An Extensive Study of User Identification via Eye Movements across Multiple Datasets

Several studies have reported that biometric identification based on eye movement characteristics can be used for authentication. This paper provides an extensive study of user identification via eye movements across multiple datasets based on an improved version of method originally proposed by George and Routray. We analyzed our method with respect to several factors that affect the identification accuracy, such as the type of stimulus, the IVT parameters (used for segmenting the trajectories into fixation and saccades), adding new features such as higher-order derivatives of eye movements, the inclusion of blink information, template aging, age and gender.We find that three methods namely selecting optimal IVT parameters, adding higher-order derivatives features and including an additional blink classifier have a positive impact on the identification accuracy. The improvements range from a few percentage points, up to an impressive 9 % increase on one of the datasets.Comment: 11 pages, 5 figures, submitted to Signal Processing: Image Communicatio

S1PR4 deficiency results in reduced germinal center formation but only marginally affects antibody production

Introduction: Splenic B cells exhibit a high expression of the G protein-coupled sphingosine-1-phosphate (S1P) receptor type 4 (S1PR4). Little is known about the functional relevance of S1PR4 expression on those cells. Methods: In this study, S1PR4-deficient mice were used to study the role of S1PR4-mediated S1P signaling in B cell motility in vitro and for the maintenance of the splenic architecture under steady state conditions as well as in polymicrobial abdominal sepsis in vivo. Finally, the impact of S1PR4 deficiency on antibody production after immunization with T cell dependent antigens was assessed. Results: Loss of S1PR4 resulted in minor alterations of the splenic architecture concerning the presence of B cell follicles. After sepsis induction, the germinal center response was severely impaired in S1PR4-deficient animals. Splenic B cells showed reduced motility in the absence of S1PR4. However, titres of specific antibodies showed only minor reductions in S1PR4-deficient animals. Discussion: These observations suggest that S1P signaling mediated by S1PR4 modifies chemokine-induced splenic B cell chemotaxis, thus modulating splenic microarchitecture, GC formation and T-cell dependent antibody production

DataSheet_1_S1PR4 deficiency results in reduced germinal center formation but only marginally affects antibody production.pdf

IntroductionSplenic B cells exhibit a high expression of the G protein-coupled sphingosine-1-phosphate (S1P) receptor type 4 (S1PR4). Little is known about the functional relevance of S1PR4 expression on those cells.MethodsIn this study, S1PR4-deficient mice were used to study the role of S1PR4-mediated S1P signaling in B cell motility in vitro and for the maintenance of the splenic architecture under steady state conditions as well as in polymicrobial abdominal sepsis in vivo. Finally, the impact of S1PR4 deficiency on antibody production after immunization with T cell dependent antigens was assessed.ResultsLoss of S1PR4 resulted in minor alterations of the splenic architecture concerning the presence of B cell follicles. After sepsis induction, the germinal center response was severely impaired in S1PR4-deficient animals. Splenic B cells showed reduced motility in the absence of S1PR4. However, titres of specific antibodies showed only minor reductions in S1PR4-deficient animals.DiscussionThese observations suggest that S1P signaling mediated by S1PR4 modifies chemokine-induced splenic B cell chemotaxis, thus modulating splenic microarchitecture, GC formation and T-cell dependent antibody production.</p