Biology subjects

Peeters, R.

Publications and source records attributed to Peeters, R..

4 recordsLinked to original sources

bioRxiv2026

Metabolic regulation of cytokine responses in diffuse large B-cell lymphoma

Aberrant communication between cells of the immune system can drive disease progression. Cytokines form the central pilar of immune cell communication and are well established factors in lymphomagenesis. An increasing body of evidence suggests that immunometabolism is tightly connected to cytokine production. However, the exact link between metabolism and cytokine responses during lymphomagenesis remains largely unknown. Here, we used established cell models representing the most common form of B-cell lymphoma, diffuse large B-cell lymphoma (DLBCL), to study the effect of metabolism on cytokine production. We found that stimulation or inhibition of the glycolysis pathway could attenuate IL-6, IL-10 and TNFa; production by DLBCL. Furthermore, we found that two different subtypes of DLBCL displayed distinct metabolic responses to IL-4. In summary, our work suggests that metabolic pathways could be involved in controlling cytokine production in DLBCL, and paves the road for further research aimed at finding specific metabolic targets that can be exploited for therapeutic intervention.

cancer biology↗

bioRxiv2026

Real-time Sub-cycle Oscillatory Beta Burst Detection

Beta-band burst activity is a key biomarker of Parkinsonian pathophysiology and a control signal for adaptive deep brain stimulation (aDBS). Existing burst detection approaches rely on bandpass filtering followed by envelope extraction and thresholding, which introduces onset/offset latency due to sliding-window estimation and can be unstable under variations in signal-to-noise ratio or threshold choice. We introduce a switching state space approach for real-time burst detection that models oscillatory activity as a superposition of latent harmonic components and explicitly represents burst and non-burst regimes. The framework performs real-time inference using a set of Kalman filters and computes posterior mode probabilities using a Markov transition prior, producing sample-by-sample burst probabilities together with phase and uncertainty estimates. In simulated data with sinusoidal beta bursts embedded in both white and pink noise, the method improved burst detection accuracy, reduced onset latency and offset latency compared with causal envelope-based baselines, and showed reduced sensitivity to threshold selection. In analysis of real sub-thalamic nucleus recordings during a grip-force task, the MSSR method recovered movement-related burst modulation consistent with prior reports. Our results indicate that state space switching provides a principled route to low-latency burst detection that may better support closed-loop stimulation strategies timed to beta bursts.

neuroscience↗

bioRxiv2024

Effect of interhemispheric zero-phase entrainment of the intrinsic mu-rhythm on behavioral and neural markers of predictive coding

Goal-directed behavior requires the integration of information from the outside world and internal (somatosensory) sources about our own actions. Expectations (or internal models) are generated from prior knowledge and constantly updated based on sensory feedback. This optimized information integration (predictive coding) results in a global behavioral advantage of anticipated action in the presence of uncertainty. Our goal was to probe the effect of phase entrainment of the sensorimotor mu-rhythm on visuomotor integration. Participants received transcranial alternating current stimulation over bilateral motor cortices (M1) while performing a visually-guided force adjustment task during functional magnetic resonance imaging. Inter-hemispheric zero-phase entrainment resulted in effector-specific modulation of performance precision and effector-generic minimization of force signal complexity paralleled by BOLD activation changes in bilateral caudate and increased functional connectivity between the right M1 and contralateral putamen, inferior parietal, and medial temporal regions. While effector-specific changes in performance precision were associated with contralateral caudate and hippocampal activation decreases, only the global reduction in force signal complexity was associated with increased functional M1 connectivity with bilateral striatal regions. We propose that zero-phase synchronization represents a neural mode of optimized information integration related to internal model updating within the recursive perception-action continuum associated with predictive coding.

neuroscience↗

bioRxiv2019

Mendelian Randomization analyses reveal a causal effect of thyroid function on stroke via atrial fibrillation

BackgroundSeveral observational studies suggest that variations in thyroid function, even within the normal range, are a risk factor for cardiovascular diseases, but it remains to be determined if these associations are causal or not. This study investigates whether the relationship between variation in normal range thyroid function, as well as hypothyroidism and hyperthyroidism, and the risk of stroke and Coronary Artery Disease (CAD) are causal and via which pathways these relations are mediated.\n\nMethods and FindingsWe performed Mendelian Randomization (MR) analyses for stroke and CAD using genetic instruments associated with TSH and FT4 levels respectively within either the normal range, hypothyroidism or hyperthyroidism. In detected associations, the potential mediatory role of known stroke and CAD risk factors was also examined. A one standard deviation increase in TSH was associated with a 5% decrease in the risk of stroke (OR=0.95, 95% CI= 0.91 to 0.99). Multivariable MR analyses indicated that this effect is mediated through atrial fibrillation (AF). Hashimotos Disease (HD) was associated with a 7% increased risk of CAD (OR=1.07, 95% CI= 1.01 to 1.13). The effect of Hashimotos Disease (HD) on CAD risk appears to be mediated via body mass index (BMI).\n\nConclusionsThese results provide important new insights into the causal relationships and mediating pathways between thyroid function, stroke and CAD. Specifically, we identify normal range TSH levels and HD as potential modifiable risk factors for stroke and CAD, respectively.

genetics↗