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Neural tube defects (NTDs) are the second most common congenital malformations in humans affecting the development of the central nervous system. Although NTD pathogenesis has not yet been fully elucidated, many risk factors, both genetic and environmental, have been extensively reported. Classically divided in two main sub‐groups (open and closed defects) NTDs present extremely variable prognosis mainly depending on the site of the lesion. Herein, we review the literature on the histological and pathological features, epidemiology, prenatal diagnosis, and prognosis, based on the type of defect, with the aim of providing important information based on NTDs classification for clinicians and scientists.

Objective Fetal hypoxia and acidemia have been reported in pregestational diabetic pregnancies in relation to poor glycaemic control, but it is still uncertain whether this is the case in apparently well-controlled gestational diabetes.Population and methods Maternal arterial and umbilical venous and arterial blood samples were collected from 37 normal (N) and 38 pregnancies complicated by gestational diabetes (GDM) at the time of caesarean section.Main outcome measures Respiratory gases, acid-base balance, lactate and glucose concentrations were measured.Results Both fetal and placental weights were significantly increased in GDM compared to N pregnancies, despite similar gestational age. Maternal biochemical parameters were similar in N and GDM but GDM fetuses were significantly more hypoxic (O 2 saturation: N 63.2 ± 13.9; GDM 53.8 ± 14.6%, P < 0.01; O 2 content: N 5.5 ± 1.4; GDM 4.8 ± 1.2 mmol/l, P < 0.05). Glucose (N 3.4 ± 0.5, GDM 3.9 ± 1.2 mmol/l, P < 0.05) and lactate (N 1.32 ± 0.49; GDM 1.64 ± 0.75 mmol/l, P < 0.05) concentrations were significantly increased in the umbilical vein in GDM compared to N fetuses. Placental histology was consistent with altered villous morphology.Conclusions Our data indicate that fetuses from gestational diabetic mothers have increased umbilical glucose concentrations despite normal maternal glucose levels and a reduction in oxygen saturation and O 2 content together with increased lactate concentration, reflecting altered fetal metabolism. These data suggest that 'good maternal metabolic control' achieved by currently used methods of monitoring glucose control is not sufficient to ensure a normal oxygenation status and metabolic milieu for the fetus in GDM pregnancies.

The placenta represents a key organ for fetal growth as it acts as an interface between mother and fetus, regulating the fetal-maternal exchange of nutrients, gases, and waste products. During pregnancy, amino acids represent one of the major nutrients for fetal life, and both maternal and fetal concentrations are significantly different in pregnancies with intrauterine growth restriction when compared to uncomplicated pregnancies. The transport of amino acids across the placenta is a complex process that includes the influx of neutral, anionic, and cationic amino acids across the microvilluos plasma membrane of the syncytiotrophoblast, the passage through the cytoplasm of the trophoblasts, and the transfer outside the trophoblasts across the basal membrane into the fetal circulation. In this paper, we review the transport mechanisms of amino acids across the placenta in normal pregnancies and in pregnancies complicated by intrauterine growth restriction.