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As bstract. The onset time for cholesterol crystal nucleation of supersaturated normal human gallbladder biles is consistently prolonged when compared with biles from patients with cholesterol gallstone disease. Investigation of the factor(s) responsible for the suspended supersaturation (metastability) of normal human biles revealed that model bile solutions of cholesterol saturation index (CSI) and molar lipid composition identical to individual gallbladder bile specimens had much shorter crystal nucleation times, i.e., exhibited decreased metastability. Unsaturated normal biles, after supplementation with lecithin, cholesterol, and sodium taurocholate to a 'standard' supersaturated lipid composition, also demonstrated nucleation times three-to 15-fold longer than the comparable standard model bile. Total lipid extracts of normal biles, however, when similarly supplemented, did not differ in nucleation time from the control model solution. Gallbladder biles were fractionated by gel chromatography and the eluted fractions were pooled into two fractions. The fractions eluting in about the first 25% of the included volume when mixed with the supersaturated standard model bile induced a modest increase in nucleation time of -1.5 times the control value. The fractions eluting in the second 25% of the included volume and which contained all ofthe bile lipids, were concentrated and supplemented with lipids to the standard composition. The nucleation times of these supPart ofthis work was presented at

In a prospective observational study, the fatty acid content of human umbilical artery and vein wall phospholipids was determined in fetuses classified according to their change in abdominal circumference during the third trimester. Three groups were identified: appropriate for gestational age (AGA; 24 infants) and small for gestational age (SGA; 38 infants) with normal antenatal growth rate, and SGA with fetal growth retardation (22 infants). The venous linoleic acid (18:2w)6) content (expressed as a percentage of the total fatty acids identified) was greater in growth retarded SGA fetuses (3.5 (0.6)%) than in SGA fetuses with a normal growth rate (3.1 (0.5)%) and AGA fetuses (3.0 (05)°/0), whereas To investigate this, we measured the umbilical artery and vein wall phospholipid fatty acid contents in AGA and SGA infants who had normal and subnormal growth rates. Methods SUBJECTSEighty four women were recruited after referral to the ultrasound department because of a suspected small fetus during the third trimester of pregnancy. In 60 subjects a SGA fetus was confirmed by an abdominal circumference less than the 10th centile for gestational age.7The remaining 24 fetuses had an abdominal circumference larger than the 10th centile for gestational age and were used as AGA controls. All fetuses were subsequently scanned at intervals of one to two weeks until delivery. All women had at least three scans and delivered after 36 weeks' gestation. All were certain of the date of their last menstrual period and had fetal size confirmed as appropriate by biparietal diameter and femur length at the 18-20 week anomaly scan. Fetal growth rate was quantified by calculating the change in SD score of abdominal circumference between the first scan after recruitment and the last before delivery. This methodology has been described in detail and been shown to identify neonatal morphometry consistent with fetal growth retardation.

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