Ever since automobiles became affordable for the average American, with the introduction of the Ford Model T in 1908, making driving safer has been a priority. While driver intoxication and distraction are the leading causes of automotive fatalities, poor road conditions increase the frequency and deadliness of these incidents. Monitoring road conditions for thousands of miles of road is a huge undertaking, one too large for human surveillance. Automated systems capable of detecting and reacting to dangerous road conditions would be life-saving. These systems could be mounted to the sides of road and notify an operator of conditions in real-time. Drivers could be warned, action taken, and many lives saved. This thesis investigated the science behind polarimetric road ice detection systems. Laboratory Mueller matrix measurements of a simulated road under differing surface conditions were collected searching for a discriminatory polarization property. These Mueller matrices were decomposed into depolarization, diattenuation, and retardance. Individual sample surface polarization properties were then calculated from these three unique matrices and compared. Simulated road samples were measured under many wavelengths and angles, which gave us a larger data library from which to observe trends. Specular and off-specular reflection responses of each sample were also collected. Four polarization properties stood out for having high separation between dry and iced measurements: Depolarization Index, Linear Diattenuation, Linear Polarizance, and Linear Retardance. Through our investigation polarimetric ice detection is possible. Continued research of the polarization properties of road ice can result in the development of a road ice detection system. Proposed deployment methods of such a system have been outlined following the analysis of the data collected in this experiment. Not only is polarimetric ice detection an exciting and novel use of polarization, it has the potential to improve road safety through real-time ice response measures.

Alternative pre-mRNA splicing is often controlled by cell signals (1-3). Membrane depolarization/calcium (Ca2+) signaling controls alternative splicing of a group of genes in neurons and endocrine cells (4-9), with important implications in memory formation or secretion of hormones and neurotransmitters (10-15). However, the underlying molecular basis remains largely unknown. In rat GH3 pituitary cells, BK potassium channels control cellular electrical firing, which is critical for the release of growth hormone and prolactin. Inclusion of the STREX exon of the Slo1 gene encoding the channel α subunit is repressed by the Ca2+/calmodulin-dependent kinase IV (CaMKIV) upon depolarization (4). We isolated CaMKIV-responsive RNA elements (CaRREs) from a library of 13-nucleotide random sequences through in vivo selection in HEK293T cells. Most elements are CA-rich or A-rich, with the heterogeneous nuclear ribonucleoprotein (hnRNP) L as a binding factor. This is consistent with the finding that CA-rich elements and hnRNP L are targeted by CaMKIV in the regulation of splicing (16). In further efforts to directly link the kinase with hnRNP L, we showed that hnRNP L is essential for the full repression of STREX by depolarization and that a highly conserved CaMKIV target serine (Ser513) of L is required. Ser513 phosphorylation enhanced L binding to the STREX CaRRE1, leading to reduced binding of the constitutive factor U2AF65 to the 3’ splice site of STREX. Mutation of Ser513 abolished both activities. Therefore, hnRNP L mediates the repression of STREX by depolarization through modulation of a key step in spliceosomal assembly. We further identified hnRNP L, L-like (LL) and PTB as repressors of STREX and other depolarization-regulated exons with differential effects. Moreover, a full response of STREX to depolarization is mediated by combinations of hnRNP L and LL or PTB. Another depolarization-responsive exon, the exon 18 of the neuregulin 1 gene, is also controlled in a similar way, with the hnRNP L Ser513 required as well. This work provides the first direct link between the Ca2+ signaling and a specific serine of a regulatory splicing factor. Elucidation of the underlying molecular mechanisms would likely help us understand the fine-tuning of hormone secretion and memory formation.

Alternative pre-mRNA splicing is often controlled by cell signals (1-3). Membrane depolarization/calcium (Ca2+) signaling controls alternative splicing of a group of genes in neurons and endocrine cells (4-9), with important implications in memory formation or secretion of hormones and neurotransmitters (10-15). However, the underlying molecular basis remains largely unknown. In rat GH3 pituitary cells, BK potassium channels control cellular electrical firing, which is critical for the release of growth hormone and prolactin. Inclusion of the STREX exon of the Slo1 gene encoding the channel α subunit is repressed by the Ca2+/calmodulin-dependent kinase IV (CaMKIV) upon depolarization (4). We isolated CaMKIV-responsive RNA elements (CaRREs) from a library of 13-nucleotide random sequences through in vivo selection in HEK293T cells. Most elements are CA-rich or A-rich, with the heterogeneous nuclear ribonucleoprotein (hnRNP) L as a binding factor. This is consistent with the finding that CA-rich elements and hnRNP L are targeted by CaMKIV in the regulation of splicing (16). In further efforts to directly link the kinase with hnRNP L, we showed that hnRNP L is essential for the full repression of STREX by depolarization and that a highly conserved CaMKIV target serine (Ser513) of L is required. Ser513 phosphorylation enhanced L binding to the STREX CaRRE1, leading to reduced binding of the constitutive factor U2AF65 to the 3’ splice site of STREX. Mutation of Ser513 abolished both activities. Therefore, hnRNP L mediates the repression of STREX by depolarization through modulation of a key step in spliceosomal assembly. We further identified hnRNP L, L-like (LL) and PTB as repressors of STREX and other depolarization-regulated exons with differential effects. Moreover, a full response of STREX to depolarization is mediated by combinations of hnRNP L and LL or PTB. Another depolarization-responsive exon, the exon 18 of the neuregulin 1 gene, is also controlled in a similar way, with the hnRNP L Ser513 required as well. This work provides the first direct link between the Ca2+ signaling and a specific serine of a regulatory splicing factor. Elucidation of the underlying molecular mechanisms would likely help us understand the fine-tuning of hormone secretion and memory formation.

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Intracellular membrane potential (Em) and force development were measured in rabbit basilar artery to help elucidate the mechanism of action of dopamine in this preparation. There was a strong correlation between membrane depolarization and contraction (r=0.95) between 3×10-7 M to 10-4 M dopamine. When the vascular muscle cells were depolarized by elevating [K]o there was a Em dependent decrease in force development in response to dopamine. Significant reduction of dopamine stimulated force development was observed when the vessel was depolarized by 5-6 mV by excess extracellular K+ and 90% inhibition was seen when the artery was depolarized to -20mv. When Ca++ influx was blocked, dopamine no longer induced force development. Such findings suggest that dopamine cotracts rabbit basilar artery by a mechanism involving membrane depolarization. This process may involve an influx of extracellular Ca++ through voltage sensitive channels.

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