The Endowment Effect in Groups with and without Strategic Incentives

The realization of market transactions often depends on decisions in groups in which members are anonymous and cannot communicate, but have interrelated outcomes. In a comprehensive study, we investigated the interaction of group effects, strategic effects and endowment effects in different group situations. We show that groups display an endowment effects for uncertain goods which is reduced by about 50% compared to the endowment effect in individuals in corresponding situations. In group situations with additional strategic incentives to overprice the endowment effect completely diminished. The strategic effects and group effects on pricing in group situations cannot be found for participants’ personal valuations of the good, whereas the endowment effect for personal valuations prevailed in both group conditions. This indicates that the endowment effect might be more fundamental than group effects and strategic effects. A paramorphic model for pricing in strategic group situations is suggested and practical implications are discussed.Decision Making, Endowment Effects, Groups, Strategic Incentives

Analysis of the DoIP Protocol for Security Vulnerabilities

DoIP, which is defined in ISO 13400, is a transport protocol stack for diagnostic data. Diagnostic data is a potential attack vector at vehicles, so secure transmission must be guaranteed to protect sensitive data and the vehicle. Previous work analyzed a draft version and earlier versions of the DoIP protocol without Transport Layer Security (TLS). No formal analysis exists for the DoIP protocol. The goal of this work is to investigate the DoIP protocol for design flaws that may lead to security vulnerabilities and possible attacks to exploit them. For this purpose, we deductively analyze the DoIP protocol in a first step and subsequently confirm our conclusions formally. For the formal analysis, we use the prover Tamarin. Based on the results, we propose countermeasures to improve the DoIP's security.We showthat the DoIP protocol cannot be considered secure mainly because the security mechanisms TLS and client authentication in the DoIP protocol are not mandatory. We propose measures to mitigate the vulnerabilities thatwe confirm to remain after activating TLS. These require only a minor redesign of the protocol

An SDN-based Approach For Defending Against Reflective DDoS Attacks

Distributed Reflective Denial of Service (DRDoS) attacks are an immanent threat to Internet services. The potential scale of such attacks became apparent in March 2018 when a memcached-based attack peaked at 1.7 Tbps. Novel services built upon UDP increase the need for automated mitigation mechanisms that react to attacks without prior knowledge of the actual application protocols used. With the flexibility that software-defined networks offer, we developed a new approach for defending against DRDoS attacks; it not only protects against arbitrary DRDoS attacks but is also transparent for the attack target and can be used without assistance of the target host operator. The approach provides a robust mitigation system which is protocol-agnostic and effective in the defense against DRDoS attacks

Message Type Identification of Binary Network Protocols using Continuous Segment Similarity

Protocol reverse engineering based on traffic traces infers the behavior of unknown network protocols by analyzing observable network messages. To perform correct deduction of message semantics or behavior analysis, accurate message type identification is an essential first step. However, identifying message types is particularly difficult for binary protocols, whose structural features are hidden in their densely packed data representation. We leverage the intrinsic structural features of binary protocols and propose an accurate method for discriminating message types. Our approach uses a similarity measure with continuous value range by comparing feature vectors where vector elements correspond to the fields in a message, rather than discrete byte values. This enables a better recognition of structural patterns, which remain hidden when only exact value matches are considered. We combine Hirschberg alignment with DBSCAN as cluster algorithm to yield a novel inference mechanism. By applying novel autoconfiguration schemes, we do not require manually configured parameters for the analysis of an unknown protocol, as required by earlier approaches. Results of our evaluations show that our approach has considerable advantages in message type identification result quality and also execution performance over previous approaches.Comment: 11 pages, 4 figures, to be published in IEEE International Conference on Computer Communications. INFOCOM. Beijing, China, 202

Secure Execution Architecture based on PUF-driven Instruction Level Code Encryption

A persistent problem with program execution, despite numerous mitigation attempts, is its inherent vulnerability to the injection of malicious code. Equally unsolved is the susceptibility of firmware to reverse engineering, which undermines the manufacturer\u27s code confidentiality. We propose an approach that solves both kinds of security problems employing instruction-level code encryption combined with the use of a physical unclonable function (PUF). Our novel Secure Execution PUF-based Processor (SEPP) architecture is designed to minimize the attack surface, as well as performance impact, and requires no significant changes to the development process. This is possible based on a tight integration of a PUF directly into the processor\u27s instruction pipeline. Furthermore, cloud scenarios and distributed embedded systems alike inherently depend on remote execution; our approach supports this, as the secure execution environment needs not to be locally available at the developers site. We implemented an FPGA-based prototype based on the OpenRISC Reference Platform. To assess our results, we performed a security analysis of the processor and evaluated the performance impact of the encryption. We show that the attack surface is significantly reduced compared to previous approaches while the performance penalty is at a reasonable factor of about 1.5

RP1 is a phosphorylation target of CK2 and is involved in cell adhesion

RP1 (synonym: MAPRE2, EB2) is a member of the microtubule binding EB1 protein family, which interacts with APC, a key regulatory molecule in the Wnt signalling pathway. While the other EB1 proteins are well characterized the cellular function and regulation of RP1 remain speculative to date. However, recently RP1 has been implicated in pancreatic cancerogenesis. CK2 is a pleiotropic kinase involved in adhesion, proliferation and anti-apoptosis. Overexpression of protein kinase CK2 is a hallmark of many cancers and supports the malignant phenotype of tumor cells. In this study we investigate the interaction of protein kinase CK2 with RP1 and demonstrate that CK2 phosphorylates RP1 at Ser(236) in vitro. Stable RP1 expression in cell lines leads to a significant cleavage and down-regulation of N-cadherin and impaired adhesion. Cells expressing a Phospho-mimicking point mutant RP1-ASP(236) show a marked decrease of adhesion to endothelial cells under shear stress. Inversely, we found that the cells under shear stress downregulate endogenous RP1, most likely to improve cellular adhesion. Accordingly, when RP1 expression is suppressed by shRNA, cells lacking RP1 display significantly increased cell adherence to surfaces. In summary, RP1 phosphorylation at Ser(236) by CK2 seems to play a significant role in cell adhesion and might initiate new insights in the CK2 and EB1 family protein association

Developing Pulmonary Vasculopathy in Systemic Sclerosis, Detected with Non-Invasive Cardiopulmonary Exercise Testing

BACKGROUND: Patients with systemic sclerosis (SSc) may develop exercise intolerance due to musculoskeletal involvement, restrictive lung disease, left ventricular dysfunction, or pulmonary vasculopathy (PV). The latter is particularly important since it may lead to lethal pulmonary arterial hypertension (PAH). We hypothesized that abnormalities during cardiopulmonary exercise testing (CPET) in patients with SSc can identify PV leading to overt PAH. METHODS: Thirty SSc patients from the Harbor-UCLA Rheumatology clinic, not clinically suspected of having significant pulmonary vascular disease, were referred for this prospective study. Resting pulmonary function and exercise gas exchange were assessed, including peakVO2, anaerobic threshold (AT), heart rate-VO2 relationship (O2-pulse), exercise breathing reserve and parameters of ventilation-perfusion mismatching, as evidenced by elevated ventilatory equivalent for CO2 (VE/VCO2) and reduced end-tidal pCO2 (PETCO2) at the AT. RESULTS: Gas exchange patterns were abnormal in 16 pts with specific cardiopulmonary disease physiology: Eleven patients had findings consistent with PV, while five had findings consistent with left-ventricular dysfunction (LVD). Although both groups had low peak VO2 and AT, a higher VE/VCO2 at AT and decreasing PETCO2 during early exercise distinguished PV from LVD. CONCLUSIONS: Previously undiagnosed exercise impairments due to LVD or PV were common in our SSc patients. Cardiopulmonary exercise testing may help to differentiate and detect these disorders early in patients with SSc

Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline

Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or (LARP4B). Individuals at high compared to those at low genetic risk (8-14 vs. 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function

Genetic Interactions with Age, Sex, Body Mass Index, and Hypertension in Relation to Atrial Fibrillation: The AFGen Consortium

It is unclear whether genetic markers interact with risk factors to influence atrial fibrillation (AF) risk. We performed genome-wide interaction analyses between genetic variants and age, sex, hypertension, and body mass index in the AFGen Consortium. Study-specific results were combined using meta-analysis (88,383 individuals of European descent, including 7,292 with AF). Variants with nominal interaction associations in the discovery analysis were tested for association in four independent studies (131,441 individuals, including 5,722 with AF). In the discovery analysis, the AF risk associated with the minor rs6817105 allele (at the PITX2 locus) was greater among subjects ≤ 65 years of age than among those > 65 years (interaction p-value = 4.0 × 10-5). The interaction p-value exceeded genome-wide significance in combined discovery and replication analyses (interaction p-value = 1.7 × 10-8). We observed one genome-wide significant interaction with body mass index and several suggestive interactions with age, sex, and body mass index in the discovery analysis. However, none was replicated in the independent sample. Our findings suggest that the pathogenesis of AF may differ according to age in individuals of European descent, but we did not observe evidence of statistically significant genetic interactions with sex, body mass index, or hypertension on AF risk

Large-scale analyses of common and rare variants identify 12 new loci associated with atrial fibrillation

Atrial fibrillation affects more than 33 million people worldwide and increases the risk of stroke, heart failure, and death. Fourteen genetic loci have been associated with atrial fibrillation in European and Asian ancestry groups. To further define the genetic basis of atrial fibrillation, we performed large-scale, trans-ancestry meta-analyses of common and rare variant association studies. The genome-wide association studies (GWAS) included 17,931 individuals with atrial fibrillation and 115,142 referents; the exome-wide association studies (ExWAS) and rare variant association studies (RVAS) involved 22,346 cases and 132,086 referents. We identified 12 new genetic loci that exceeded genome-wide significance, implicating genes involved in cardiac electrical and structural remodeling. Our results nearly double the number of known genetic loci for atrial fibrillation, provide insights into the molecular basis of atrial fibrillation, and may facilitate the identification of new potential targets for drug discovery