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Introduction: The main objective of the study will be to evaluate the effects of two widely used standardized mindfulness-based programs [Mindfulness-Based Stress Reduction (MBSR) and Compassion Cultivation Training (CCT)], on epigenetic, neurobiological, psychological, and physiological variables. Methods: The programs will be offered in an intensive retreat format in a general population sample of healthy volunteer adults. During a 7-day retreat, participants will receive MBSR and CCT in a crossover design where participants complete both programs in random order. After finishing their first 3-day training with one of the two programs, participants will be assigned to the second 3-day training with the second program. The effects of the MBSR and CCT programs, and their combination, will be measured by epigenetic changes (i.e., DNA methylation biomarkers), neurobiological and psychophysiological measures (i.e., EEG resting state, EKG, respiration patterns, and diurnal cortisol slopes), self-report questionnaires belonging to different psychological domains (i.e., mindfulness, compassion, well-being, distress, and general functioning), and stress tasks (i.e., an Arithmetic Stress Test and the retrieval of negative autobiographical memories). These measures will be collected from both groups on the mornings of day 1 (pre-program), day 4 (after finishing the first program and before beginning the second program), and day 7 (post-second program). We will conduct a 3-month and a 12-month follow-up using only the set of self-report measures. Discussion: This study aims to shed light on the neurobiological and psychological mechanisms linked to meditation and compassion in the general population. The protocol was registered at clinicaltrials.gov (Identifier: NCT05516355; August 23, 2022). [ABSTRACT FROM AUTHOR]

Summary: Chronic lymphocytic leukaemia (CLL) is not only characterised by driver genetic alterations but by extensive epigenetic changes. Over the last decade, epigenomic studies have described the DNA methylome, chromatin accessibility, histone modifications and the three‐dimensional (3D) genome architecture of CLL. Beyond its regulatory role, the DNA methylome contains imprints of the cellular origin and proliferative history of CLL cells. These two aspects are strong independent prognostic factors. Integrative analyses of chromatin marks have uncovered novel regulatory elements and altered transcription factor networks as non‐genetic means mediating gene deregulation in CLL. Additionally, CLL cells display a disease‐specific pattern of 3D genome interactions. From the technological perspective, we are currently witnessing a transition from bulk omics to single‐cell analyses. This review aims at summarising the major findings from the epigenomics field as well as providing a prospect of the present and future of single‐cell analyses in CLL. [ABSTRACT FROM AUTHOR]

Common Variable Immunodeficiency (CVID) is characterized by impaired antibody production and poor terminal differentiation of the B cell compartment, yet its pathogenesis is still poorly understood. We first reported the occurrence of epigenetic alterations in CVID by high-throughput methylation analysis in CVID-discordant monozygotic twins. Data from a recent whole DNA methylome analysis throughout different stages of normal B cell differentiation allowed us to design a new experimental approach. We selected CpG sites for analysis based on two criteria: one, CpGs with potential association with the transcriptional status of relevant genes for B cell activation and differentiation; and two, CpGs that undergo significant demethylation from naïve to memory B cells in healthy individuals. DNA methylation was analyzed by bisulfite pyrosequencing of specific CpG sites in sorted naïve and memory B cell subsets from CVID patients and healthy donors. We observed impaired demethylation in two thirds of the selected CpGs in CVID memory B cells, in genes that govern B cell-specific processes or participate in B cell signaling. The degree of demethylation impairment associated with the extent of the memory B cell reduction. The impaired demethylation in such functionally relevant genes as AICDA in switched memory B cells correlated with a lower proliferative rate. Our new results reinforce the hypothesis of altered demethylation during B cell differentiation as a contributing pathogenic mechanism to the impairment of B cell function and maturation in CVID. In particular, deregulated epigenetic control of AICDA could play a role in the defective establishment of a post-germinal center B cell compartment in CVID. [ABSTRACT FROM AUTHOR]

The affiliation for the seventh author is incorrect. The correct affiliations are not indicated. Pablo Roca is not affiliated with #1 and #6 but with: Faculty of Health Sciences, Universidad Villanueva, Spain and Valencian International University, Valencia, Spain.By Gustavo G. Diez; Ignacio Martin-Subero; Rosaria M. Zangri; Marta Kulis; Catherine Andreu; Ivan Blanco; Pablo Roca; Pablo Cuesta; Carola García; Jesús Garzón; Carlos Herradón; Miguel Riutort; Shishir Baliyan; César Venero and Carmelo VázquezReported by Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author [Extracted from the article]