Background: The purpose of this study was to assess the efficacy of a lifestyle intervention on cardiorespiratory fitness in Latino youth with obesity and prediabetes. <br/>Methods: Participants (n=50) in this study were taken from a larger randomized controlled trial (n=180, BMI ≥ 95th percentile). Youth participated in a 6-month lifestyle intervention that included physical activity (60 minutes, 3x/week) and nutrition and wellness classes (60 minutes, 1x/week) delivered to families at the Lincoln Family YMCA in Downtown Phoenix. The primary outcome was cardiorespiratory fitness measured at baseline and post-intervention.<br/>Results: The mean BMI for the sample was 33.17 ± 4.54 kg/m2, which put the participants in the 98.4th percentile. At baseline, the mean VO2max was 2737.02 ± 488.89 mL/min. The mean relative VO2max was 30.65 ± 3.87 mL/kg/min. VO2max values significantly increased from baseline to post-intervention (2737.022 ± 483.977 mL/min vs 2932.654 ± 96.062 mL/min, p<0.001). <br/>Conclusion: Culturally-grounded, family-focused lifestyle interventions are a promising approach for improving cardiorespiratory fitness in high-risk youth at risk for diabetes.
Fluoroquinolone antibiotics have been known to cause severe, multisystem adverse side effects, termed fluoroquinolone toxicity (FQT). This toxicity syndrome can present with adverse effects that vary from individual to individual, including effects on the musculoskeletal and nervous systems, among others. The mechanism behind FQT in mammals is not known, although various possibilities have been investigated. Among the hypothesized FQT mechanisms, those that could potentially explain multisystem toxicity include off-target mammalian topoisomerase interactions, increased production of reactive oxygen species, oxidative stress, and oxidative damage, as well as metal chelating properties of FQs. This review presents relevant information on fluoroquinolone antibiotics and FQT and explores the mechanisms that have been proposed. A fluoroquinolone-induced increase in reactive oxygen species and subsequent oxidative stress and damage presents the strongest evidence to explain this multisystem toxicity syndrome. Understanding the mechanism of FQT in mammals is important to aid in the prevention and treatment of this condition.