How Officers Create Guardianship: An Agent-based Model of Policing

Crime is a complex phenomenon, emerging from the interactions of offenders, victims, and their environment, and in particular from the presence or absence of capable guardians. Researchers have historically struggled to understand how police officers create guardianship. This presents a challenge because, in order to understand how to advise the police, researchers must have an understanding of how the current system works. The work presents an agent-based model that simulates the movement of police vehicles, using a record of real calls for service and real levels of police staffing in spatially explicit environments to emulate the demands on the police force. The GPS traces of the simulated officers are compared with real officer movement GPS data in order to assess the quality of the generated movement patterns. The model represents an improvement on existing standards of police simulation, and points the way toward more nuanced understandings of how police officers influence the criminological environment

Developing an online cooperative police patrol routing strategy

A cooperative routing strategy for daily operations is necessary to maintain the effects of hotspot policing and to reduce crime and disorder. Existing robot patrol routing strategies are not suitable, as they omit the peculiarities and challenges of daily police patrol including minimising the average time lag between two consecutive visits to hotspots, as well as coordinating multiple patrollers and imparting unpredictability to patrol routes. In this research, we propose a set of guidelines for patrol routing strategies to meet the challenges of police patrol. Following these guidelines, we develop an innovative heuristic-based and Bayesian-inspired real-time strategy for cooperative routing police patrols. Using two real-world cases and a benchmark patrol strategy, an online agent-based simulation has been implemented to testify the efficiency, flexibility, scalability, unpredictability, and robustness of the proposed strategy and the usability of the proposed guidelines

The Puck Stops Here: Evolving Social Norms of Helmet Usage in the National Hockey League

Since the mid 1960s, the use of safety helmets in the National Hockey League (NHL) went from virtually nil to almost universal adoption. Despite horrific injuries sustained by players early in the history of the sport, widespread helmet adoption did not take place immediately. Using the NHL as an example, this paper examines the process of emerging norms in a social group, considering peer influence and exogenous policy impacts. The historical circumstances surrounding the NHL helmet usage policy changes are presented, along with a brief survey of the social science modeling of cultural norms. The study presents a peer-influence model in which players helmet usage decisions are influenced by their immediate social network and an exogenous mandate requiring helmet usage for new players. Model results are compared to actual NHL helmet usage trends based on data extracted by review of NHL game footage. The results show eventual dominance of helmet usage, but without the wide fluctuations in the actual historical adoption trends. The study is of interest to policy makers comparing interventionist strategies versus social network based approaches for influencing cultural norms of behavior

Social phobia following maprotiline: the first case report

This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Characterization of Endothelial Progenitor Cell Interactions with Human Tropoelastin.

The deployment of endovascular implants such as stents in the treatment of cardiovascular disease damages the vascular endothelium, increasing the risk of thrombosis and promoting neointimal hyperplasia. The rapid restoration of a functional endothelium is known to reduce these complications. Circulating endothelial progenitor cells (EPCs) are increasingly recognized as important contributors to device re-endothelialization. Extracellular matrix proteins prominent in the vessel wall may enhance EPC-directed re-endothelialization. We examined attachment, spreading and proliferation on recombinant human tropoelastin (rhTE) and investigated the mechanism and site of interaction. EPCs attached and spread on rhTE in a dose dependent manner, reaching a maximal level of 56±3% and 54±3%, respectively. EPC proliferation on rhTE was comparable to vitronectin, fibronectin and collagen. EDTA, but not heparan sulfate or lactose, reduced EPC attachment by 81±3%, while full attachment was recovered after add-back of manganese, inferring a classical integrin-mediated interaction. Integrin αVβ3 blocking antibodies decreased EPC adhesion and spreading on rhTE by 39±3% and 56±10% respectively, demonstrating a large contribution from this specific integrin. Attachment of EPCs on N-terminal rhTE constructs N25 and N18 accounted for most of this interaction, accompanied by comparable spreading. In contrast, attachment and spreading on N10 was negligible. αVβ3 blocking antibodies reduced EPC spreading on both N25 and N18 by 45±4% and 42±14%, respectively. In conclusion, rhTE supports EPC binding via an integrin mechanism involving αVβ3. N25 and N18, but not N10 constructs of rhTE contribute to EPC binding. The regulation of EPC activity by rhTE may have implications for modulation of the vascular biocompatibility of endovascular implants

Identification of a novel splice variant form of the influenza a virus m2 ion channel with an antigenically distinct ectodomain

Segment 7 of influenza A virus produces up to four mRNAs. Unspliced transcripts encode M1, spliced mRNA2 encodes the M2 ion channel, while protein products from spliced mRNAs 3 and 4 have not previously been identified. The M2 protein plays important roles in virus entry and assembly, and is a target for antiviral drugs and vaccination. Surprisingly, M2 is not essential for virus replication in a laboratory setting, although its loss attenuates the virus. To better understand how IAV might replicate without M2, we studied the reversion mechanism of an M2-null virus. Serial passage of a virus lacking the mRNA2 splice donor site identified a single nucleotide pseudoreverting mutation, which restored growth in cell culture and virulence in mice by upregulating mRNA4 synthesis rather than by reinstating mRNA2 production. We show that mRNA4 encodes a novel M2-related protein (designated M42) with an antigenically distinct ectodomain that can functionally replace M2 despite showing clear differences in intracellular localisation, being largely retained in the Golgi compartment. We also show that the expression of two distinct ion channel proteins is not unique to laboratory-adapted viruses but, most notably, was also a feature of the 1983 North American outbreak of H5N2 highly pathogenic avian influenza virus. In identifying a 14th influenza A polypeptide, our data reinforce the unexpectedly high coding capacity of the viral genome and have implications for virus evolution, as well as for understanding the role of M2 in the virus life cycle

Negative life events and suicide risk in college students: Conditional indirect effects of hopelessness and self-compassion

Objective: Suicide risk is a significant public health concern for college students and may be exacerbated by hopelessness resulting from negative life events (NLE), yet may be ameliorated by self-compassion. We examined the mediating role of hopelessness in the relation between NLE and suicidal behavior, and the moderating influence of self-compassion on all model paths. Participants: Participants were 338 undergraduates (89% white; 67% female). Data were collected from December 2014 to December 2015. Methods: Participants completed the Life Events Checklist for College Students, Beck Hopelessness Inventory, Self-Compassion Scale, and Suicidal Behaviors Questionnaire – Revised. Results: Negative life events were related to greater hopelessness and, in turn, to more suicidal behavior, yet self-compassion attenuated this effect. Conclusions: Self-compassion may buffer the NLE–hopelessness linkage, thereby reducing suicide risk among college students. Therapeutic promotion of self-compassion, and reduction of hopelessness, may be important suicide prevention strategies on college campuses

Stimulus-Dependent Adjustment of Reward Prediction Error in the Midbrain

Previous reports have described that neural activities in midbrain dopamine areas are sensitive to unexpected reward delivery and omission. These activities are correlated with reward prediction error in reinforcement learning models, the difference between predicted reward values and the obtained reward outcome. These findings suggest that the reward prediction error signal in the brain updates reward prediction through stimulus–reward experiences. It remains unknown, however, how sensory processing of reward-predicting stimuli contributes to the computation of reward prediction error. To elucidate this issue, we examined the relation between stimulus discriminability of the reward-predicting stimuli and the reward prediction error signal in the brain using functional magnetic resonance imaging (fMRI). Before main experiments, subjects learned an association between the orientation of a perceptually salient (high-contrast) Gabor patch and a juice reward. The subjects were then presented with lower-contrast Gabor patch stimuli to predict a reward. We calculated the correlation between fMRI signals and reward prediction error in two reinforcement learning models: a model including the modulation of reward prediction by stimulus discriminability and a model excluding this modulation. Results showed that fMRI signals in the midbrain are more highly correlated with reward prediction error in the model that includes stimulus discriminability than in the model that excludes stimulus discriminability. No regions showed higher correlation with the model that excludes stimulus discriminability. Moreover, results show that the difference in correlation between the two models was significant from the first session of the experiment, suggesting that the reward computation in the midbrain was modulated based on stimulus discriminability before learning a new contingency between perceptually ambiguous stimuli and a reward. These results suggest that the human reward system can incorporate the level of the stimulus discriminability flexibly into reward computations by modulating previously acquired reward values for a typical stimulus