A case of pseudoaneurysm of the marginal artery of Drummond post-open abdominal aortic aneurysm (AAA) repair.

We present the first published account of a pseudoaneurysm of the Marginal artery of Drummond (MAoD) following an emergency open surgical repair of an inflammatory abdominal aortic aneurysm, in which the inferior mesenteric artery was ligated. This was hypothesized to be an iatrogenic injury secondary to retraction of the colonic mesentery during dissection of the aneurysm neck. The risk of pseudoaneurysm growth and rupture versus bowel ischaemia were evaluated in the post-operative phase.

KAT6B is required for histone 3 lysine 9 acetylation and SOX gene expression in the developing brain.

Heterozygous mutations in the histone lysine acetyltransferase gene () underlie neurodevelopmental disorders, but the mechanistic roles of KAT6B remain poorly understood. Here, we show that loss of KAT6B in embryonic neural stem and progenitor cells (NSPCs) impaired cell proliferation, neuronal differentiation, and neurite outgrowth. Mechanistically, loss of KAT6B resulted in reduced acetylation at histone H3 lysine 9 and reduced expression of key nervous system development genes in NSPCs and the developing cortex, including the SOX gene family, in particular , which is a key driver of neural progenitor proliferation, multipotency and brain development.

A Literature Review of Methods of Perioperative Pain Management in Thoracic Outlet Decompression.

Objectives: Post-operative pain control in thoracic outlet decompression (TOD) is difficult due to the complex innervation of the anatomical region. Poor post-operative pain control has been associated with worse patient experiences and prolonged inpatient stays. This study aims to identify evidence-based peri-operative analgesic strategies for thoracic outlet decompression.

Loss of PHF6 causes spontaneous seizures, enlarged brain ventricles and altered transcription in the cortex of a mouse model of the Börjeson-Forssman-Lehmann intellectual disability syndrome.

Börjeson-Forssman-Lehmann syndrome (BFLS) is an X-linked intellectual disability and endocrine disorder caused by pathogenic variants of plant homeodomain finger gene 6 (PHF6). An understanding of the role of PHF6 in vivo in the development of the mammalian nervous system is required to advance our knowledge of how PHF6 mutations cause BFLS. Here, we show that PHF6 protein levels are greatly reduced in cells derived from a subset of patients with BFLS.