Neural plate microvillus lengthening in rat embryos grown in various concentrations of glucose and further studies of the mechanism.

Glucose is an important cellular nutrient, and in the early embryo, which is dependent mostly on anaerobic glycolysis, it is even more essential. Based on tissue culture cells in which glucose utilization has become membrane-limited, a concept has been developed that the tip of the microvilli is the entrance compartment for glucose and that the shaft sets up a diffusion barrier. An increase in length of the microvillus is associated with decreased entry of phosphorylated hexose into the cells. Our previous findings of lengthening of the microvilli of the neural plate cells after 40 min exposure to glucose at room temperature have been extended to a 17 hr whole embryo culture system. In cultures where the final concentration of glucose was 20 and 24 mg/dl there was embryonic death. In those cultures ending with 29-137 mg/dl of glucose the embryos developed normally. Those grown in dialyzed serum supplemented with B vitamins and glucose grew equally as well as those in whole rat serum. Somite numbers attained did not change with increasing glucose concentration but a modest increase in micromoles of glucose used per embryo was found, suggesting the presence of another source of energy at lower glucose concentrations. The average glucose utilization per gram of protein per hour was 844 mumol in these day 9.5-10 embryos and this compares to 733 mumol previously found using uniformly labeled 14C glucose on day 10.3. Lactate production averaged 85% of the glucose utilized. Pyruvate did not support growth in the absence of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Twin fetuses with abnormalities that overlap with three midline malformation complexes.

Twin fetuses aborted at an estimated gestational age of 145 days were concordant for oral, facial, skeletal, and central nervous system malformations. The twins were discordant for other anomalies including cardiac defects, polydactyly, and malrotated short bowel. The combination of malformations observed overlaps with that of the oral-facial-digital syndrome, hydrolethalus syndrome, and Pallister-Hall syndrome. The problem of phenotypic overlap between these syndromes is discussed.

A selection of candidate compounds for in vitro teratogenesis test validation.

The Consensus Workshop on In Vitro Teratogenesis Testing recommended that test validation be facilitated by a listing of agents with defined teratogenicity; subsequently, a panel was convened to review and select such agents. This communication established a list of 47 compounds or conditions which demonstrate a wide range of teratogenicity in vivo. The agents were chosen primarily on the strength of the literature base denoting their in vivo effects. The tables note a number of general biological and toxicological characteristics for each agent, and the details of representative in vivo teratology studies are summarized and referenced. This list is intended to serve as a base for in vitro teratogenesis test validation and should prove useful in developing and identifying those systems which will contribute to a more effective testing program.

Maternal hyperthermia as a possible cause of anencephaly.

Mothers of anencephalic infants were asked about febrile illness and sauna bathing during their pregnancies. In 7 of 63 affected pregnancies (11%), a history of maternal hyperthermia near the presumed time of anterior neural-groove closure was given. 5 had fever with a maximum recorded temperature ranging from 38.9 to 40.0 degrees C, each case being secondary to a different type of illness. The other 2 had possible hyperthermia episodes as a consequence of sauna bathing, with no infectious agent involved. The frequencies of hyperthermia at the same period of gestation in two control groups were 0% and 0.1%. This excess frequency of maternal hyperthermia at the period of anterior neural-groove closure, and the differing natures of its causes, imply that hyperthermia itself may be an aetiological factor in anencephaly.