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As women's labor-force participation and earnings have grown, so has the likelihood that wives outearn their husbands. A common concern is that these couples may be at heightened risk of divorce. Yet with the rise of egalitarian marriage, wives' relative earnings may be more weakly associated with divorce than in the past. We examine trends in the association between wives' relative earnings and marital dissolution using data from the 1968–2009 Panel Study of Income Dynamics. We find that wives' relative earnings were positively associated with the risk of divorce among couples married in the late 1960s and 1970s, and that this was especially true for wives who outearned their husbands, but this was no longer the case for couples married in the 1990s. Change was concentrated among middle-earning husbands and those without college degrees, a finding consistent with the economic squeeze of the middle class over this period.
Background/Objectives: Sharing the bed with a partner is common among adults and impacts sleep quality with potential implications for mental health. However, hitherto findings are contradictory and particularly polysomnographic data on co-sleeping couples are extremely rare. The present study aimed to investigate the effects of a bed partner's presence on individual and dyadic sleep neurophysiology.
Methods: Young healthy heterosexual couples underwent sleep-lab-based polysomnography of two sleeping arrangements: individual sleep and co-sleep. Individual and dyadic sleep parameters (i.e., synchronization of sleep stages) were collected. The latter were assessed using cross-recurrence quantification analysis. Additionally, subjective sleep quality, relationship characteristics, and chronotype were monitored. Data were analyzed comparing co-sleep vs. individual sleep. Interaction effects of the sleeping arrangement with gender, chronotype, or relationship characteristics were moreover tested.
Results: As compared to sleeping individually, co-sleeping was associated with about 10% more REM sleep, less fragmented REM sleep (p = 0.008), longer undisturbed REM fragments (p = 0.0006), and more limb movements (p = 0.007). None of the other sleep stages was significantly altered. Social support interacted with sleeping arrangement in a way that individuals with suboptimal social support showed the biggest impact of the sleeping arrangement on REM sleep. Sleep architectures were more synchronized between partners during co-sleep (p = 0.005) even if wake phases were excluded (p = 0.022). Moreover, sleep architectures are significantly coupled across a lag of ± 5min. Depth of relationship represented an additional significant main effect regarding synchronization, reflecting a positive association between the two. Neither REM sleep nor synchronization was influenced by gender, chronotype, or other relationship characteristics.
Conclusion: Depending on the sleeping arrangement, couple's sleep architecture and synchronization show alterations that are modified by relationship characteristics. We discuss that these alterations could be part of a self-enhancing feedback loop of REM sleep and sociality and a mechanism through which sociality prevents mental illness.
Limbic encephalitis (LE) is an autoimmune syndrome often associated with temporal lobe epilepsy. Recent research suggests that particular structural changes in LE depend on the type of the associated antibody and occur in both mesiotemporal gray matter and white matter regions. However, it remains questionable to what degree conventional diffusion tensor imaging (DTI)-methods reflect alterations in white matter microstructure, since these methods do not account for crossing fibers. To address this methodological shortcoming, we applied fixel-based analysis as a novel technique modeling distinct fiber populations. For our study, 19 patients with LE associated with autoantibodies against glutamic acid decarboxylase 65 (GAD-LE, mean age = 35.9 years, 11 females), 4 patients with LE associated with autoantibodies against leucine-rich glioma-inactivated 1 (LGI1-LE, mean age = 63.3 years, 2 females), 5 patients with LE associated with contactin-associated protein-like 2 (CASPR2, mean age = 57.4, 0 females), 20 age- and gender-matched control patients with hippocampal sclerosis (19 GAD-LE control patients: mean age = 35.1 years, 11 females; 4 LGI1-LE control patients: mean age = 52.6 years, 2 females; 5 CASPR2-LE control patients: mean age = 42.7 years, 0 females; 10 patients are included in more than one group) and 33 age- and gender-matched healthy control subjects (19 GAD-LE healthy controls: mean age = 34.6 years, 11 females; 8 LGI1-LE healthy controls: mean age = 57.0 years, 4 females, 10 CASPR2-LE healthy controls: mean age = 57.2 years, 0 females; 4 subjects are included in more than one group) underwent structural imaging and DTI at 3 T and neuropsychological testing. Patient images were oriented according to lateralization in EEG resulting in an affected and unaffected hemisphere. Fixel-based metrics fiber density (FD), fiber cross-section (FC), and fiber density and cross-section (FDC = FD · FC) were calculated to retrieve information about white matter integrity both on the micro- and the macroscale. As compared to healthy controls, patients with GAD-LE showed significantly (family-wise error-corrected, p < 0.05) lower FDC in the superior longitudinal fascicle bilaterally and in the isthmus of the corpus callosum. In CASPR2-LE, lower FDC in the superior longitudinal fascicle was only present in the affected hemisphere. In LGI1-LE, we did not find any white matter alteration of the superior longitudinal fascicle. In an explorative tract-based correlation analysis within the GAD-LE group, only a correlation between the left/right ratio of FC values of the superior longitudinal fascicle and verbal memory performance (R = 0.64, Holm-Bonferroni corrected p < 0.048) remained significant after correcting for multiple comparisons. Our results underscore the concept of LE as a disease comprising a broad and heterogeneous group of entities and contribute novel aspects to the pathomechanistic understanding of this disease that may strengthen the role of MRI in the diagnosis of LE.
Advertising arbitrage
(2020)
Arbitrageurs with a short investment horizon gain from accelerating price discovery by advertising their private information. However, advertising many assets may overload investors' attention, reducing the number of informed traders per asset and slowing price discovery. So arbitrageurs optimally concentrate advertising on just a few assets, which they overweight in their portfolios. Unlike classic insiders, advertisers prefer assets with the least noise trading. If several arbitrageurs share information about the same assets, inefficient equilibria can arise, where investors' attention is overloaded and substantial mispricing persists. When they do not share, the overloading of investors' attention is maximal.
In fifteen European countries, China, and the US, stocks and business equity as a share of total household assets are represented by an increasing and convex function of income/wealth. A parsimonious model fitted to the data shows why background labor- income risk can explain much of this risk-taking pattern. Uncontrollable labor-income risk stresses middle-income households more because labor income is a larger fraction of their total lifetime resources compared with the rich. In response, middle-income households re-duce (controllable) financial risk. Richer households, having less pressure, can afford more risk-taking. The poor take low risk because they avoid jeopardizing their subsistence consumption.
Die wesentliche Glaubenslehre des Islam ist das Bekenntnis der Einheit Gottes (Tawḥīd). Jalāluddīn Rūmī (g. 1273) erzählt in einer der längsten Geschichten seiner Maṯnawī die geistige Entwicklung des Menschen, bis er von Zwiespalt, Zweifel und Sorge befreit wird und so Tawḥīd, d.h. Einheit und Frieden in sich erreicht. Die Geschichte des Wüstenarabers (A‛rābī) und seiner Frau, welche in diesem Artikel behandelt wird, legt die Stufen der geistigen Reise, das Voranschreiten der Seele zur Einheit und hierbei das Verhältnis von Vernunft und Seele des Menschen, die als ein Ehepaar versinnbildlicht werden, dar.
The innate immune system is the first line of host defense that senses invading pathogens by various surveillance mechanisms, involving pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs). Furthermore, in response to stress, tissue injury or ischemia, cells release endogenous danger-associated molecular patterns (DAMPs) which activate PRRs in order to prompt an effective immune response. Activation of PRRs by DAMPs initiates signaling transduction pathways which drive sterile inflammation by the production of pro-inflammatory effector molecules. Biglycan, a class I small leucine-rich proteoglycan (SLRP), is proteolytically released from the extracellular matrix (ECM) in response to tissue stress and injury or de novo synthesized by activated macrophages. In its soluble form, biglycan operates as an ECM-derived DAMP and triggers a potent inflammatory response by engaging TLR2 and TLR4 on immune cells. By selective utilization of TLR2/4 and the TLR adaptor molecules adaptor molecule myeloid differentiation primary response gene 88 (MyD88) or TIR domain-containing adaptor-inducing interferon-β (TRIF) biglycan differentially regulates the production of TLR downstream mediators or inflammatory molecules. In this way, biglycan triggers the activation of mitogen-activated protein kinase (MAPK) p38, extracellular signal-regulated kinase (Erk) and nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) in a primarily MyD88-dependent manner. In contrast, biglycan induces the expression of (C–C motif) ligand (CCL)5 and chemokine (C-X-C motif) ligand (CXCL)10 over TLR4/TRIF, heat shock protein 70 (HSP70) production over TLR2 and the synthesis of tumor necrosis factor (TNF)-α, CCL2 and CCL20 by utilizing TLR2/4/MyD88. As a consequence, biglycan promotes the recruitment of immune cells such as neutrophils, T cells, B cells and macrophages into the inflamed tissue. Research over the past years showed that biglycan-induced inflammation is involved in the pathogenesis of various inflammatory diseases such as lupus nephritis (LN), sepsis and renal ischemia/reperfusion injury (IRI), whereby genetic deletion of biglycan or TLR2/4 alleviated disease outcome. Unfortunately, the selective interaction of biglycan to TLRs and TLR adaptors complicates the identification of an efficient pharmacological target in biglycan-mediated inflammation. Yet, the necessity of possible co-receptors in biglycan signaling such as cluster of differentiation 14 (CD14) which was found in a high molecular complex with biglycan was not addressed so far.
In the first part of the present study, by utilizing primary peritoneal murine macrophages we demonstrated that the biglycan-induced expression and synthesis of TNF-α and CCL2 via TLR2/4/MyD88, CCL5 through TLR4/TRIF and HSP70 over TLR2 is blunted in CD14 deficient mice, proving that CD14 is essential in TLR2- and TLR4-mediated biglycan signaling. Pre-incubation of macrophages with an anti-CD14 antibody significantly reduced the protein levels of TNF-α, CCL2, CCL5 and HSP70. In line with these data, pharmacological inhibition of CD14 alleviated the transcriptional activation of NF-κB by biglycan in HEK-Blue cells expressing hTLR2/CD14 as well as hTLR4/CD14/MD2 supporting CD14-dependency for biglycan/TLR2/4 signaling. Western blot analysis of phosphorylated p38, p44/42 and NF-κB in WT and CD14 deficient mice revealed that activation of biglycan-mediated TLR downstream signaling is CD14-dependent. Accordingly, biglycan-induced activation and nuclear translocation of p38, p44/42 and NF-κB was blocked in Cd14-/- mice as analyzed by confocal microscopy. Co-immunoprecipitation studies combined with microscale thermophoresis analysis showed that biglycan is in complex with CD14 in macrophages and in vitro binds directly with high affinity to CD14, thereby sustaining the concept that CD14 is a novel co-receptor in biglycan-mediated inflammation. Additionally, we provided proof-of-principle of our concept in an in vivo mouse model of renal IRI. Transient overexpression of biglycan in WT mice exacerbated the expression and production of TNF-α, CCL2, CCL5 and HSP70 in a CD14-dependent manner. Interestingly, pLIVE or pLIVE-hBGN-injected Cd14-/- mice displayed lower chemo- and cytokine levels in reperfused kidneys as compared to respective WT controls during renal IRI (30 h), indicating a renoprotective effect by CD14 deficiency. Flow cytometry analysis of kidney homogenates underlined the pivotal effect of CD14 in biglycan signaling as biglycan-mediated infiltration of CD11b- and F4/80-positive renal macrophages was abolished in Cd14-/- mice. Additionally, pLIVE or pLIVE-hBGN-injected CD14 deficient mice displayed lower numbers of renal CD11b- and F4/80-positive cells during renal IRI compared to WT mice. Analysis of F4/80- and CD38-positive cells isolated from mononuclear cell extracts from kidney homogenates of pLIVE or pLIVE-hBGN-injected WT and Cd14-/- mice revealed that biglycan triggers the polarization of pro-inflammatory M1 macrophages in a CD14-dependent manner. In line with this, Cd14-/- mice, either injected with pLIVE or pLIVE-hBGN, showed less F4/80- and CD38-positive cells during renal IRI than the respective WT control. As a corroboration of our data PAS-stained renal sections of pLIVE- or pLIVE-hBGN-injected WT or Cd14-/- mice uncovered that biglycan worsens tubular damage in IRI-subjected mice via CD14. At the same time, tubular damage was significantly reduced in IRI-subjected Cd14-/- mice as compared to WT mice. In correlation with these data, serum creatine levels were increased in pLIVE-hBGN-injected WT mice during renal IRI. In contrast, serum creatine levels were significantly less increased in pLIVE- or pLIVE-hBGN-injected Cd14-/- mice than in WT littermate controls. In conclusion we demonstrated that CD14 is a new high affinity ligand for biglycan-mediated pro-inflammatory signaling over TLR2 and TLR4 in macrophages. In vivo, soluble biglycan triggers the expression of various inflammatory mediators by utilizing the co-receptor CD14. Ablation of CD14 abolishes biglycan-induced renal macrophage infiltration and M1 macrophage polarization as well as overall kidney function by reduced tubular damage and serum creatinine levels. Therefore, this study identifies CD14 as a promising therapeutic target to ameliorate biglycan-induced inflammation.
...
Chiralität ist in der belebten Natur ein omnipräsentes Phänomen und beschreibt die Symmetrieeigenschaft eines Objektes, dass dieses von seinem Spiegelbild unterscheidbar ist. Die bisherigen Untersuchungen der Wechselwirkung zwischen chiralen Molekülen und Licht fokussieren sich auf das Regime der Ein- und Multiphoton-Ionisation und wird mit dieser Arbeit um Untersuchungen im Starkfeldregime erweitert. Im Rahmen dieser Arbeit wurden Experimente an einzelnen chiralen Molekülen in starken Laserfeldern vorbereitet, durchgeführt, analysiert und alle geladenen Fragmente in Koinzidenz untersucht.
Die Präsentation der Ergebnisse orientierte sich an der Reihenfolge, in der auch die Datenauswertung von Vielteilchenaufbrüchen vonstattengeht: Zunächst wurde der Dichroismus in den Photoionen (PICD) auf chirale Signale in integraler differentieller Form untersucht, dann wurde die Asymmetrien in den Elektronenverteilungen vorgestellt und abschließend die Zusammenhänge zwischen den Ionen- und Elektronenverteilungen aufgezeigt.
Kapitel 6 untersuchte die (differentielle) Ionisations- und Fragmentationswahrscheinlichkeit von verschiedenen chiralen Molekülen. Die in Kapitel 6.1 präsentierten Daten verknüpften erstmals den bereits in der Literatur diskutierten Zirkulardichroismus in den Zählraten von Photoionen (PICD) mit dem signalstärkeren differentiellen PICD in der Einfachionisation von Methyloxiran. Dissoziiert das Molekül nach der Ionisation rasch genug, gewährt der Impulsvektor des geladenen Fragments Zugang zu einer Fragmentationsachse. Durch die Auflösung nach einer Molekülachse ist der beobachtete PICD fast eine Größenordnung stärker, als der über alle Raumrichtungen integrierte.
In steigender Komplexität wurde in Kapitel 6.2 eine Fragmentation in vier Teilchen von Molekülen aus einem racemischen Gemisch von CHBrClF untersucht. Über die Auswertung eines Spatproduktes aus den Impulsvektoren konnte für jedes Molekül dessen Händigkeit bestimmt und der vollständig differentielle PICD untersucht werden. Durch das Festhalten einer Fragmentationsachse (analog zu Kapitel 6.1) konnten um einen Faktor vier stärkere PICD-Signale und durch das Auflösen nach der vollständigen Molekülorientierung die Signalstärke des PICD um einen Faktor von etwa 16 in den Bereich einiger Prozente gebracht werden. Leider übersteigt die theoretische Beschreibung dieses Prozesses den aktuellen Stand der Forschung weit. Daher kann nicht ausgeschlossen werden, dass nicht ein Beitrag zur PICD-Signalverstärkung auch aus der Dynamik der sequentiellen vielfachen Ionisation stammt.
Die untersuchte Reaktion in Kapitel 6.3 war der Fünf-Teilchenaufbruch der achiralen Ameisensäure. In der Messung aller ionischen Fragmente konnten analog zu dem vorherigen Kapitel die internen Koordinaten sowie die Orientierung des Moleküls ermittelt werden. Tatsächlich wurde von einer chiralen Fragmentation der achiralen Ameisensäure berichtet. Welches Enantiomer in der Fragmentation beobachtet wird, hängt maßgeblich von der Molekülorientierung relativ zum ionisierenden Laserpuls ab. Diese Erkenntnis könnte zu neuen Ansätzen für Laserkatalysierte enantioselektive Reaktionen führen. Darüber hinaus konnte gezeigt werden, dass die beobachtete Händigkeit des Moleküls nicht nur von seiner Orientierung, sondern auch von der Helizität des ionisierenden Laserpulses abhängt. Dieser differentielle PICD an der Ameisensäure zeigte sich neben einer sehr großen Signalstärke von über 20 % auch als sensitive Probe für die molekulare Struktur.
In Kapitel 7 wurden die Untersuchungen an den 3-dimensionalen Impulsverteilungen der Photoelektronen vorgestellt. Zunächst wird hierzu auf die allgemeine Form des Dichroismus in den Photoelektronen (PECD) im Starkfeldregime eingegangen und die vorherrschenden Symmetrien des Ionisationsregimes herausgearbeitet (Kapitel 7.1). Mit leicht steigender Komplexität konnte eine klare Verbindung zwischen der Asymmetrie in der Elektronenverteilung und dem Schicksal des zurückbleibenden molekularen Ions anhand der Einfachionisation von Methyloxiran herausgearbeitet werden (Kapitel 7.2). Dies hat eine wichtige Auswirkung auf die Nutzbarkeit des PECD im Starkfeldregime als Analysemethode für Chemie und Pharmazie: Der über alle Fragmentationskanäle integrierte PECD ist sensitiv auf die Gewichtung der Fragmente und damit auch auf beispielsweise die maximale Laserintensität. Die Daten legen nahe, dass die Abhängigkeit des PECD von dem Fragmentationskanal auf die unterschiedliche Auswahl von Subensembles molekularer Orientierungen zurückzuführen ist.
Bei Verwendung von elliptisch polarisiertem Licht treten gegenüber der zirkularen Polarisation eine Reihe neuer Effekte auf (Kapitel 7.3). Zunächst zeigt der PECD auch im Starkfeldregime eine nicht lineare Sensitivität auf den Polarisationszustand, welche sich auch als Funktion des Elektronentransversalimpulses und dem Fragmentationskanal ändert. Somit ist die Verwendung von elliptisch polarisiertem Licht bestens für die chirale Erkennung geeignet, wie inzwischen auch in der Literatur bestätigt wurde. Darüber hinaus führt die gebrochene Rotationssymmetrie bei elliptisch polarisiertem Licht zu einer Elektronenimpulsverteilung, welche selbst chiral ist: Der PECD variiert je nach Winkel φ in der Polarisationsebene, wobei die Extrema des PECD nicht mit den Maxima der Zählraten übereinstimmen. Als neue chirale Beobachtungsgröße konnten wir eine enantiosensitive und vorwärts-/rückwärtsasymmetrische Rotation der Zählratenmaxima einführen. Als abgeleitete Größe aus derselben drei-dimensionalen Elektronenverteilung ist diese Beobachtungsgröße jedoch untrennbar verknüpft mit dem ϕ-abhängigen PECD.
Kapitel 8 verknüpfte das (partielle) Wissen um die molekulare Orientierung und den PICD mit den Asymmetrien der Elektronenverteilung für die Messung der fünffach-Ionisation von Ameisensäure (Kapitel 8.1), der vierfach-Ionisation von CHBrClF (Kapitel 8.2) und der Einfachionisation von Methyloxiran (Kapitel 8.3). Im Datensatz der Ameisensäure und dem des CHBrClF zeigte die molekulare Orientierung einen größeren Einfluss auf die Asymmetrie in der Elektronenverteilung als das Enantiomer oder die Helizität des Lichtes. Diese Verknüpfung zwischen Molekülorientierung und Elektronenasymmetrie überträgt die Asymmetrien des PICD auf die Elektronenverteilung. Die Messung an Methyloxiran relativiert diesen Zusammenhang jedoch in dem dieser in dieser Stärke nur bei manchen Fragmentationskanälen auftritt. Offenbar ist die Übertragung der Asymmetrie der differentiellen Ionisationswahrscheinlichkeit nur einer der Mechanismen, welcher zu Elektronasymmetrien im Starkfeldregime führt.
Gliflozins are inhibitors of the renal proximal tubular sodium-glucose co-transporter-2 (SGLT-2), that inhibit reabsorption of urinary glucose and they are able to reduce hyperglycemia in patients with type 2 diabetes. A renoprotective function of gliflozins has been proven in diabetic nephropathy, but harmful side effects on the kidney have also been described. In the current project, primary highly purified human renal proximal tubular epithelial cells (PTCs) have been shown to express functional SGLT-2, and were used as an in vitro model to study possible cellular damage induced by two therapeutically used gliflozins: empagliflozin and dapagliflozin. Cell viability, proliferation, and cytotoxicity assays revealed that neither empagliflozin nor dapagliflozin induce effects in PTCs cultured in a hyperglycemic environment, or in co-medication with ramipril or hydro-chloro-thiazide. Oxidative stress was significantly lowered by dapagliflozin but not by empagliflozin. No effect of either inhibitor could be detected on mRNA and protein expression of the pro-inflammatory cytokine interleukin-6 and the renal injury markers KIM-1 and NGAL. In conclusion, empa- and dapagliflozin in therapeutic concentrations were shown to induce no direct cell injury in cultured primary renal PTCs in hyperglycemic conditions.
In higher concentrations, the blood pressure regulating hormone angiotensin II leads to vasoconstriction, hypertension, and oxidative stress by activating NADPH oxidases which are a major enzymatic source of reactive oxygen species (ROS). With the help of knockout animals, the impact of the three predominant NADPH oxidases present in the kidney, i.e., Nox1, Nox2 and Nox4 on angiotensin II-induced oxidative damage was studied. Male wildtype (WT) C57BL/6 mice, Nox1-, Nox2- and Nox4-deficient mice were equipped with osmotic minipumps, delivering either vehicle (PBS) or angiotensin II, for 28 days. Angiotensin II increased blood pressure and urinary albumin levels significantly in all treated mouse strains. In Nox1 knockout mice these increases were significantly lower than in WT, or Nox2 knockout mice. In WT mice, angiotensin II also raised systemic oxidative stress, ROS formation and DNA lesions in the kidney. A local significantly increased ROS production was also found in Nox2 and Nox4 knockout mice but not in Nox1 knockout mice who further had significantly lower systemic oxidative stress and DNA damage than WT animals. Nox2 and Nox4 knockout mice had increased basal DNA damage, concealing possible angiotensin II-induced increases. In conclusion, in the kidney, Nox1 seemed to play a role in angiotensin II-induced DNA damage.
The specific temporal evolution of bacterial and phage population sizes, in particular bacterial depletion and the emergence of a resistant bacterial population, can be seen as a kinetic fingerprint that depends on the manifold interactions of the specific phage–host pair during the course of infection. We have elaborated such a kinetic fingerprint for a human urinary tract Klebsiella pneumoniae isolate and its phage vB_KpnP_Lessing by a modeling approach based on data from in vitro co-culture. We found a faster depletion of the initially sensitive bacterial population than expected from simple mass action kinetics. A possible explanation for the rapid decline of the bacterial population is a synergistic interaction of phages which can be a favorable feature for phage therapies. In addition to this interaction characteristic, analysis of the kinetic fingerprint of this bacteria and phage combination revealed several relevant aspects of their population dynamics: A reduction of the bacterial concentration can be achieved only at high multiplicity of infection whereas bacterial extinction is hardly accomplished. Furthermore the binding affinity of the phage to bacteria is identified as one of the most crucial parameters for the reduction of the bacterial population size. Thus, kinetic fingerprinting can be used to infer phage–host interactions and to explore emergent dynamics which facilitates a rational design of phage therapies.
Background: Ataxia telangiectasia (A-T) is a rare autosomal-recessive multisystem disorder characterized by pronounced cerebellar ataxia, telangiectasia, cancer predisposition and altered body composition. In addition, evidence is rising for endocrine dysfunction.
Objectives: To determine the evolution of diabetes and its prevalence in a larger A-T cohort.
Methods: A retrospective analysis of the patient charts of 39 subjects from the Frankfurt A-T cohort was performed between August 2002 and 2018 concerning HbA1c and oral glucose tolerance (OGTT). The median follow-up period was 4 years (1–16 years). In addition, in 31 A-T patients aged 1 to 38 years HbA1c and fasting glucose were studied prospectively from 2018 to 2019.
Results: In the retrospective analysis, we could demonstrate a longitudinal increase of HbA1c. The prospective analysis showed a significant increase of HbA1c and fasting glucose with age (r = 0.79, p ≤ 0.0001). OGTT has a good sensitivity for insulin resistance screening, whereas HbA1c can be used to evaluate individual courses and therapy response. Seven out of 39 (17.9%) patients suffered from diabetes. Metformin did not always lead to sufficient diabetes control; one patient was treated successfully with repaglinide.
Conclusion: Diabetes is a common finding in older A-T patients and often starts in puberty. Our data clearly demonstrate the need for an annual diabetes screening in patients > 12 years.
Background: The newly introduced German pediatric screening examination at the end of the third year of life (U7a) incorporates visual function testing in particular; there is no ophthalmic screening during childhood in Germany. The purpose of this study is to investigate the relationship between participation in U7a and visual function at the preschool health examination (PHE) in the sixth year of life. Methods: This study evaluated PHE data from school enrollment years 2009/2010 to 2014/2015 of Rhineland-Palatinate, Germany. Visual acuity (VA) at PHE was assessed with Rodenstock visual acuity test device (tumbling E) wearing glasses if present. The relationship between participation in U7a and VA <0.7 at PHE was calculated for reduced monocular and binocular VA using multiple logistic regression adjusted for potential confounders. Results: Data from 189,704 children (91,041 girls) in 35 out of 36 districts were included. The first children to participate in U7a were enrolled in 2011/2012 school year. In total, 90,339 children (47.6%) had U7a before PHE, while 99,365 (52.4%) had not. VA <0.7 in at least one eye was measured at PHE in 8429 (4.4%) children, and in both eyes in 4345 (2.3%) children. Participation in U7a was not associated with VA <0.7 at PHE (odds ratio 0.99; 95% confidence interval: 0.94–1.04). Conclusions: The proportion of children with VA <0.7 at PHE was high. No beneficial effect of newly introduced German U7a pediatric screening examination was found for reduced VA at PHE.
Background: Children who are frequently aggressive or lack empathy show various deficits in their social information processing. Several findings suggest that children with conduct problems (CP) show a tendency to interpret ambiguous situations as hostile (hostile attribution bias) and have difficulties to disengage from negative stimuli (attentional bias). The role that additional callous-unemotional traits (CU-traits) play in these biases is yet unclear. Investigating both attentional and attributional aspects of social information processing in children can help us to understand where anomalies in the processing pathway occur and whether the biases are associated with CP and CU-traits separately or in an interactive manner.
Methods: We compared three groups of children: (a) 25 children with CP and low levels of CU-traits (b) 25 children with CP and elevated levels of CU-traits (c) 50 gender (68% male), age (8–17 years) and intelligence score-matched typically developing children, on a pictorial emotional stroop task and a hostile attribution bias task.
Results: In contrast to our predictions, there were no significant group differences regarding attentional biases or hostile attribution biases. Boys with CP and high levels of CU-traits showed a significantly higher hostile attribution bias compared to girls with CP and high levels of CU-traits. The attention bias to angry stimuli significantly correlated with the hostile attribution bias. Compared to the control group the CP group with low levels of CU-traits showed a significantly stronger association between the attention bias to angry stimuli and the hostile attribution bias.
Conclusions: The current study provides evidence that boys with CP and high levels of CU-traits interpret ambiguous situations as more hostile than girls do. Our results further provide indications that the interaction of attentional and attributional biases in children with CP might contribute to their increased aggressive behavior.
Making agriculture sustainable is a global challenge. In the European Union (EU), the Common Agricultural Policy (CAP) is failing with respect to biodiversity, climate, soil, land degradation as well as socio‐economic challenges.
The European Commission's proposal for a CAP post‐2020 provides a scope for enhanced sustainability. However, it also allows Member States to choose low‐ambition implementation pathways. It therefore remains essential to address citizens' demands for sustainable agriculture and rectify systemic weaknesses in the CAP, using the full breadth of available scientific evidence and knowledge.
Concerned about current attempts to dilute the environmental ambition of the future CAP, and the lack of concrete proposals for improving the CAP in the draft of the European Green Deal, we call on the European Parliament, Council and Commission to adopt 10 urgent action points for delivering sustainable food production, biodiversity conservation and climate mitigation.
Knowledge is available to help moving towards evidence‐based, sustainable European agriculture that can benefit people, nature and their joint futures.
The statements made in this article have the broad support of the scientific community, as expressed by above 3,600 signatories to the preprint version of this manuscript. The list can be found here (https://doi.org/10.5281/zenodo.3685632).
A free Plain Language Summary can be found within the Supporting Information of this article.
Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9pat) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an imprinting disorder.
Über problematische Straßennamen und Denkmäler wird politisch debattiert. Wie der öffentliche Raum aussieht, wird gemeinhin nicht als juristische Frage behandelt. Trotzdem taucht die Frage, was die Gesellschaft im öffentlichen Raum sehen will, auch als rechtliches Argument auf. Wann erkennt der Diskurs solche Fragen politischer Ästhetik als juristisches Argument an? Und welche Bedingungen entscheiden darüber?
In Offenbach am Main wurde im Herbst 2018 eine Fahrradstraßen-Teststrecke eröffnet, die Teil des Vorhabens ist, die Stadt fahrradfreundlicher zu gestalten. Um herauszufinden, inwiefern das Design dieser Teststrecke einen Einfluss darauf ausübt, wie die Fahrradstraße von den Verkehrsteilnehmenden wahrgenommen und genutzt wird, wurden im Rahmen dieser Forschungsarbeit im Mai 2019 zwei Fokusgruppengespräche mit Nutzer*innen durchgeführt. In den Fokusgruppen wurden unter der Betrachtung der Fragestellung unterschiedliche Konzeptvorschläge der Offenbacher Hochschule für Gestaltung (HfG) thematisiert. In der Forschungsarbeit wird herausgearbeitet, wieso es sinnvoll ist, das Design der gebauten Umwelt näher zu betrachten und vor allem es gezielt zu verändern, wenn es darum geht, mehr Stadtbewohner*innen zum Fahrradfahren und hiermit zu einem umweltfreundlicheren Fortbewegen zu motivieren. Basierend auf den Ausführungen von JENSEN (2014, 2016) zum Mobilitätsdesign und unter Verwendung seines staging mobilities frameworks konnten die Erfahrungen der Teilnehmenden der Fokusgruppen ausgewertet und erste Aussagen über den Einfluss des Designs auf die Wahrnehmung und Nutzung der Teststrecke getroffen werden.