58 research outputs found
Mechanisms of Hearing Loss after Blast Injury to the Ear
Given the frequent use of improvised explosive devices (IEDs) around the world, the study of traumatic blast injuries is of
increasing interest. The ear is the most common organ affected by blast injury because it is the bodyï¾’s most sensitive
pressure transducer. We fabricated a blast chamber to re-create blast profiles similar to that of IEDs and used it to develop a
reproducible mouse model to study blast-induced hearing loss. The tympanic membrane was perforated in all mice after
blast exposure and found to heal spontaneously. Micro-computed tomography demonstrated no evidence for middle ear or
otic capsule injuries; however, the healed tympanic membrane was thickened. Auditory brainstem response and distortion
product otoacoustic emission threshold shifts were found to be correlated with blast intensity. As well, these threshold
shifts were larger than those found in control mice that underwent surgical perforation of their tympanic membranes,
indicating cochlear trauma. Histological studies one week and three months after the blast demonstrated no disruption or
damage to the intra-cochlear membranes. However, there was loss of outer hair cells (OHCs) within the basal turn of the
cochlea and decreased spiral ganglion neurons (SGNs) and afferent nerve synapses. Using our mouse model that
recapitulates human IED exposure, our results identify that the mechanisms underlying blast-induced hearing loss does not
include gross membranous rupture as is commonly believed. Instead, there is both OHC and SGN loss that produce auditory
dysfunction
Effect of valdecoxib pretreatment on pain and secondary hyperalgesia: a randomized controlled trial in healthy volunteers [ISRCTN05282752, NCT00260325]
BACKGROUND: Induction of the COX-2 isoenzyme appears to play a major role in the genesis of central sensitization after nociceptive stimulation. This study aimed to investigate the efficacy of a single, oral dose of the specific COX-2 inhibitor-valdecoxib in attenuating the central sensitization – induced secondary hyperalgesia in a heat/capsaicin pain model in healthy volunteers. METHODS: The study was a randomized, double blind, placebo controlled, crossover, single dose efficacy trial using 20 healthy volunteers. Two hours following placebo or 40 mg, PO valdecoxib, participants underwent skin sensitization with heat/capsaicin, as well as supra-threshold pain and re-kindling measurements according to an established, validated pain model. Subjects rated pain intensity and unpleasantness on a visual analog scale and the area of secondary hyperalgesia was serially mapped. RESULTS: The area of secondary hyperalgesia produced after 40 mg of valdecoxib was no different than that after placebo. Furthermore, there were no significantly relevant differences when volunteers were treated with valdecoxib or placebo in relation to either cold- or hot pain threshold or the intensity of pain after supra-threshold, thermal pain stimulation. CONCLUSION: We demonstrated that a single, oral dose of valdecoxib when does not attenuate secondary hyperalgesia induced by heat/capsaicin in a cutaneous sensitization pain model in healthy volunteers
Effect of BRAFmutational status on expression profiles in conventional papillary thyroid carcinomas
Exploring the relationship between governance mechanisms in healthcare and health workforce outcomes: a systematic review
Neurochemical, immunological and pharmacological assessments in a transgenic mouse model of the endocrine changes in depression
Malabsorption associated with extreme malnutrition: importance of replacing plasma albumin.
Diarrhea in the intensive care unit: the role of hypoalbuminemia and the response to a chemically defined diet (case reports and review of the literature).
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