in controlling cancer dissemination and metastasis in oral cancer patients.</p