Measurement and Pricing of Risk in Insurance Markets

The theory and practice of risk measurement provides a point of intersection between risk management, economic theories of choice under risk, financial economics, and actuarial pricing theory. This article provides a review of these interrelationships, from the perspective of an insurance company seeking to price the risks that it underwrites. We examine three distinct approaches to insurance risk pricing, all being contingent on the concept of risk measures. Risk measures can be interpreted as representations of risk orderings, as well as absolute (monetary) quantifiers of risk. The first approach can be called an “axiomatic” one, whereby the price for risks is calculated according to a functional determined by a set of desirable properties. The price of a risk is directly interpreted as a risk measure and may be induced by an economic theory of price under risk. The second approach consists in contextualizing the considerations of the risk bearer by embedding them in the market where risks are traded. Prices are calculated by equilibrium arguments, where each economic agent's optimization problem follows from the minimization of a risk measure. Finally, in the third approach, weaknesses of the equilibrium approach are addressed by invoking alternative valuation techniques, the leading paradigm among which is arbitrage pricing. Such models move the focus from individual decisiontakers to abstract market price systems and are thus more parsimonious in the amount of information that they require. In this context, risk measures, instead of characterizing individual agents, are used for determining the set of price systems that would be viable in a market

Holistic health record for Hidradenitis suppurativa patients.

Hidradenitis suppurativa (HS) is a recurrent inflammatory skin disease with a complex etiopathogenesis whose treatment poses a challenge in the clinical practice. Here, we present a novel integrated pipeline produced by the European consortium BATMAN (Biomolecular Analysis for Tailored Medicine in Acne iNversa) aimed at investigating the molecular pathways involved in HS by developing new diagnosis algorithms and building cellular models to pave the way for personalized treatments. The objectives of our european Consortium are the following: (1) identify genetic variants and alterations in biological pathways associated with HS susceptibility, severity and response to treatment; (2) design in vitro two-dimensional epithelial cell and tri-dimensional skin models to unravel the HS molecular mechanisms; and (3) produce holistic health records HHR to complement medical observations by developing a smartphone application to monitor patients remotely. Dermatologists, geneticists, immunologists, molecular cell biologists, and computer science experts constitute the BATMAN consortium. Using a highly integrated approach, the BATMAN international team will identify novel biomarkers for HS diagnosis and generate new biological and technological tools to be used by the clinical community to assess HS severity, choose the most suitable therapy and follow the outcome.This work was supported by a Biomolecular Analyses for Tailored Medicine in AcneiNversa (BATMAN) project, funded by ERA PerMed (JTC_2018) through the Italian Ministry of Health, the “Fondazione Regionale per la Ricerca Biomedica” (FRRB), the Slovenian Ministry of Education, Science, and Sport (MIZŠ), the Austrian Science fund (I 4229), the Federal Ministry of Education and Research Germany (BMBF), and ANR automate (ANR-20-CE15-0018-01). This work was also supported by and by a grant from the Institute for Maternal and Child Health IRCCS ‘Burlo Garofolo/Italian Ministry of Health (RC16/2018) and by a Starting Grant (SG-2019-12369421) founded by the Italian Ministry of Health. Figures were created with BioRender.com

Tratado de obstetricia

Na port.: Con 614 figuras en negro y colo

The effects of apnea on the haemostaseologic system in healthy male test persons

In der hier vorliegenden Arbeit wurde der Einfluss von akutem Sauerstoffmangel auf die Blutgerinnung und die Thrombozytenaktivität bei 15 männlichen, gesunden Probanden untersucht. Das obstruktive Schlafapnoesyndrom, welches durch wiederholte Phasen von Apnoe und Hypopnoe gekennzeichnet ist, prädisponiert für kardiovaskuläre Erkrankungen und ist ein großer Risikofaktor für thromboembolische Ereignisse. Es wird vermutet, dass dieses mit einer Gerinnungsaktivierung durch den akuten Sauerstoffmangel, der mit den Apnoephasen einhergeht, zusammenhängt. Anhand dieser Vorstellung wurde ein Versuchsaufbau generiert, der im Kleinen eine Situation wie bei einem OSAS simulieren sollte. Die Probanden wurden an zwei aufeinander folgenden Tagen einbestellt und der Versuch durchgeführt. Per Zufall wurde entschieden, ob zunächst der Luftanhalteversuch oder die Kontrolle durchgeführt wurde. Der Proband legte sich hin, es erfolgte die erste Blutentnahme, dann der Luftanhalteversuch (4x30 Sekunden Luftanhalten, jeweils im Wechsel mit 4x30 Sekunden Atmen, zum Schluss einmal solange wie möglich Luftanhalten), sofort im Anschluss erfolgte die nächste Blutentnahme und nach 30 Minuten die letzte Blutentnahme. Der Kontrolltag wurde in der gleichen Abfolge durchgeführt, nur der Luftanhalteversuch fehlte. Es wurden die Herzfrequenz und die Sauerstoffsättigung bestimmt. Als Marker für das thrombozytäre System wurden die Thrombozytenzahl und die Thrombozytenaktivität anhand des MPC bestimmt. TPZ, PTT, Fibrinogen und Faktor VIII wurden als Marker für das Gerinnungssytem bestimmt. Um eine erhöhte Thromboseneigung nachzuweisen, wurden PAI-1 und die D-Dimere bestimmt. Ein weiterer, relativ neuer Parameter, das ETP, als Marker für eine Hypo- bzw. Hyperkoagulabilität, wurde ebenfalls bestimmt. Das ETP gilt als neuer Ansatz in der Gerinnungsdiagnostik, da mit diesem Parameter das Hämostasesystem als Ganzes untersucht wird. Es wird die Menge an gebildetem Thrombin gemessen. Die Herzfrequenz sank im Mittel von 75 auf 63 Schlägen pro Minute ab. Die Sauerstoffsättigung sank im Mittel von 99% auf 94% ab. Es wurde keine gesteigerte Thrombozytenaktivität gemessen. Das MPC, welches ein Parameter für die Thrombozytenaktivierung ist, blieb unverändert. Die Thrombozytenzahl änderte sich nur geringfügig und in einem physiologisch nicht relevanten Ausmaß. Die PTT als Maß für das endogene Gerinnungssystem blieb unverändert. Die TPZ als Maß für das exogene Gerinnungssystem erfuhr keine wesentlichen Änderungen. Auch der Faktor VIII erfuhr ebenfalls keine signifikante Änderung. Das Fibrinogen zeigte keine biologisch relevanten Änderungen während des Luftanhalteversuchs. Sowohl PAI-1 als auch die D-Dimere, als Maß für eine Thrombophilie, blieben unverändert. Das ETP, als Maß für die Gesamtkoagulabilität, erfuhr während des Versuches keine Änderungen. Für gesunde männliche Probanden konnte damit weder eine Thrombozytenaktivierung noch eine Gerinnungsaktivierung bei akutem Sauerstoffmangel in dieser Versuchsanordnung nachgewiesen werden.In this thesis we evaluated the influence of apnea on platelets and some parameters of blood coagulation in 15 healthy male volunteers as a model to study sleep apnea. Obstructive sleep apnea syndrome (OSAS), which is characterised by recurrent phases of apnea und hypopnea, predisposes for cardiovascular diseases and is recognised as a risk factor for thromboembolic events. It is suspected that these effects are a consequence of an activation of the coagulation system due to acute hypoxia resulting from recurring phases of apnea and hypopnea during sleep. We thus constructed a model that was supposed to imitate a situation in patients with OSAS. The test person was summoned on two following days and on one day the actual experiment was performed. On one day the subjects constituted their own control group and on the other day they participated the hypoxia experiment or vice versa. The subject rested in supine position after which the first phlebotomy was performed. Then the test person had to hold their breath (4x30 seconds of apnoic period interrupted by 30 seconds of normal breathing, with a last apnoic phase of breath-holding as long as possible). After the last procedure the second blood sample was taken and after 30 minutes the last blood sample was obtained. On the second day the test persons lay in a supine position and the blood samples obtained at the same times as the previous day. We measured the heart rate and the oxygen saturation. As a marker for the thrombocytic system we performed a thrombocyte count and measured the mean platelet component (MPC) as a marker for thrombocyte activation. Thromboplastin time (PT), activated partial Thromboplastin time (aPTT), fibrinogen and factor VIII were quantified. Thrombophilia markers (PAI-1 and D-Dimer) were also measured. A relatively new parameter, endogenous thrombin potential (ETP), which is both a marker for hypo- and hypercoagulability, was evaluated. ETP examines the system of hemostasis as a whole by measuring the total thrombin generation. The heart rate fell from 75 to 63 beats per minute. The saturation of the oxygen fell from 99% to 94%. We did not find an increased activity of the thrombocytes. The MPC as a marker for the activation of the thrombocytes did not change. The total number of thrombocytes only changed marginally and was not thought to be physiologically relevant. The aPTT (endogenous pathway of the coagulation system) did not undergo any changes. The PT (exogenous system of the coagulation) did not change in a significant way as well. No significant changes in the activities of fibrinogen or factor VIII were noticed during the apnea experiment. PAI-1 as well as the D-Dimer as a mirror of thromophilia and thrombosis did not show any signs of relevant change. ETP (total thrombingeneration) as a marker for the coagulability did not undergo any changes during the experiment. Thus, we could not measure either an activation of the thrombocytes or an activation of the coagulation system of the blood during acute oxygen shortage in male, healthy test persons in these experiments