Background Histone lactylation has been recently described as a novel histone post-translational modification linking cellular metabolism to epigenetic regulation. Results Given the expected relevance of this modification and current limited knowledge of its function, we generate genome-wide datasets of H3K18la distribution in various in vitro and in vivo samples, including mouse embryonic stem cells, macrophages, adipocytes, and mouse and human skeletal muscle. We compare them to profiles of well-established histone modifications and gene expression patterns. Supervised and unsupervised bioinformatics analysis shows that global H3K18la distribution resembles H3K27ac, although we also find notable differences. H3K18la marks active CpG island-containing promoters of highly expressed genes across most tissues assessed, including many housekeeping genes, and positively correlates with H3K27ac and H3K4me3 as well as with gene expression. In addition, H3K18la is enriched at active enhancers that lie in proximity to genes that are functionally important for the respective tissue. Conclusions Overall, our data suggests that H3K18la is not only a marker for active promoters, but also a mark of tissue specific active enhancers.
PurposeChildren living with disabilities are at high risk of malnutrition but have long been marginalised in malnutrition treatment programmes and research. The 2013 WHO guidelines for severe acute malnutrition (SAM) mention disability but do not contain specific details for treatment or support. This study assesses inclusion of children living with disabilities in national and international SAM guidelines.MethodsNational and international SAM guidelines available in English, French, Spanish or Portuguese were sourced online and via direct enquiries. Regional guidelines or protocols subspecialising in a certain patient group (eg, people living with HIV) were excluded. Eight scoping key informant interviews were conducted with experts involved in guideline development to help understand possible barriers to formalising malnutrition guidance for children living with disabilities.Results71 malnutrition guidelines were reviewed (63 national, 8 international). National guidelines obtained covered the greater part of countries with a high burden of malnutrition. 85% of guidelines (60/71) mention disability, although mostly briefly. Only 4% (3/71) had a specific section for children living with disabilities, while the remaining lacked guidance on consistently including them in programmes or practice. Only one guideline mentioned strategies to include children living with disabilities during a nutritional emergency. Most (99%,70/71) did not link to other disability-specific guidelines. Of the guidelines that included children living with disabilities, most only discussed disability in general terms despite the fact that different interventions are often needed for children with different conditions. Interviews pointed towards barriers related to medical complexity, resource constraints, epidemiology (eg, unrecognised burden), lack of evidence and difficulty of integration into existing guidelines.ConclusionChildren living with disabilities are under-recognised in most SAM guidelines. Where they are recognised, recommendations are very limited. Better evidence is urgently needed to identify and manage children living with disabilities in malnutrition programmes. More inclusion in the 2022 update of the WHO malnutrition guidelines could support this vulnerable group.
Implantation depth of the Core Valve(®) into the LVOT was associated with post-procedural PM requirement. Thereby, a cut-off value of 6mm, as measured by 64-slice CT, proved useful to define patients at risk for PM requirement.
Since it was first described >20 yr ago, the SPOC domain (Spen paralog and ortholog C-terminal domain) has been identified in many proteins all across eukaryotic species. SPOC-containing proteins regulate gene expression on various levels ranging from transcription to RNA processing, modification, export, and stability, as well as X-chromosome inactivation. Their manifold roles in controlling transcriptional output implicate them in a plethora of developmental processes, and their misregulation is often associated with cancer. Here, we provide an overview of the biophysical properties of the SPOC domain and its interaction with phosphorylated binding partners, the phylogenetic origin of SPOC domain proteins, the diverse functions of mammalian SPOC proteins and their homologs, the mechanisms by which they regulate differentiation and development, and their roles in cancer.
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