[Show abstract][Hide abstract] ABSTRACT: Background: Scope of practice in audiology encompasses proficiency in visual inspection of ear canal and tympanic membrane (TM) as well as otoscopy interpretation skills to determine normal versus abnormal conditions of outer and middle ear. Audiology students can develop skills in otoscopy through education and supervised training. Studies have shown that additional otoscopy training increased skills in medical students and general practitioners. However, educational and supervised practices targeting otoscopy competency during audiology graduate coursework are lacking. Also, no studies have attempted to determine otoscopy skills among audiology students. Purpose: To determine the effectiveness of the otoscopy training model on clinical competency and confidence level of audiology students in performing and interpreting otoscopy. Research Design: A combination of experimental treatment design with random assignment of treatment and control groups and delayed treatment for control group. Study Sample: Thirty-two first- and second-year audiology graduate students who were enrolled in a pediatric audiology class participated in this study. Students were randomly assigned to the control (n = 16, 14 females) or experimental (n = 16, 14 females) group. Intervention: Participants in the experimental group received supplementary otoscopy training including didactic otoscopy lectures as well as clinical training using manikin ears. The control group received the same pretest and posttest and then completed a third assessment (posttest 2) after receiving the same training. Data Collection and Analysis: An evaluation of knowledge and skills regarding otoscopy between groups and time was conducted at three times: (a) pretraining, (b) upon completion of training for the experimental group, (c) upon completion of training by the control group. The evaluation consisted of a written exam, a clinical exam, and a self-perception rating of confidence. Both written exam scores and clinical exam scores (otoscopy manikin) were analyzed via two-way analyses of variance (ANOVAs), whereas chi-square (χ²) statistic was conducted to evaluate the effects of training on the confidence level of students of both groups. Results: Experimental and control groups demonstrated significant increased overall competency in otoscopy following the otoscopy training model with didactic and laboratory components. Posttest confidence ratings showed increases in all groups, and there were no significant differences between groups. Conclusions: The need for supplementary otoscopy training was warranted by low knowledge and clinical competency in otoscopy skills of audiology students as measured by pretest mean scores. After completing the training, both experimental and control groups showed significant improvement in knowledge and competency. Results also suggest that perceived confidence ratings may be misleading in determining students' clinical otoscopy skills.
Journal of the American Academy of Audiology 10/2013; 24(9):859-66. · 1.63 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Objective/Background.- The goal of this study was to better understand the cellular mechanisms involved in proton stimulation of calcitonin gene-related peptide (CGRP) secretion from cultured trigeminal neurons by investigating the effects of 2 antimigraine therapies, onabotulinumtoxinA and rizatriptan. Stimulated CGRP release from peripheral and central terminating processes of trigeminal ganglia neurons is implicated in migraine pathology by promoting inflammation and nociception. Based on models of migraine pathology, several inflammatory molecules including protons are thought to facilitate sensitization and activation of trigeminal nociceptive neurons and stimulate CGRP secretion. Despite the reported efficacy of triptans and onabotulinumtoxinA to treat acute and chronic migraine, respectively, a substantial number of migraineurs do not get adequate relief with these therapies. A possible explanation is that triptans and onabotulinumtoxinA are not able to block proton-mediated CGRP secretion. Methods.- CGRP secretion from cultured primary trigeminal ganglia neurons was quantitated by radioimmunoassay while intracellular calcium and sodium levels were measured in neurons via live cell imaging using Fura-2 AM and SBFI AM, respectively. The expression of acid-sensing ion channel 3 (ASIC3) was determined by immunocytochemistry and Western blot analysis. In addition, the involvement of ASICs in mediating proton stimulation of CGRP was investigated using the potent and selective ASIC3 inhibitor APETx2. Results.- While KCl caused a significant increase in CGRP secretion that was significantly repressed by treatment with ethylene glycol tetraacetic acid (EGTA), onabotulinumtoxinA, and rizatriptan, the stimulatory effect of protons (pH 5.5) was not suppressed by EGTA, onabotulinumtoxinA, or rizatriptan. In addition, while KCl caused a transient increase in intracellular calcium levels that was blocked by EGTA, no appreciable change in calcium levels was observed with proton treatment. However, protons did significantly increase the intracellular level of sodium ions. Under our culture conditions, ASIC3 was shown to be expressed in most trigeminal ganglion neurons. Importantly, proton stimulation of CGRP secretion was repressed by pretreatment with the ASIC3 inhibitor APETx2, but not the transient receptor potential vanilloid-1 antagonist capsazepine. Conclusions.- Our findings provide evidence that proton regulated release of CGRP from trigeminal neurons utilizes a different mechanism than the calcium and synaptosomal-associated protein 25-dependent pathways that are inhibited by the antimigraine therapies, rizatriptan and onabotulinumtoxinA.
Headache The Journal of Head and Face Pain 09/2012; · 2.94 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Intranasal noninhaled delivery of carbon dioxide (CO₂) is efficacious in the symptomatic treatment of seasonal allergic rhinitis. The goal of this study was to determine whether and how 100% CO₂ inhibits mast cell degranulation, thereby possibly contributing to the reduction of symptoms in seasonal allergic rhinitis.
Peritoneal mast cells isolated from rats and labelled with sulforhodamine-B (SFRM-B) were used to determine whether CO₂ treatment could block mast cell degranulation and histamine release in response to 48/80. In addition, the effect of CO₂ on intracellular calcium levels in unstimulated and stimulated mast cells was determined by fluorescent microscopy.
Treatment with 48/80 caused >90% of mast cells containing SFRM-B to degranulate, resulting in a marked decrease in the fluorescent intensity within the mast cells, and simultaneously causing a significant increase in histamine release. Significantly, the stimulatory effect of 48/80 on fluorescent intensity and histamine levels was greatly inhibited (>95%) to near control levels by pretreatment with 100% CO₂. Treatment with 48/80 also caused a robust transient increase in intracellular calcium, whereas pretreatment with CO₂ repressed the increase in calcium (>70%) in response to 48/80.
Results from this study provide the first evidence of a unique regulatory mechanism by which CO₂ inhibits mast cell degranulation and histamine release by repressing stimulated increases in intracellular calcium. Thus, our data provide a plausible explanation for the reported therapeutic benefit of noninhaled intranasal delivery of 100% CO₂ to treat allergic rhinitis.
[Show abstract][Hide abstract] ABSTRACT: To investigate the mechanism by which adenosine triphosphate (ATP) causes sensitization of trigeminal neurons and how dihydroergotamine (DHE) represses this modulatory effect.
Dihydroergotamine is an effective treatment of migraine. The cellular mechanisms of action of DHE in treating migraine attacks remain unclear.
In this study, neonatal rat trigeminal ganglia cultures were used to investigate effects of ATP, alpha, beta-methyl ATP (α,β-meATP), and DHE on intracellular calcium levels and calcitonin gene-related peptide (CGRP) secretion.
Pretreatment with ATP or α,β-meATP caused sensitization of neurons, via P2X(3) receptors, such that a subthreshold amount of potassium chloride (KCl) significantly increased intracellular calcium levels and CGRP secretion. Pretreatment with DHE repressed increases in calcium and CGRP secretion in response to ATP-KCl or α,β-meATP-KCl treatment. Importantly, these inhibitory effects of DHE were blocked with an α(2) -adrenoceptor antagonist and unaffected by a 5HT(1B/D) receptor antagonist. DHE also decreased neuronal membrane expression of the P2X(3) receptor.
Our findings provide evidence for a novel mechanism of action for DHE that involves blocking ATP-mediated sensitization of trigeminal neurons, repressing stimulated CGRP release, and decreasing P2X(3) membrane expression via activation of α(2) -adrenoceptors.
Headache The Journal of Head and Face Pain 10/2010; 50(9):1424-39. · 2.94 Impact Factor