This new staging system for IP provides information about prognosis (as operationally defined by RR) for IP managed by advanced endoscopic techniques. In contrast, other staging systems for IP reflect surgeon's judgment rather than outcomes data. This new classification for IP provides important objective data for preoperative planning and patient counseling.
Frontal recess pneumatization patterns differ in the Korean and Caucasian adult populations. Because corresponding differences in skull base length were not identified, these differences seem likely to reflect other factors. Such information has clinical significance for frontal recess surgery in these patient populations.
Osteitis involves inflammatory changes in the underlying bone that may lead to recalcitrant CRS. Osteitis is associated with worsened measures of disease severity such as CT, endoscopy, and olfactory scores, and affects the degree of improvement in quality-of-life measures after both medical and surgical treatment. Future studies directed at characterizing the underlying molecular mechanisms including earlier and precise identification may improve our ability to treat this significant aspect of CRS.
Acoustic trauma was recently shown to induce an inflammatory response in the ear characterized by rapid entry of macrophages in the spiral ligament. The current study seeks to elucidate the mechanisms involved in summoning macrophages to the cochlear lateral wall and the role macrophages play in noiseinduced injury or repair. CCL2 and its primary receptor, CCR2, are the most widely validated effectors of monocyte chemotaxis in vivo. CCL2 -/-and CCR2 -/-mice have been used extensively in studies of monocyte activation in neuronal injury. However, the function of CCL2 and CCR2 in the cochlea has not been studied. The present study examines the role of CCL2 and CCR2 in acoustic injury. CCL2-/-and CCR2 -/-mice on a CX3CR1 +/GFP background were exposed to octave band noise (8-16 kHz) for 2 h to determine the effect of CCL2 and CCR2 on monocyte migration into the cochlea, threshold shift, and cell survival. We found that threshold shift was unchanged in the two knockout mouse strains when compared to the background strain (CX3CR1 +/GFP ). Surprisingly, we found that monocyte migration was also unchanged, despite the absence of CCL2 or CCR2. However, there was a dramatic increase in noise-induced hair cell death in the CCR2 -/-strain. This observation suggests that CCR2, independent of CCL2, plays a protective role in the cochlea after noise, and neither ligand nor receptor is necessary for monocyte migration. Possible mechanisms of neuroprotection by CCR2 are discussed.
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