Publications by authors named "A E Mullick"
Myocardial infarction (MI) mobilizes macrophages, the central protagonists of tissue repair in the infarcted heart. Although necessary for repair, macrophages also contribute to adverse remodeling and progression to heart failure. In this context, specific targeting of inflammatory macrophage activation may attenuate maladaptive responses and enhance cardiac repair.
View Article and Find Full Text PDFObjectives: Non-pneumatic compression devices (NPCDs) rely on shape-memory alloy technology that allows patients to ambulate and remain active during lymphedema treatment. This study examines the effect of the NPCD on foot and ankle swelling.
Methods: This was a prospective, non-randomized study of patients with phlebolymphedema (venous insufficiency-related lymphedema) treated with a novel NPCD for 4 weeks.
Article Synopsis
- Pharmacological inhibition of megalin in mice helps reduce atherosclerosis, but the study aimed to see if specifically deleting megalin in renal proximal tubule cells (PTCs) could have similar effects against hypercholesterolemia-induced atherosclerosis.
- The experiments involved creating mice with and without megalin (PTC-LRP2 -/-) and inducing atherosclerosis by using a Western diet, but results showed that deleting megalin did not reduce atherosclerosis in any mice.
- Instead, male PTC-LRP2 -/- mice exhibited severe kidney issues, including CD68+ cell infiltration and tubular atrophy, indicating that high-fat diets can lead to kidney damage independent of cholesterol levels, while female P
Background: Calmodulinopathies are rare inherited arrhythmia syndromes caused by dominant heterozygous variants in , , or , which each encode the identical CaM (calmodulin) protein. We hypothesized that antisense oligonucleotide (ASO)-mediated depletion of an affected calmodulin gene would ameliorate disease manifestations, whereas the other 2 calmodulin genes would preserve CaM level and function.
Methods: We tested this hypothesis using human induced pluripotent stem cell-derived cardiomyocyte and mouse models of pathogenic variants.
Article Synopsis
- A study was conducted to examine if deleting megalin from renal proximal tubule cells (PTCs) would reduce atherosclerosis in mice with high cholesterol levels.
- The results showed that this deletion did not reduce atherosclerosis but caused kidney issues, such as inflammation and tubular atrophy, particularly in male mice on a Western diet.
- Overall, the findings suggest that while megalin deletion doesn’t impact atherosclerosis, it leads to specific kidney problems influenced by diet, especially in males.