Social Media und Geschlecht in der Offenen Kinder- und Jugendarbeit

Social Media spielt in den Lebenswelten von Kindern und Jugendlichen bekanntermassen eine bedeutsame Rolle und die entsprechenden Plattformen können als sozialisationsrelevant begriffen werden. Um identitätsbildende Prozesse, etwa im Zusammenhang mit geschlechtlicher Selbstverortung oder sexueller Orientierung, nachvollziehen zu können, ist eine Auseinandersetzung mit den Medienpraktiken von Kindern und Jugendlichen von hoher Relevanz. Dies betrifft auch das pädagogische Handlungsfeld der Offenen Kinder- und Jugendarbeit, das jungen Menschen als ausserschulisches Tätigkeitsfeld Bildungsgelegenheiten bietet und dabei die Heterogenität der Zielgruppe bestmöglich zu berücksichtigen hat. In diesem Schnittfeld verortet sich der Beitrag, indem er nach der Bedeutung der Kategorien Geschlecht und Sexualität im Kontext der Nutzung von Social Media-Plattformen durch Jugendliche fragt und anhand einer qualitativen Studie relevante Aspekte herausarbeitet, welche Anknüpfungspunkte für eine sich als inklusiv verstehende Medienbildung bieten können

Multi-species population indices for sets of species including rare, disappearing or newly occurring species

NI is funded by Natural Environment Research Council award NE/R016429/1 as part of the UK-SCAPE programme delivering National Capability.Multi-species indices (MSI) are widely used as ecological indicators and as instruments to inform environmental policies. Many of these indices combine species-specific estimates of relative population sizes using the geometric mean. Because the geometric mean is not defined when values of zero occur, usually only commoner species are included in MSIs and zero values are replaced by a small non-zero value. The latter can exhibit an arbitrary influence on the geometric mean MSI. Here, we show how the compound Poisson and the negative binomial model can be used in such cases to obtain an MSI that has similar features to the geometric mean, including weighting halving and doubling of a species’ population equally. In contrast to the geometric mean, these two statistical models can handle zero values in population sizes and thus accommodate newly occurring and temporarily or permanently disappearing species in the MSI. We compare the MSIs obtained by the two statistical models with the geometric mean MSI and measure sensitivity to changes in evenness and to population trends in rare and abundant species. Additionally, we outline sources of uncertainty and discuss how to measure them. We found that, in contrast to the geometric mean and the negative binomial MSI, the compound Poisson MSI is less sensitive to changes in evenness when total abundance is constant. Further, we found that the compound Poisson model can be influenced more than the other two methods by trends of species showing a low interannual variance. The negative binomial MSI is less sensitive to trends in rare species compared with the other two methods, and similarly sensitive to trends in abundant species as the geometric mean. While the two new MSIs have the advantage that they are not arbitrarily influenced by rare, newly appearing and disappearing species, both do not weight all species equally. We recommend replacing the geometric mean MSI with either compound Poisson or negative binomial when there are species with a population size of zero in some years having a strong influence on the geometric mean MSI. Further, we recommend providing additional information alongside the MSIs. For example, it is particularly important to give an evenness index in addition to the compound Poisson MSI and to indicate the number of disappearing and newly occurring species alongside the negative binomial MSI.Publisher PDFPeer reviewe

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

Handlungskonzept zu Social Media und Geschlecht in der Offenen Kinder- und Jugendarbeit

Das Handlungskonzept liefert Wissen rund um Social Media, Geschlecht und Sexualität für die pädagogische Praxis der Offenen Kinder- und Jugendarbeit

Peroxisome Proliferator-Activated Receptor-γ Modulates the Response of Macrophages to Lipopolysaccharide and Glucocorticoids

Although glucocorticoids (GC) represent the most frequently used immunosuppressive drugs, their effects are still not well understood. In our previous studies, we have shown that treatment of monocytes with GC does not cause a global suppression of monocytic effector functions, but rather induces differentiation of a specific anti-inflammatory phenotype. The anti-inflammatory role of peroxisome proliferator-activated receptor (PPAR)-γ has been extensively studied during recent years. However, a relationship between GC treatment and PPAR-γ expression in macrophages has not been investigated so far. Studies using PPAR-γ-deficient mice have frequently provided controversial results. A potential reason is the use of primary cells, which commonly represent inhomogeneous populations burdened with side effects and influenced by bystander cells. To overcome this constraint, we established ER-Hoxb8-immortalized bone marrow-derived macrophages from Ppargfl/fl and LysM-Cre Ppargfl/fl mice in this study. In contrast to primary macrophages, the ER-Hoxb8 system allows the generation of a homogeneous and well-defined population of resting macrophages. We could show that the loss of PPAR-γ resulted in delayed kinetic of differentiation of monocytes into macrophages as assessed by reduced F4/80, but increased Ly6C expression in early phases of differentiation. As expected, PPAR-γ-deficient macrophages displayed an increased pro-inflammatory phenotype upon long-term LPS stimulation characterized by an elevated production of pro-inflammatory cytokines TNF-α, IL1-β, IL-6, IL-12 and a reduced production of anti-inflammatory cytokine IL-10 compared to PPAR-γ WT cells. Moreover, PPAR-γ-deficient macrophages showed impaired phagocytosis. GC treatment of macrophages led to the upregulation of PPAR-γ expression. However, there were no differences in GC-induced suppression of cytokines between both cell types, implicating a PPAR-γ-independent mechanism. Intriguingly, GC treatment resulted in an increased in vitro migration only in PPAR-γ-deficient macrophages. Performing a newly developed in vivo cell-tracking experiment, we could confirm that GC induces an increased recruitment of PPAR-γ KO, but not PPAR-γ WT macrophages to the site of inflammation. Our findings suggest a specific effect of PPAR-γ on GC-induced migration in macrophages. In conclusion, we could demonstrate that PPAR-γ exerts anti-inflammatory activities and shapes macrophage functions. Moreover, we identified a molecular link between GC and PPAR-γ and could show for the first time that PPAR-γ modulates GC-induced migration in macrophages