The clinical predictors of sleepiness correlated with the multiple sleep latency test in an Asian Singapore population.

STUDY OBJECTIVES: To explore the clinical predictors of sleepiness as objectively determined by the Multiple Sleep Latency Test with the Epworth Sleepiness Scale, age, body mass index, and overnight polysomnographic parameters at a tertiary referral center Sleep Disorders Unit. DESIGN: Retrospective, consecutive case series review. SETTING: A multidisciplinary sleep disorders unit in Singapore General Hospital, a tertiary-care university-affiliated hospital. PATIENTS: 72 consecutive patients evaluated for sleep disorders with overnight polysomnograms and Multiple Sleep Latency Tests between March 2002 and September 2002. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Mean sleep latency on the Multiple Sleep Latency Test was 9.0 +/- 4.4 minutes, and mean Epworth Sleepiness Scale score was 10.8 +/- 5.8. On univariate analysis, mean sleep latency on the Multiple Sleep Latency Test showed a significant negative correlation with the Epworth Sleepiness Scale score, apnea-hypopnea index, body mass index, arousal index, and time spent below 90% oxygen saturation during overnight polysomnography. After performing multiple linear regression, only Epworth Sleepiness Scale score and apnea-hypopnea index remained significantly correlated (P = .039 and P = .008, respectively). An Epworth Sleepiness Scale score of 8 or above predicted a mean sleep latency on the Multiple Sleep Latency Test of less than 10 minutes with a sensitivity of 73.9% and specificity of 50.0%. CONCLUSIONS: The Epworth Sleepiness Scale and apnea-hypopnea index are useful predictors of sleepiness in our Asian Singapore population.

Modest promoter methylation of E-cadherin gene in sporadic colorectal cancers: a quantitative analysis.

Although E-cadherin expression is frequently reduced in colorectal cancers (CRCs), this does not appear to be due to gene mutation or allele loss. We investigated the hypothesis that promoter methylation could be responsible for suppression of E-cadherin expression in 142 pairs of sporadic CRCs and respective normal mucosae. E-cadherin expression was examined by Western blot. E-cadherin methylation at two promoter regions was quantitatively measured by methylation specific real time PCR (MethyLight). We found that E-cadherin protein levels were significantly lower in CRCs, even in Dukes' A tumors, compared to normal mucosae. Decreased E-cadherin protein expression in CRCs was an independent poor prognostic factor in multivariate disease-free survival analysis. However, the extent of DNA methylation was extremely modest at both regions of the E-cadherin promoter. There was no correlation between DNA methylation and E-cadherin protein levels in either tumors or matched normal tissues. These findings suggested that suppression of E-cadherin expression in CRCs is a significant event and is possibly involved in both carcinoma development and progression. However, our data did not support a crucial role of promoter methylation of the E-cadherin gene in the remarkable downregulation of E-cadherin expression in CRCs. Methylated E-cadherin gene as a CRC biomarker therefore needs further validation.