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Biology subjects

Verstraeten, B.

Publications and source records attributed to Verstraeten, B..

3 recordsLinked to original sources

Going around phase defects: reliable phase mapping for realistic data

Phase mapping is a widespread method for identifying rotational electrical activity sustaining cardiac arrhythmias. However, conventional implementations assume that the cardiac phase map is continuous, leading to ill-defined phase indices in regions affected by functional conduction block, fibrosis, or anatomical boundaries. These regions of discontinuous or undefined phase, termed phase defects, lead to both false positive and false negative detections of rotational drivers. This work introduces an improved phase mapping implementation termed extended phase mapping that explicitly detects and accounts for phase defects, enabling robust calculation of the phase index around them. Extended phase mapping is applied to (1) simulated excitation patterns using the Fenton-Karma model, (2) experimental optical mapping data of rat ventricular fibrillation, and (3) a clinical CARTO activation map of atrial tachycardia. Across all datasets, the extended approach eliminates erroneous detections and resolves previously missed rotations. Our results demonstrate that proper treatment of phase defects yields a unified and physiologically consistent characterization of all rotational drivers including near-complete and anatomical reentries. Therefore, we propose replacing the classical notion of phase singularities with critical phase defects as the fundamental entities governing rotational dynamics in cardiac tissue. Author summaryDetecting rotating electrical activity in the heart is crucial for understanding and treating abnormal heart rhythms. A common method, phase mapping, assigns a timing phase to each region of the heart to identify these rotations. However, in regions affected by scars, blocked conduction, or anatomical boundaries, the phase can become undefined or discontinuous. These so-called phase defects make current methods unreliable, causing false detections or missed rotations. In this study, we introduce an extended method that explicitly identifies phase defects and calculates phase indices around them. We test this approach using computer simulations, experimental recordings from animal hearts, and clinical heart-mapping data. Across all datasets, it eliminates false detections and reveals previously overlooked rotational activity. By properly accounting for phase defects, the extended phase mapping method provides a more reliable and complete characterization of heart rhythms, offering a physiologically meaningful framework for studying electrical dynamics in cardiac tissue.

biophysics↗

Type 1 immunity enables neonatal thymic ILC1 production

Thymic atrophy occurs following type 1 inflammatory conditions like viral infection and sepsis, resulting in cell death and disruption of T-cell development. However, it remains undetermined whether the thymus actively contributes to the immune response. Thus, we cultured neonatal thymus ex vivo with the type 1 cytokines IL-12 plus IL-18, resulting in a rapid shift from steady-state T-cell development to the production, expansion, and thymic exit of CXCR6+CD62L- type 1 innate lymphoid cells (ILC1s). Single-cell RNA-sequencing and functional assays identified these cells as embryonic-wave-derived KLRG1+ ILC1s that mainly differentiated from immature neonatal thymic ILC1s. Confocal 3D imaging confirmed neonatal thymic ILC1 expansion during MCMV infection. Furthermore, thymic grafts revealed in vivo thymic ILC1 egress and type 1 inflammation-induced homing of thymus-derived KLRG1+ ILC1s to the liver and peritoneal cavity. Altogether, our data reveal a novel thymic function where type 1 immunity enables the production and peripheral homing of thymic-derived ILC1s. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=185 SRC="FIGDIR/small/530451v1_ufig1.gif" ALT="Figure 1"> View larger version (56K): org.highwire.dtl.DTLVardef@d768corg.highwire.dtl.DTLVardef@1e20d77org.highwire.dtl.DTLVardef@1e206bforg.highwire.dtl.DTLVardef@292108_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

Genome-wide shifts in histone modifications at early stage of rice infection with Meloidogyne graminicola

Epigenetic processes play a crucial role in the regulation of plant stress responses, but their role in plant-pathogen interactions remains poorly understood. Although histone modifying enzymes have been observed to be deregulated in galls induced by root-knot nematodes (RKN, Meloidogyne graminicola) in rice, their influence on plant defence and their genome-wide impact have not been comprehensively investigated. In this study, we applied 3 chemical inhibitors of histone modifying enzymes on rice 24h before inoculation with RKN. Despite their distinct described effects on histone modifications, application of different concentrations led in all cases to reduced susceptibility to RKN. Infection assays on two overexpression lines of histone lysine methyltransferases and one histone deacetylase showed contrasting results in susceptibility, indicating that each histone mark has a specific role in plant defence against RKN in rice. At genome-wide level, three histone marks, H3K9ac, H3K9me2 and H3K27me3 were studied by chromatin-immunoprecipitation (ChIP)-sequencing on RKN-induced galls at 3 days post inoculation. While levels of H3K9ac and H3K27me3 were strongly enriched, H3K9me2 was generally depleted in galls versus control root tips. Differential histone peaks were generally associated with plant defence related genes. In conclusion, our results indicate that histone modifications respond dynamically to RKN infection, and specifically target plant-defence related genes. One-sentence summaryPost-translational histone modifications show a dynamic genome-wide response to root-knot nematode infection in rice and are specifically associated with plant defence genes.

plant biology↗