Adnan Abbasi

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Scholarly Contributions

Journals/Publications

• Abbasi, A., & Thatipelli, S. (2021). 397 Health Insurance Status in Subjects at High Risk for Obstructive Sleep Apnea. Sleep, 44(Supplement_2), A158-A158. doi:10.1093/sleep/zsab072.396
• Thatipelli, S., & Abbasi, A. A. (2020). 0846 Reports of Sleep Symptoms in Young Adults of College Age. Sleep, 43(Supplement_1), A322-A322. doi:10.1093/sleep/zsaa056.842
• Pusalavidyasagar, S., & Abbasi, A. (2019). 0482 Distribution of Fat in Pre- and Post-Menopausal Females with Sleep Related Breathing Disorder. Sleep, 42(Supplement_1), A193-A193. doi:10.1093/sleep/zsz067.480
• Peterson, N. E., Abbasi, A., & Pusalavidyasagar, S. (2018). 0595 Sleep Disordered Breathing In Heart Failure Patients Post LVAD Placement. Sleep, 41(suppl_1), A221-A221. doi:10.1093/sleep/zsy061.594
• Abbasi, A. A. (2015). Clinical and Demographic Factors Associated With Tobacco Smoking in United States Military Veterans Returning From Iraq and Afghanistan. Chest. doi:10.1378/chest.2281668
• Abbasi, A. A., Meyer, K. C., Xiang, Z., & Tsao, F. H. (2012). Neutrophil necrosis and annexin 1 degradation associated with airway inflammation in lung transplant recipients with cystic fibrosis. BMC Pulmonary Medicine. doi:10.1186/1471-2466-12-44
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  Abstract Background Neutrophils sequestered in lower respiratory tract secretions in the inflamed lung may undergo apoptosis and/or necrosis and release toxic cellular contents that can injure airways or parenchyma. This study examined the viability of neutrophils retrieved from the proximal airways of lung transplant recipients with bacterial tracheobronchitis. Methods Integrity and stability of intracellular proteins in neutrophils from proximal airways and peripheral blood from lung transplant recipients with bacterial tracheobronchitis were analyzed via Western blot analysis and determination of neutrophil viability by morphologic appearance and flow cytometry. Results Neutrophils in tracheobronchial secretions from lung transplant recipients with cystic fibrosis who had normal chest radiographic imaging but bronchoscopic evidence of purulent tracheobronchitis post-transplant were necrotic and associated with degradation of intracellular protein annexin 1. The neutrophil influx was compartmentalized to large airways and not detected in peripheral bronchoalveolar airspaces sampled via bronchoalveolar lavage. Peripheral blood neutrophils from healthy subjects cultured in vitro demonstrated that annexin 1 degradation, particularly to a 33 kDa annexin 1 breakdown product (A1-BP), was associated with neutrophil necrosis, but not apoptosis. Although annexin 1 degradation was not specific to neutrophil necrosis, it was a sensitive marker of intracellular protein degradation associated with neutrophil necrosis. Annexin 1 degradation to 33 kDa A1-BP was not observed in peripheral blood neutrophils from healthy subjects, but annexin 1 appeared to be degraded in peripheral blood neutrophils of lung transplant recipients despite a normal morphologic appearance of these cells. Conclusions Neutrophils were necrotic from the proximal airways of lung transplant recipients with bacterial tracheobronchitis, and this process may begin when neutrophils are still in the systemic circulation prior to sequestration in inflamed airways. Annexin 1 degradation to 33 kDa A1-BP may be useful as a sensitive marker to detect neutrophil necrosis.
• Abbasi, A. A., Ramar, K., Olson, E. N., Tippmann-Peikert, M., Slocumb, N. L., & Morgenthaler, T. I. (2012). Nocturnal moaning and groaning—catathrenia or nocturnal vocalizations. Sleep and Breathing. doi:10.1007/s11325-011-0503-3
• Abbasi, A. A., Dempsey, J. A., Meyer, K. C., Rice, A. J., Haverkamp, H. C., Sonetti, D. A., Xiang, Z., & Wetter, T. J. (2002). Role of lung inflammatory mediators as a cause of exercise-induced arterial hypoxemia in young athletes. Journal of Applied Physiology. doi:10.1152/japplphysiol.01095.2001
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  We examined whether lung inflammatory mediators are increased during exercise and whether pharmacological blockade can prevent exercise-induced arterial hypoxemia (EIAH) in young athletes. Seventeen healthy athletes (9 men, 8 women; age 23 +/- 3 yr) with varying degrees of EIAH completed maximal incremental treadmill exercise tests after administration of fexofenadine, zileuton, and nedocromil sodium or placebo in a randomized double-blind crossover study. Lung function, arterial blood gases, and inflammatory metabolites in plasma, urine, and induced sputum were assessed. Drug administration did not improve EIAH or gas exchange during exercise. At maximal exercise, oxygen saturation fell to 91.4 +/- 2.6% (drug trial) and 91.9 +/- 2.1% (placebo trial) and alveolar-arterial oxygen difference widened to 28.1 +/- 6.3 Torr (drug trial) and 29.3 +/- 5.7 Torr (placebo trial). Oxygen consumption, ventilation, and other exercise variables were similarly unaffected by drug treatment. Although plasma histamine increased with exercise, values did not differ between trials, and urinary leukotriene E(4) and 11beta-prostaglandin F(2alpha) levels were unchanged after exercise. Postexercise sputum revealed no significant changes in markers of inflammation. These results demonstrate that EIAH in young athletes is not attenuated with acute administration of drugs targeting histamine and bioactive lipids. We conclude that airway inflammation is of insufficient magnitude to cause impairments in gas exchange and does not appear to be linked to EIAH in healthy young athletes.

Proceedings Publications

• Abbasi, A., & Gibbs, A. (2020). Cold Hand, Large Clot: A Case of Arterial and Venous Thrombi in a Patient with Idiopathic Pulmonary Fibrosis Treated with Nintedanib. In ATS.
• Puthalapattu, S., Abbasi, A., Meyer, P., & Gibbs, A. (2020). Vaping Pure Luck: A Case of Nicotine Vaping-Related Lung Injury. In ATS conference.
• Abbasi, A. A., Dempsey, J. A., Meyer, K. C., Rice, A. J., Haverkamp, H. C., Sonetti, D. A., Xiang, Z., & Wetter, T. J. (2002). Role of lung inflammatory mediators as a cause of exercise-induced arterial hypoxemia in young male and female athletes. In Journal of Applied Physiology - Abstract publication.
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  We examined whether lung inflammatory mediators are increased during exercise and whether pharmacologic blockade can prevent exercise-induced exercise hypoxemia (EIAH) in young athletes. Seventeen healthy athletes (9 males, 8 females; age 23 ± 3 yr) with varying degrees of EIAH completed maximal incremental treadmill exercise tests after administration of fexofenadine, zileuton, and nedocromil sodium or placebo in a randomized double-blind crossover study. Maximal flow volume loops, total respiratory resistance, and exhaled nitric oxide were obtained both preand post-exercise. Arterial blood gases were measured during exercise. Inflammatory metabolites in plasma, urine, and cell counts and mediator levels in induced sputum were measured before and after exercise. Drug administration did not improve EIAH or gas exchange during exercise. At maximal exercise, oxygen saturation fell to 91.4 ± 2.6% (drug trial) and 91.9 ± 2.1% (placebo trial) and alveolar to arterial oxygen difference (AaDO2) widened to 28.1 ± 6.3 mmHg (drug trial) and 29.3 ± 5.7 mmHg (placebo trial). Oxygen consumption, ventilation and other exercise variables were similarly unaffected by drug treatment. Although plasma histamine increased with exercise, values did not differ between drug and placebo trials and urinary leukotriene E4 and 11$-Prostaglandin F2 levels were unchanged after exercise. Post-exercise sputum did not reveal significant changes in markers of inflammation. These results demonstrate that EIAH in young athletes is not attenuated with acute administration of drugs that target histamine and bioactive lipids. We conclude that airway inflammation is of insufficient magnitude to cause impairments in gas exchange and does not appear to be linked to EIAH in healthy young athletes.

Poster Presentations

• Abbasi, A. (2019, Spring). Distribution of Fat in Pre-and Post-Menopausal Females with Sleep Disordered Breathing. American Academy of Sleep Medicine.