University Transportation Center for Railway Safety
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[McAllen] Photograph of First Aero Squadron Airplane
First Aero Squadron airplane at Army Air Field.https://scholarworks.utrgv.edu/hidalgohist_aa/1316/thumbnail.jp
[Pharr] Photograph of Fire at Dixie Petroleum Products
Fire at Dixie Petroleum Products.https://scholarworks.utrgv.edu/hidalgohist_aa/1274/thumbnail.jp
[Mercedes] Photograph of Karle Family in Horse Drawn Carriage
Karle family in a horse drawn carriage.https://scholarworks.utrgv.edu/hidalgohist_aa/1415/thumbnail.jp
[Brownsville] Photograph of St. Louis, Brownsville, and Mexico Depot
St. Louis, Brownsville, and Mexico railroad depot.https://scholarworks.utrgv.edu/hidalgohist_aa/1366/thumbnail.jp
[McAllen] Photograph of Landseekers on Wagon
Landseekers on a wagon loaded with wood.https://scholarworks.utrgv.edu/hidalgohist_aa/1305/thumbnail.jp
Detection and parameter estimation of supermassive black hole ringdown signals using a pulsar timing array
Gravitational wave (GW) searches using pulsar timing arrays (PTAs) are commonly assumed to be limited to a GW frequency of ≲4 ×10−7 Hz given by the Nyquist rate associated with the average observational cadence of 2 weeks for a single pulsar. However, by taking advantage of asynchronous observations of multiple pulsars, a PTA can detect GW signals at higher frequencies. This allows a sufficiently large PTA to detect and characterize the ringdown signals emitted following the merger of supermassive binary black holes (SMBBHs), leading to stringent tests of the no-hair theorem in the mass range of such systems. Such large-scale PTAs are imminent with the advent of the FAST telescope and the upcoming era of the Square Kilometer Array (SKA). To scope out the data analysis challenges involved in such a search, we propose a likelihood-based method coupled with particle swarm optimization and apply it to a simulated large-scale PTA comprised of 100 pulsars, each having a timing residual noise standard deviation of 100 nsec, with randomized observation times. Focusing on the dominant (2, 2) mode of the ringdown signal, we show that it is possible to achieve a 99% detection probability with a false alarm probability below 0.2% for an optimal signal-to-noise ratio (SNR) \u3e10. This corresponds, for example, to an equal-mass nonspinning SMBBH with an observer frame chirp mass =9.52 ×109⊙ at a luminosity distance of =420 Mpc
The Influence of Stroke Characteristics on GAD-7 and PHQ-9 Scores: A Retrospective Analysis in the Rio Grande Valley
Background: Strokes, also known as cerebral infarctions, are life-threatening emergencies. They involve blockage of blood flow to the brain and require prompt and critical management to prevent permanent damage or death. The long-term effects of a stroke may include impaired speech, restricted physical mobility, as well as depression and anxiety. The prevalence of anxiety and depression after a stroke is estimated between 20-25% and 20-40% of patients respectively. Just as it is imperative to treat strokes as they transpire, it is equally important to initiate appropriate rehabilitation and therapy targeting post-stroke psychiatric outcomes. The Patient Health Questionnaire 9 (PHQ-9) and the Generalized Anxiety Disorder 7 (GAD-7) are standardized and commonly used questionnaires screening for depression and anxiety symptoms, providing enlightening insight into the mental health status of patients. The purpose of this study is to perform a retrospective analysis of mental health outcomes of stroke patients in the Rio Grande Valley within the past five years and investigate any particular stroke characteristics that may be tied to worsening outcomes.
Methods: Patient chart data from 2019 to 2024 was gathered from several UTHealth RGV sites. This data included patient demographics, year of diagnosis, and the specific ICD-10 code each patient was diagnosed with. ICD-10 stroke codes included in the data request are as follows: Ischemic = I63, Hemorrhagic = I61. Patients who were also co-diagnosed with anxiety and/or depression were also included with the following codes: Anxiety = F41.0, F41.1, etc, Depression = F33.0, F33.1, F33.2, etc. Specific PHQ-9 and GAD-7 scores were also gathered for these patients if applicable. Initial descriptive analysis was conducted through Microsoft Excel while measures of statistical association will be further evaluated through SPSS.
Results: In total, 1704 patients were diagnosed with a stroke, 1526 (89.5%) met the criteria of being diagnosed with an ischemic stroke while 178 (10.4%) unique patients were diagnosed with a hemorrhagic stroke. Within the ischemic stroke group, 128 patients were assigned ICD-10 codes associated with only anxiety, 16 patients with only depression, 10 with both anxiety and depression, and 1372 without a diagnosis of either. In the hemorrhagic stroke group, 15 patients had only anxiety, 1 had only depression, 3 had both, and 159 had neither. Results from GAD-7, PHQ-9, and stroke location are to follow.
Conclusion: The results of this study were greatly limited by the lack of GAD-7 and PHQ-9 scores for patients despite being diagnosed with the relevant ICD-10 code. It is possible that providers based their diagnosis on clinical features rather than the questionnaires. It is also a possibility that patients were not screened for either anxiety or depression. Therefore, future clinical management should include screening for both anxiety and depression due to their prevalence in stroke patients
Structural Studies of Zinc Cations Modulating the N-terminal of Synapse-Associated Protein 102 (SAP102)
Neurological disorders are diseases of the central or peripheral nervous system caused by dysfunction in the brain, spinal cord, or other nervous tissue. Due to the dynamic nature of neurons and their highly specialized structure and function, piecing together the underlying cause of these disorders is difficult. The dysfunction of neuronal synapses, which are specialized structures that allow the transfer of information between neurons--either electrically or chemically--are believed to contribute to brain diseases. More specifically, excitatory glutamatergic synapses have been implicated in causing neuronal cell death under conditions of excess glutamate. Thus, glutamate receptors like the NMDA receptors and their regulations have become the subject of extensive research because of their potential as future therapies. The MAGUK (Membrane-Associated Guanylate Kinase) protein family, which consists of PSD93, PSD95, SAP97, and SAP102, functions to regulate the localization and function of these key receptors. SAP102 is a highly mobile MAGUK predominate in early synaptogenesis and its N-terminus contains a concentrated cluster of cysteine and histidine residues for metal binding. This study investigates the effect of zinc cations on modulating N-terminal domain of SAP102 (SAP102NT) to further elucidate the role that zinc cations may play in the central nervous system through a direct interaction with SAP102. The SAP102NT proteins were overexpressed and purified by affinity chromatography. The experiments of Zn2+ binding with SAP102NT were performed by fluorescence and NMR titrations and further confirmed by mutagenesis assays. The results show that zinc binds tightly to the N-terminus of SAP-102 with a binding affinity (Kd) in the micromolar range, suggesting that zinc is likely to serve a functional modulator of SAP-102 at synaptic sites implicated in its function of regulating glutamate receptors
UCA1 as a Key Regulator of the Warburg Effect during Anoikis Resistance in Colorectal Cancer Metastasis
Colorectal carcinoma (CRC) is the second leading cause of cancer-related mortality in the United States. While localized CRC has a 90% five-year survival rate, this drops sharply to 14% upon metastasis. Metastasis occurs in approximately 40–50% of CRC cases and requires cancer cells to acquire anoikis resistance—a critical adaptation allowing survival after detachment from the extracellular matrix, enabling migration and colonization of secondary sites. Understanding the molecular mechanisms driving anoikis resistance, particularly those linked to altered glucose metabolism, is essential for developing targeted therapies for metastatic CRC.
Cancer cells frequently exhibit the Warburg Effect, a metabolic adaptation favoring glycolysis over oxidative phosphorylation even in the presence of oxygen. This shift supports tumor cell proliferation and may enhance survival under anchorage-independent conditions. Our preliminary findings suggest that the long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1), which is overexpressed in CRC and associated with poor prognosis, plays a central role in glucose metabolism and metastasis.
To investigate UCA1’s function, we utilized isogenic CRC cell lines derived from primary (SW480) and metastatic (SW620) tumors. Stable UCA1-overexpressing (SW480+UCA1) and UCA1-knockdown (SW620+shUCA1) models were developed. Phenotypic assays demonstrated that UCA1 overexpression enhances invasion, migration, proliferation, and colony formation, while its knockdown reduces these traits. Additionally, UCA1 overexpression was linked to increased glucose uptake, lactate production, and anchorage-independent survival, indicating its role in metabolic reprogramming to promote anoikis resistance.
Furthermore, studies evaluate UCA1’s impact under anchorage-independent conditions by assessing changes in cell cycle progression, pro-survival signaling, and stemness markers. Glucose metabolism will also be analyzed using Seahorse XFp metabolic profiling. These findings may uncover UCA1 as a critical regulator of CRC metastasis and a potential therapeutic target
HIV and Bacterial LPS Synergistically Activate AIM2 Inflammasome in Primary Human Oral Keratinocytes
Background: HIV infection profoundly disrupts the oral microbiome, increasing the presence of Gram-negative bacteria such as Porphyromonas gingivalis (P. gingivalis), which is detected in over 80% of cases. P. gingivalis secretes lipopolysaccharide (LPS), a potent immune stimulant that can damage primary human oral keratinocytes (HOK) even in antiretroviral therapy (cART) treated people with HIV (PWH). HOK cells respond to bacterial and viral stimuli by activating inflammasome complexes, including AIM2, a DNA-sensing inflammasome protein. While LPS alone is known to trigger canonical and non-canonical pathways, leading to inflammasome activation, our study investigates how HIV exposure synergizes with LPS to induce the inflammatory response in HOK. We hypothesize that HIV exposure primes HOK cells to enhance AIM2 activation in response to LPS, contributing to increased chronic inflammation and immune dysregulation - among PWH.
Methods: HOK were treated with different P. gingivalis LPS (pgLPS) concentrations (1 ng, 10 ng, 100 ng, 1 μg) for 96 hours, and gene expression changes in NLRP3, CASPASE 1, AIM2, CASPASE 4, and CASPASE 5 were analyzed via qPCR. Additionally, HOK were exposed to HIV for 24 hours, followed by 24-hour LPS treatment, to assess the impact of HIV on LPS-induced inflammation.
Results: In cells treated with LPS alone, NLRP3, CASPASE 4, and CASPASE 5 increased by ~1.5-fold at 1 ng of LPS. At 10 ng, NLRP3 increased 1.4-fold, CASPASE 1 increased 3.5-fold, and AIM2 increased 2.5-fold. At 100 ng, NLRP3 rose 2.4-fold, CASPASE 1 increased 2.6-fold, and AIM2 reached 3.2-fold. At 1 μg, CASPASE 4 increased 2-fold and AIM2 3-fold. Pre-exposure to HIV-1 followed by 1 ng LPS led to a 10-fold increase in CASPASE 5 and an 8-fold increase in AIM2 (p=0.0013). At 10 ng, CASPASE 5 and AIM2 increased 9-fold (p\u3c0.0001). At 100 ng, all three genes increased 2-fold. HIV alone caused a 3-fold increase in AIM2 with no other changes
Conclusion: Our study established that there is a synergistic effect of HIV and LPS in driving AIM2 inflammasome activation in HOK cells. While LPS alone upregulated AIM2 in a dose-dependent manner, HIV pre-exposure significantly increased the AIM2 activation and other associated proteins such as CASPASEs, especially at lower LPS concentrations. This heightened activation, along with increased CASPASE 5 expression, suggests HIV primes HOK for enhanced inflammasome responses, potentially contributing to persistent inflammation in oral cavity. AIM2 emerges as a key player and potential therapeutic target for reducing chronic inflammation among PWH