Biomedical subjects

Graciela E Silva

Publications and source records attributed to Graciela E Silva.

3 recordsLinked to original sources

PubMed2007

Comparison between reported and recorded total sleep time and sleep latency in 6- to 11-year-old children: the Tucson Children's Assessment of Sleep Apnea Study (TuCASA).

Research comparing parental report of sleep times to objectively obtained polysomnographic evidence of sleep times in schoolchildren is lacking. This report compares habitual sleep time and objectively recorded sleep time and sleep latency with parental reports of sleep time immediately after a night of polysomnography in elementary schoolchildren. Unattended home polysomnograms (PSG) were obtained from 480 children. On the night of the PSG, a parent was asked to complete a Sleep Habits Questionnaire, which inquired about the habitual total sleep time (HABTST) and habitual sleep onset latency (HABSOL) of his/her child on both school days and nonschool days. On the morning after the PSG, the parent was asked to estimate the total sleep time (ESTTST) and sleep onset latency (ESTSOL) of his/her child on the night of the recording. Comparisons were made to actual total sleep time (PSGTST) and sleep latency (PSGSOL) on the PSG. The sample was comprised of 50% girls, 42.3% Hispanic, and 53% aged 6-8 years. The mean HABTST, ESTTST, and PSGTST were 578, 547, and 480 min, respectively. HABTST was greater than both ESTST and PSGTST (p < 0.001). Moreover, ESTTST was greater than PSGTST (p < 0.001). The mean HABSOL, ESTSOL, and PSGSOL were 15, 17, and 11 min. ESTSOL was longer than PSGSOL (p < 0.001). There were no gender differences. However, Hispanic parents reported significantly less HABTST in their children than Caucasian parents (566 vs 587 min, p < 0.001). Parents of schoolchildren in this population-based sample substantially overestimated their children's actual total sleep time and sleep onset latency.

Adult↗

PubMed2004

Asthma as a risk factor for COPD in a longitudinal study.

BACKGROUND: For several years, asthma and COPD have been regarded as distinct entities, with distinct clinical courses. However, despite distinctive physiologic features at the time of diagnosis, and different risk factors, the two diseases over time may develop features that are quite similar. STUDY OBJECTIVE: To evaluate the association between physician-diagnosed asthma and the subsequent development of COPD in a cohort of 3,099 adult subjects from Tucson, AZ. DESIGN AND METHODS: A prospective observational study. Participants completed up to 12 standard respiratory questionnaires and 11 spirometry lung function measurements over a period of 20 years. Survival curves (with time to development of COPD as the dependent variable) were compared between subjects with asthma and subjects without asthma at the initial survey. RESULTS: Subjects with active asthma (n = 192) had significantly higher hazard ratios than inactive (n = 156) or nonasthmatic subjects (n = 2751) for acquiring COPD. As compared with nonasthmatics, active asthmatics had a 10-times-higher risk for acquiring symptoms of chronic bronchitis (95% confidence interval [CI], 4.94 to 20.25), 17-times-higher risk of receiving a diagnosis of emphysema (95% CI, 8.31 to 34.83), and 12.5-times-higher risk of fulfilling COPD criteria (95% CI, 6.84 to 22.84), even after adjusting for smoking history and other potential confounders. CONCLUSIONS: Physician-diagnosed asthma is significantly associated with an increased risk for CB, emphysema, and COPD.

Adult↗

PubMed2003

A longitudinal study of alpha1-antitrypsin phenotypes and decline in FEV1 in a community population.

BACKGROUND: It is well-known that the homozygous deficiency of alpha(1)-antitrypsin, phenotype PiZZ, is associated with an increased risk of COPD. However, studies evaluating the association between the heterozygous forms of the alpha(1)-antitrypsin phenotype PiMZ and rapid decline in lung function, both in patient and community populations, have yielded conflicting results. STUDY OBJECTIVE: To assess the relationship between alpha(1)-antitrypsin phenotypes and decline in FEV(1) values of 2,016 adult subjects in a community population in Tucson, AZ. DESIGN AND METHODS: Prospective cohort study. Standardized questionnaires and lung function measurements were administered 1.5 to 2 years apart during 12 surveys. RESULTS: The frequency distribution for PiMM, PiMS, and PiMZ phenotypes did not differ significantly by physician-confirmed diagnoses of emphysema, chronic bronchitis, or asthma. There was no statistically significant difference in mean FEV(1) slope values between PiMM, PiMS, and PiMZ phenotypes (-22.5, -21, and -7 mL per year, respectively). After controlling for smoking and other potential confounders, the FEV(1) slope was associated with an initial FEV(1) level and age for the initial questionnaire but not with the different phenotypes. Selecting cutoff values, we identified rapidly declining and nondeclining subgroups, based on the percent predicted changes in FEV(1). They also were not associated with alpha(1)-antitrypsin phenotypes. CONCLUSIONS: We conclude that the data from this longitudinal community study suggest that having the PiMZ phenotype is not a significant risk factor for an accelerated decline in FEV(1).

Adult↗