Biology subjects

Ioannidis, K.

Publications and source records attributed to Ioannidis, K..

4 recordsLinked to original sources

bioRxiv2026

Modeling spheroid assembly dynamics and mechanical stress generation in magnetic-based biofabrication

Magnetic biofabrication enables rapid assembly of multicellular spheroids but still lacks a basis for predictive control over structure and mechanical environment. Here, we combine experiments and an individual spheroid-based model to study magnetic assembly of periosteum-derived spheroids. Spheroids are treated as discrete particles interacting through magnetic forces, contact mechanics, and interfacial friction, with parameters obtained from independent measurements. This model quantitatively captures assembly dynamics arising from magnetic force patterns and viscous drag with the well surface. The spatial distribution of magnetic forces, determined by magnet geometry and positioning, predicts the size and morphology of magnetic assembloids, including disk- and ring-like structures. Magnetic assembly further generates heterogeneous compressive stresses that depend on magnet geometry and spheroid number. Radial stresses arise collectively through inter-spheroid interactions, whereas vertical stresses are mainly determined by magnetic loading of individual spheroids. These results establish a minimal physical framework for magnetic biofabrication and provide a basis for predictive control of both tissue structure and mechanical microenvironment.

bioengineering↗

bioRxiv2025

Inflammatory profiles of transdiagnostic symptom dimensions in healthy females

BackgroundPsychiatric disorders are increasingly conceptualised as heterogeneous categories with transdiagnostic underlying mechanisms that cut across multiple diagnoses and vary within a single diagnosis. Inflammation induced by psychosocial stress is one particularly potent example: previous research suggests that inflammatory profiles may correspond to symptom subgroups rather than traditional diagnostic categories. However, robust identification of transdiagnostic symptoms linked to specific inflammatory profiles remains rare. In this study, we examined the relationship between inflammatory profiles (at baseline and after a stress induction) and transdiagnostic symptom dimensions in females, who show higher prevalence of stress-related disorders such as anxiety and depression. MethodsA modest but relatively homogenous healthy female sample, between the ages of 18 and 35, was recruited (N=26). We obtained venous blood samples, at baseline and after a combined physiological and social stress induction, to measure full blood counts, plasma cytokines and peripheral blood mononuclear cells (PBMCs; for cell stimulation and intracellular flow cytometry analysis). Participants completed a battery of psychiatric self-report questions, from which we modelled three transdiagnostic factor scores. Finally, we used Bayesian regressions to evaluate the predictive contribution of transdiagnostic factors to inflammatory markers (at baseline and stress-induced), as well as to the principal components of inflammatory measures (derived from a principal component analysis (PCA) of the inflammatory data). ResultsWe identified specific relationships between inflammatory profiles and transdiagnostic symptom dimensions. Higher scores on a social withdrawal factor were associated with greater baseline neutrophil (95% highest density interval (HDI) = [0.06, 1.32]; BF10 = 2.92) and monocyte counts (95% HDI = [0.29, 1.46]; BF10 = 19.08), whereas higher anxious-depression scores were associated with a lower baseline monocyte count (95% HDI = [-0.96, -0.02]; BF10 = 1.81) and a greater inflammatory response to stress (e.g., change in neutrophil scores from pre- to post stress induction: (95% HDI = [0.18, 2.14]); BF10 = 5.66). We also found evidence for an association between the social withdrawal factor and an immune principal component most strongly weighted by monocytes, basophils, and IL-6 (95% HDI = [-1.14, -0.01]; BF10 = 1.88). ConclusionsWe find preliminary evidence that different transdiagnostic psychiatric symptom dimensions map onto specific inflammatory profiles, both at baseline and after a stress induction. This represents a proof-of-principle for the use of data-driven and hypothesis-driven approaches to identify and link transdiagnostic factors with inflammatory changes, which may be of use to future studies with larger, clinical populations, or for testing in the context of stratified interventions.

immunology↗

bioRxiv2021

Cortical dopamine reduces the impact of motivational biases governing automated behaviour

Motivations shape our behaviour: the promise of reward invigorates, while in the face of punishment, we hold back. Abnormalities of motivational processing are implicated in clinical disorders characterised by excessive habits and loss of top-down control, notably substance and behavioural addictions. Striatal and frontal dopamine have been hypothesised to play complementary roles in the respective generation and control of these motivational biases. However, while dopaminergic interventions have indeed been found to modulate motivational biases, these previous pharmacological studies used regionally non-selective pharmacological agents. Here, we tested the hypothesis that frontal dopamine controls the balance between Pavlovian, bias-driven automated responding and instrumentally learned action values. Specifically, we examined whether selective enhancement of cortical dopamine either (i) enables adaptive suppression of Pavlovian control when biases are maladaptive; or (ii) non-specifically modulates the degree of bias-driven automated responding. Healthy individuals (n=35) received the catechol-o-methyltransferase (COMT) inhibitor tolcapone in a randomized, double-blind, placebo-controlled cross-over design, and completed a motivational Go NoGo task known to elicit motivational biases. In support of hypothesis (ii), tolcapone globally decreased motivational bias. Specifically, tolcapone improved performance on trials where the bias was unhelpful, but impaired performance in bias-congruent conditions. These results indicate a non-selective role for cortical dopamine in the regulation of motivational processes underpinning top-down control over automated behaviour. The findings have direct relevance to understanding neurobiological mechanisms underpinning addiction and obsessive-compulsive disorders, as well as highlighting a potential trans-diagnostic novel mechanism to address such symptoms.

neuroscience↗

bioRxiv2021

Effect of SARS-CoV-2 proteins on vascular permeability

SARS-CoV-2 infection leads to severe disease associated with cytokine storm, vascular dysfunction, coagulation, and progressive lung damage. It affects several vital organs, seemingly through a pathological effect on endothelial cells. The SARS-CoV-2 genome encodes 29 proteins, whose contribution to the disease manifestations, and especially endothelial complications, is unknown. We cloned and expressed 26 of these proteins in human cells and characterized the endothelial response to overexpression of each, individually. Whereas most proteins induced significant changes in endothelial permeability, nsp2, nsp5_c145a (catalytic dead mutant of nsp5) and nsp7 also reduced CD31, and increased von Willebrand factor expression and IL-6, suggesting endothelial dysfunction. Using propagation-based analysis of a protein-protein interaction (PPI) network, we predicted the endothelial proteins affected by the viral proteins that potentially mediate these effects. We further applied our PPI model to identify the role of each SARS-CoV-2 protein in other tissues affected by COVID-19. Overall, this work identifies the SARS-CoV-2 proteins that might be most detrimental in terms of endothelial dysfunction, thereby shedding light on vascular aspects of COVID-19.

cell biology↗