Be alarmed. Some reflections about the COVID-19 risk communication in Germany

2020 Informa UK Limited, trading as Taylor & Francis Group. This article addresses six typical communication traps regarding COVID-19 which can also be observed with respect to other risk topics. First, we argue that risk communication can slide into what is known as \u27risk kitsch\u27. This refers to the misconception that avoiding risk automatically results in safety. However, the avoidance of one risk always leads to other risks. Life without risk is not possible. We go on to scrutinize the unquestioning belief in numbers. It would seem that describing risks in terms of numbers promises to overcome chaos, provide order, and create a sense of agency over the threatening health risks. However, is this really so? Don\u27t numbers also lie, lead astray, or misrepresent? The third issue we examine is the impact of pictures and individual cases on risk perception. What key picture-or rather what particular graphic-shapes the risk perception of COVID-19? What message does it convey? Does it bias and mislead us? The fourth issue involves the use of COVID-19 modeling studies which aim to provide answers to a number of essential questions: How bad can it get? What does it depend on? What can be done? Yet it is clear that not all assumptions underlying modeling computations are valid. Information content is not necessarily the same as reality content. The fifth section examines the question of how politics can navigate through the crisis. Is it navigating with a faulty compass? How defective is the compass? We then consider the question of morality, which is a crucial issue during a pandemic with its life- and-death stakes. Are moral evaluations always helpful? Or does a rigorously moral discourse hinder the necessary consideration of alternative options in dealing with the pandemic? Finally, we will draw some conclusions. What could better risk communication on COVID-19 look like? What can be improved, and how?

Microprocessor-based long term cardiorespirography. II. Status evaluation in term and premature newborns

Peer Reviewe

Disease progression and search for monogenic diabetes among children with new onset type 1 diabetes negative for ICA, GAD- and IA-2 Antibodies

Background: To investigate disease progression the first 12 months after diagnosis in children with type 1 diabetes negative (AAB negative) for pancreatic autoantibodies [islet cell autoantibodies(ICA), glutamic acid decarboxylase antibodies (GADA) and insulinoma-associated antigen-2 antibodies (IA-2A)]. Furthermore the study aimed at determining whether mutations in KCNJ11, ABCC8, HNF1A, HNF4A or INS are common in AAB negative diabetes. Materials and methods: In 261 newly diagnosed children with type 1 diabetes, we measured residual β-cell function, ICA, GADA, and IA-2A at 1, 6 and 12 months after diagnosis. The genes KCNJ11, ABCC8, HNF1A, HNF4A and INS were sequenced in subjects AAB negative at diagnosis. We expressed recombinant K-ATP channels in Xenopus oocytes to analyse the functional effects of an ABCC8 mutation. Results: Twenty-four patients (9.1%) tested AAB negative after one month. Patients, who were AAB-negative throughout the 12-month period, had higher residual β-cell function (P = 0.002), lower blood glucose (P = 0.004), received less insulin (P = 0.05) and had lower HbA1c (P = 0.02) 12 months after diagnosis. One patient had a heterozygous mutation leading to the substitution of arginine at residue 1530 of SUR1 (ABCC8) by cysteine. Functional analyses of recombinant K-ATP channels showed that R1530C markedly reduced the sensitivity of the K-ATP channel to inhibition by MgATP. Morover, the channel was highly sensitive to sulphonylureas. However, there was no effect of sulfonylurea treatment after four weeks on 1.0-1.2 mg/kg/24 h glibenclamide. Conclusion: GAD, IA-2A, and ICA negative children with new onset type 1 diabetes have slower disease progression as assessed by residual beta-cell function and improved glycemic control 12 months after diagnosis. One out of 24 had a mutation in ABCC8, suggesting that screening of ABCC8 should be considered in patients with AAB negative type 1 diabetes. </p