Prediction of large for gestational age birth weights in diabetic mothers based on early third-trimester sonography.

OBJECTIVES: The purpose of this study was to evaluate the ability of early third-trimester sonography to predict large for gestational age (LGA) birth weights in women with diabetes mellitus. METHODS: We identified women with nonanomalous singleton gestations and pregestational and gestational diabetes mellitus who underwent sonographic examinations between gestational ages of 28 weeks and 32 weeks 6 days and subsequently delivered at 37 weeks or later. Using a cohort study design, we compared data from women with an estimated fetal weight at or above the 75th percentile (exposed group) with data from those with an estimated fetal weight below the 75th percentile (unexposed group). The primary outcome variable was LGA birth weight, defined as a birth weight of greater than 90% for gestational age. RESULTS: Eighty-six women met inclusion criteria over a 3-year period: 40 were in the exposed group, and 46 were in the unexposed group. The mean body mass indices ± SD at delivery were similar for both groups: 35.4 ± 8.2 kg/m(2) exposed versus 35.0 ± 8.2 kg/m(2) unexposed (P = .80). There was no difference in the number of women with gestational diabetes mellitus: 40% exposed versus 39% unexposed (P = .90). Neonates whose early third-trimester estimated fetal weight was at or above the 75th percentile were significantly more likely to be LGA at birth compared with neonates whose early third-trimester estimated fetal weight was below the 75th percentile: 65% exposed versus 15% unexposed (P < .001; odds ratio, 10.3; 95% confidence interval, 3.7-29.1). There was no significant difference in cesarean delivery rates: 60% exposed versus 44% unexposed (P = .13) CONCLUSIONS: Measurements obtained by early third-trimester sonographic fetal biometry are reasonably predictive of fetal LGA birth weights at term.

Transcriptional profiling identifies two members of the ATP-binding cassette transporter superfamily required for sterol uptake in yeast.

In contrast to lipoprotein-mediated sterol uptake, free sterol influx by eukaryotic cells is poorly understood. To identify components of non-lipoprotein-mediated sterol uptake, we utilized strains of Saccharomyces cerevisiae that accumulate exogenous sterol due to a neomorphic mutation in the transcription factor, UPC2. Two congenic upc2-1 strains, differing quantitatively in aerobic sterol uptake due to a modifying mutation in the HAP1 transcription factor, were compared using DNA microarrays. We identified 9 genes as responsive to UPC2 that were also induced under anaerobiosis, when sterol uptake is essential. Deletion mutants in these genes were assessed for sterol influx in the upc2-1 background. UPC2 itself was up-regulated under these conditions and was required for aerobic sterol influx. Deletion of the ATP-binding cassette transporters YOR011w (AUS1) or PDR11, or a putative cell wall protein encoded by DAN1, significantly reduced sterol influx. Sodium azide and vanadate inhibited sterol uptake, consistent with the participation of ATP-binding cassette transporters. We hypothesized that the physiological role of Aus1p and Pdr11p is to mediate sterol uptake when sterol biosynthesis is compromised. Accordingly, expression of AUS1 or PDR11 was required for anaerobic growth and sterol uptake. We proposed similar molecules may be important components of sterol uptake in all eukaryotes.