Little has been reported about how to improve health care access and delivery for adolescents and adults with autism spectrum disorder. To understand the contributions to the health disparities in the autism spectrum disorder population, we conducted two independent research approaches to learn about current medical needs. A retrospective chart review was performed to evaluate medical comorbidities and medication use. A focus group was also created to address barriers faced in providing medical care. Of 126 charts reviewed, 49% (n = 62) had intellectual disability, 49% (n = 62) had attention-deficit hyperactivity disorder, 52% (n = 65) had anxiety, 41% (n = 52) had obesity, 31% (n = 39) with a history of aggressive behavior, 31% (n = 31) had depression, 22% (n = 28) had seizures, and 9% (n = 11) had hypertension. A Medical Regimen Complexity Index score was determined to examine medication use trends in the autism spectrum disorder population. Medical Regimen Complexity Index scores were significantly higher for patients with intellectual disability, patients with seizures, and patients with a history of aggressive behavior. Both the focus group and our pre-visit assessment identified the waiting room and waiting time as barriers to care. Understanding the comorbidities, polypharmacy, and medical barriers should provide a better understanding of the current health care access and delivery needs of adolescents and adults with autism spectrum disorder.
Activator of G protein Signaling 1 (AGS1) and Ras homologue enriched in striatum (Rhes) define a new group of Ras-like monomeric G proteins whose signaling properties and physiological roles are just beginning to be understood. Previous results suggest that AGS1 and Rhes exhibit distinct preferences for heterotrimeric G proteins, with AGS1 selectively influencing Galphai and Rhes selectively influencing Galphas. Here, we demonstrate that AGS1 and Rhes trigger nearly identical modulation of N-type Ca(2+) channels (Ca(V)2.2) by selectively altering Galphai-dependent signaling. Whole-cell currents were recorded from HEK293 cells expressing Ca(V)2.2 and Galphai- or Galphas-coupled receptors. AGS1 and Rhes reduced basal current densities and triggered tonic voltage-dependent (VD) inhibition of Ca(V)2.2. Additionally, each protein attenuated agonist-initiated channel inhibition through Galphai-coupled receptors without reducing channel inhibition through a Galphas-coupled receptor. The above effects of AGS1 and Rhes were blocked by pertussis toxin (PTX) or by expression of a Gbetagamma-sequestering peptide (masGRK3ct). Transfection with HRas, KRas2, Rap1A-G12V, Rap2B, Rheb2, or Gem failed to duplicate the effects of AGS1 and Rhes on Ca(V)2.2. Our data provide the first demonstration that AGS1 and Rhes exhibit similar if not identical signaling properties since both trigger tonic Gbetagamma signaling and both attenuate receptor-initiated signaling by the Gbetagamma subunits of PTX-sensitive G proteins. These results are consistent with the possibility that AGS1 and Rhes modulate Ca(2+) influx through Ca(V)2.2 channels under more physiological conditions and thereby influence Ca(2+)-dependent events such as neurosecretion.
Asthma and EIB are common etiologies of dyspnea in athletes, both competitive and recreational. However, VCD is also common and can coexist with either asthma or EIB. Vocal cord dysfunction may contribute to exercise-related respiratory symptoms more frequently in middle school- and high school-aged athletes than in college athletes. Effective treatment of dyspnea requires appropriate identification and treatment of all disorders. Classic symptoms of stridor and/or hoarseness are often not present in athletes with VCD. Accurate diagnosis of asthma, EIB, and VCD requires objective testing and can prevent exposure of patients to medications that are ineffective and have potential adverse side effects. Furthermore, there is need for increased awareness of VCD as a common cause of respiratory complaints in athletes, either as a single diagnosis or in combination with EIB, especially in females, as well as middle school and high school athletes.
Perennial allergic rhinitis (PAR) often causes sleep disturbances and associated daytime somnolence, thus resulting in a poor quality of life. Various clinical interventions in patients suffering from the disorder seek to improve symptoms and quality of life. Additional studies are needed to establish whether the alleviation of PAR symptoms, particularly the reduction of congestion, will improve sleep quality and reduce daytime somnolence. This study seeks to determine whether treatment with montelukast is more effective than placebo in reducing nasal congestion and sleep disturbances, resulting in reduced daytime somnolence and fatigue in patients with PAR. Thirty-one subjects were enrolled in a double-blinded, placebo-controlled study using Balaam's design. Patients were treated with montelukast or placebo. Collected subjective data included a daily diary recording nasal symptoms, sleep issues, and daytime fatigue, the Functional Outcomes of Sleep Questionnaire, the Epworth Sleepiness Scale, Juniper's Rhinoconjunctivitis Quality of Life Questionnaire, the Rhinitis Severity Scale, the Calgary Sleep Apnea Quality of Life Index, and Trail Making tests. Subjects treated with montelukast, compared with placebo, showed a statistically significant improvement in daytime somnolence (p = 0.0089) and daytime fatigue (p = 0.0087), with both factors improving with montelukast and worsening with placebo. In a small cohort of subjects, montelukast, when compared with placebo, improved the symptoms of PAR and reduced the fatigue and daytime somnolence associated with the disorder.
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