The pharyngoesophageal high pressure zone (PE-HPZ) was measured prelaryngectomy and postlaryngectomy with a new force-summing probe that accounts for sphincter pressure asymmetry. A total of 31 patients were studied six times each. Postoperatively, pressures dropped from 130+/-24 mm Hg to 66+/-9 mm Hg. After a standardized, intensive laryngectomy rehabilitation program, 12 of 19 postoperative patients acquired acceptable esophageal speech and 7 did not. Speakers and nonspeakers were found to have nearly identical PE-HPZ pressures (speakers = 70+/-10 mm Hg, nonspeakers = 59+/-18 mm Hg). Differences in sphincter length or relaxation likewise did not discriminate between these two groups. We conclude that PE-HPZ pressure is not a critical determinant of the acquisition of esophageal speech.
Dibromoacetic acid (DBA) and bromodichloromethane (BDCM), by-products of chlorine disinfection of water, were provided in drinking water in range-finding reproductive/developmental toxicity studies (rats) and a developmental toxicity study (BDCM) in rabbits. Studies included absorption and biodisposition of DBA and BDCM, including passage into placentas, amniotic fluid, fetuses (rats and rabbits), or milk (rats). The DBA and BDCM range-finding reproductive/developmental toxicity studies each included 50 Sprague-Dawley rats/sex/group. DBA (0, 125, 250, 500, or 1000 ppm) or BDCM (0, 50, 150, 450, or 1350 ppm) was provided in drinking water 14 days premating through gestation and lactation (63 to 70 days). The developmental toxicity range-finding study included 25 time-mated New Zealand white rabbits/group given 0, 50, 150, 450, or 1350 ppm BDCM in drinking water on gestation days (GDs) 6 through 29. Satellite groups (6 male, 17 female rats/group/study and 4 rabbits/group) were used for bioanalytical sampling. Rats and rabbits had exposure-related reduced water consumption caused by apparent taste aversion to DBA or BDCM, especially in the parental animals at the two highest exposure levels (500 and 1000 ppm DBA; 450 and 1350 ppm BDCM). Female rats consumed slightly higher mg/kg/day doses of DBA than male rats, especially during gestation and lactation; weanling rats consumed the highest mg/kg/day doses. DBA produced detectable and quantifiable concentrations in plasma, placentas, amniotic fluid, and milk. Plasma samples confirmed that rats drink predominately during the dark; this drinking pattern, not accumulation, produced detectable plasma concentrations for 18 to 24 hours/day. No quantifiable concentrations of BDCM occurred in plasma, placentas, amniotic fluid, or milk, suggesting that BDCM is rapidly degraded or metabolized in vivo. DBA (500 and 1000 ppm, rats) and BDCM (450 and 1350 ppm, rats and rabbits) produced secondary toxicity in the parental generation by reducing water consumption, which caused severe exposure-related apparent dehydration, reduced feed intake and weight gain. Reproductive and developmental parameters were essentially unaffected (mating possibly reduced [DBA at 1000 ppm]; exposure-related decreases in body weights of pups secondary to reduced water and feed consumption [DBA at 250, 500, and 1000 ppm; BDCM at 150, 450, and 1350 ppm]). No effects on development of rabbit fetuses occurred at BDCM concentrations as high as 1350 ppm. Results from these preliminary studies, in which DBA and BDCM were provided in the drinking water at concentrations thousands of times higher than those to which humans are exposed, suggest that neither DBA nor BDCM are reproductive/developmental risks for humans.
Computer-assisted curve-fitting techniques were used to describe quantitative and qualitative characteristics of normal tympanometric shape. The data base consisted of sets of triplicate tympanograms, obtained at 2-week intervals, from 7 2 ears of children with normal middle ears enrolled in the first through the fifth grades. A nonlinear equation produced significantly better prediction of normal tympanograms (R2 = 0.70) than did linear equations (R2 -= 0.44).bringing into question the use of the latter in determining normality. The complexity of applying curve fitting in clinical practice led to the development of a qualitative technique to determine normality. An initial application of the technique as a screen in 7 6 ears subjected to myringotomy produced a sensitivity of 96% and a specificity of 83% with respect to identification of the presence of middle ear fluid.A tympanogram is a record of the energy transfer characteristics of the middle ear as a function of pressure changes in the external canal. For a variety of reasons, shape seems to be of more clinical value than absolute indexes of energy tran~fer,~ although there is no consensus regarding description of shape. The most commonly used system of typing was introduced by Jerger4 and is based on the presence or absence of a peak and its location.Others have examined tympanometric shape more quantitatively. Liden et a1.8 proposed a system in which a tympanogram would be described by ( 1) the differences between energy transfer at +200 mm H 2 0 and -200 mm H20, (2) the width in millimeters of H20 of the tympanogram between its one-half of maximum energy transfer points, and (3) the pressure at which maximum energy transfer occurred. Brooks' addressed himself to a tympanogram's "gradient," calculated by dividing the change in energy transfer over a 100 mm H20 range in the area of the peak by the maximum change in energy transfer over the entire tympanogram. It is noted that ' Portions of this investigation were supported by Grason-Stadler.Inc., and Grant RFP-NIH-NINCDS-79-12 from the National Institute of Neurological and Communicative Disorders and Stroke.
Lee et al. (2005) misquoted our hypothesis (Gates et al. 2000) and, not unexpectedly, differed in their conclusion about the effect of noise on cochlear aging. We described actual shifts in noise-damaged ears and found a significant effect. In contrast, Lee et al. (2005) described predicted shifts in noise-exposed ears and found a similar pattern albeit not statistically significant. Although these are different concepts, the similarity in the primary graphs in both reports (Figures 1 and 2) suggests a substantial degree of parallelism.A convincing case can be made that if Lee et al. (2005) had simply followed their subjects longer and had an adequate sample size, their conclusions would have been similar to ours. We had an IS year, not a 6.4-yr follow-up and nearly twice the sample size. Moreover, few of their cases had audiometric evidence of noise damage. Thus, their conclusion that noiseexposed ears do not age differently than nonexposed ears may be underpowered and premature.We look forward to a re-evaluation of their cases after longer follow-up and predict that their data will support ours despite the difference in experimental design. We clearly showed that noise-damaged ears do change with age in adjacent frequency regions differently than nondamaged ears.
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