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Full-Text Articles in Life Sciences

Impact Of Collateral Enlargement On Smooth Muscle Phenotype, Alexander Jerome Bynum Dec 2011

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 Jun 2011

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.


Modulation Of Hypoglossal Motoneurons By Nitric Oxide, Justin Philip Benoit May 2011

Modulation Of Hypoglossal Motoneurons By Nitric Oxide, Justin Philip Benoit

Master's Theses

Obstructive sleep apnea (OSA)- the occurrence of repetitive episodes of airway obstruction during sleep- is considered a major health problem affecting up to 9% of adults in the United States (Parish & Somers, 2004). The hypoglossal motor nucleus (HMN) controls genioglossus muscle tone and is critically important for maintaining airway patency; loss of excitatory input to the HMN during sleep results in disfacilitation of hypoglossal motoneurons, increased airway resistance and contributes to the development of OSA (Horner R. L., 2007). However, a fundamental question of sleep medicine that remains unresolved is what mechanisms help maintain airway patency during sleep? A …


The Role Of T-Type Calcium Channels In Vascular Smooth Muscle Cell Cycle Regulation, Abigail Prier Jan 2011

The Role Of T-Type Calcium Channels In Vascular Smooth Muscle Cell Cycle Regulation, Abigail Prier

Master's Theses

Results from previous experiments have provided evidence for T-type channel expression in adult pulmonary artery smooth muscle cells (PASMCs) using electrophysiology and qRT-PCR. Studies have also shown that when T-type channels are blocked, either pharmacological or with small hairpin RNA targeted against T-type channel Cav3.1 subunit, mRNA levels are reduced and cell proliferation is inhibited. These results suggest a connection between T-type calcium channels and cell proliferation. In this thesis, Cav3.1 and its possible interplay with cyclin D, an early marker of the cell cycle, was investigated. The time course of cyclin D's translocation to the nucleus to begin the …