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Full-Text Articles in Biomedical Engineering and Bioengineering
Mechanisms For Regenerative Intervertebral Disc Healing During Early Growth In Mice, Danielle N. D'Erminio
Mechanisms For Regenerative Intervertebral Disc Healing During Early Growth In Mice, Danielle N. D'Erminio
Dissertations and Theses
Annulus Fibrosus (AF) defects of intervertebral discs (IVDs) cause painful disability, for example when herniated tissue compresses against adjacent nerves. Discectomy, the current standard of treatment to address herniation, does not repair AF defects and can result in re-herniation and recurrent pain. As such there is a need for improved AF repair strategies. It has previously been established that neonatal mice functionally regenerate following severe AF injury providing a model of successful innate AF repair processes that contrasts the poor healing of adult mice. This dissertation focuses on identifying mechanisms of AF regenerative healing in neonatal mice subjected to severe …
Sex Differences In Collateral Remodeling Following Hindlimb Arterial Occlusion, Laura Burckhardt
Sex Differences In Collateral Remodeling Following Hindlimb Arterial Occlusion, Laura Burckhardt
Master's Theses
Clinical evidence indicates a higher incidence of peripheral arterial occlusive disease and associated likelihood of critical limb ischemia in women, as well as worse prognosis and decreased survival post myocardial infarction. Therefore, understanding the possible differences in underlying vascular compensation mechanisms is crucial. With arterial occlusions, necrosis and tissue injury can be naturally mitigated by the collateral circulation, improving patient prognosis. Previous sex-comparison studies describing differences in vascular remodeling are inconsistent. Therefore, the aim of this study was to describe the effect of arterial occlusion on collateral remodeling in healthy male and healthy reproductive-stage female mice. At 7 days following …
Impact Of Collateral Enlargement On Smooth Muscle Phenotype, Alexander Jerome Bynum
Impact Of Collateral Enlargement On Smooth Muscle Phenotype, Alexander Jerome Bynum
Master's Theses
Peripheral Artery Disease is a very serious disease characterized by an arterial occlusion due to atherosclerotic plaques. In response to an arterial occlusion, arteriogenesis occurs, causing smooth muscle cells to transition from a contractile to synthetic state. Also following an arterial occlusion, functional impairment was seen in the collateral circuit. An immunofluorescence protocol was developed in order to assess the impact of collateral enlargement (arteriogenesis) on smooth muscle phenotype at various time points. Smooth muscle α-actin was used to mark all smooth muscle cells, Ki-67 was used to label proliferating smooth muscle cells, and a fluorescent nuclear stain was used …
Ischemia Impairs Vasodilation In Skeletal Muscle Resistance Artery, Kyle Remington Struthers
Ischemia Impairs Vasodilation In Skeletal Muscle Resistance Artery, Kyle Remington Struthers
Master's Theses
Functional vasodilation in arterioles is impaired with chronic ischemia. We sought to examine the impact of chronic ischemia and age on skeletal muscle resistance artery function. To examine the impact of chronic ischemia, the femoral artery was resected from young (2-3mo) and adult (6-7mo) mice and the profunda femoris artery diameter was measured at rest and following gracilis muscle contraction 14 days later using intravital microscopy. Functional vasodilation was significantly impaired in ischemic mice (14.4±4.6% vs. 137.8±14.3%, p<0.0001 n=8) and non-ischemic adult mice (103.0±9.4% vs. 137.8±14.3%, p=0.05 n=10). In order to analyze the cellular mechanisms of the impairment, a protocol was developed to apply pharmacological agents to the experimental preparation while maintaining tissue homeostasis. Endothelial and smooth muscle dependent vasodilation were impaired with ischemia, 39.6 ± 13.6% vs. 80.5 ± 11.4% and 43.0 ± 11.7% vs. 85.1 ± 10.5%, respectively. From this data, it can be supported that smooth muscle dysfunction is the reason for the observed impairment in arterial vasodilation.