Biology subjects

Schumann, A.

Publications and source records attributed to Schumann, A..

6 recordsLinked to original sources

bioRxiv2026

Increases in therapist-patient physiological synchrony after dog-patient contact in canine-assisted psychotherapy: an exploratory pilot study

Introduction: Canine-assisted psychotherapy (CAP) introduces a therapy dog into the therapist-patient relationship and may influence interpersonal processes underlying therapeutic change. This exploratory pilot study investigated whether direct patient-dog contact is associated with changes in autonomic arousal and therapist-patient physiological synchrony. Methods: Skin conductance was recorded from 18 patients with depressive disorders and one therapist during 53 routine CAP sessions. A total of 192 episodes of direct patient-dog contact were identified from video recordings. Three-minute periods before and after each contact onsets were compared. Skin conductance level (SCL), skin conductance fluctuations (SCF), and therapist-patient physiological synchrony were assessed using zero-lag correlation and maximum cross-correlation. Sliding-window analyses examined temporal changes in synchrony, while randomly selected pseudo-events served as controls. Results: SCL increased significantly following dog contact in both patients and the therapist, whereas SCF rate over 3 min did not change significantly. Therapist-patient physiological synchrony increased significantly after dog contact, as indicated by both zero-lag correlation and maximum cross-correlation. Sliding-window analyses confirmed these increases and showed a reduction in the temporal lag between the two physiological signals. Importantly, increases in synchrony were significantly greater following genuine dog-contact events than following pseudo-events. Discussion: Direct physical contact between patients and therapy dogs is followed by increased autonomic arousal and enhanced therapist-patient physiological synchrony. These findings suggest that dog-patient contact may function as an interactional event that promotes physiological coordination and interpersonal attunement within the therapeutic dyad.

physiology↗

bioRxiv2026

Disturbed mitochondrial energy production in methylmalonic aciduria is cell-type and variant-dependent

Methylmalonic aciduria (MMA) is caused by deficiency of methylmalonyl-CoA mutase (MMUT), which catalyses the final step of propionate catabolism and fuels the tricarboxylic acid cycle for energy production. Previous studies reported disrupted mitochondrial homeostasis in MMA, including reduced mitochondrial membrane potential and increased oxidative stress, especially in energetically demanding and chronically affected tissues like brain and kidneys. However, how these changes impact mitochondrial energy production remains unclear. Here, we systematically investigated mitochondrial energy production using extracellular flux analysis in cellular models of MMA, including 293T cells, patient-derived fibroblasts, urine-derived epithelial kidney cells and induced pluripotent stem cells (iPSCs) as well as iPSC-derived neurons harbouring either complete loss (knockout, KO) or pathogenic missense variants in MMUT. We found no impact on mitochondrial energy production in MMUT-KO 293T cells and fibroblasts compared to controls. In contrast, fibroblasts and 293T cells expressing the pathogenic MMUT-p.N219Y variant showed decreased energy production. This corresponds to the altered mitochondrial membrane potential in 293T cells, but contrasts with their unchanged mitochondrial abundance. Depletion of glucose, glutamine and pyruvate from the media or provision of each individually as sole fuel source exacerbated the phenotype of MMUT-p.N219Y clones, but did not induce a phenotype in MMUT-KO 293T cells. Finally, we confirmed reduced mitochondrial energy production in patient-derived kidney cells but found no evidence in MMUT-p.N219Y iPSCs and their derived neurons. Overall, our work suggests that the impact of MMUT-deficiency on mitochondrial energy production is cell type- and variant-dependent. Further investigations should clarify molecular mechanisms and their clinical impact.

cell biology↗

bioRxiv2025

Zebrafish facility report on implementation of artificial plants as structural enrichment

There is a broad consensus that husbandry conditions of laboratory animals need constant improvement to guarantee optimal animal welfare and research data quality. Zebrafish (Danio rerio) as one of the main animal models in biomedicine and toxicology are currently kept in barren tanks in most experimental setups, as well as in animal husbandry. Structural enrichment with artificial plants is currently discussed as a potential refinement measure to provide a more diverse environment. It was shown, that this can reduce stress and improve cognitive abilities, survival rate and fertility in these animals. Still, concerns remain regarding its long-term benefits and drawbacks. Therefore, we introduced artificial plants in our husbandry tanks, and evaluated over a one-year period if in our specific system, the benefits would outweigh the risks. Comparing six different lines of zebrafish raised in enriched tanks or under our standard conditions, we saw no significant difference in terms of sex ratio, fertility or pathogen burden. Enrichment increased the survival rate of 4 % during upbringing, albeit not statistically significant due to high variation. When analyzing zebrafish behavior in their 8 L home-tanks, we found less zebrafish in areas close to the plants but rather a preference for the open water in the middle or opposite side of the tank. This effect was even more pronounced at lower holding densities of less than 4 fish per liter. In summary, we found that introducing structural enrichment to our zebrafish facility carried low cost and no detrimental effects for the animals but at the same time benefits were difficult to determine in our readouts as our survival rates already were very high without these measures. We like to encourage other animal facilities to evaluate enrichment measures to ensure a broader discussion on long-term benefits of structural enrichment in zebrafish husbandry systems.

animal behavior and cognition↗

bioRxiv2024

Lipid A phosphoethanolamine transferase-mediated site-selective modifications show association with colistin resistance phenotypes and fitness

Genes encoding lipid A modifying phosphoethanolamine transferases (PETs) are genetically diverse and can confer resistance to colistin and antimicrobial peptides. To better understand the functional diversity of PETs, we characterized three canonical mobile colistin resistance (mcr) alleles (mcr-1, -3, -9), one intrinsic pet (eptA), and two mcr-like genes (petB, petC). Using an isogenic expression system, we show that mcr-1 and mcr-3 are phenotypically similar by conferring colistin resistance with lower fitness costs. mcr-9, which is phylogenetically closely related to mcr-3, and eptA only provide fitness advantages in the presence of sub-inhibitory concentrations of colistin and significantly reduce fitness in media only. PET-B and PET-C were phenotypically distinct from bonafide PETs; neither conferred colistin resistance or caused considerable fitness cost in Escherichia coli. Strikingly, we found for the first time that different PETs selectively modify different phosphates of lipid A - MCR-1, MCR-3, and PET-C selectively modify the 4-phosphate, while MCR-9 and EptA modify the 1-phosphate. 4-phosphate modifications facilitated by MCR-1 and -3 are associated with high levels of colistin resistance and low toxicity. Our results suggest that PETs have a wide phenotypic diversity and that high level colistin resistance is associated with specific lipid A modification patterns that has been largely unexplored thus far. IMPORTANCERising levels of resistance to increasing numbers of antimicrobials has led to the revival of last resort antibiotic colistin. Unfortunately, resistance to colistin is also spreading in the form of mcr genes, making it essential to (i) improve identification of resistant bacteria to allow clinicians to prescribe effective drug regimens and (ii) develop new combination therapies effective at targeting resistant bacteria. Our results demonstrate that PETs, including MCR variants, are site-selective in E. coli, with site-selectivity correlating with the level of resistance and fitness costs conferred by certain PETs. Site-selectivity associated with a given PET may not only help predict colistin resistance phenotypes, but may also provide an avenue to (i) improved drug regimens and (ii) development of new combination therapies to better combat colistin resistant bacteria.

microbiology↗

bioRxiv2023

Escherichia coli B-strains are intrinsically resistant to colistin and not suitable for characterization and identification of mcr genes

Antimicrobial resistance is an increasing threat to human and animal health. Due to the rise of multi- and extreme drug resistance, last resort antibiotics, such as colistin, are extremely important in human medicine. While the distribution of colistin resistance genes can be tracked through sequencing methods, phenotypic characterization of putative antimicrobial resistance (AMR) genes is still important to confirm the phenotype conferred by different genes. While heterologous expression of AMR genes (e.g., in E. coli) is a common approach, so far, no standard method for heterologous expression and characterization of mcr genes exists. E. coli B-strains, designed for optimum protein expression, are frequently utilized. Here we report that four E. coli B-strains are intrinsically resistant to colistin (MIC 8 - 16 g/mL). Additionally, the three tested B-strains that encode T7 RNA show growth defects when transformed with empty or gene-expressing pET17b plasmids and grown in the presence of IPTG; K-12 or B-strains without T7 RNA polymerase do not show these growth defects. The E. coli Shuffle T7 express strain carrying empty pET17b also showed a heteroresistance phenotype when exposed to colistin in the presence of IPTG. These phenotypes could explain why B-strains were erroneously reported as colistin susceptible. Analysis of existing genome data identified one nonsynonymous change in each pmrA and pmrB in all four E. coli B-strains; the E121K change in PmrB has previously been linked to intrinsic colistin resistance. We conclude that E. coli B-strains are not appropriate heterologous expression hosts for identification and characterization of mcr genes.

microbiology↗

bioRxiv2020

The influence of heart rate variability biofeedback on cardiac regulation and functional brain connectivity

BackgroundHeart rate variability (HRV) biofeedback has a beneficial impact on perceived stress and emotion regulation. However, its impact on brain function is still unclear. In this study, we aimed to investigate the effect of an 8-week HRV-biofeedback intervention on functional brain connectivity in healthy subjects. MethodsHRV biofeedback was carried out in five sessions per week, including four at home and one in our lab. A control group played jump nrun games instead of the training. Functional magnetic resonance imaging was conducted before and after the intervention in both groups. To compute resting state functional connectivity (RSFC), we defined regions of interest in the ventral medial prefrontal cortex (VMPFC) and a total of 260 independent anatomical regions for network-based analysis. Changes of RSFC of the VMPFC to other brain regions were compared between groups. Temporal changes of HRV during the resting state recording were correlated to dynamic functional connectivity of the VMPFC. ResultsFirst, we corroborated the role of the VMPFC in cardiac autonomic regulation. We found that temporal changes of HRV were correlated to dynamic changes of prefrontal connectivity, especially to the middle cingulate cortex, left anterior insula, right amygdala, supplementary motor area, dorsal and ventral lateral prefrontal regions. The biofeedback group showed a drop in heart rate by 5.5 beats/min and an increased RMSSD as a measure of HRV by 10.1ms (33%) after the intervention. Functional connectivity of the VMPFC increased mainly to the right anterior insula, the dorsal anterior cingulate cortex and the dorsolateral prefrontal cortex after biofeedback intervention when compared to changes in the control group. Network-based statistic showed that biofeedback had an influence on a broad functional network of brain regions. ConclusionOur results show that increased vagal modulation induced by HRV-biofeedback is accompanied by changes in functional brain connectivity during resting state.

neuroscience↗