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Background Obesity has been associated with increased risk of antenatal depression, but little is known about this relationship. This study tested whether socio-economic status (SES) influences the relationship between obesity and antenatal depression. Methods Data were taken from the Screening for Pregnancy Endpoints (SCOPE) cohort. BMI was calculated from measured height and weight at 15±1 weeks' gestation. Underweight women were excluded. SES was indicated by self-reported household income (dichotomised around the median: low SES ≤£45,000; high SES >£45,000). Antenatal depression was defined as scoring ≥13 on the Edinburgh Postnatal Depression Scale at both 15±1 and 20±1 weeks' gestation, to identify persistently elevated symptoms of depression. Results Five thousand five hundred and twenty two women were included in these analyses and 5.5% had persistently elevated antenatal depression symptoms. There was a significant interaction between SES and BMI on the risk of antenatal depression (p=0.042). Among high SES women, obese women had approximately double the odds of antenatal depression than normal weight controls (AOR 2.11, 95%CI 1.16–3.83, p=0.014, adjusted for confounders). Among low SES women there was no association between obesity and antenatal depression. The interaction effect was robust to alternative indicators of SES in sensitivity analyses. Limitations 1) Antenatal depression was assessed with a self-reported screening measure; and 2) potential mediators such as stigma and poor body-image could not be examined. Conclusions Obesity was only associated with increased risk of antenatal depression among high SES women in this sample. Healthcare professionals should be aware that antenatal depression is more common among low SES women, regardless of BMI category., Highlights • High SES obese women had twice the odds of antenatal depression than high SES normal weight controls. • There was no significant association between obesity and antenatal depression among low SES women. • Antenatal depression was substantially more common among low SES women, regardless of BMI category.

Preeclampsia, which affects approximately 5% of pregnancies, is a leading cause of maternal and perinatal death. The causes of preeclampsia remain unclear, but there is evidence for inherited susceptibility. Genome-wide association studies (GWAS) have not identified maternal sequence variants of genome-wide significance that replicate in independent data sets. We report the first GWAS of offspring from preeclamptic pregnancies and discovery of the first genome-wide significant susceptibility locus (rs4769613; P = 5.4 × 10(-11)) in 4,380 cases and 310,238 controls. This locus is near the FLT1 gene encoding Fms-like tyrosine kinase 1, providing biological support, as a placental isoform of this protein (sFlt-1) is implicated in the pathology of preeclampsia. The association was strongest in offspring from pregnancies in which preeclampsia developed during late gestation and offspring birth weights exceeded the tenth centile. An additional nearby variant, rs12050029, associated with preeclampsia independently of rs4769613. The newly discovered locus may enhance understanding of the pathophysiology of preeclampsia and its subtypes.

OBJECTIVE: To develop a prediction model for term infants born large for gestational age (LGA) by customised birthweight centiles.METHODS: International prospective cohort of nulliparous women with singleton pregnancy recruited to the Screening for Pregnancy Endpoints (SCOPE) study. LGA was defined as birthweight above the 90th customised centile, including adjustment for parity, ethnicity, maternal height and weight, fetal gender and gestational age. Clinical risk factors, ultrasound parameters and biomarkers at 14-16 or 19-21 weeks were combined into a prediction model for LGA infants at term using stepwise logistic regression in a training dataset. Prediction performance was assessed in a validation dataset using area under the Receiver Operating Characteristics curve (AUC) and detection rate at fixed false positive rates.RESULTS: The prevalence of LGA at term was 8.8% (n = 491/5628). Clinical and ultrasound factors selected in the prediction model for LGA infants were maternal birthweight, gestational weight gain between 14-16 and 19-21 weeks, and fetal abdominal circumference, head circumference and uterine artery Doppler resistance index at 19-21 weeks (AUC 0.67; 95%CI 0.63-0.71). Sensitivity of this model was 24% and 49% for a fixed false positive rate of 10% and 25%, respectively. The addition of biomarkers resulted in selection of random glucose, LDL-cholesterol, vascular endothelial growth factor receptor-1 (VEGFR1) and neutrophil gelatinase-associated lipocalin (NGAL), but with minimal improvement in model performance (AUC 0.69; 95%CI 0.65-0.73). Sensitivity of the full model was 26% and 50% for a fixed false positive rate of 10% and 25%, respectively.CONCLUSION: Prediction of LGA infants at term has limited diagnostic performance before 22 weeks but may have a role in contingency screening in later pregnancy.

This paper presents a case study of a semiconductor laser with a saturable absorber (SLSA) and an external optical feedback loop. The system is modeled by the Yamada rate equations to which a feedback term has been added. Starting from the bifurcation analysis of the SLSA alone, the influence of feedback strength and delay time is investigated by means of a numerical bifurcation analysis. The emphasis is on excitable dynamics and self-sustained oscillations in the presence of the feedback loop.

Ultradian pulsatile hormone secretion underlies the activity of most neuroendocrine sys- tems, including the hypothalamo-pituitary adrenal (HPA) and gonadal (HPG) axes, and this pulsatile mode of signalling permits the encoding of information through both amplitude and frequency modulation. Thus in the HPA axis, glucocorticoid pulse ampli- tude increases in anticipation of waking, and in the HPG axis changing gonadotrophin- releasing hormone (GnRH) pulse frequency is the primary means by which the body alters its reproductive status during development. The prevalence of hormone pulsatility raises two crucial questions: how are ultradian pulses encoded (or generated) by these systems, and how are these pulses decoded (or interpreted) at their target sites? We have looked at mechanisms within the HPA axis responsible for encoding the pulsatile mode of glucocorticoid signalling that we observe in vivo. We review evidence regard- ing the ‘hypothalamic pulse generator’ hypothesis, and present an alternative model for pulse generation which involves steroid feedback-dependent endogenous rhythmic ac- tivity throughout the HPA axis. We also consider the second question concerning the decoding of hormone pulsatility, taking the HPG axis as a model system, and focussing on molecular mechanisms of frequency decoding by pituitary gonadotrophs.

The hypothalamic-pituitary-adrenal (HPA) axis is a neuroendocrine system that regulates the circulating levels of vital glucocorticoid hormones. The activity of the HPA axis is characterized not only by a classic circadian rhythm but also by an ultradian pattern of discrete pulsatile release of glucocorticoids. A number of psychiatric and metabolic diseases are associated with changes in glucocorticoid pulsatility, and it is now clear that glucocorticoid responsive genes respond to these rapid fluctuations in a biologically meaningful way. Theoretical modeling has enabled us to identify and explore potential mechanisms underlying the ultradian activity in this axis, which to date have not been successfully identified. We demonstrate that the combination of delay and feedforward and feedback loops in the pituitary-adrenal system is sufficient to give rise to ultradian pulsatility in the absence of an external ultradian source from a supra-pituitary site. Moreover, our model enables us to predict the different patterns of glucocorticoid release mediated by changes in hypophysial-portal corticotrophin-releasing hormone (CRH) levels, with results that parallel our experimental in vivo data. Since the vast majority of hormones are secreted in ultradian patterns, and most endocrine systems involve excitatory/inhibitory pathways and delays, our theoretical approach could provide a basis for understanding the origin and reg- ulation of the ultradian rhythmicity seen in many other endocrine systems

This study has examined the incidence of thyroid dysfunction during pregnancy and up to six months postpartum in 65 women attending an antenatal clinic in the West of Scotland. Five were found to be positive for thyroid antibodies at presentation and in these the antibody titre fluctuated during pregnancy and in the post partum period. One patient developed thyroglobulin antibodies post partum. Mean total T3 and total T4 levels rose during pregnancy but had normalised by six weeks post partum. The changes in FT4 and TBG levels observed during pregnancy did not normalise until after six weeks post partum. Only one patient developed any biochemical evidence of thyrotoxicosis post partum and this was not found to be associated with the presence of thyroid antibodies. No patient showed any evidence of hypothyroidism.