Malicious Bayesian Congestion Games

In this paper, we introduce malicious Bayesian congestion games as an extension to congestion games where players might act in a malicious way. In such a game each player has two types. Either the player is a rational player seeking to minimize her own delay, or - with a certain probability - the player is malicious in which case her only goal is to disturb the other players as much as possible. We show that such games do in general not possess a Bayesian Nash equilibrium in pure strategies (i.e. a pure Bayesian Nash equilibrium). Moreover, given a game, we show that it is NP-complete to decide whether it admits a pure Bayesian Nash equilibrium. This result even holds when resource latency functions are linear, each player is malicious with the same probability, and all strategy sets consist of singleton sets. For a slightly more restricted class of malicious Bayesian congestion games, we provide easy checkable properties that are necessary and sufficient for the existence of a pure Bayesian Nash equilibrium. In the second part of the paper we study the impact of the malicious types on the overall performance of the system (i.e. the social cost). To measure this impact, we use the Price of Malice. We provide (tight) bounds on the Price of Malice for an interesting class of malicious Bayesian congestion games. Moreover, we show that for certain congestion games the advent of malicious types can also be beneficial to the system in the sense that the social cost of the worst case equilibrium decreases. We provide a tight bound on the maximum factor by which this happens.Comment: 18 pages, submitted to WAOA'0

Investigating the Role of T-Cell Avidity and Killing Efficacy in Relation to Type 1 Diabetes Prediction

During the progression of the clinical onset of Type 1 Diabetes (T1D), high-risk individuals exhibit multiple islet autoantibodies and high-avidity T cells which progressively destroy beta cells causing overt T1D. In particular, novel autoantibodies, such as those against IA-2 epitopes (aa1-577), had a predictive rate of 100% in a 10-year follow up (rapid progressors), unlike conventional autoantibodies that required 15 years of follow up for a 74% predictive rate (slow progressors). The discrepancy between these two groups is thought to be associated with T-cell avidity, including CD8 and/or CD4 T cells. For this purpose, we build a series of mathematical models incorporating first one clone then multiple clones of islet-specific and pathogenic CD8 and/or CD4 T cells, together with B lymphocytes, to investigate the interaction of T-cell avidity with autoantibodies in predicting disease onset. These models are instrumental in examining several experimental observations associated with T-cell avidity, including the phenomenon of avidity maturation (increased average T-cell avidity over time), based on intra- and cross-clonal competition between T cells in high-risk human subjects. The model shows that the level and persistence of autoantibodies depends not only on the avidity of T cells, but also on the killing efficacy of these cells. Quantification and modeling of autoreactive T-cell avidities can thus determine the level of risk associated with each type of autoantibodies and the timing of T1D disease onset in individuals that have been tested positive for these autoantibodies. Such studies may lead to early diagnosis of the disease in high-risk individuals and thus potentially serve as a means of staging patients for clinical trials of preventive or interventional therapies far before disease onset

Accuracy of syndrome definitions based on diagnoses in physician claims

<p>Abstract</p> <p>Background</p> <p>Community clinics offer potential for timelier outbreak detection and monitoring than emergency departments. However, the accuracy of syndrome definitions used in surveillance has never been evaluated in community settings. This study's objective was to assess the accuracy of syndrome definitions based on diagnostic codes in physician claims for identifying 5 syndromes (fever, gastrointestinal, neurological, rash, and respiratory including influenza-like illness) in community clinics.</p> <p>Methods</p> <p>We selected a random sample of 3,600 community-based primary care physicians who practiced in the fee-for-service system in the province of Quebec, Canada in 2005-2007. We randomly selected 10 visits per physician from their claims, stratifying on syndrome type and presence, diagnosis, and month. Double-blinded chart reviews were conducted by telephone with consenting physicians to obtain information on patient diagnoses for each sampled visit. The sensitivity, specificity, and positive predictive value (PPV) of physician claims were estimated by comparison to chart review.</p> <p>Results</p> <p>1,098 (30.5%) physicians completed the chart review. A chart entry on the date of the corresponding claim was found for 10,529 (95.9%) visits. The sensitivity of syndrome definitions based on diagnostic codes in physician claims was low, ranging from 0.11 (fever) to 0.44 (respiratory), the specificity was high, and the PPV was moderate to high, ranging from 0.59 (fever) to 0.85 (respiratory). We found that rarely used diagnostic codes had a higher probability of being false-positives, and that more commonly used diagnostic codes had a higher PPV.</p> <p>Conclusions</p> <p>Future research should identify physician, patient, and encounter characteristics associated with the accuracy of diagnostic codes in physician claims. This would enable public health to improve syndromic surveillance, either by focusing on physician claims whose diagnostic code is more likely to be accurate, or by using all physician claims and weighing each according to the likelihood that its diagnostic code is accurate.</p

In search of quality evidence for lifestyle management and glycemic control in children and adolescents with type 2 diabetes: A systematic review

<p>Abstract</p> <p>Background</p> <p>Our purpose was to evaluate the impact of lifestyle behavior modification on glycemic control among children and youth with clinically defined Type 2 Diabetes (T2D).</p> <p>Methods</p> <p>We conducted a systematic review of studies (randomized trials, quasi-experimental studies) evaluating lifestyle (diet and/or physical activity) modification and glycemic control (HbA1c). Our data sources included bibliographic databases (EMBASE, CINAHL^®, Cochrane Library, Medline^®, PASCAL, PsycINFO^®, and Sociological Abstracts), manual reference search, and contact with study authors. Two reviewers independently selected studies that included any intervention targeting diet and/or physical activity alone or in combination as a means to reduce HbA1c in children and youth under the age of 18 with T2D.</p> <p>Results</p> <p>Our search strategy generated 4,572 citations. The majority of citations were not relevant to the study objective. One study met inclusion criteria. In this retrospective study, morbidly obese youth with T2D were treated with a very low carbohydrate diet. This single study received a quality index score of < 11, indicating poor study quality and thus limiting confidence in the study's conclusions.</p> <p>Conclusions</p> <p>There is no high quality evidence to suggest lifestyle modification improves either short- or long-term glycemic control in children and youth with T2D. Additional research is clearly warranted to define optimal lifestyle behaviour strategies for young people with T2D.</p

Etiopathogenesis of type 1 diabetes mellitus: prognostic factors for the evolution of residual β cell function

Type 1A diabetes mellitus (T1ADM) is a progressive autoimmune disease mediated by T lymphocytes with destruction of beta cells. Up to now, we do not have precise methods to assess the beta cell mass, "in vivo" or "ex-vivo". The studies about its genetic susceptibility show strong association with class II antigens of the HLA system (particularly DQ). Others genetics associations are weaker and depend on the population studied. A combination of precipitating events may occur at the beginning of the disease. There is a silent loss of immune-mediated beta cells mass which velocity has an inverse relation with the age, but it is influenced by genetic and metabolic factors. We can predict the development of the disease primarily through the determination of four biochemically islet auto antibodies against antigens like insulin, GAD65, IA2 and Znt8. Beta cell destruction is chronically progressive but at clinical diagnosis of the disease a reserve of these cells still functioning. The goal of secondary disease prevention is halt the autoimmune attack on beta cells by redirecting or dampening the immune system. It is remains one of the foremost therapeutic goals in the T1ADM. Glycemic intensive control and immunotherapeutic agents may preserve beta-cell function in newly diagnosed patients with T1ADM. It may be assessed through C-peptide values, which are important for glycemic stability and for the prevention of chronic complications of this disease. This article will summarize the etiopathogenesis mechanisms of this disease and the factors can influence on residual C-peptide and the strategies to it preservation

Mitral valve surgery for mitral regurgitation caused by Libman-Sacks endocarditis: a report of four cases and a systematic review of the literature

Libman-Sacks endocarditis of the mitral valve was first described by Libman and Sacks in 1924. Currently, the sterile verrucous vegetative lesions seen in Libman-Sacks endocarditis are regarded as a cardiac manifestation of both systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS). Although typically mild and asymptomatic, complications of Libman-Sacks endocarditis may include superimposed bacterial endocarditis, thromboembolic events, and severe valvular regurgitation and/or stenosis requiring surgery. In this study we report two cases of mitral valve repair and two cases of mitral valve replacement for mitral regurgitation (MR) caused by Libman-Sacks endocarditis. In addition, we provide a systematic review of the English literature on mitral valve surgery for MR caused by Libman-Sacks endocarditis. This report shows that mitral valve repair is feasible and effective in young patients with relatively stable SLE and/or APS and only localized mitral valve abnormalities caused by Libman-Sacks endocarditis. Both clinical and echocardiographic follow-up after repair show excellent mid- and long-term results

The extractive industries and development: The resource curse at the micro, meso and macro levels

The resource curse literature has necessarily evolved in a rather fragmented way. While economists, political economists and political scientists have largely focused on the role of mineral abundance in long-term growth with the analysis largely confined to the country (macro) or regional (meso) level, anthropologists, sociologists and other social scientists have explored the development impacts of extractive industries at the community (micro) level. While this has provided a rigorous and comprehensive exploration of extractive industries and their impacts, causal factors that bridge and/or leap-frog these levels tend not to be accounted for. In this paper we examine the evolution of the literature across disciplinary lines and different levels of scale to assess the current status of resource curse debates. In so doing, we aim to explore how an integration of the various multi-scale approaches can help address the persistent problem of the resource curse