[Investigation of risk factors for hearing impairment in premature infants].

OBJECTIVE: To investigate the risk factors for hearing impairment in premature infants. METHODS: A total of 895 premature infants who were admitted to the neonatal intensive care unit from January to December 2010 were evaluated using distortion product otoacoustic emission to detect hearing impairment. The failure rates in initial screening and secondary screening were recorded. The risk factors for failure to pass hearing screenings were elucidate using multivariate logistic regression analysis. RESULTS: The failure rate in initial screening was 38.4%, and the failure rate in secondary screening was 18.3%. In the auditory brainstem response test conducted at three months after birth, the failure rate was 22.2%. In premature infants with a gestational age of 28-29(+6) weeks, 60.5% did not pass the initial screening; 48.1% of the premature infants with a birth weight of 1 001-1 499 g failed the initial screening; 70.0% of the premature infants with a birth weight of ≤1 000 g failed the initial screening; 53.8% of the premature infants who had severe asphyxia failed the initial screening; 45.0% of the premature infants who used invasive ventilation failed the initial screening; 47.9% of the premature infants with a total bilirubin of ≥340 µmol/L failed the initial screening; 54.6% of the premature infants with septicemia failed the initial screenings. The multivariate logistic regression analysis revealed the following independent risk factors for failing the initial and secondary hearing screenings: gestational age, birth weight, hyperbilirubinemia and septicemia. CONCLUSIONS: Premature infants are susceptible to hearing impairment because they have immature organs and tissues and incomplete blood-brain barrier function and are sensitive to such factors as hyperbilirubinemia and infection. Early hearing screening and follow-up are necessary for premature infants to ensure timely interventions.

Partial least squares based identification of Duchenne muscular dystrophy specific genes.

Large-scale parallel gene expression analysis has provided a greater ease for investigating the underlying mechanisms of Duchenne muscular dystrophy (DMD). Previous studies typically implemented variance/regression analysis, which would be fundamentally flawed when unaccounted sources of variability in the arrays existed. Here we aim to identify genes that contribute to the pathology of DMD using partial least squares (PLS) based analysis. We carried out PLS-based analysis with two datasets downloaded from the Gene Expression Omnibus (GEO) database to identify genes contributing to the pathology of DMD. Except for the genes related to inflammation, muscle regeneration and extracellular matrix (ECM) modeling, we found some genes with high fold change, which have not been identified by previous studies, such as SRPX, GPNMB, SAT1, and LYZ. In addition, downregulation of the fatty acid metabolism pathway was found, which may be related to the progressive muscle wasting process. Our results provide a better understanding for the downstream mechanisms of DMD.