Place, Prestige, Price, and Promotion: How International Students Use Social Networks To Learn About Universities Abroad

This qualitative study aims to explore the social media component of international student’s college choice process for studying abroad.  One of the emerging evidence was that participants applied social media specific criteria, such as the number of “likes”, the number of followers, and the ratio of followers to following to rank Higher Education Institutions (HEI) and measure their prestige.  Another emerging finding was that participants with no connections abroad relied exclusively on social media for their college choice decisions and without social media would not even consider an option of transferring abroad.   Videos and pictures offered by social network sites (SNS) provided emotional benefits by helping “to see” an unknown reality, develop sense of belonging, diminish apprehensions of moving abroad, and solidify the choice of HEI, while traditional sources of promotion, such as websites, were perceived as not trustworthy. Higher education professionals could hire individuals with proven expertise in social media to create consistent and meaningful content on different social media platforms to connect with potential international candidates.   

The Internet AS-Level Topology: Three Data Sources and One Definitive Metric

We calculate an extensive set of characteristics for Internet AS topologies extracted from the three data sources most frequently used by the research community: traceroutes, BGP, and WHOIS. We discover that traceroute and BGP topologies are similar to one another but differ substantially from the WHOIS topology. Among the widely considered metrics, we find that the joint degree distribution appears to fundamentally characterize Internet AS topologies as well as narrowly define values for other important metrics. We discuss the interplay between the specifics of the three data collection mechanisms and the resulting topology views. In particular, we show how the data collection peculiarities explain differences in the resulting joint degree distributions of the respective topologies. Finally, we release to the community the input topology datasets, along with the scripts and output of our calculations. This supplement should enable researchers to validate their models against real data and to make more informed selection of topology data sources for their specific needs.Comment: This paper is a revised journal version of cs.NI/050803

BGP Hijacking Classification

Recent reports show that BGP hijacking has increased substantially. BGP hijacking allows malicious ASes to obtain IP prefixes for spamming as well as intercepting or blackholing traffic. While systems to prevent hijacks are hard to deploy and require the cooperation of many other organizations, techniques to detect hijacks have been a popular area of study. In this paper, we classify detected hijack events in order to document BGP detectors output and understand the nature of reported events. We introduce four categories of BGP hijack: typos, prepending mistakes, origin changes, and forged AS paths. We leverage AS hegemony-a measure of dependency in AS relationship-to identify forged AS paths in a fast and efficient way. Besides, we utilize heuristic approaches to find common operators\u27 mistakes such as typos and AS prepending mistakes. The proposed approach classifies our collected ground truth into four categories with 95.71% accuracy. We characterize publicly reported alarms (e.g. BGPMon) with our trained classifier and find 4%, 1%, and 2% of typos, prepend mistakes, and BGP hijacking with a forged AS path, respectively

Protein Kinase C inhibition ameliorates functional endothelial insulin resistance and Vascular Smooth Muscle Cell hypersensitivity to insulin in diabetic hypertensive rats

<p>Abstract</p> <p>Objective</p> <p>Insulin resistance, diabetes, and hypertension are considered elements of metabolic syndrome which is associated with vascular dysfunction. We investigated whether inhibition of protein kinase C (PKC) would affect vascular function in diabetic hypertensive (DH) rats.</p> <p>Methods</p> <p>A combination of type 2 diabetes and arterial hypertension was produced in male Sprague Dawley rats by intrauterine protein deprivation (IUPD) followed by high salt diet. At the age of 32 weeks, DH rats were treated for 2 weeks with the angiotensin-converting enzyme inhibitor captopril (Capto, 30 mg/kg), PKC inhibitor ruboxistaurin (RBX, 50 mg/kg) or vehicle (n = 8 per group) and blood pressure was monitored using telemetry. At the end of experiments, femoral arteries were dissected, and vascular reactivity was evaluated with isovolumic myography.</p> <p>Results</p> <p>The IUPD followed by high salt diet resulted in significant elevation of plasma glucose, plasma insulin, and blood pressure. Endothelium-dependent vascular relaxation in response to acetylcholine was blunted while vascular contraction in response to phenylephrine was enhanced in the DH rats. Neither Capto nor RBX restored endothelium-dependent vascular relaxation while both suppressed vascular contraction. Ex-vivo incubation of femoral arteries from control rats with insulin induced dose-response vasorelaxation while insulin failed to induce vasorelaxation in the DH rat arteries. In the control arteries treated with endothelial nitric oxide synthase inhibitor L-NAME, insulin induced vasoconstriction that was exacerbated in DH rats. Capto and RBX partially inhibited insulin-stimulated vascular contraction.</p> <p>Conclusion</p> <p>These findings suggest that PKC inhibition ameliorates functional endothelial insulin resistance and smooth muscle cell hypersensitivity to insulin, but does not restore acetylcholine-activated endothelium-dependent vasodilation in DH rats.</p

Factor XIII A-Subunit V34L Variant Affects Thrombus Cross-Linking in a Murine Model of Thrombosis

Objective-Factor XIII (FXIII) cross-links fibrin upon activation by thrombin. Activation involves cleavage at residue 37 by thrombin, releasing an activation peptide. A common polymorphism (valine to leucine variant at residue 34, V34L), located in the activation peptide, has been associated with increased activation rates and paradoxically a protective effect in cardiovascular disease. There is, currently, no data available on the effects of V34L from in vivo models of thrombosis. We examined the effect of FXIII V34L on clot formation and cross-linking in vivo. Approach and Results-We generated a panel of full-length recombinant human FXIII-A2 variants with amino acid substitutions in the activation peptide to investigate the effect of these variants on activation rate, and we used wild-type, V34L, and alanine to glycine variant at residue 33 variants to study the effects of varying FXIII activation rate on thrombus formation in a murine model of FeCl3 injury. FXIII activation assay showed that residues 29, 30, 33, and 34 play a critical role in thrombin interaction. Full-length recombinant human FXIII-A2 V34L has significant effects on clot formation, structure, and lysis in vitro, using turbidity assay. This variant influenced fibrin cross-linking but not size of the thrombus in vivo. Conclusions-Mutations in the activation peptide of full-length recombinant FXIII regulate activation rates by thrombin, and V34L influences in vivo thrombus formation by increased cross-linking of the clot

AS-level topology collection through looking glass servers

While accurate and complete modeling of the Internet topol-ogy at the Autonomous System (AS) level is critical for future protocol design, performance evaluation, simulation and analysis, still it remains a challenge to construct its ac-curate representation. In this paper, we collect BGP route announcements of ASes from Looking glass (LG) servers. By querying LG servers, we build an AS topology estimate of around 116 K AS links, from which we discover 11 K new AS links and 686 new ASes. We conclude that collecting BGP traces from LG servers can help enhance the current view of the AS topology from the BGP collector projects (e.g., RouteViews)

RiPKI: The Tragic Story of RPKI Deployment in the Web Ecosystem

Previous arXiv version of this paper has been published under the title "When BGP Security Meets Content Deployment: Measuring and Analysing RPKI-Protection of Websites", Proc. of Fourteenth ACM Workshop on Hot Topics in Networks (HotNets), New York:ACM, 2015Previous arXiv version of this paper has been published under the title "When BGP Security Meets Content Deployment: Measuring and Analysing RPKI-Protection of Websites", Proc. of Fourteenth ACM Workshop on Hot Topics in Networks (HotNets), New York:ACM, 2015Web content delivery is one of the most important services on the Internet. Access to websites is typically secured via TLS. However, this security model does not account for prefix hijacking on the network layer, which may lead to traffic blackholing or transparent interception. Thus, to achieve comprehensive security and service availability, additional protective mechanisms are necessary such as the RPKI, a recently deployed Resource Public Key Infrastructure to prevent hijacking of traffic by networks. This paper argues two positions. First, that modern web hosting practices make route protection challenging due to the propensity to spread servers across many different networks, often with unpredictable client redirection strategies, and, second, that we need a better understanding why protection mechanisms are not deployed. To initiate this, we empirically explore the relationship between web hosting infrastructure and RPKI deployment. Perversely, we find that less popular websites are more likely to be secured than the prominent sites. Worryingly, we find many large-scale CDNs do not support RPKI, thus making their customers vulnerable. This leads us to explore business reasons why operators are hesitant to deploy RPKI, which may help to guide future research on improving Internet security

Matrix metalloproteinases at key junctions in the pathomechanism of stroke

Matrix metalloproteinases play a crucial role in the remodelling of the extracellular matrix through direct degradation of its structural proteins and control of extracellular signaling. The most common cause of ischemic brain damage is an atherothrombotic lesion in the supplying arteries. The progress of the atherosclerotic plaque development and the related thrombotic complications are mediated in part by matrix metalloproteinases. In addition to their role in the underlying disease, various members of this protease family are upregulated in the acute phase of ischemic brain damage as well as in the post-ischemic brain recovery following stroke. This review summarizes the current understanding of the matrix metalloproteinase-related molecular events at three stages of the ischemic cerebrovascular disease (in the atherosclerotic plaque, in the neurovascular unit of the brain and in the regenerating brain tissue)