The PTPN22 C1858T gene variant is associated with proinsulin in new-onset type 1 diabetes

<p>Abstract</p> <p>Background</p> <p>The protein tyrosine phosphatase nonreceptor type 2 (<it>PTPN22</it>) has been established as a type 1 diabetes susceptibility gene. A recent study found the C1858T variant of this gene to be associated with lower residual fasting C-peptide levels and poorer glycemic control in patients with type 1 diabetes. We investigated the association of the C1858T variant with residual beta-cell function (as assessed by stimulated C-peptide, proinsulin and insulin dose-adjusted HbA_1c), glycemic control, daily insulin requirements, diabetic ketoacidosis (DKA) and diabetes-related autoantibodies (IA-2A, GADA, ICA, ZnT8Ab) in children during the first year after diagnosis of type 1 diabetes.</p> <p>Methods</p> <p>The C1858T variant was genotyped in an international cohort of children (n = 257 patients) with newly diagnosed type 1 diabetes during 12 months after onset. We investigated the association of this variant with liquid-meal stimulated beta-cell function (proinsulin and C-peptide) and antibody status 1, 6 and 12 months after onset. In addition HbA_1cand daily insulin requirements were determined 1, 3, 6, 9 and 12 months after diagnosis. DKA was defined at disease onset.</p> <p>Results</p> <p>A repeated measurement model of all time points showed the stimulated proinsulin level is significantly higher (22%, p = 0.03) for the T allele carriers the first year after onset. We also found a significant positive association between proinsulin and IA levels (est.: 1.12, p = 0.002), which did not influence the association between <it>PTPN22 </it>and proinsulin (est.: 1.28, p = 0.03).</p> <p>Conclusions</p> <p>The T allele of the C1858T variant is positively associated with proinsulin levels during the first 12 months in newly diagnosed type 1 diabetes children.</p

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?