Aromatase expression in atypical ductal hyperplasia in women.

PURPOSE: To determine the levels of aromatase in atypical ductal hyperplasia (ADH) lesions, tissue surrounding the ADH, and in dense and non-dense normal breast tissue. We postulated that excess aromatase in breast tissue might, through production of increased estrogen, drive the carcinogenic process. Estrogens and their metabolites are thought to contribute to the development of breast cancer through estrogen receptor-mediated mechanisms and genotoxic effects of estrogen metabolites. ADH is a benign lesion of the breast which is associated with substantially increased risk for subsequent development of breast cancer. After 25 years, approximately 30% of women with ADH develop breast cancer. In women with three or more separate ADH lesions at the same time, 47% will develop breast cancer over that time period. Another important risk factor for breast cancer is the presence of mammographically dense breast tissue. METHODS: We utilized quantitative immunochemical analysis of aromatase in biopsy tissue to test this possibility. Previously published results comparing dense with non-dense breast tissue in normal women (Vachon et al. Breast Cancer Res Treat 125:243-252, 2011) were used for comparisons with ADH. A well-characterized histochemical H-score was employed for quantitative assessment of aromatase in the various tissue studied. RESULTS: The H-score of aromatase staining was statistically significantly higher (p = 0.003) in the ADH epithelium than surrounding epithelial tissue. In order of H-score from highest to lowest were ADH, issue surrounding ADH, dense normal and non-dense normal breast tissues. The levels of aromatase in a subset of women with ADH who went on to develop breast cancer were not higher than in women who did not. CONCLUSIONS: We suggest from these studies that overexpression of aromatase in breast tissue and its resultant increase in estradiol levels may contribute to the later development of breast cancer in women with ADH.

Centrosome-related genes, genetic variation, and risk of breast cancer.

Centrosome amplification has been detected in premalignant lesions and in situ tumors in the breast and in over 70% of invasive breast tumors, and has been associated with aneuploidy and tumor development. Based on these observations, the contribution of commonly inherited genetic variation in candidate genes related to centrosome structure and function to breast cancer risk was evaluated in an association study. Seven-hundred and 82 single nucleotide polymorphisms (SNPs) from 101 centrosomal genes were analyzed in 798 breast cancer cases and 843 controls from the Mayo Clinic Breast Cancer Study to assess the association between these SNPs (both individually and combined) and risk of breast cancer in this population. Eleven SNPs out of 782 from six genes displayed associations with breast cancer risk (P < 0.01). Haplotypes in five genes also displayed significant associations with risk. A two SNP combination of rs10145182 in NIN and rs2134808 in the TUBG1 locus (P-interaction = 0.00001), suggested SNPs in mediators of microtubule nucleation from the centrosome contribute to breast cancer. Evaluation of the simultaneous significance of all SNPs in the centrosome pathway suggested that the centrosome pathway is highly enriched (P = 4.76 × 10(-50)) for SNPs that are associated with breast cancer risk. Collections of weakly associated genetic variants in the centrosome pathway, rather than individual highly significantly associated SNPs, may account for a putative role for the centrosome pathway in predisposition to breast cancer.

Intraoperative ventilator settings and acute lung injury after elective surgery: a nested case control study.

BACKGROUND: While acute lung injury (ALI) is among the most serious postoperative pulmonary complications, its incidence, risk factors and outcome have not been prospectively studied. OBJECTIVE: To determine the incidence and survival of ALI associated postoperative respiratory failure and its association with intraoperative ventilator settings, specifically tidal volume. DESIGN: Prospective, nested, case control study. SETTING: Single tertiary referral centre. PATIENTS: 4420 consecutive patients without ALI undergoing high risk elective surgeries for postoperative pulmonary complications. MEASUREMENTS: Incidence of ALI, survival and 2:1 matched case control comparison of intraoperative exposures. RESULTS: 238 (5.4%) patients developed postoperative respiratory failure. Causes included ALI in 83 (35%), hydrostatic pulmonary oedema in 74 (31%), shock in 27 (11.3%), pneumonia in nine (4%), carbon dioxide retention in eight (3.4%) and miscellaneous in 37 (15%). Compared with match controls (n = 166), ALI cases had lower 60 day and 1 year survival (99% vs 73% and 92% vs 56%; p<0.001). Cases were more likely to have a history of smoking, chronic obstructive pulmonary disease and diabetes, and to be exposed to longer duration of surgery, intraoperative hypotension and larger amount of fluid and transfusions. After adjustment for non-ventilator parameters, mean first hour peak airway pressure (OR 1.07; 95% CI 1.02 to 1.15 cm H(2)O) but not tidal volume (OR 1.03; 95% CI 0.84 to 1.26 ml/kg), positive end expiratory pressure (OR 0.89; 95% CI 0.77 to 1.04 cm H(2)O) or fraction of inspired oxygen (OR 1.0; 95% CI 0.98 to 1.03) were associated with ALI. CONCLUSION: ALI is the most common cause of postoperative respiratory failure and is associated with markedly lower postoperative survival. Intraoperative tidal volume was not associated with an increased risk for early postoperative ALI.

The temporal relationship between speech auditory brainstem responses and the acoustic pattern of the phoneme /ba/ in normal-hearing adults.

OBJECTIVE: To investigate the temporal relationship between speech auditory brainstem responses and acoustic pattern of the phoneme /ba/. METHODS: Speech elicited auditory brainstem responses (Speech ABR) to /ba/ were recorded in 23 normal-hearing subjects. Effect of stimulus intensity was assessed on Speech ABR components latencies in 11 subjects. The effect of different transducers on electromagnetic leakage was also measured. RESULTS: Speech ABR showed a reproducible onset response (OR) 6ms after stimulus onset. The frequency following response (FFR) waveform mimicked the 500Hz low pass filtered temporal waveform of phoneme /ba/ with a latency shift of 14.6ms. In addition, the OR and FFR latencies decreased with increasing stimulus intensity, with a greater rate for FFR (-1.4ms/10dB) than for OR (-0.6ms/10dB). CONCLUSIONS: A close relationship was found between the pattern of the acoustic stimulus and the FFR temporal structure. Furthermore, differences in latency behaviour suggest different generation mechanisms for FFR and OR. SIGNIFICANCE: The results provided further insight into the temporal encoding of basic speech stimulus at the brainstem level in humans.

Pilot study of the impact of letrozole vs. placebo on breast density in women completing 5 years of tamoxifen.

Breast density, a strong risk factor for breast cancer, is reduced by the anti-estrogen, tamoxifen (TAM). We examined whether aromatase inhibitor (AI) therapy results in further reductions in breast density among women completing 5 years of TAM. Among a sample of women with early-onset breast cancer who were randomized to letrozole (LET)(n=56) or placebo (PLAC)(n=48) after 5 years of TAM, we examine the change in percent density at 9-15 months as well as a per-year change in PD by treatment group. There was no difference in the adjusted mean change (-1.0%, LET; -0.3%, PLAC (P=0.58)) or the percentage change (-2.7%, LET; -3.0%, PLAC (P=0.96)) in PD between treatment groups at 9-15 months. Results were similar for longitudinal change (-0.68% per year, LET; -0.12% per year, PLAC (P=0.23)). Breast density does not appear to be a clinically relevant biomarker in women who already have low PD following 5 years of TAM.

Genetic services for familial cancer patients: a survey of National Cancer Institute cancer centers.

In the past decade, significant progress has been made in understanding the genetic component of familial cancers. Genes associated with familial colon and breast cancers have recently been isolated and molecular diagnostic tests are expected to become available in the near future. Clinicians now have the opportunity to recognize and counsel individuals with elevated risk of cancer by identifying risk factors and genes associated with cancer predisposition. The rapid advances in molecular technology are a direct challenge to the medical community and cancer centers to supply specialized clinical services for familial cancers. We sought to ascertain the activities of cancer centers in the development of programs and the provision of genetic services for familial cancer. We surveyed 41 centers with National Cancer Institute (NCI) cancer center support grants. One half of the centers responding (17 of 34) reported that they provide some genetic services for familial cancer. About one half of these 17 centers (eight [57%] of 14; the three remaining clinics that responded had incomplete information on this indicator) see a variety of patient types on a small scale (fewer than 100 patients per year), and most provide four basic clinical evaluations: medical evaluation, cancer risk assessment, genetic counseling, and pedigree analysis. Staffing of each center varied widely, as did the types of screening services offered (including molecular diagnostic testing). Several centers (six [35%] of 17) indicated that they were in the developmental stages for serving familial cancer patients, and many seem to be increasing their activities in this area. The remaining 17 NCI-supported centers that responded, however, currently provide no genetic services for familial cancers. The results of this survey suggest that there is interest in developing clinical programs for familial cancers by NCI-supported cancer centers, but most of these programs are in developmental stages. A base line has been established to monitor future progress for the provision of cancer genetic services.

Genetic analysis of mammographic breast density in adult women: evidence of a gene effect.

BACKGROUND: The appearance of the female breast viewed by mammography varies considerably from one individual to another because of underlying differences in the relative proportions of fat, connective tissue, and glandular epithelium that combine to create a characteristic pattern of breast density. An association between mammographic patterns and family history of breast cancer has previously been reported. However, this association has not been found in all studies, and few data are available on possible genetic components contributing to mammographic breast density. PURPOSE: Our purpose was to estimate familial correlations and perform complex genetic segregation analyses to test the hypothesis that the transmission of a major gene influences mammographic breast density. METHODS: As part of a cohort study (initiated in 1944) of families with a history of breast cancer, the probands' female relatives who were older than 40 years were asked to obtain a routine mammogram. The mammograms of 1370 women from 258 independent families were analyzed. The fraction of the breast volume occupied by radiographically dense tissue was estimated visually from video displays of left or right mediolateral oblique views by one radiologist experienced in mammography who had no knowledge of individual relationships to the probands. Data on breast cancer risk factors were obtained through telephone interviews and mailed questionnaires. Unadjusted and adjusted familial correlations in breast density were calculated, and complex genetic segregation analyses were performed. RESULTS: Sister-sister correlations in breast density (unadjusted and adjusted for age and either body mass index, menopausal status, hormone replacement therapy, waist-to-hip ratio, number of live births, alcohol consumption, or cigarette smoking status) were all statistically significant (r = .16-.27; all P<.05 [two-sided]). Estimated mother-daughter correlations were smaller in magnitude (r = .01-.17) and not statistically significant. Segregation analyses indicate that a major autosomal gene influences breast density. The mendelian transmission of a dominant gene provided the best fit to the data; however, hypotheses involving the inheritance of either a recessive gene or a codominant gene could not be ruled out. The mendelian dominant hypothesis, accounting for 29% of the variability in breast density, suggests that approximately 12% of the population would be expected to carry at least one variant allele of this putative gene. Women who inherit the variant allele would have a mean breast density about twice that of the rest of the population. CONCLUSIONS: Our preliminary findings suggest that, in this cohort of women at risk of breast cancer, mammographic breast density may be genetically influenced.

Lung cancer risk reduction after smoking cessation: observations from a prospective cohort of women.

PURPOSE: We conducted this study because the duration of excess lung cancer risk among former smokers has been inconsistently reported, doubt has been raised regarding the population impact of smoking cessation, and differential risk reduction by histologic cell type after smoking cessation needs to be confirmed. METHODS: The Iowa Women's Health Study is a prospective cohort study of 41,836 Iowa women aged 55 to 69 years. In 1986, mailed questionnaires were used to collect detailed smoking history. Age-adjusted lung cancer incidence through 1999 was analyzed according to years of smoking abstinence. Relative risks were estimated using Cox regression analysis. RESULTS: There were 37,078 women in the analytic cohort. Compared with the never smokers, former smokers had an elevated lung cancer risk (relative risk, 6.6; 95% confidence interval, 5.0 to 8.7) up to 30 years after smoking cessation for all former smokers. However, a beneficial effect of smoking cessation was observed among recent and distant former smokers. The risk of adenocarcinoma remained elevated up to 30 years for both former heavier and former lighter smokers. CONCLUSION: The risk for lung cancer is increased for both current and former smokers compared with never smokers and declines for former smokers with increasing duration of abstinence. The decline in excess lung cancer risk among former smokers is prolonged compared with other studies, especially for adenocarcinoma and for heavy smokers, suggesting that more emphasis should be placed on smoking prevention and lung cancer chemoprevention.

Racial differences in primary cytogenetic abnormalities in multiple myeloma: a multi-center study.

We examined four clinically assessed cytogenetic subtypes (t(11;14), t(4;14), monosomy 13/del13q and monosomy 17/del17p in 292 black patients with newly diagnosed multiple myeloma (MM) from four medical centers, who had fluorescent in situ hybridization testing results available in their medical records. We then compared the prevalence of these abnormalities with a previously characterized Mayo Clinic cohort of 471 patients with MM. We found a significant difference in the prevalence of the t(11;14) immunoglobulin heavy chain (IgH) translocation between blacks and whites, 6.5% versus 17.6%, respectively, P<0.0001. Blacks also had lower rates of the t(4;14) IgH translocation, (5.5% versus 10%); monosomy 13/del13q (29.1 versus 49.3%); and monosomy 17/del17p (7.9% versus 13%). Consequently, 63.4% of blacks versus 34.6% of whites did not have any of the four abnormalities that we studied, P<0.001. As almost all MM is associated with either an IgH translocation or trisomies, we hypothesize that MM in blacks is associated with either excess prevalence of either the trisomic (hyperdiploid) form of MM or an IgH translocation besides t(11;14) or t(4;14). We conclude that there are significant differences in the cytogenetic subtypes of MM that occur in blacks and whites.

Association of diet and mammographic breast density in the Minnesota breast cancer family cohort.

Mammographic breast density is a significant risk factor for breast cancer. The present report analyzes the association of breast density and dietary factors in 1508 women in a historical cohort study of breast cancer families in Minnesota. Diet was assessed by a semiquantitative food frequency questionnaire. Percent breast density was estimated visually by a radiologist experienced in mammography. The association of percent breast density with quartiles of energy-adjusted dietary intakes was examined in analysis of covariance models adjusting for potential confounding effects of age, body mass index, and other covariates as well as correcting for familial correlation. Analyses were performed on all women combined and were also stratified by menopausal status. Among premenopausal women, percent breast density was positively associated with intakes of polyunsaturated fat, polyunsaturated:saturated fat ratio, and vitamins C and E and was inversely associated with saturated fat and total dairy intake. Among postmenopausal women, vitamin B12 was linearly associated with increased breast density. The positive associations for vitamin C and B12 were attributable to supplement intake only. There was a suggestive positive trend between breast density and daily alcohol consumption in both premenopausal and postmenopausal women. After adjustment for other sources of alcohol, only wine intake among postmenopausal women was significant such that white wine showed a positive association and red wine an inverse association with percent breast density. There was no association with other examined dietary factors. The cross-sectional differences in breast density across levels of dietary factors were small in magnitude but may have implications for breast cancer risk.

Cigarette smoking increases risk for breast cancer in high-risk breast cancer families.

Most epidemiological studies of cigarette smoking and breast cancer have failed to demonstrate a strong association. Only one study has been performed on women at high genetic risk, and smoking was reported to be a protective factor. To further explore this observation, we examined the association of cigarette smoking with the risk of breast cancer in a historical cohort study of high-risk breast cancer families. A total of 426 families ascertained through a consecutive series of breast cancer patients (probands) between 1944 and 1952 were followed through 1996. Occurrence of breast cancer and detailed smoking histories for sisters, daughters, granddaughters, nieces, and marry-ins were obtained through telephone interviews between 1991 and 1996. Cox proportional hazards regression, accounting for age, birth cohort, and other risk factors, was used to calculate relative risks and 95% confidence intervals (CIs) of breast cancer. All of the models were constructed within strata defined by relationship to the index case (proband), with nonsmokers designated as the referent group. Of the 426 families in the cohort, 132 had at least three incident breast and/or ovarian cancers in the biological relatives at the end of the follow-up period. Among sisters and daughters in these 132 high-risk families, those who ever smoked were at 2.4-fold increased risk of breast cancer (95% CI, 1.2-5.1) relative to never-smokers. No association between breast cancer and smoking was observed among nieces and granddaughters of probands or among marry-ins. When the analysis was restricted to 35 families at highest genetic risk (each containing five breast and/or ovarian cancers), smoking became an even stronger risk factor. Among sisters and daughters, ever-smokers were at 5.8-fold greater risk than nonsmokers (95% CI, 1.4-23.9). Among nieces and granddaughters, the risk of breast cancer associated with smoking was increased 60% (95% CI, 0.8-3.2). These results suggest that smoking may increase risk for breast cancer in families with multiple cases of breast or ovarian cancer, especially those with the strongest apparent familial predisposition.

Fifty-year follow-up of cancer incidence in a historical cohort of Minnesota breast cancer families.

A family history of breast cancer is well established as a risk factor for the disease. Because family history is a dynamic rather than a static characteristic, longitudinal studies of entire families can be very instructive in quantifying the significance of risk classification. The Minnesota Breast Cancer Family Study is a historical cohort study of relatives of a consecutive series of 426 breast cancer cases (probands) identified between 1944 and 1952. The incidence of cancer and the measurement of risk factors in sisters, daughters, granddaughters, nieces, and marry-ins was determined through telephone interviews and mailed questionnaires. Ninety-eight percent of eligible families were recruited, and 93% of members participated. A total of 9073 at-risk women were studied: 56% were biological relatives of the case probands, whereas the others were related through marriage. Through 1996, 564 breast cancers were identified in nonprobands. Compared to the rate of breast cancer among marry-ins (188 cases), sisters and daughters of the probands were at a 1.9-fold greater age-adjusted risk (128 cases; 95% confidence interval, 1.4-2.4); granddaughters and nieces were at a 1.5-fold greater risk (248 cases, 95% confidence interval, 1.2-1.8). The breast cancer risk since 1952 was not distributed equally across families: although all biological relatives had a family history of breast cancer, 166 families (39%) experienced no additional cases. Most of the cases occurred among a subset of families: 21 families had 5 breast or ovarian cancers, 8 had 6, 2 had 7, and 4 had > or =8. There was no evidence of significantly increased risk for cancer at other sites, including the ovaries, cervix, uterus, colon, pancreas, stomach, or lymphatic tissue, although there was some evidence that stomach cancer in previous generations may help define the susceptible subset. These families contain four to five generations of validated occurrences of cancer, thus minimizing the uncertainty of genetic risk inherent in a disease with a late and variable age at onset. The patterns of breast cancer in these multigeneration families is consistent with the influence of autosomal dominant susceptibility in a subset, low penetrance genes in another, and purely environmental influences in the remainder.

The effects of theophylline and 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (RO 20-1724) on protein secretion from rat parotid gland.

1 The effects of two chemically distinct cyclic nucleotide phosphodiesterase (PDE) inhibitors on protein secretion from superfused rat parotid gland were studied.2 In the presence of 1.0 mM Ca(2+), Ro 20-1724 (10 muM), an imidazolidinone derivative, increased the secretory response to isoprenaline 100% and the isoprenaline-dependent accumulation of adenosine cyclic 3',5'-monophosphate (cyclic AMP) 300-400%. At this concentration Ro 20-1724 alone did not cause protein secretion, accumulation of cyclic AMP or significantly inhibit PDE activity in cell-free preparations from parotid gland.3 In the absence of added Ca(2+) and in the presence of 1.0 mM EGTA, Ro 20-1724 inhibited the secretory response to isoprenaline 65% while increasing isoprenaline-dependent cyclic AMP accumulation 200%.4 In the presence of Ca(2+), theophylline (10 mM) stimulated protein secretion but did not cause the accumulation of cyclic AMP. When combined with isoprenaline the rate of secretion was greater than the sum of the effects of the individual drugs but there was no effect of theophylline on the isoprenaline-dependent accumulation of cyclic AMP.5 Theophylline-stimulated protein secretion is increased by omitting Ca(2+) from the superfusion medium without any detectable change in cyclic AMP accumulation. Under these conditions Ro 20-1724 inhibits theophylline-stimulated protein secretion and the maximum rate of protein secretion in the presence of isoprenaline and theophylline is no greater than that seen with either agent alone.6 It is concluded that the theophylline effects do not result from inhibition of PDE. It is suggested that the primary action of both drugs on parotid gland acinar cells is to alter the distribution of intracellular Ca(2+). Ro 20-1724 may also inhibit Ca(2+)/calmodulin activated enzymes such as PDE.

Soccer accidents in the French Rhône-Alpes Soccer Association.

The analysis of 6153 accidents reported to the insurance company of the French Rhône-Alpes Soccer Association, for the 1980-81 season was undertaken, providing a survey of acute pathology in French soccer accidents and an estimation of the cost of this pathology to French society. Findings from this study include: injuries--ankle sprain is the most common; fractures prevail in the young players pathology; exposure--the average risk is one accident for 20 matches; the highest risk is for the senior category; collisions with opponents is the main cause of accidents; the first 5 minutes of the second half have a peak of accidents; the players exposure is roughly the same whatever their position on the ground; risk--winter should not increase the risk if the matches are played under good conditions; the risk is unevenly distributed according to the level of practice; cost--the cost for France over 1 year was estimated at US$20,000,000 and the total number of sick leave days at 2000 years; games with several accidents are very common in January and for the adult category. Consequently, tightening up the safety measures would be a very good investment.

Circadian variation of food intake and digestive tract contents in the rat.

The variation of food intake and digestive tract contents over a period of 24 hours was measured in the free feeding rat kept under a 12:12 hr light:dark cycle (lights on at 0700 hr). After a cessation between 0700 and 1000 hr, the rate of food intake increased progressively during daytime followed by a marked increase and a plateau after lights went off. In the dark, dry matter in the stomach was almost ten times the levels of the light phase. In the major part of the high feeding period, the rates of food intake and gastric emptying equilibrated. Dry matter content of the intestine also followed circadian variations that were specific for each segment. The time-to-time content of the mid-gut segment was closely related to gastric emptying. The extent of dry matter absorption in the proximal intestine decreased continuously from the time lights went on and reached a minimum at 22 hr. Absorption in the distal segments was much less subjected to variation over 24 hours. In the free feeding situation, the changes induced by the light cycle on the rhythm of food intake were accompanied by marked modifications of digestive tract contents including those of the intestine. Data indicate a close relationship between gastric function and the middle portion of the intestine.

Mechanical and structural properties of milk protein edible films cross-linked by heating and gamma-irradiation.

The mechanical properties of cross-linked edible films based on calcium caseinate and two type of whey proteins (commercial and isolate) were investigated. Cross-linking of the proteins was carried out using thermal and radiative treatments. Size-exclusion chromatography performed on the cross-linked proteins showed that gamma-irradiation increased the molecular weight of calcium caseinate, while it changed little for the whey proteins. However, heating of the whey protein solution induced cross-linking. For both cross-linked proteins, the molecular weight distribution was >/=2 x 10(3) kDa. Combined thermal and radiative treatments were applied to protein formulations with various ratios of calcium caseinate and whey proteins. Whey protein isolate could replace up to 50% of calcium caseinate without decreasing the puncture strength of the films. Films based on commercial whey protein and calcium caseinate were weaker than those containing whey protein isolate. Electron microscopy showed that the mechanical characteristics of these films are closely related to their microstructures.

Model for understanding the influence of some parameters in cochlear implantation.

Considering the recognition performance obtained by an implanted patient, the authors have developed models to explain the decrease in performance when the number of open channels on the prosthesis is increased. The French cochlear implant Chorimac was used in this experiment. Two models have been developed. The first is monodimensional and the second is multidimensional. They respectively represent an increase in information and its superposition. Results suggest that for the patient, the superposition factor prevails and is detrimental to recognition. Its elimination should be a major goal. A good selection of electrodes in a relatively small number seems to be the best policy. This is already done in some cochlear implants. Some other parameters in the signal that seem worth being analyzed are introduced.

Acoustical recognition of laryngeal pathology: a comparison of two strategies based on sets of features.

The efficiency of sets of acoustical features discriminating pathological voices from control voices is reported. Two strategies were compared. The first (called the 'distance strategy') was built upon a statistical distance of voice features to reference values obtained for a set of healthy (reference) voices. The second strategy (called the 'range strategy') is based on the position inside or outside normal ranges established from a reference population; results based on this strategy were presented in a previous paper. Reference values were calculated from a database of 200 healthy voices distributed into 10-year age groups ranging from 20 to 70. Comparisons were made using a second database of 220 voices, including 65 control, 51 functional dysphonia, 50 with nodules on the vocal folds and 54 recurrent nerve palsy. The phonetic material was compared of 17 French vowels: 11 vowels in a sentence, three isolated vowels and three segments (beginning, middle and end) of the sustained vowel /a/. Four acoustical features were considered for each vowel: the voice fundamental (f0) and the first three formant frequencies. Acoustical features were calculated on an ILS (Interactive Laboratory System) analysis system (workstation). The separation of each pathological group from the control group, using sets of acoustical features, was statistically assessed. From the strategy point of view, results indicated that (i) the fundamental frequency f0 was the best measure to separate normal from pathological voices with the distance strategy; (ii) when the formants were taken, the range strategy performed better in separating the voices. For classification of pathologies, the best separation coefficients were obtained with nodules and the worst with recurrent nerve palsy. Overall, it was seen that the separation between control and pathological voices was most efficient when measured using the distance strategy for f0. The range strategy was useful with formant frequencies.

Acoustical recognition of laryngeal pathology using the fundamental frequency and the first three formants of vowels.

The recognition of laryngeal pathology by analysis of the voice is investigated. The fundamental frequency and the first three formants are considered. The recognition strategy is based on comparison with normal ranges calculated over 200 ordinary voices, grouped in ten age classes ranging from 20 to 70 years, for males and females. 220 test voices are studied divided into four groups: normal voices, functional dysphonia, nodules and recurrent nerve palsy. Each subject is marked according to his/her normal range. Parameters (or items) are calculated on the Interactive Laboratory System workstation. The vocalic material is composed of 11 vowels taken from a sentence. Results are given in terms of the number of values out of the normal ranges. Statistical analysis considers both parameter ability and error rates in pathology recognition. Pathology recognition shows the following error percentages: 23% for dysphonia, 14% for nodules and 33% for recurrent nerve palsy. Parameters do not show the same efficiency for voice pathology characterisation. Formants appear to be better than the fundamental frequency.

Evaluation of cochlear implanted children's voices.

Cochlear implant (CI) is a good means in developing communication in deaf children. Nevertheless, compared to children with the same age, CI patients' voices are far from being similar. In this work, the voice of CI children has been compared with the voice of corresponding normal children (same age, same sex) included in the main stream. Six girls and two boys participated to the experiment. The phonetic material was a paragraph of the French standard text La bise et le soleil (The North Wind and the Sun). An objective and a subjective analysis of the voice were done and parameters were compared between both groups of people (implantees and control). Studied parameters were voice pitch, intensity, fluency, pauses, articulation and pleasantness in the objective analysis, and voice pitch, formants, and duration for the objective study. It appeared that intensity variations were different between control and implanted subjects. Also voice formants were not situated in the same region regarding the normal ranges, but differences were difficult to assess. Globally, the main change was in the speaking duration. This method is open for further studies and points out some relevant items for an efficient use in rehabilitation sessions.