Robust One Period Option Modelling

AMS classifications: 90C15; 90C20; 90C90; 49M29;return on investment;option pricing models;optimization;portfolio investment

2016 Jeffrey M. Hoeg Award Lecture: Immune Checkpoints in Atherosclerosis: Toward Immunotherapy for Atheroprotection

Innate and adaptive immune effector mechanisms, in conjunction with hyperlipidemia, are important drivers of atherosclerosis. The interaction between the different immune cells and the secretion of cytokines and chemokines determine the progression of atherosclerosis. The activation or dampening of the immune response is tightly controlled by immune checkpoints. Costimulatory and coinhibitory immune checkpoints represent potential targets for immune modulatory therapies for atherosclerosis. This review will discuss the current knowledge on immune checkpoints in atherosclerosis and the clinical potential of immune checkpoint targeted therapy for atherosclerosis

Robust One Period Option Modelling

AMS classifications: 90C15; 90C20; 90C90; 49M29;

UB als Learning Space

Vanouds hebben bibliotheken instructie verzorgd voor studenten en anderen om informatie te leren zoeken en vinden. In de elektronische omgeving zijn deze informatievaardigheden nog meer van belang. UKB, het samenwerkingsverband tussen universiteitsbibliotheken en de KB, heeft de werkgroep Learning Spaces ingesteld om voorstellen te doen voor de verdere ontwikkeling van de informatievoorziening in de elektronische leeromgeving

Lymphocytic tumor necrosis factor receptor superfamily co-stimulatory molecules in the pathogenesis of atherosclerosis

Purpose of reviewThe role of lymphocytes in the chronic inflammatory disease atherosclerosis has emerged over the past decade. Co-stimulatory molecules of the heterogeneous tumor necrosis factor receptor superfamily play a pivotal role in lymphocyte activation, proliferation and differentiation. Here we describe the immune modulatory properties and mechanisms of four tumor necrosis factor receptor superfamily members in atherosclerosis.Recent findingsCD40/CD40L, OX40L/OX40, CD70/CD27 and CD137/CD137L are present in human atherosclerotic plaques and have shown strong immune modulatory functions in atherosclerosis, resulting in either atherogenic or atheroprotective effects in mouse models of atherosclerosis.SummaryInsight into the immune modulatory mechanisms of co-stimulatory interactions in atherosclerosis can contribute to clinical exploitation of these interactions in the treatment of cardiovascular disease

CD40-CD40L: Linking pancreatic, adipose tissue and vascular inflammation in type 2 diabetes and its complications

Numerous epidemiological studies have consistently demonstrated the strong association between type 2 diabetes mellitus (T2DM) and an increased risk to develop cardiovascular disease. The pathogenesis of T2DM and its complications are characterized by pancreatic, adipose tissue and vascular inflammation. CD40 and CD40L, members of the tumour necrosis factor (receptor) TNF(R) family, are well known for their role in immunity and inflammation. Here we give an overview on the role of CD40-CD40L interactions in the pathogenesis of T2DM with a special focus on pancreatic, adipose tissue and vascular inflammation. In addition, we explore the role of soluble CD40L (sCD40L) as a potential biomarker for the development of cardiovascular disease in T2DM subjects. Finally, the therapeutic potential of CD40-CD40L inhibition in T2DM is highlighted

Immunotherapy and cardiovascular diseases: novel avenues for immunotherapeutic approaches

As current therapies for cardiovascular disease (CVD), predominantly based on lipid lowering, still face an unacceptable residual risk, novel treatment strategies are being explored. Besides lipids, inflammatory processes play a major role in the pathogenesis of atherosclerosis, the underlying cause of the majority of CVD. The first clinical trials targeting the interleukin-1 beta-inflammasome axis have shown that targeting this pathway is successful in reducing cardiovascular events but did not decrease overall CVD mortality. Hence, novel and improved immunotherapeutics to treat CVD are being awaited