Publications by authors named "M A Momoh"
[This corrects the article DOI: 10.1371/journal.pone.
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- Myomectomy for Jehovah's Witnesses poses challenges due to their refusal of blood transfusions, requiring careful surgical planning.
- A patient's successful procedure involved a multidisciplinary effort to conserve blood, utilizing acute normovolemic hemodilution (ANH) and precise surgical techniques.
- The case emphasizes the need for healthcare providers to respect patients' beliefs while demonstrating ANH as an effective strategy for managing blood loss in complex surgeries.
Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation.
Am J Physiol Gastrointest Liver Physiol
December 2024
Functional loss of the motor protein myosin Vb (MYO5B) induces various defects in intestinal epithelial function and causes a congenital diarrheal disorder, namely, microvillus inclusion disease (MVID). Utilizing the MVID model mice (MYO5BΔIEC) and [MYO5B(G519R)], we previously reported that functional MYO5B loss disrupts progenitor cell differentiation and enterocyte maturation that result in villus blunting and deadly malabsorption symptoms. In this study, we determined that both absence and a point mutation of MYO5B impair lipid metabolism and alter mitochondrial structure, which may underlie the progenitor cell malfunction observed in the MVID intestine.
View Article and Find Full Text PDFBackground & Aims: Intestinal tuft cells have recently been the interest of studies in several human gastrointestinal diseases. However, the impact of tuft cell deletion on intestinal physiological functions are not fully understood. This study investigated the effects of acute tuft cell loss on nutrient absorption and cell lineage differentiation.
View Article and Find Full Text PDFArticle Synopsis
- - Functional loss of the motor protein MYO5B leads to serious intestinal issues, including microvillus inclusion disease (MVID), characterized by progenitor cell dysfunction and malabsorption symptoms.
- - Research using MVID model mice showed that both the absence and mutation of MYO5B disrupt lipid metabolism and mitochondrial structure, resulting in reduced fatty acid oxidation and altered energy metabolism.
- - Treatment with Compound-1, which targets LPAR5, was found to improve intestinal function and weight loss in mice with MYO5B mutations, suggesting a potential therapeutic approach for treating MVID.