We measured the cord serum levels of thyroid‐stimulating hormone (TSH), thyroxine (T4) and triiodothyronine (T3) in 922 neonates delivered by mothers who had no thyroid disorders. The T4 and T3 levels increased progressively from the 27th to the 40th week of gestation. However, the TSH levels varied widely and had no correlation with gestational age, because they were affected by the mode of delivery. The mean cord serum TSH level in neonates delivered by vacuum extraction was 16.3 ±10.0 µUml (n = 30), which was significantly higher than the level following normal vaginal delivery (9.5 ± 6.0µ U/ml, n = 622) (p < 0.005). The mean cord serum TSH level following elective caesarean section was 6.5 ± 3.1µ U/ml (n = 79), and this was significantly lower than after normal vaginal delivery (p< 0.005). TSH levels in high‐risk neonates were significantly higher than in neonates without risk factors. A significant positive correlation was found between the duration of the second stage of labor and the cord serum TSH level (r = 0.45, n = 412, p<0.01). However, there was no correlation between the cord serum TSH level and the congenital hypothyroidism screening TSH level (r = 0.01, n = 468). We conclude that the cord serum TSH level reflects delivery stress and that an elevated level does not influence the congenital hypothyroidism screening TSH test in which blood is obtained at five days of life.

Apert syndrome is characterized by craniosynostosis, midfacial hypoplasia and bilateral syndactyly. We document in detail the intrauterine natural history of Apert syndrome by serial sonographic examination. Ultrasound examination of a 19-week fetus revealed an abnormal appearance of the skull. The subsequent examination including transvaginal brain scanning demonstrated a deformed occipital part of the cerebrum and lateral ventricles, frontal bossing, a low nasal bridge and an abnormal appearance of the fetal hands and feet. The distortion of the fetal profile became progressively worse with advancing gestation. Towards the end of pregnancy, anterior prominence of the cerebrum, ventricles and corpus callosum was demonstrated and mild non-progressive ventriculomegaly was seen. The female 3152-g newborn with the typical facial appearance of Apert syndrome, bilateral syndactyly of the fingers and toes and isolated cleft palate was delivered at 37 weeks. Postnatal three-dimensional computed tomography scan demonstrated the fusion of the coronal suture and a wide mid-line calvarial defect, and cranial magnetic resonance imaging confirmed the prenatal sonographic findings. Although the karyotype was normal, genomic DNA analysis of the fibroblast growth factor receptor 2 revealed Ser252Trp, which is specified in the mutational basis of Apert syndrome. The time course of the prenatal findings in this case may help increase understanding of the intrauterine natural history of Apert syndrome.

Lactic dehydrogenase (LDH) activity in the anterior, middle and posterior hypothalamus has been studied in adult female rats during the different phases of the oestrous cycle. Differences in LDH activity were found in the middle and posterior hypothalamus. LDH activity in the middle hypothalamus was significantly higher between 5:30 a. m. and 7:00 a. m. on the day of pro-oestrus than during the other phases (P < 0.01). (Rats were exposed to a controlled light schedule of 12 hours of light daily from 10 p. m. to 10 a. m.). LDH activity in the posterior hypothalamus was higher between 5:30 a. m. and 7:00 a. m. on the day of pro-oestrus than during the other phases. But this difference was not statistically significant. Ovulation which should occur during that night was blocked, when the rats were anaesthetized by pentobarbital between 5:30 a. m. and 7:00 a. m. during pro-oestrus. These findings indicate that the rise in LDH activity of the middle hypothalamus during the critical period may be related to the release of the luteinizing hormone releasing factor.

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