Speech recognition as a function of the number of electrodes used in the SPEAK cochlear implant speech processor.

Speech recognition was measured in listeners with the Nucleus-22 SPEAK speech processing strategy as a function of the number of electrodes. Speech stimuli were analyzed into 20 frequency bands and processed according to the usual SPEAK processing strategy. In the normal clinical processor each electrode is assigned to represent the output of one filter. To create reduced-electrode processors the output of several adjacent filters were directed to a single electrode, resulting in processors with 1, 2, 4, 7, 10, and 20 electrodes. The overall spectral bandwidth was preserved, but the number of active electrodes was progressively reduced. After a 2-day period of adjustment to each processor, speech recognition performance was measured on medial consonants, vowels, monosyllabic words, and sentences. Performance with a single electrode processor was poor in all listeners, and average performance increased dramatically on all test materials as the number of electrodes was increased from 1 to 4. No differences in average performance were observed on any test in the 7-, 10-, and 20-electrode conditions. On sentence and consonant tests there was no difference between average performance with the 4-electrode and 20-electrode processors. This pattern of results suggests that cochlear implant listeners are not able to make full use of the spectral information on all 20 electrodes. Further research is necessary to understand the reasons for this limitation and to understand how to increase the amount of spectral information in speech received by implanted listeners.

Seismic analysis for design or retrofit of gravity bridge abutments

Depending on their seismic resistance, existing bridge abuments may be vulnerable to earthquake. Seismic resistance may be quantified in terms of a threshold acceleration level beyond which permanent deformation will occur. During a seismic event, whenever the ground acceleration exceds the threshold, permanent deformation accumulates. The current displacement-based design procedure considers only the possibility of a sliding mode of failure between the abutment and foundation soil The procedure allows one to estimate the amount of permanent horizontal displacement given relevant earthquake parameters, and tthe seismic resistance of the bridge abutment. The results from these tests verify the analytic procedurrre for predicting critical threshold acceleration based on simple theory. Computation of predicted displacements and rotation are reasonable. Thus it is now possible, with this analytic tool, to evaluate the seismic vulnerability of existing abutments. This is demostrated for a representative sample of 40 bridges with free-standing abutments from New York State.It appears that significant numbers are at risk from an earthquake with peak accelerations above 0.15g. The results indicate that extending this easy screening procedure to other areas in the East and Midwest in moderate earthquake zones would be worthwhile. The also relates directly to design recommendations to increease the seismic capacity of both existing bridge abutments and new designs. Not only can the critical threshold acceleration be made higher with passive restraint footing keys, piles or tiebacks but girder seats, knock-off walls and transverse restraint can be designed to reduce damage in extreme events.(AU)

Seismic analysis and design of bridge abutments considering sliding and rotation

Current displacement based seismic design of gravity retaining walls utilizes a sliding block idealization, and considers only a translation mode of deformation. However, results from recent studies demostrate the possibility of seismic loss of bearing capacity and subsequent rotation or mixed mode of deformation. The purpose of the task described herein is to generalize the sliding block procedure to determine seismic displacements of walls and bridge abutments to include mixed-mode behavior with rotation due bearing capacity movement.(AU)

Comparison of urinary 6-beta-cortisol and the erythromycin breath test as measures of hepatic P450IIIA (CYP3A) activity.

The production of 14CO2 in the breath from an intravenous dose of [14C-N-methyl]-erythromycin (the erythromycin breath test [ERMBT]) and the measurement of the ratio of 6-beta-cortisol to free cortisol (6-beta-F/FF) in the urine have each been proposed as means of measuring hepatic P450IIIA catalytic activity in patients. We found that there was a significant correlation between the results of each test (r = 0.59, p less than 0.001) in 47 patients who were without liver disease and who were not taking medications believed to influence P450IIIA catalytic activity. In the 24 of these patients who were subsequently treated with the P450IIIA substrate cyclosporine, the ERMBT result was highly correlated with the mean trough cyclosporine blood level observed; however, there was no correlation between urinary 6-beta-F/FF and the cyclosporine blood levels. In a separate study of a patient during the anhepatic phase of liver transplantation surgery, the ERMBT result decreased by greater than 85%, whereas urinary 6-beta-F/FF decreased by just 50%. We conclude that the ERMBT and urinary 6-beta-F/FF do not always provide similar information about P450IIIA catalytic activity in patients, possibly because of extrahepatic production of 6-beta-F. Of the two tests, the ERMBT appears to provide the most relevant information for cyclosporine administration.

The effect of long-acting analog of luteinizing hormone-releasing hormone on growth hormone secretory dynamics in children with precocious puberty.

Long-acting preparations of LHRH (LHRHa), such as leuprolide acetate, have been shown to selectively and reversibly suppress the clinical and biochemical features of central precocious puberty (CPP). The withdrawal of gonadal sex steroids results in a decline of growth velocity and a decrease in the rate of bone age maturation, with resultant improvement in predicted adult stature. The purpose of this study was to define GH secretory dynamics in children treated with leuprolide acetate. Twelve-hour nocturnal GH studies were performed in five children (four girls and one boy) with CPP before and after 6 months of treatment with leuprolide acetate. Mean GH levels, GH secretory rate, and number of GH secretory episodes were determined. Secretory profiles were analyzed using the Cluster program. Growth velocity, somatomedin-C, and dehydroepiandrosterone sulfate were measured before and after 6 months of therapy. By 6 months of therapy, there was a significant decrease in mean growth velocity from 10.5 +/- 3.3 to 6.7 +/- 1.6 cm/yr. Somatomedin-C levels remained the same at 46.90 +/- 9.51 and 52.5 +/- 12.40 nmol/L. Levels of dehydroepiandrosterone sulfate remained unchanged at 118.6 +/- 71.4 and 139.0 +/- 61.3 mumol/L at 0 and 6 months of the study. By 6 months, there was a significant decrease in mean GH levels from 13.6 +/- 5.3 to 6.4 +/- 3.4 micrograms/L (P less than 0.05). Total GH levels decreased from 1367.9 +/- 687.3 to 447.0 +/- 186.5 ng/12 h. The number of GH secretory episodes remained the same at 5.4 +/- 1.5 and 4.8 +/- 1.0/12 h at 0 and 6 months of study. Therefore, the decrease in GH that occurs during the withdrawal of gonadal sex steroids with LHRHa in children with CPP is an amplitude-modulated phenomenon, as the number of secretory peaks remains unchanged.

Normative data for adrenal steroidogenesis in a healthy pediatric population: age- and sex-related changes after adrenocorticotropin stimulation.

The normal response to a single 0.25-mg dose of ACTH-(1-24) is not well established in infancy or childhood. We report the adrenal steroidogenic responses of 17-hydroxypregnenolone (17OH Preg), 17-hydroxyprogesterone (17OH Prog), 11-deoxycortisol, cortisol, deoxycorticosterone, dehydroepiandrosterone (DHEA), DHEA sulfate, androstenedione (A'dione), and testosterone in 102 healthy children who were divided into 5 groups: group 1 (less than 1 yr old; n = 22), group 2 (1-5 yr old; n = 22), group 3 (6-12 yr old; n = 15), group 4 (early-midpuberty; n = 21), and group 5 (late puberty; n = 22). Baseline and stimulated levels of 17OH Preg were significantly higher in group 1 infants than in group 2 children (P less than 0.01). Baseline levels of 17OH Prog increased in late puberty (P less than 0.01). Baseline and stimulated levels of DHEA rose in late puberty (group 5 vs. group 3, P less than 0.01). DHEA levels in late pubertal females were higher than those in their male counterparts (P less than 0.01). DHEA sulfate levels did not change after ACTH administration in any age group. Baseline and stimulated levels of A'dione rose significantly before the onset of puberty in female children (group 2 vs. group 3, P less than 0.01). The calculated ratio of 17OH Preg/17OH Prog in group 1 was significantly higher than that in other groups of children (P less than 0.01). The calculated, baseline DHEA/A'dione ratio was higher in group 1 than in older children (P less than 0.01). Stimulated ratios were higher in late pubertal females than in males (P less than 0.01). In both sexes baseline and stimulated ratios of 17OH Prog/deoxycorticosterone increased in puberty, such that late pubertal children had higher levels than prepubertal children (P less than 0.01). These data confirm the need for interpretation ACTH stimulation test data to be based upon age- and sex-specific norms.

Effects of growth hormone therapy on circadian osteocalcin rhythms in idiopathic short stature.

The effects of GH administration on the circadian osteocalcin (Oc) rhythm were determined in four prepubertal children with idiopathic short stature (height, less than 5th percentile; growth velocity, less than 50th percentile for age). Each child underwent 24-h sequential blood sampling on three occasions: immediately before the initiation of GH treatment, 6 months later, and at the end of 12 months of treatment. The growth rate increased more than 50% over baseline in three of the four children during at least one of the 6-month periods. Insulin-like growth factor-I levels increased during treatment in all of the children. Twenty-four-hour Oc levels increased on 7 of the 8 treatment days evaluated. When mean 24-h Oc patterns for each of the 3 study days were derived by averaging across individual subjects at each time point and then compared, we noted an upward shift in the entire pattern during treatment (t = 13.2 at P less than 0.001 and t = 5.9 at P less than 0.001 for 6 and 12 month comparisons vs. the pretreatment day, respectively). This was more easily appreciated after the data were smoothed using the method of running means. There was, in addition, a progressive improvement in the shape of the Oc pattern compared to a normative model derived from a study of healthy adult men. The correlation between the model and the pre-GH day was 0.46, that between the model and the 6 months of GH day was 0.77, and that between the model and the 12 months of GH day was 0.96. Cross-correlation analyses showed that the peak correlation between the 2 treatment days and the model occurred at zero lag. In contrast, the peak correlation between the pre-GH day and the model or the pre-GH day and either of the 2 treatment days occurred when the pre-GH series was lagged by 2-3 h. Thus, an additional finding is the synchronization of the Oc series that occurred during treatment. We conclude that GH treatment increases Oc concentrations in children with idiopathic short stature by affecting its circadian rhythm. This rise in Oc values may not necessarily reflect an increase in growth velocity.