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As we draw closer and closer to a complete deregulation in this sector, looking back on the complex evolution undergone by air transport and its market may be a useful exercise. The intrinsic danger of its trend toward globalisation is due to the fact that there is still no strict monitoring of fleets that can truly guarantee man's safety. With reference to the relation between ethics and economics, the companies in charge of running airports and airlines must join forces in order to prevent aircrafts that have not passed the most rigorous test from flying over cities and countries. Sadly, this is not yet the case. Furthermore, national government and transport authorities ought to give top-most priority to the task of monitoring both the secondary market of aircrafts and spare parts and the reliability of operator.

Biotechnology's promises has been widely recognized as a major enterprise accelerating the commodification of the biological. After the 9/11 events and the subsequent anthrax letters, biotechnologies have additionally been described as contributing to the construction of biosecurity risks. This paper proposes to investigate the collaboration between the FBI and the DIYbio (Do-It-Yourself biology) network as a case study illustrating the productive entanglement of biological risks and promises. To do so, the paper explores the social construction of risks and promises associated with the vision of distributed biotechnologies as enacted in this collaboration. We argue that the FBI needs to police the DIYbio network in order to disseminate a specific notion of bioterrorist risk, while, in a counter-intuitive manner, the DIYbio network benefits from being policed by the FBI as it helps them disseminate their socio-technological vision. If the entanglement of technoscientific risks and promises is a well established finding of the STS literature, our case study suggests that such entanglement now additionally comprises the sphere of biosecurity and the promises of a distributed biotechnology available to everyone.

In recent years, new methods to engage citizens in deliberative processes of governments and institutions have been studied. Such methodologies have become a necessity to assure the efficacy and longevity of policies. Several tools and solutions have been proposed while trying to achieve such a goal. The dual problem to citizen engagement is how to provide policy-makers with useful and actionable insights stemming from those processes. In this paper, we propose a research featuring a method and implementation of a crowdsourcing and co-creation technique that can provide value to both citizens and policy-makers engaged in the policy-making process. Thanks to our methodology, policy-makers can design challenges for citizens to partake, cooperate and provide their input. We also propose a web-based tool that allow citizens to participate and produce content to support the policy-making processes through a gamified interface that focuses on emotional and vision-oriented content.

Acknowledgements We thank Sabine Kafert-Kasting, Hannover Medical School, who participated in the writing and technical editing of the manuscript. Conflict of interest: C.G.T. holds patents in the field of cardiovascular disease. M.G. and T.T. hold patents in the field of non-coding RNAs and therapeutic applications thereof. T.T. is the founder and shareholder of Cardior Pharmaceuticals GmbH. T.T. reports fees/support from Novo Nordisk, Takeda, Amicus Therapeutics, Böhringer Ingelheim, and Sanofi-Genzyme (outside the scope of this position paper). S.H. reports personal fees from Astra Zeneca as a consultant preclinical development, personal fees from Cellprothera, as well as grants from Pfizer outside the submitted work. All other authors have nothing to disclose. Funding This work was supported by the British Heart Foundation, in particular, BHF Project Grant No. PG/17/64/33205 (to D.D.); European Union Commission's Seventh Framework program (GA 305507 [HOMAGE] to S.H.) and EU Horizon 2020 project CARDIOREGENIX (GA 825670 to T.T.); ERA-Net-CVD project MacroERA (01KL1706 to S.H.); IMI2-CARDIATEAM (No. 821508 to S.H.); Netherlands Cardiovascular Research Initiative—an initiative with support of the Dutch Heart Foundation (CVON2016-Early HFPEF, 2015-10; CVON She-PREDICTS, 2017-21; and CVON Arena-PRIME, 2017-18 to S.H.; CVON 2018-28 & 2012-06 Heart Brain Connection; and CVON-Dosis 2014-20 to J.v.d.V., A.H., A.L., and D.H.); Research Foundation Flanders FWO (G091018N and G0B5930N to S.H.); Deutsche Forschungsgemeinschaft (KFO311/TH903/20 to T.T.); AIRC (IG 2016 19032 to S.Z.); Dutch Federation of University Medical Centres, the Netherlands Organisation for Health Research and Development and the Royal Netherlands Academy of Sciences, and the Netherlands Organization for Sciences-ZonMW (VICI 91818602 to J.v.d.V.) as well as Project NETDIAMOND (POCI-01-0145-FEDER-016385), supported by European Structural and Investment Funds, Lisbon's Regional Operational Program 2020 and national funds from the Portuguese Foundation for Science and Technology (to I. F.-P.). ; Peer reviewed ; Publisher PDF

JV is supported by the Netherlands Cardiovascular Research Initiative, an initiative with support of the Dutch Heart Foundation, CVON2014-40 DOSIS. SH has received funding from the European Union Commission's Seventh Framework programme under grant agreement N° 305507 (HOMAGE), N° 602904 (FIBROTARGETS) and FP7-Health-2013- Innovations-1 N° 602156 (HECATOS). . We acknowledge the support from the Netherlands Cardiovascular Research Initiative, an initiative with support of the Dutch Heart Foundation, CVON2011-ARENA, CVON2016-Early HFPEF, and ShePREDICTS. This research is cofinanced as a PPP-allowance Research and Innovation by the Ministry of Economic Affairs within Top Sector Life sciences & Health. This research was co-funded by the C3 project "Vision Core Leuven" of the Leuven University ; Peer reviewed ; Publisher PDF

Dilated cardiomyopathy (DCM) frequently affects relatively young, economically, and socially active adults, and is an important cause of heart failure and transplantation. DCM is a complex disease and its pathological architecture encounters many genetic determinants interacting with environmental factors. The old perspective that every pathogenic gene mutation would lead to a diseased heart, is now being replaced by the novel observation that the phenotype depends not only on the penetrance—malignancy of the mutated gene—but also on epigenetics, age, toxic factors, pregnancy, and a diversity of acquired diseases. This review discusses how gene mutations will result in mutation-specific molecular alterations in the heart including increased mitochondrial oxidation (sarcomeric gene e.g. TTN), decreased calcium sensitivity (sarcomeric genes), fibrosis (e.g. LMNA and TTN), or inflammation. Therefore, getting a complete picture of the DCM patient will include genomic data, molecular assessment by preference from cardiac samples, stratification according to co-morbidities, and phenotypic description. Those data will help to better guide the heart failure and anti-arrhythmic treatment, predict response to therapy, develop novel siRNA-based gene silencing for malignant gene mutations, or intervene with mutation-specific altered gene pathways in the heart. ; The authors acknowledge the support from the Netherlands Cardiovascular Research Initiative, with support of the Dutch Heart Foundation, CVON2011-ARENA, CVON2018-ARENA PRIME, CVON2016-Early HFPEF, and CVON 2017-ShePREDICTS to S.H. S.H. received funding from the European Union Commission's Seventh Framework programme under grant agreement N 305507 (HOMAGE), N 602904 (FIBROTARGETS), and FP7-Health-2013- Innovations-1 N 602156 (HECATOS). E.A. received support from the EU funded project INHERITANCE (n241924), from the Italian Ministry of Health, from the Cariplo Foundation, and from the Magica Onlus Charity. A.B. received support from the Erasme Foundation (ULB) and ...

Acknowledgements S.H. acknowledges the support from the Netherlands Cardiovascular Research Initiative, an initiative with support of the Dutch Heart Foundation, CVON2016-Early HFPEF, 2015-10, and CVON She-PREDICTS, grant 2017-21, CVON-Arena-PRIME, European Union Commission's Seventh Framework programme under grant agreement n. 305507 (HOMAGE) and n. 602904 (FIBROTAR-GETS). D.D. acknowledges support from the British Heart Foundation grants PG/15/108/31928 and FS/16/39/32174, the Josephine Lansdell British Medical Association 2015Award and Tenovus Scotland, G13.10. A.R.L. is supported by the Leducq Foundation Cardio-Oncology Network. Conflict of interest: none declared ; Peer reviewed ; Publisher PDF