Print‐Light‐Synthesis of Gold Thin Film Electrodes for Electrochemical Sensing

The one-step fabrication of gold films by inkjet printing of a gold precursor ink and its photochemical reduction by exposure to UV light is presented. Inkjet printing creates on a substrate with high control micrometer-thin reaction volumes in which upon direct high-intensity light irradiation, the gold precursor reduces to pure and well-adhered Au particles, while all other ink components escape in the gas phase, without the need for any further post-treatment. The Au precursor ink does neither contain stabilizing agents, such as polymers or surfactants, nor sacrificial compounds, such as photoinitiators, to initiate and accelerate the reduction. This economic and green process is known as Print-Light-Synthesis (PLS) and is herein used to create gold patterns of thin compact Au films and separated Au nanoparticles. Gold loadings are in the μg cm−2 range and precisely controlled, thanks to the inkjet printing parameters. The gold films are characterized by spectroscopic and electrochemical methods. Finally, the applicability of Au films as electrochemical sensors is demonstrated for the detection of 1,4-butanediol in comparison to a commercial screen-printed Au electrode. The PLS Au electrode shows a 20 times higher sensitivity and opens new possibilities for disposable electrode production

Relapse of drunk driving and association with traffic accidents, alcohol-related problems, and biomarkers of impulsivity

Objective: Individual biological predispositions should play a role in risky driving behaviour. Platelet monoamine oxidase (MAO) activity, dopamine transporter gene (DAT1) and neuropeptide S receptor 1 (NPSR1) gene polymorphisms have been identified as markers of impulsivity, alcohol use and excessive risk-taking. We aimed to find out how this knowledge on neurobiology of impulsivity applies to drunk driving and traffic behaviour in general. Methods: We have longitudinally examined the behaviour of drunk drivers (n=203) and controls (n=211) in traffic, in association with their alcohol-related problems, personality measures and the three biomarkers. We analysed differences between the subjects based on whether they had committed driving while impaired by alcohol (DWI) violation in a 10-year time period after recruitment or not and investigated further, what kind of predictive value do the different biomarkers have in committing DWI and other traffic violations and accidents. Results: The original drunk drivers group had lower platelet MAO activity but further DWI was not significantly associated with this measure. Being a NPSR1 T-allele carrier contributed to the risk of repeatedly committing DWI. DAT1 9R carriers in contrast were involved in more traffic accidents by their own fault (active accidents), compared to 10R homozygotes in the whole sample. All groups with DWI also had significantly more alcohol-related problems and higher scores in maladaptive impulsivity compared to controls without DWI. Conclusions: Established biological markers of alcohol use and impulsivity can be reliably associated with everyday traffic behaviour and help in contributing to the understanding of the need for more personalized prevention activities

Family environment interacts with CRHR1 rs17689918 to predict mental health and behavioral outcomes

Background: Corticotrophin-releasing hormone receptor-1 gene (CRHR1) variants have been implicated in mental health. However, little is known of the effects of CRHR1 on long-term mental health and behavior in presence of environmental stressors. We assess the effects of CRHR1 variant (rs17689918)-by-environment interactions on emotionality and behavioral traits, including anxiety, depression, aggression and antisocial behaviors. We also determine effects of rs17689918-by-environment-by-sex interactions on the above-mentioned outcomes. Methods: Genotypic assessments were carried out in 564 children (mean age 10 years, 52.5% females) from the ongoing longitudinal Estonian Children Personality Behaviour and Health Study (ECPBHS). Information on stressful life events and family relationships were available at baseline and information on behavioral and mental health outcomes (self- and parent-reports) were available at follow-up ages of 18 and 25 years. ANOVAs were used to determine associations of two-way CRHR1-by-environment and three-way CRHR1-by-sex-by-environment interactions on behavioral and mental health outcomes. Results: Two-way CRHR1 interaction effects showed associations between low familial warmth and hostility in individuals with the GG genotype. Associations of low familial warmth with aggression, of higher number of stressful life events with aggression, and of stressful live events with anxious-depressive symptoms were noted in male A-allele carriers and female GG homozygotes. Conclusion: CRHR1-by-familial environment interactions influence both outwardly-directed aggression as well as mood and anxiety disorder symptoms in a sex-specific manner. The type of environmental stressor can also influence effects of CRHR1 on behavioral and mental health outcomes

Brain-Derived Neurotrophic Factor (Val66Met) and Serotonin Transporter (5-HTTLPR) Polymorphisms Modulate Plasticity in Inhibitory Control Performance Over Time but Independent of Inhibitory Control Training

Several studies reported training-induced improvements in executive function tasks and also observed transfer to untrained tasks. However, the results are mixed and there is large interindividual variability within and across studies. Given that training-related performance changes would require modification, growth or differentiation at the cellular and synaptic level in the brain, research on critical moderators of brain plasticity potentially explaining such changes is needed. In the present study, a pre-post-follow-up design (N=122) and a three-weeks training of two response inhibition tasks (Go/NoGo and Stop-Signal) was employed and genetic variation (Val66Met) in the brain-derived neurotrophic factor (BDNF) promoting differentiation and activity-dependent synaptic plasticity was examined. Because Serotonin (5-HT) signaling and the interplay of BDNF and 5-HT are known to critically mediate brain plasticity, genetic variation in the 5-HT transporter (5-HTTLPR) was also addressed. The overall results show that the kind of training (i.e., adaptive vs. non-adaptive) did not evoke genotype-dependent differences. However, in the Go/NoGo task, better inhibition performance (lower commission errors) were observed for BDNF Val/Val genotype carriers compared to Met-allele ones supporting similar findings from other cognitive tasks. Additionally, a gene-gene interaction suggests a more impulsive response pattern (faster responses accompanied by higher commission error rates) in homozygous l-allele carriers relative to those with the s-allele of 5-HTTLPR. This, however, is true only in the presence of the Met-allele of BDNF, while the Val/Val genotype seems to compensate for such non-adaptive responding. Intriguingly, similar results were obtained for the Stop-Signal task. Here, differences emerged at post-testing, while no differences were observed at T1. In sum, although no genotype-dependent differences between the relevant training groups emerged suggesting no changes in the trained inhibition function, the observed genotype-dependent performance changes from pre- to post measurement may reflect rapid learning or memory effects linked to BDNF and 5-HTTLPR. In line with ample evidence on BDNF and BDNF-5-HT system interactions to induce (rapid) plasticity especially in hippocampal regions and in response to environmental demands, the findings may reflect genotype-dependent differences in the acquisition and consolidation of task-relevant information, thereby facilitating a more adaptive responding to task-specific requirements

Relevance of Host Cell Surface Glycan Structure for Cell Specificity of Influenza A Viruses

first_page settings Order Article Reprints Open AccessHypothesis Relevance of Host Cell Surface Glycan Structure for Cell Specificity of Influenza A Viruses by Markus Kastner 1,†,‡, Andreas Karner 1,†,§ [ORCID] , Rong Zhu 1,† [ORCID] , Qiang Huang 2 [ORCID] , Andreas Geissner 3,4,‖, Anne Sadewasser 5,¶, Markus Lesch 6, Xenia Wörmann 6, Alexander Karlas 6,**, Peter H. Seeberger 3,4 [ORCID] , Thorsten Wolff 5 [ORCID] , Peter Hinterdorfer 1 [ORCID] , Andreas Herrmann 7 and Christian Sieben 8,9,* [ORCID] 1 Institute for Biophysics, Johannes Kepler University Linz, 4020 Linz, Austria 2 State Key Laboratory of Genetic Engineering, Shanghai Engineering Research Center of Industrial Microorganisms, MOE Engineering Research Center of Gene Technology, School of Life Sciences, Fudan University, Shanghai 200438, China 3 Department for Biomolecular Systems, Max Planck Institute for Colloids and Interfaces, 14476 Potsdam, Germany 4 Institute of Chemistry and Biochemistry, Freie Universität Berlin, 14195 Berlin, Germany 5 Division of Influenza and other Respiratory Viruses, Robert Koch-Institute, 13353 Berlin, Germany 6 Molecular Biology Department, Max Planck Institute for Infection Biology, 10117 Berlin, Germany 7 Institut für Chemie und Biochemie, Freie Universität Berlin, Altensteinstraße 23a, 14195 Berlin, Germany 8 Nanoscale Infection Biology Group, Department of Cell Biology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany 9 Institute for Genetics, Technische Universität Braunschweig, 38106 Braunschweig, Germany * Author to whom correspondence should be addressed. † These authors contributed equally to this work. ‡ Current address: Materials Characterization Lab (MCL), Materials Research Institute (MRI), Pennsylvania State University, University Park, PA 16802, USA. § Current address: University of Applied Sciences Upper Austria, School of Medical Engineering and Applied Social Sciences, Garnisonstr. 21, 4020 Linz, Austria. ‖ Current address: Department of Chemistry, University of British Columbia, 2036 Main Mall, Vancouver, BC V6T 1Z1, Canada. ¶ Current address: Secarna Pharmaceuticals GmbH & Co. KG, Am Klopferspitz 19, 82152 Planegg, Germany. ** Current address: Viral Vectors and Gene Therapeutics, ProBioGen AG, 13086 Berlin, Germany. Viruses 2023, 15(7), 1507; https://doi.org/10.3390/v15071507 Received: 9 May 2023 / Revised: 21 June 2023 / Accepted: 28 June 2023 / Published: 5 July 2023 (This article belongs to the Special Issue Physical Virology - Viruses at Multiple Levels of Complexity) Download Browse Figures Review Reports Versions Notes Abstract Influenza A viruses (IAVs) initiate infection via binding of the viral hemagglutinin (HA) to sialylated glycans on host cells. HA’s receptor specificity towards individual glycans is well studied and clearly critical for virus infection, but the contribution of the highly heterogeneous and complex glycocalyx to virus–cell adhesion remains elusive. Here, we use two complementary methods, glycan arrays and single-virus force spectroscopy (SVFS), to compare influenza virus receptor specificity with virus binding to live cells. Unexpectedly, we found that HA’s receptor binding preference does not necessarily reflect virus–cell specificity. We propose SVFS as a tool to elucidate the cell binding preference of IAVs, thereby including the complex environment of sialylated receptors within the plasma membrane of living cells