School hearing screening programme in the UK: practice and performance.

BACKGROUND: Paediatric audiology services and screening programmes are currently under review. AIMS AND METHODS: To investigate current practice and performance of the school hearing screening programme (SHSP) by means of a questionnaire. RESULTS: SHSP was found to detect previously unrecognised hearing loss at low cost. Wide variation in practice was shown, and the majority of services had no computerised system for data collection. CONCLUSION: There is a need for nationally agreed protocols and quality assurance procedures.     

Perceptions of vulnerability 3 1/2 years after problems of feeding and crying behavior in early infancy

The long-term consequences for infants with problems of feeding and crying behavior remain unknown. The purpose of this research was to determine whether such children are later perceived by their parents as vulnerable and more often have behavior problems and have different personalities than children without problems in infancy. The implications of managing such problems by changing milk formulas is explored. Mothers of 379 infants were enrolled in the postpartum period. Information about problems of feeding and crying behavior was obtained at 4 months. Thirty-six percent of the infants had problems and the formula had been changed for 17%. At 3 1/2 years, 320 (84%) mothers completed a questionnaire. Children who had had problems were more often perceived as vulnerable (relative risk [RR] 1.86; 95% confidence interval [CI] 1.09, 3.19) and more often had behavior problems (RR 1.78; 95% CI 1.03, 3.07). There were no differences in personality. Children whose problems had been managed by changing milk formulas were more often perceived as vulnerable (RR 2.18; 95% CI 1.05, 4.53). Although allergies were reported significantly more often for those children who had had problems, there were no differences in the prevalence of asthma or eczema. Problems of feeding and crying behavior in early infancy and the way they are managed may have long-term implications for the child.     

New epidemiologic evidence confirming that bias does not explain the aspirin/Reye's syndrome association

To determine the validity of the aspirin/Reye's syndrome association, we developed an epidemiologic investigation to assess the effects of five potential sources of bias. A case-control study incorporated procedures to avoid temporal precedence and susceptibility bias. These included classifying cases as having monophasic or biphasic patterns of illness and matching for severity of symptoms at zero-time. To evaluate the effect of a potential recall bias, an "alternate-condition" control group was enrolled. A medical record review study was conducted to assess the potential for diagnostic bias, and a blanket surveillance of all hospitals in a region was conducted to evaluate reporting bias. Twenty-four case subjects and 48 matched controls were enrolled. Eight-eight percent of case subjects and only 17% of controls had received aspirin prior to the onset of Reye's syndrome (matched odds ratio, 35; 95% confidence interval, 4.2 to 288). Further analyses demonstrated that the association could not be attributed to the five potential sources of bias.     

Impaired Microvascular Function in Normal Children: Effects of Adiposity and Poor Glucose Handling

Clustering of cardiovascular risk factors is thought to occur early in life. The endothelium is an important regulator of microvascular function. We investigated the relationship between microvascular function and cardiovascular risk factors in 145 normal, healthy children aged 11-14 years. Skin microvascular responses, measured using laser Doppler imaging, to iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), were negatively correlated with percentage body fat ( r =−0.20, P < 0.05 and r =−0.18, P < 0.05, respectively). Subjects were stratified into quintiles based on 2-h, post-feeding glucose levels. Subjects in the upper glucose quintile (range 7.4-11.4 mmol l⁻¹) showed significantly lower vasodilatation to both ACh (   P < 0.005  ) and SNP (   P < 0.02  ) than those in the lower quintile (range 3.9-4.9 mmol l⁻¹). Waist-to-hip ratio and the fasting insulin resistance index were significantly greater in subjects in the upper quintile than those in the lower quintile ( P < 0.001 and P < 0.05, respectively). Additionally, in subjects in the upper glucose quintile, fasting triglyceride correlated with fasting insulin ( r = 0.59, P < 0.001) and with the fasting insulin resistance index ( r = 0.49, P < 0.009), and plasma levels of cholesterol and 2-h glucose were also correlated ( r = 0.40, P < 0.05). In a cross-section of normal children, microvascular function was negatively associated with adiposity. Additionally, in a subgroup of subjects, there was a clustering of high post-feeding glucose, impaired microvascular function, increased insulin resistance and higher central fat distribution. These findings suggest that risk factors for adult cardiovascular disease begin to cluster in normal children, which might have important consequences for development of atherosclerosis later in life.     

Evidence for involvement of a tumor suppressor gene on 1p in malignant peripheral nerve sheath tumors

Malignant peripheral nerve sheath tumors (MPNST) are rare soft-tissue malignancies. The genetic basis of these tumors is still poorly understood. Cytogenetic analyses predominantly revealed complex karyotypes, precluding the identification of recurrent chromosomal changes. We report loss of 1p material in a near-diploid karyotype with few or no additional structural chromosome changes in two sporadic cases of MPNST, indicating an important role of 1p loss in MPNST development. In one of these two tumors, a distal 1p deletion (1p31.2 approximately pter) was detected suggesting involvement of a tumor suppressor gene located within this distal region of 1p. Further evidence for recurrent 1p loss in MPNST was obtained by interphase fluorescence in situ hybridization, which showed loss of 1p material in 3 out of 13 tumors. These findings together with data from the literature suggest that loss of a tumor suppressor gene located within distal 1p is implicated in the pathogenesis of MPNST.