BEMDEC: An Adaptive and Robust Methodology for Digital Image Feature Extraction

The intriguing study of feature extraction, and edge detection in particular, has, as a result of the increased use of imagery, drawn even more attention not just from the field of computer science but also from a variety of scientific fields. However, various challenges surrounding the formulation of feature extraction operator, particularly of edges, which is capable of satisfying the necessary properties of low probability of error (i.e., failure of marking true edges), accuracy, and consistent response to a single edge, continue to persist. Moreover, it should be pointed out that most of the work in the area of feature extraction has been focused on improving many of the existing approaches rather than devising or adopting new ones. In the image processing subfield, where the needs constantly change, we must equally change the way we think. In this digital world where the use of images, for variety of purposes, continues to increase, researchers, if they are serious about addressing the aforementioned limitations, must be able to think outside the box and step away from the usual in order to overcome these challenges. In this dissertation, we propose an adaptive and robust, yet simple, digital image features detection methodology using bidimensional empirical mode decomposition (BEMD), a sifting process that decomposes a signal into its two-dimensional (2D) bidimensional intrinsic mode functions (BIMFs). The method is further extended to detect corners and curves, and as such, dubbed as BEMDEC, indicating its ability to detect edges, corners and curves. In addition to the application of BEMD, a unique combination of a flexible envelope estimation algorithm, stopping criteria and boundary adjustment made the realization of this multi-feature detector possible. Further application of two morphological operators of binarization and thinning adds to the quality of the operator

PIKFYVE Modulation Mitigates TDP-43-Dependent Disease Phenotypes in a Drosophila Model of Amyotrophic Lateral Sclerosis

Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease affecting both upper and lower motor neuron and marked by progressive muscle weakness. However, the pathogenic mechanisms underlying motor neuron death remain unclear. Currently there is no cure for ALS. Therapies fully capable of mitigating complex disease processes are not well developed and greatly needed. So far, three drugs Riluzole, Radicava and recently Terasemtiv, have been approved for ALS, but none of them are very effective. Recently, a small molecule modulator of vesicle trafficking (Apilimod) has been reported to rescue patients motor neuron survival and improve the degree of degeneration in mouse model of ALS based on C9ORF72 mutations. Here, I used a Drosophila model of ALS to test the therapeutic potential of Apilimod and its target, PIKFYVE, in TDP-43 proteinopathy. My results show that PIKFYVE knock down (PIKFYVE RNAi) in motor neurons rescue locomotor dysfunction caused by TDP-43. Consistent with the PIKFYVE knockdown results, Apilimod also rescues TDP-43-dependent locomotor dysfunction. PIKFYVE knockdown was also able to slightly improve lifespan in TDP-43 mutants. These findings confirm that PIKFYVE may provide a useful, albeit limited therapeutic target for TDP-43 proteinopathy.Release after 07/14/202

Uncovering Dominant-Satellite Relationships in the U.S. Soybean Basis: Temporal Causation and Spatial Dependence

This study examines the degree to which market information is shared in discovering the local basis. The analysis draws from tests of temporal causation and spatial dependence of weekly county-level soybean basis values across 13 markets. Time series analysis shows that local soybean basis levels have some tendency to follow basis levels at export locations (Toledo and U.S. Gulf). Processing centers tend to show the most independence in basis discovery. Spatial statistics suggest a similar phenomenon in which basis values at interior locations are highly correlated with neighboring locations. The patterns of spatial correlation appear consistent throughout the growing season

TDP-43 proteinopathy alters the ribosome association of multiple mRNAs including the glypican Dally-like protein (Dlp)/GPC6

Amyotrophic lateral sclerosis (ALS) is a genetically heterogeneous neurodegenerative disease in which 97% of patients exhibit cytoplasmic aggregates containing the RNA binding protein TDP-43. Using tagged ribosome affinity purifications in Drosophila models of TDP-43 proteinopathy, we identified TDP-43 dependent translational alterations in motor neurons impacting the spliceosome, pentose phosphate and oxidative phosphorylation pathways. A subset of the mRNAs with altered ribosome association are also enriched in TDP-43 complexes suggesting that they may be direct targets. Among these, dlp mRNA, which encodes the glypican Dally like protein (Dlp)/GPC6, a wingless (Wg/Wnt) signaling regulator is insolubilized both in flies and patient tissues with TDP-43 pathology. While Dlp/GPC6 forms puncta in the Drosophila neuropil and ALS spinal cords, it is reduced at the neuromuscular synapse in flies suggesting compartment specific effects of TDP-43 proteinopathy. These findings together with genetic interaction data show that Dlp/GPC6 is a novel, physiologically relevant target of TDP-43 proteinopathy. © 2021, The Author(s).Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Progenitor cell release plus exercise to improve functional performance in peripheral artery disease: The PROPEL Study

Functional impairment, functional decline, and mobility loss are major public health problems in people with lower extremity peripheral artery disease (PAD). Few medical therapies significantly improve walking performance in PAD. We describe methods for the PROgenitor cell release Plus Exercise to improve functionaL performance in PAD (PROPEL) Study, a randomized controlled clinical trial designed to determine whether granulocyte-macrophage colony stimulating factor (GM-CSF) combined with supervised treadmill walking exercise improves six-minute walk distance more than GM-CSF alone, more than supervised treadmill exercise alone, and more than placebo plus attention control in participants with PAD, respectively. PROPEL Study participants are randomized to one of four arms in a 2 by 2 factorial design. The four study arms are GM-CSF plus supervised treadmill exercise, GM-CSF plus attention control, placebo plus supervised exercise therapy, or placebo plus attention control. The primary outcome is change in six-minute walk distance at 12-week follow-up. Secondary outcomes include change in brachial artery flow-mediated dilation (FMD), change in maximal treadmill walking time, and change in circulating CD34+ cells at 12-week follow-up. Outcomes are also measured at six-week and six-month follow-up. Results of the PROPEL Study will have important implications for understanding mechanisms of improving walking performance and preventing mobility loss in the large and growing number of men and women with PAD