| 1. |
- Mishra, Nivedita, et al.
(author)
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Memcached : An Experimental Study of DDoS Attacks for the Wellbeing of IoT Applications
- 2021
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In: Sensors. - : MDPI. - 1424-8220. ; 21:23
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Journal article (peer-reviewed)abstract
- Distributed denial‐of‐service (DDoS) attacks are significant threats to the cyber world because of their potential to quickly bring down victims. Memcached vulnerabilities have been targeted by attackers using DDoS amplification attacks. GitHub and Arbor Networks were the victims of Memcached DDoS attacks with 1.3 Tbps and 1.8 Tbps attack strengths, respectively. The bandwidth amplification factor of nearly 50,000 makes Memcached the deadliest DDoS attack vector to date. In recent times, fellow researchers have made specific efforts to analyze and evaluate Memcached vulnerabilities; however, the solutions provided for security are based on best practices by users and service providers. This study is the first attempt at modifying the architecture of Memcached servers in the context of improving security against DDoS attacks. This study discusses the Memcached protocol, the vulnerabilities associated with it, the future challenges for different IoT applications associated with caches, and the solutions for detecting Memcached DDoS attacks. The proposed solution is a novel identification‐pattern mechanism using a threshold scheme for detecting volume‐based DDoS attacks. In the undertaken study, the solution acts as a pre‐emptive measure for detecting DDoS attacks while maintaining low latency and high throughput.
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| 2. |
- Brorson, Håkan, et al.
(author)
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Excisional Procedures: Liposuction
- 2016
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In: Principles and practice of lymphedema surgery. - 9780323298971 - 9780323298971 ; , s. 107-112
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Book chapter (peer-reviewed)
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| 3. |
- Collins, Justin, et al.
(author)
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Live streaming of robotic surgery from leading educational centres enables a global approach to surgical teaching
- 2016
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In: Journal of Urology. - : Ovid Technologies (Wolters Kluwer Health). - 0022-5347 .- 1527-3792. ; 195:4, s. E116-E116
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Journal article (other academic/artistic)abstract
- Following recently published EAU Policy on Live Surgical Events (LSE's) it is assured that live surgery will be ongoing at conferences in the immediate future. However, the panel reached >80% consensus view that performing at a home institution may be safer. The committee also identified issues with a ‘travelling surgeon’ performing complex surgery in an unfamiliar environment with a surgical team that is not experienced with the intricacies of surgeons techniques. LSE's from home institutions remove or minimize these negative aspects.
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| 4. |
- Lessard, Christopher J., et al.
(author)
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Variants at multiple loci implicated in both innate and adaptive immune responses are associated with Sjogren's syndrome
- 2013
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In: Nature Genetics. - : NATURE PUBLISHING GROUP, 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA. - 1061-4036 .- 1546-1718. ; 45:11, s. 1284-
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Journal article (peer-reviewed)abstract
- Sjogrens syndrome is a common autoimmune disease (affecting similar to 0.7% of European Americans) that typically presents as keratoconjunctivitis sicca and xerostomia. Here we report results of a large-scale association study of Sjogrens syndrome. In addition to strong association within the human leukocyte antigen (HLA) region at 6p21 (P-meta = 7.65 x 10(-114)), we establish associations with IRF5-TNPO3 (P-meta = 2.73 x 10(-19)), STAT4 (Pmeta = 6.80 x 10-15), IL12A (P-meta = 1.17 x 10(-10)), FAM167ABLK (P-meta = 4.97 x 10(-10)), DDX6-CXCR5 (P-meta = 1.10 x 10(-8)) and TNIP1 (P-meta = 3.30 x 10(-8)). We also observed suggestive associations (P-meta andlt; 5 x 10(-5)) with variants in 29 other regions, including TNFAIP3, PTTG1, PRDM1, DGKQ, FCGR2A, IRAK1BP1, ITSN2 and PHIP, among others. These results highlight the importance of genes that are involved in both innate and adaptive immunity in Sjogrens syndrome.
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| 5. |
- Li, He, et al.
(author)
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Identification of a Sjögren's syndrome susceptibility locus at OAS1 that influences isoform switching, protein expression, and responsiveness to type I interferons
- 2017
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In: PLOS Genetics. - : PUBLIC LIBRARY SCIENCE. - 1553-7390 .- 1553-7404. ; 13:6
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Journal article (peer-reviewed)abstract
- Sjogren's syndrome (SS) is a common, autoimmune exocrinopathy distinguished by keratoconjunctivitis sicca and xerostomia. Patients frequently develop serious complications including lymphoma, pulmonary dysfunction, neuropathy, vasculitis, and debilitating fatigue. Dysregulation of type I interferon (IFN) pathway is a prominent feature of SS and is correlated with increased autoantibody titers and disease severity. To identify genetic determinants of IFN pathway dysregulation in SS, we performed cis-expression quantitative trait locus (eQTL) analyses focusing on differentially expressed type I IFN-inducible transcripts identified through a transcriptome profiling study. Multiple cis-eQTLs were associated with transcript levels of 2'-5'-oligoadenylate synthetase 1 (OAS1) peaking at rs10774671 (PeQTL = 6.05 x 10(-14)). Association of rs10774671 with SS susceptibility was identified and confirmed through meta-analysis of two independent cohorts (P-meta = 2.59 x 10(-9); odds ratio = 0.75; 95% confidence interval = 0.66-0.86). The risk allele of rs10774671 shifts splicing of OAS1 from production of the p46 isoform to multiple alternative transcripts, including p42, p48, and p44. We found that the isoforms were differentially expressed within each genotype in controls and patients with and without autoantibodies. Furthermore, our results showed that the three alternatively spliced isoforms lacked translational response to type I IFN stimulation. The p48 and p44 isoforms also had impaired protein expression governed by the 3' end of the transcripts. The SS risk allele of rs10774671 has been shown by others to be associated with reduced OAS1 enzymatic activity and ability to clear viral infections, as well as reduced responsiveness to IFN treatment. Our results establish OAS1 as a risk locus for SS and support a potential role for defective viral clearance due to altered IFN response as a genetic pathophysiological basis of this complex autoimmune disease.
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