Publications by authors named "M Rabinovitch"
Background: Computational modeling indicated that pathological high shear stress (HSS; 100 dyn/cm) is generated in pulmonary arteries (PAs; 100-500 µm) in congenital heart defects causing PA hypertension (PAH) and in idiopathic PAH with occlusive vascular remodeling. Endothelial-to-mesenchymal transition (EndMT) is a feature of PAH. We hypothesize that HSS induces EndMT, contributing to the initiation and progression of PAH.
View Article and Find Full Text PDFCongenital heart defects (CHD) arise in part due to inherited genetic variants that alter genes and noncoding regulatory elements in the human genome. These variants are thought to act during fetal development to influence the formation of different heart structures. However, identifying the genes, pathways, and cell types that mediate these effects has been challenging due to the immense diversity of cell types involved in heart development as well as the superimposed complexities of interpreting noncoding sequences.
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- Major advances have been made in understanding the cellular and molecular mechanisms involved in various types of pulmonary hypertension, but survival rates are still low, highlighting the need for better healthcare interventions.
- Recent discussions from the 7th World Symposium on Pulmonary Hypertension emphasize the importance of new findings in pathology and pathophysiology, questioning their relevance to different forms of the condition.
- The exploration of omics and technological advancements aims to improve our understanding of pulmonary vascular remodelling and to enhance patient care, drug development, and research in this area.
Article Synopsis
- * A meta-analysis identified eight genetic loci linked to Raynaud's syndrome, with specific genes like ADRA2A, NOS3, and IRX1 showing important roles in blood vessel behavior and gene expression.
- * The research utilized CRISPR gene editing and functional assays, revealing how these genes influence blood vessel contraction in response to cold, emphasizing the complexity of genes in understanding this syndrome.
The discovery and replacement of lung surfactant have helped increase survival rates for neonatal respiratory distress syndrome in extremely premature infants.
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