A5090090406- Pulmonary Hypertension Research and Treatments
- interferon and immune responses
- Monoclonal and Polyclonal Antibodies Research
- RNA and protein synthesis mechanisms
- High Altitude and Hypoxia
- Protein Structure and Dynamics
- Chemokine receptors and signaling
- Eicosanoids and Hypertension Pharmacology
- Biochemical and Structural Characterization
- Birth, Development, and Health
- Neuroscience of respiration and sleep
- Advanced Graph Theory Research
- Peptidase Inhibition and Analysis
- Acute Myocardial Infarction Research
- Enzyme Structure and Function
- Antiplatelet Therapy and Cardiovascular Diseases
- Data Management and Algorithms
- Analytical Methods in Pharmaceuticals
- Anesthesia and Pain Management
- Coronary Interventions and Diagnostics
- Protease and Inhibitor Mechanisms
- Protein purification and stability
- Inflammatory mediators and NSAID effects
- Immune Cell Function and Interaction
- Cancer, Hypoxia, and Metabolism
University of New Mexico
2019-2024
Radiology Associates of Albuquerque
2024
Eastern New Mexico University
2018-2023
The imbalance between pro-inflammatory T helper 17 (T H 17) cells and anti-inflammatory regulatory (Tregs) has been implicated in multiple inflammatory autoimmune conditions, but the effects of chronic hypoxia (CH) on this balance have yet to be explored. CH-exposed mice an increased prevalence lungs with no change Tregs. This is significant because it precedes development pulmonary hypertension (PH), are a major contributor CH-induced PH. While Tregs shown attenuate or prevent certain types...
Chronic hypoxia (CH)-induced pulmonary hypertension (PH) results, in part, from T helper-17 (TH17) cell-mediated perivascular inflammation. However, the antigen(s) involved is unknown. Cellular immunity to collagen type V (col V) develops after ischemia-reperfusion injury during lung transplant and mediated by naturally occurring (n)TH17 cells. Col5a1 gene codifies for α1-helix of col V, which normally hidden immune system within I extracellular matrix. COL5A1 promoter analysis revealed...
ABSTRACT Purpose Chronic, high-altitude hypoxic exposure increases the risk of pulmonary hypertension (PH). Emerging evidence shows maternal exercise may improve offspring resistance to disease throughout life. The purpose this study is determine if mitigates chronic hypoxic-induced changes in indicative PH development. Methods Female adult C57BL/6J mice were randomly allocated nonexercise or conditions. Exercise consisted voluntary running wheel for 4 wk during perinatal period. Three days...
Charged residues on the surface of proteins are critical for both protein stability and interactions. However, many contain binding regions with a high net charge that may destabilize but useful to oppositely charged targets. We hypothesized these domains would be marginally stable, as electrostatic repulsion compete favorable hydrophobic collapse during folding. Furthermore, by increasing salt concentration, we predict folds stabilized mimicking some interactions take place target binding....
Charged residues on the surface of proteins are critical for both protein stability and interactions. However, many contain binding regions with a high net-charge that may destabilize but useful to oppositely charged targets. We hypothesized these domains would be marginally stable, as electrostatic repulsion compete favorable hydrophobic collapse during folding. Furthermore, by increasing salt concentration we predict folds stabilized mimicking some interactions take place target binding....
The distinguishing chromatic number of a graph $G$ is the smallest colors needed to properly color vertices so that trivial automorphism only symmetry preserves coloring. We investigate for Hamiltonian circulant graphs with maximum degree at most 4.
Pulmonary hypertension (PH) caused by chronic hypoxia (CH) is a multifaceted disease most often sleep apnea, prolonged high-altitude exposure, or obstructive pulmonary (COPD), with minimal treatment options, leading to right heart failure and death. One major contributor in the pathogenesis of PH that requires more characterization accompanying immune response.Our previous studies have demonstrated importance inflammation self-immunity CH-induced PH. We pulmonary-perivascular localization...
Chronic hypoxia (CH)-induced pulmonary hypertension (PH) is a progressive and often fatal consequence of chronic lung diseases, exposure to high altitude sleep apnea. PH results from arterial remodeling, enhanced vasoreactivity, Th17 cell-mediated perivascular inflammation. Naturally occurring “nTH17” cells, can be detected in fetal life are homeostatic equilibrium with natural T regulatory cells. nTH17 cells specific for limited range self-antigens, including type V collagen (colV). ColV...
The residue of a graph is the number zeros left after iteratively applying Havel-Hakimi algorithm to its degree sequence. Favaron, Mah\'{e}o, and Sacl\'{e} showed that lower bound on independence number. Maxine heuristic reduces an independent set size $M$. It has been shown given $G$, $M$ bounded between for any application heuristic. We improve upon forbidden subgraph classification graphs such equal by Barrus Molnar in 2015.
Hypoxic pulmonary hypertension (PH) can be caused by chronic obstructive lung diseases, acute injury, sleep apnea, and high altitude. Hallmarks for PH include recruitment of immune cells to the perivascular region lungs, thickening arterial walls, elevated vascular resistance pressure, right ventricular remodeling, ultimately causing heart failure death. We previously reported that hypoxia (CH) leads an upregulation pro-inflammatory Th17 but does not alter T regulatory (Treg) cell numbers...
Hypoxic pulmonary hypertension (PH) can be caused by lung disease, injury, and chronic hypoxia (CH) exposure. Hallmarks for PH include recruitment of immune cells to the perivascular region lungs, thickening arterial walls, elevated vascular resistance pressure, right ventricular remodeling. These signature signs are what lead heart failure ultimately death. We have previously reported that 21 days CH leads both an upregulation collagen type V (Col V) as well natural T helper 17 (nTh17)...