Vitamin D, pre-eclampsia, and preterm birth among pregnancies at high risk for pre-eclampsia: an analysis of data from a low-dose aspirin trial.

OBJECTIVE: To examine the relation between maternal vitamin D status and risk of pre-eclampsia and preterm birth in women at high risk for pre-eclampsia. DESIGN: Analysis of prospectively collected data and blood samples from a trial of prenatal low-dose aspirin. SETTING: Thirteen sites across the USA. POPULATION: Women at high risk for pre-eclampsia. METHODS: We measured 25-hydroxyvitamin D [25(OH)D] concentrations in stored maternal serum samples drawn at 12-26 weeks' gestation (n = 822). We used mixed effects models to examine the association between 25(OH)D and risk of pre-eclampsia and preterm birth, controlling for confounders including prepregnancy BMI and race. MAIN OUTCOME MEASURES: Pre-eclampsia and preterm birth. RESULTS: Twelve percent of women were vitamin D deficient [25(OH)D <30 nmol/l]. Women with 25(OH)D <30 versus ≥75 nmol/l had a 2.4-fold (95% CI 1.0-5.6) higher risk of early-onset pre-eclampsia (<35 weeks' gestation) after confounder adjustment. Women with 25(OH)D <50 nmol/l had a 1.8-fold (95% CI 1.0-3.2) increased risk of preterm birth at <35 weeks compared with women who had 25(OH)D ≥75 nmol/l, which was driven by indicated preterm births at <35 weeks' gestation [25(OH)D <50 versus ≥75 nmol/l adjusted RR 2.5 (95% CI 1.1-5.8)]. There was no association between vitamin D status and pre-eclampsia or preterm birth at <37 weeks. CONCLUSION: Maternal vitamin D status in the second trimester was inversely associated with risk of early-onset pre-eclampsia and preterm birth at <35 weeks in women at high risk for pre-eclampsia. TWEETABLE ABSTRACT: Vitamin D is inversely related to risk of pre-eclampsia and preterm birth at <35 weeks in high-risk pregnancies.

A collaborative EDNAP exercise on SNaPshot™-based mtDNA control region typing.

A collaborative European DNA Profiling (EDNAP) Group exercise was undertaken to assess the performance of an earlier described SNaPshot™-based screening assay (denoted mini-mtSNaPshot) (Weiler et al., 2016) [1] that targets 18 single nucleotide polymorphism (SNP) positions in the mitochondrial (mt) DNA control region and allows for discrimination of major European mtDNA haplogroups. Besides the organising laboratory, 14 forensic genetics laboratories were involved in the analysis of 13 samples, which were centrally prepared and thoroughly tested prior to shipment. The samples had a variable complexity and comprised straightforward single-source samples, samples with dropout or altered peak sizing, a point heteroplasmy and two-component mixtures resulting in one to five bi-allelic calls. The overall success rate in obtaining useful results was high (97.6%) given that some of the participating laboratories had no previous experience with the typing technology and/or mtDNA analysis. The majority of the participants proceeded to haplotype inference to assess the feasibility of assigning a haplogroup and checking phylogenetic consistency when only 18 SNPs are typed. To mimic casework procedures, the participants compared the SNP typing data of all 13 samples to a set of eight mtDNA reference profiles that were described according to standard nomenclature (Parson et al., 2014) [2], and indicated whether these references matched each sample or not. Incorrect scorings were obtained for 2% of the comparisons and derived from a subset of the participants, indicating a need for training and guidelines regarding mini-mtSNaPshot data interpretation.

Regulation of operant ethanol-reinforced behavior is genetically independent of regulation of withdrawal severity in WSP and WSR mice.

Selectively bred withdrawal seizure prone (WSP1 and WSP2) and withdrawal seizure resistant (WSR1 and WSR2) mice were used to test the extent to which severity of ethanol withdrawal response is predictive of the reinforcing effects of ethanol. Mice were systematically introduced to ethanol under a fixed ratio 1 (FR 1) schedule using adjunctive drinking methods. There were no significant differences in ethanol consumption between the lines during training. Subsequently, responding for ethanol concentrations of 8%, 0% (vehicle control), and 8% retest under a FR 1 schedule in the absence of food induction was measured. Group data showed that ethanol did not serve as a reinforcer in the test phase within any of the four lines, and there were no significant line differences in rate of responding, intake, or blood ethanol concentrations (BEC). Mice were next tested for responding for ethanol under a FR 4 schedule. Again, ethanol did not serve as a reinforcer for any of the four groups, and there were no significant differences between the lines. However, further analysis showed that there were individual differences in responding within each group, some animals were apparently reinforced by ethanol, while others showed no reinforcement and some appeared to avoid ethanol. There was no systematic pattern within or between groups for these individual differences in responding. Thus, both the group results as well as the behavior patterns of individual animals are consistent with the conclusion that genes regulating rewarding effects of ethanol appear to be segregating randomly across groups and are independent of genes mediating ethanol withdrawal severity.(ABSTRACT TRUNCATED AT 250 WORDS)