On-line monitoring of VoIP quality using IPFIX

The main goal of VoIP services is to provide a reliable and high-quality voice transmission over packet networks. In order to prove the quality of VoIP transmission, several approaches were designed. In our approach, we are concerned about on-line monitoring of RTP and RTCP traffic. Based on these data, we are able to compute main VoIP quality metrics including jitter, delay, packet loss, and finally R-factor and MOS values. This technique of VoIP quality measuring can be directly incorporated into IPFIX monitoring framework where an IPFIX probe analyses RTP/RTCP packets, computes VoIP quality metrics, and adds these metrics into extended IPFIX flow records. Then, these extended data are stored in a central IPFIX monitoring system called collector where can be used for monitoring purposes. This paper presents a functional implementation of IPFIX plugin for VoIP quality measurement and compares the results with results obtained by other tools

Quality Analysis of VoIP Calls

Tato bakalářská práce se zabývá metodami pro hodnocení kvality hovorů VoIP. Je zde vysvětlen rozbor protokolu RTP/RTCP a následné počítání statistik potřebných pro určení kvality hovorů. V této práci je také popsána metoda, která byla implementována do pluginů pro sondu FlowMon. Budete zde seznámeni s výsledky a s porovnáním s ostatními programy.This bachelor's thesis focuses on methods for evaluating quality of VoIP calls. You can read about analysis of RTP/RTCP packets and use this knowledge for computing statistics required for assessing quality of VoIP calls. Also, I explain the method, which is implemented in plugins that work in FlowMon probe. Finally, you will see the results compared to the other programs.

With a Little Help from Your Friends: Collaboration with Vendors During Smart Grid Incident Response Exercises

The introduction of Information and Communications Technology (ICT) into conventional power grids has resulted in a digitalized smart grid, enabling a more efficient and robust operation. However, it can also lead to increased risk and new threats due to more complex systems and longer supply chains. Recent events indicate that the electrical power grid is an attractive target, promoting the need for well-prepared incident management processes that involve external vendors. This paper addresses this through the development of scenarios for collaborative preparedness exercises, and an investigation into which factors may contribute to making it easier to include vendors in preparedness exercises.acceptedVersio

Clinical effect of obesity on N-terminal pro-B-type natriuretic peptide cut-off concentrations for the diagnosis of acute heart failure

AIMS Obese patients have lower natriuretic peptide concentrations. We hypothesized that adjusting the concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP) for obesity could further increase its clinical utility in the early diagnosis of acute heart failure (AHF). METHODS AND RESULTS This hypothesis was tested in a prospective diagnostic study enrolling unselected patients presenting to the emergency department with acute dyspnoea. Two independent cardiologists/internists centrally adjudicated the final diagnosis using all individual patient information including cardiac imaging. NT-proBNP plasma concentrations were applied: first, using currently recommended cut-offs; second, using cut-offs lowered by 33% with body mass index (BMI) of 30-34.9 kg/m$^{2}$ and by 50% with BMI ≥ 35 kg/m$^{2}$ . Among 2038 patients, 509 (25%) were obese, of which 271 (53%) had AHF. The diagnostic accuracy of NT-proBNP as quantified by the area under the receiver-operating characteristic curve was lower in obese versus non-obese patients (0.890 vs. 0.938). For rapid AHF rule-out in obese patients, the currently recommended cut-off of 300 pg/ml achieved a sensitivity of 96.7% (95% confidence interval [CI] 93.8-98.2%), ruling out 29% of patients and missing 9 AHF patients. For rapid AHF rule-in, the age-dependent cut-off concentrations (age 75 years: 1800 pg/ml) achieved a specificity of 84.9% (95% CI 79.8-88.9%). Proportionally lowering the currently recommended cut-offs by BMI increased sensitivity to 98.2% (95% CI 95.8-99.2%), missing 5 AHF patients; reduced the proportion of AHF patients remaining in the 'gray zone' (48% vs. 26%; p = 0.002), achieving a specificity of 76.5% (95% CI 70.7-81.4%). CONCLUSIONS Adjusting NT-proBNP concentrations for obesity seems to further increase its clinical utility in the early diagnosis of AHF

How does risk flow in the credit default swap market?

We develop a framework to analyse the credit default swap (CDS) market as a network of risk transfers among counterparties. From a theoretical perspective, we introduce the notion of flow-of-risk and provide sufficient conditions for a bow-tie network architecture to endogenously emerge as a result of intermediation. This architecture shows three distinct sets of counterparties: (i) Ultimate Risk Sellers (URS), (ii) Dealers (indirectly connected to each other), (iii) Ultimate Risk Buyers (URB). We show that the probability of widespread distress due to counterparty risk is higher in a bow-tie architecture than in more fragmented network structures. Empirically, we analyse a unique global dataset of bilateral CDS exposures on major sovereign and financial reference entities in 2011–2014. We find the presence of a bow-tie network architecture consistently across both reference entities and time, and that the flow-of-risk originates from a large number of URSs (e.g. hedge funds) and ends up in a few leading URBs, most of which are non-banks (in particular asset managers). Finally, the analysis of the CDS portfolio composition of the URBs shows a high level of concentration: in particular, the top URBs often show large exposures to potentially correlated reference entities

Complex aetiology of an apparently Mendelian form of Mental Retardation

<p>Abstract</p> <p>Background</p> <p>Mental Retardation is a common heterogeneous neurodevelopment condition, which causes are still largely elusive. It has been suggested that half of the phenotypic variation of intelligence is explained by genetic variation. And genetic or inherited factors indeed account for most of the cases of mental retardation with an identifiable cause. However, only a few autosomal genes have been mapped and identified to date. In this report, the genetic causes for an apparently recessive form of mental retardation, in a large nordern swedish pedigree, are investigated.</p> <p>Methods</p> <p>After extensive evaluation of the patients, which ruled out recognizable patterns of malformation and excluded known causes of MR, a comprehensive genome-wide linkage analysis, with 500 microsatellite markers, was performed in 24 members of this family. Additionally, a genome-wide copy number analysis, using an affimetrix 250 K SNP chip, was performed in this pedigree.</p> <p>Results</p> <p>No significant LOD score was found with either parametric and non-parametric linkage analysis. The highest scores are located at chromosomes 13, 15 and 17. Genome-wide copy number analysis identified no clear cause for the disorder; but rather, several variants were present in the family members, irrespective of their affected status.</p> <p>Conclusion</p> <p>These results suggest that mental retardation in this family, unlikely what was expected, has a heterogeneous aetiology; and that several lower effect genes variants might be involved. To demonstrate such effects, our family may be too small. This study also indicates that the ascertainment of the cause of MR may be challenging, and that a complex aetiology may be present even within a pedigree, constituting an additional obstacle for genetic counselling. Variants in genes involved in molecular mechanisms of cellular plasticity, in genes involved in the development of underlying neural architectures, and in genes involved in neurodevelopment and in the ongoing function of terminally differentiated neurons may underlie the phenotypic variation of intelligence and explain instances of intellectual impairment.</p

DNA Polymerase Epsilon Deficiency Causes IMAGe Syndrome with Variable Immunodeficiency.

During genome replication, polymerase epsilon (Pol ε) acts as the major leading-strand DNA polymerase. Here we report the identification of biallelic mutations in POLE, encoding the Pol ε catalytic subunit POLE1, in 15 individuals from 12 families. Phenotypically, these individuals had clinical features closely resembling IMAGe syndrome (intrauterine growth restriction [IUGR], metaphyseal dysplasia, adrenal hypoplasia congenita, and genitourinary anomalies in males), a disorder previously associated with gain-of-function mutations in CDKN1C. POLE1-deficient individuals also exhibited distinctive facial features and variable immune dysfunction with evidence of lymphocyte deficiency. All subjects shared the same intronic variant (c.1686+32C>G) as part of a common haplotype, in combination with different loss-of-function variants in trans. The intronic variant alters splicing, and together the biallelic mutations lead to cellular deficiency of Pol ε and delayed S-phase progression. In summary, we establish POLE as a second gene in which mutations cause IMAGe syndrome. These findings add to a growing list of disorders due to mutations in DNA replication genes that manifest growth restriction alongside adrenal dysfunction and/or immunodeficiency, consolidating these as replisome phenotypes and highlighting a need for future studies to understand the tissue-specific development roles of the encoded proteins