Chikungunya virus has become a global health threat, spreading to the industrial world of Europe and the Americas; no treatment or prophylactic vaccine is available. Since the late 1960s much effort has been put into the development of a vaccine, and several heterogeneous strategies have already been explored. Only two candidates have recently qualified to enter clinical phase II trials, a chikungunya virus-like particle-based vaccine and a recombinant live attenuated measles virus-vectored vaccine.This review focuses on the current status of vaccine development against chikungunya virus in humans and discusses the diversity of immunization strategies, results of recent human trials and promising vaccine candidates.

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Background Despite the increasing use of potent P2Y12 inhibitors, further atherothrombotic events still impair the prognosis of many acute coronary syndrome (ACS) patients. This may in part be attributable to intact platelet aggregation via the human thrombin receptors protease‐activated receptor (PAR)‐1 and PAR‐4. Objective We studied PAR mediated platelet aggregation in ACS patients following percutaneous coronary intervention (PCI) with stent implantation in a cross‐sectional study. Methods Platelet aggregation to ADP as well as to the PAR‐1 agonist SFLLRN and the PAR‐4 agonist AYPGKF was assessed by multiple electrode aggregometry in 194 ACS patients on dual antiplatelet therapy with aspirin and either prasugrel (n = 114) or ticagrelor (n = 80) 3 days after PCI. Results Based on the consensus cutoff value, high on‐treatment residual platelet reactivity to ADP (HRPR ADP) was observed in only 2 prasugrel‐treated patients. Both patients with HRPR ADP had also a normal response to SFLLRN and AYPGKF. Among the 112 prasugrel‐treated patients with adequate P2Y12 inhibition, 50 patients (45%) still had a normal response to SFLLRN, and 70 patients (63%) still had a normal response to AYPGKF. Among the 80 ticagrelor‐treated patients with adequate P2Y12 inhibition, 25 patients (31%) still had a normal response to SFLLRN, and 50 (63%) still had a normal response to AYPGKF. Conclusion Normal platelet aggregation via PAR‐1 and PAR‐4 is preserved in many patients with adequate P2Y12 inhibition by prasugrel and ticagrelor. The present findings may at least in part explain adverse ischemic events despite potent P2Y12 inhibition.

BackgroundCase-Based Learning (CBL) has seen widespread implementation in undergraduate education since the early 1920s. Ample data has shown CBL to be an enjoyable and motivational didactic tool, and effective in assisting the expansion of declarative and procedural knowledge in academia. Although a plethora of studies apply multiple choice questions (MCQs) in their investigation, few studies measure CBL or case-based blended learning (CBBL)-mediated changes in students’ procedural knowledge in practice or employ comparison or control groups in isolating causal relationships.MethodsUtilizing the flexibilities of an e-learning platform, a CBBL framework consisting of a) anonymized patient cases, b) case-related textbook material and online e-CBL modules, and c) simulated patient (SP) contact seminars, was developed and implemented in multiple medical fields for undergraduate medical education. Additionally, other fields saw a solo implementation of e-CBL in the same format. E- cases were constructed according to the criteria of Bloom’s taxonomy.In this study, Objective Structured Clinical Examination (OSCE) results from 1886 medical students were analyzed in total, stratified into the following groups: medical students in 2013 (n = 619) before CBBL implementation, and after CBBL implementation in 2015 (n = 624) and 2016 (n = 643).ResultsA significant improvement (adjusted p = .002) of the mean OSCE score by 1.02 points was seen between 2013 and 2015 (min = 0, max = 25).ConclusionE-Case-Based Learning is an effective tool in improving performance outcomes and may provide a sustainable learning platform for many fields of medicine in future.

Platelet–endothelial interactions have a critical role in microcirculatory function, which maintains tissue homeostasis. The subtle equilibrium between platelets and the vessel wall is disturbed by the coronavirus disease 2019 (COVID-19), which affects all three components of Virchow’s triad (endothelial injury, stasis and a hypercoagulable state). Endotheliitis, vasculitis, glycocalyx degradation, alterations in blood flow and viscosity, neutrophil extracellular trap formation and microparticle shedding are only few pathomechanisms contributing to endothelial damage and microthrombosis resulting in capillary plugging and tissue ischemia. In the following opinion paper, we discuss major pathological processes leading to microvascular endothelial activation and thrombosis formation as a possible major adverse factor driving the deterioration of patient disease course in severe COVID-19.