The impact of lockdown stress and loneliness during the COVID-19 pandemic on mental health among university students in Germany

The COVID-19 pandemic led to a shutdown of universities in Germany. In a longitudinal design, we compared mental health (depression, anxiety, somatic complaints) of university students in Germany before (June to August 2019) and in the course of the COVID-19 pandemic (June 2020) and determined the impact of pandemic-related stress and loneliness on students’ mental health in self-report online surveys. We investigated 443 participants (mean age 22.8 years), among them 77% female, and 10.4% medical students. A small increase of depression mean scores was observed (F(1,420) = 5.21; p = .023), anxiety and somatic complaints have not significantly changed. There was a medium increase in loneliness from pre-pandemic scores to the pandemic situation (F(1,423) = 30.56; p < .001). Analyzed with regression analyses, current loneliness and pre-pandemic distress represented the strongest associations with mental health during the pandemic. Additionally, health-related concerns during the pandemic were associated with symptoms of depression [b = 0.21; 95%CI(0.08; 0.34); t = 3.12; p = .002], anxiety [b = 0.07; 95%CI(0.01; 0.12); t = 2.50; p = .013], somatic complaints [b = 0.33; 95%CI(0.18; 0.47); t = 4.49; p < .001], and loneliness [b = 0.10; 95%CI(0.03; 0.17); t = 2.74; p = .006]. Social stress due to the pandemic situation was associated with loneliness [b = 0.38; 95%CI(0.32; 0.45); t = 11.75; p < .001]. The results imply that university students represent a risk group for psychosocial long-term ramifications of the pandemic

Antecedents and moderation effects of maladaptive coping behaviors among German university students

Prolonging working hours and presenteeism have been conceptualized as self-endangering coping behaviors in employees, which are related to health impairment. Drawing upon the self-regulation of behavior model, the goal achievement process, and Warr's vitamin model, we examined the antecedents and moderation effects regarding quantitative demands, autonomy, emotion regulation, and self-motivation competence of university students' self-endangering coping behaviors (showing prolonging working hours and presenteeism). Results from a cross-sectional survey of 3,546 German university students indicate that quantitative demands are positively related and autonomy has a u-shape connection with self-endangering coping. Emotion regulation was shown to be a protective factor for prolonging working hours. Moreover, self-motivation moderated the relationship between quantitative demands and prolonging of working hours, but not in the assumed direction. Self-motivation showed a systematic positive relationship with prolonging of working hours, but no relationship with presenteeism. Autonomy moderated the relationship of quantitative demands with both self-endangering behaviors. We found no moderating effects for emotion regulation of quantitative demands or autonomy and self-endangering behaviors. Besides further practical implications, the results suggest that lecturers should design their courses accordingly with less time pressure and university students should be trained in the use of autonomy

Challenge Accepted! a Critical Reflection on How to Perform a Health Survey Among University Students—An Example of the Healthy Campus Mainz Project

Background: Universities represent an important setting of everyday life for health promotion. The Healthy Campus Mainz project aims to develop an evidence-based and comprehensive student health management program covering physical, mental, and social health promotion. Hence, an initial health survey was performed in order to identify the students' health concerns and resources. Up until now, it remains unclear which topics to choose in a health survey among university students and which strategies can be recommended to receive an acceptable response rate or representative student sample within a university setting. The present paper contributes to the call for the present research topic “Public Health Promotion in University Students” by describing methods for health assessment. Therefore, the current paper aims to give an empirical example on how to perform a health survey among university students, focusing on (1) choosing topics for the survey and (2) methodological considerations of how to reach the target population.Methods: An online questionnaire including around 270 items was developed covering a comprehensive set of health topics. Participants were recruited via the university email. Mixed channels for survey promotion, such as lecture visits and social media, were used, accompanied by different monetary and non-monetary incentives. Descriptive analyses were performed to describe the sample.Results: A total of 5,006 participants (out of 31,213 registered students) viewed the first page of the questionnaire; of whom, 4,714 continued further. After a manual data cleaning according to the predefined criteria, the final sample was 4,351, demonstrating a response rate of 13.9%. Students from different study disciplines participated. However, some study disciplines showed a low participation rate, hence, making the results not free from some bias.Discussion: This survey is exceptional as it integrates a great variety of health aspects. The incentive strategy demonstrated promising results. Future research should try to improve target-group-specific recruitment strategies for the traditionally underrepresented groups, such as males and specific study disciplines. This would not only include advancing marketing strategies, but also refining the incentive strategy

Sequential neuromodulation of Hebbian plasticity offers mechanism for effective reward-based navigation

Spike timing-dependent plasticity (STDP) is under neuromodulatory control, which is correlated with distinct behavioral states. Previously we reported that dopamine, a reward signal, broadens the time window for synaptic potentiation and modulates the outcome of hippocampal STDP even when applied after the plasticity induction protocol (Brzosko et al., 2015). Here we demonstrate that sequential neuromodulation of STDP by acetylcholine and dopamine offers an efficacious model of reward-based navigation. Specifically, our experimental data in mouse hippocampal slices show that acetylcholine biases STDP towards synaptic depression, whilst subsequent application of dopamine converts this depression into potentiation. Incorporating this bidirectional neuromodulation-enabled correlational synaptic learning rule into a computational model yields effective navigation towards changing reward locations, as in natural foraging behavior. Thus, temporally sequenced neuromodulation of STDP enables associations to be made between actions and outcomes and also provides a possible mechanism for aligning the time scales of cellular and behavioral learning.Medical Research Council Studentship Zuzanna Brzosko Wolfram Schultz Ole Paulsen Engineering and Physical Sciences Research Council Studentship Sara Zannone Claudia Clopath Wellcome 095495 Wolfram Schultz Biotechnology and Biological Sciences Research Council BB/N013956/1 Claudia Clopath Wellcome 200790/Z/16/Z Claudia Clopath Biotechnology and Biological Sciences Research Council BB/N019008/1 Ole Paulse

An Integrated Transcriptomic and Meta-Analysis of Hepatoma Cells Reveals Factors That Influence Susceptibility to HCV Infection

Hepatitis C virus (HCV) is a global problem. To better understand HCV infection researchers employ in vitro HCV cell-culture (HCVcc) systems that use Huh-7 derived hepatoma cells that are particularly permissive to HCV infection. A variety of hyper-permissive cells have been subcloned for this purpose. In addition, subclones of Huh-7 which have evolved resistance to HCV are available. However, the mechanisms of susceptibility or resistance to infection among these cells have not been fully determined. In order to elucidate mechanisms by which hepatoma cells are susceptible or resistant to HCV infection we performed genome-wide expression analyses of six Huh-7 derived cell cultures that have different levels of permissiveness to infection. A great number of genes, representing a wide spectrum of functions are differentially expressed between cells. To focus our investigation, we identify host proteins from HCV replicase complexes, perform gene expression analysis of three HCV infected cells and conduct a detailed analysis of differentially expressed host factors by integrating a variety of data sources. Our results demonstrate that changes relating to susceptibility to HCV infection in hepatoma cells are linked to the innate immune response, secreted signal peptides and host factors that have a role in virus entry and replication. This work identifies both known and novel host factors that may influence HCV infection. Our findings build upon current knowledge of the complex interplay between HCV and the host cell, which could aid development of new antiviral strategies

Medical conditions in autism spectrum disorders

Autism spectrum disorder (ASD) is a behaviourally defined syndrome where the etiology and pathophysiology is only partially understood. In a small proportion of children with the condition, a specific medical disorder is identified, but the causal significance in many instances is unclear. Currently, the medical conditions that are best established as probable causes of ASD include Fragile X syndrome, Tuberous Sclerosis and abnormalities of chromosome 15 involving the 15q11-13 region. Various other single gene mutations, genetic syndromes, chromosomal abnormalities and rare de novo copy number variants have been reported as being possibly implicated in etiology, as have several ante and post natal exposures and complications. However, in most instances the evidence base for an association with ASD is very limited and largely derives from case reports or findings from small, highly selected and uncontrolled case series. Not only therefore, is there uncertainty over whether the condition is associated, but the potential basis for the association is very poorly understood. In some cases the medical condition may be a consequence of autism or simply represent an associated feature deriving from an underlying shared etiology. Nevertheless, it is clear that in a growing proportion of individuals potentially causal medical conditions are being identified and clarification of their role in etio-pathogenesis is necessary. Indeed, investigations into the causal mechanisms underlying the association between conditions such as tuberous sclerosis, Fragile X and chromosome 15 abnormalities are beginning to cast light on the molecular and neurobiological pathways involved in the pathophysiology of ASD. It is evident therefore, that much can be learnt from the study of probably causal medical disorders as they represent simpler and more tractable model systems in which to investigate causal mechanisms. Recent advances in genetics, molecular and systems biology and neuroscience now mean that there are unparalleled opportunities to test causal hypotheses and gain fundamental insights into the nature of autism and its development

Ultrastructural and ERG Findings in Mice With Adenomatous Polyposis Coli Gene Disruption

Purpose: In order to continue the previous morphological studies of eyes from mice with adenomatous polyposis coli (APC) gene mutation at codon 1638, we determined the ultrastructural and electrophysiologic characteristics of these eyes. Methods: Thirty-eight eyes from 20 mice heterozygous for APC gene mutation and 22 eyes from 11 wild-type mice were examined by light microscopy. Six APC-modified eyes without light microscopic abnormalities, four APC-modified eyes with focal light microscopic abnormalities, and four wild-type eyes were examined by electron microscopy. Electroretinograms were recorded from four APC-modified and three wild-type mice. Results: Four of 38 APC-modified eyes demonstrated ultrastructural evidence of focal RPE cells with increased melanosome production and atrophy. Other areas of the RPE in these four eyes demonstrated no ultrastructural abnormalities. Three APC-modified eyes demonstrated electron and light microscopic evidence of RPE hyperplasia. Electron microscopic examination of APC-modified eyes without light microscopic evidence of abnormalities demonstrated no ultrastructural differences from age-matched controls. Electroretinography demonstrated no differences in the b-wave or c-wave amplitudes between APC-modified and wild-type mice. Conclusions: While light microscopic RPE alterations are observed in these APC-modified mice, the absence of a generalized, ultrastructural murine RPE defect is in contradistinction to observations in electron microscopic investigations of humans with colonic polyposis, pigmented ocular fundus lesions, and APC gene mutations between codons 463 and 1444. Our results in mice with APC mutation at codon 1638, however, are consistent with a previously identified association between the expression of pigmented ocular fundus lesions and region-specific mutation in the human APC gene. The APC protein may possess a physiologic function for both retinal and RPE development

Retinal Pigment Epithelium Abnormalities in Mice With Adenomatous Polyposis Coli Gene Disruption

Objective: To examine eyes from mice with targeted adenomatous polyposis coli (APC) gene disruption to determine if retinal pigment epithelium (RPE) abnormalities replicate the human counterpart. Methods: Thirty-two eyes from 16 mice heterozygous for APC gene disruption (chain-termination mutation in codon 1638 of exon 15) and 12 control eyes were examined by light microscopy. Results: Fifteen of 32 eyes from 12 of 16 APC-disrupted mice demonstrated abnormalities of the RPE and retina. The RPE abnormalities included RPE coloboma, unifocal and multifocal RPE hypertrophy, RPE hyperplasia, and RPE duplication with invasion in the areas of outer and inner segments. Retinal abnormalities included outer nuclear layer duplication and outer nuclear layer atrophy. There were no RPE and retinal abnormalities seen in the control eyes. Conclusions: This study is consistent with the hypothesis that the APC gene is critical in the regulation of RPE proliferation and development. These findings also demonstrate that mutation of the APC gene in codon 1638, a location beyond the previously described critical region for human RPE abnormalities, leads to perturbation in the mouse RPE and retina. Further study of this murine model and the APC/RPE relationship may provide insight into regulatory mechanisms for RPE proliferation