Poster Session #2: UC South Ballroom
Presentation Type
Poster - Campus Access Only
Faculty Mentor’s Full Name
John Quindry
Faculty Mentor’s Department
Health and Human Performance
Abstract / Artist's Statement
Purpose: Duchenne Muscular Dystrophy (DMD) is an incurable disease affecting one in 2,500 boys. DMD is caused by insufficient dystrophin content, resulting in muscle function loss. Individuals are left wheelchair bound until death due to respiratory or cardiac failure. To study DMD treatments, different mouse models have been developed but lack clinical relevance, emphasizing the need for novel mouse models. The study purpose was to characterize pulmonary function in a new mouse model, the D2J (control) and D2 (dystrophin deficient). Mice were examined to quantify respiratory function at four months of age.
Methods: Mouse respiratory function was measured using whole body plethysmography (WBP). Using Buxco WBP, untreated four-month-old male D2J (n=10) and D2 (n=10) mice were placed in independent chambers. A pressure sensitive diaphragm allowed assessment of respiratory rate, tidal volume (ml), minute ventilation (ml/min), expiratory and inspiratory times (s), peak inspiratory and expiratory flows (ml/s), and relaxation time (s). Methods derived from Quindry et. al. were applied within a common 2-hour time frame and mice were habituated to the WBP before data collection. Specifically, mice were habituated to the chamber for 12 minutes and data collection continued for an additional 20 minutes.
Significance: The dystrophin deficient D2 mice had a higher respiration rate (p=0.035) and shorter inspiratory time (p=0.046) compared to the D2J strain. Most importantly, minute ventilation was not different between groups. No other differences existed for tidal volume, expiratory time, peak inspiratory and expiratory flows, or relaxation times. Overall, respiratory function is similar between 4-month-old dystrophic D2 and D2J mouse strains.
Category
Life Sciences
Respiratory Function Comparison in Young D2 and D2J Mice
UC South Ballroom
Purpose: Duchenne Muscular Dystrophy (DMD) is an incurable disease affecting one in 2,500 boys. DMD is caused by insufficient dystrophin content, resulting in muscle function loss. Individuals are left wheelchair bound until death due to respiratory or cardiac failure. To study DMD treatments, different mouse models have been developed but lack clinical relevance, emphasizing the need for novel mouse models. The study purpose was to characterize pulmonary function in a new mouse model, the D2J (control) and D2 (dystrophin deficient). Mice were examined to quantify respiratory function at four months of age.
Methods: Mouse respiratory function was measured using whole body plethysmography (WBP). Using Buxco WBP, untreated four-month-old male D2J (n=10) and D2 (n=10) mice were placed in independent chambers. A pressure sensitive diaphragm allowed assessment of respiratory rate, tidal volume (ml), minute ventilation (ml/min), expiratory and inspiratory times (s), peak inspiratory and expiratory flows (ml/s), and relaxation time (s). Methods derived from Quindry et. al. were applied within a common 2-hour time frame and mice were habituated to the WBP before data collection. Specifically, mice were habituated to the chamber for 12 minutes and data collection continued for an additional 20 minutes.
Significance: The dystrophin deficient D2 mice had a higher respiration rate (p=0.035) and shorter inspiratory time (p=0.046) compared to the D2J strain. Most importantly, minute ventilation was not different between groups. No other differences existed for tidal volume, expiratory time, peak inspiratory and expiratory flows, or relaxation times. Overall, respiratory function is similar between 4-month-old dystrophic D2 and D2J mouse strains.