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. Human complement C7 and C9 in fetal and newborn sera. Using specific immune sera, C7, C9, and C3 activator were detected in sera from human fetuses more than 16 weeks old and in newborn samples. Levels of C9 in cord sera ranged between 10 and 300/o of those present in sera from adult subjects. The mean value of C3 activator was about half that in maternal blood. The mean level of C7 in newborns was nearly 700o of the amount in normal adults.The availability of antibodies to specific components of human complement (C) and the analysis of in vitro cultures of fetal tissues have made it possible to study the onset and site of synthesis of these proteins during fetal life (Adinolfi, 1972;Rosen, 1974). The studies of the ontogeny of complement so far published have shown that Cl, C3, C4, and C5 are produced by the human fetus at an early stage of gestation (Adinolfi and Gardner, 1967;Adinolfi, Gardner, and Wood, 1968;Gitlin and Biasucci, 1969; Colten, 1972, Kohler;1973).We report preliminary results of our investigations on the presence and estimation of C3 activator, C7, and C9 in sera from human fetuses and newborns. Materials and methodsTwenty-four samples of cord blood were collected by syringe from the umbilical vein. Blood from normal adult individuals was taken by venepuncture. Serum was separated from clotted blood as soon as possible and the samples stored at -20°for no more than 2 months before being used. Blood was also collected by cardiac puncture from 5 fetuses whose ages, calculated from crown-rump length, ranged between 14 and 25 weeks. Most of the fetuses were obtained from therapeutic abortions.Immune serum against C3 activator (factor B) was obtained from Behringwerke (Marburg, Germany) and it was raised against one of the breakdown products of factor B. The rabbit immune sera against C7 and C9 were made by injection of precipitin lines cut from immunoelectrophoretic plates using anti-C7 and anti-C9 (kindly donated by Dr. H. Y. Muiller-Eberhard, Received 9 December 1974. U.S.A.). Both antisera gave only one line of precipitation when tested by double diffusion in agar gel.The presence of C7 and C9 in fetal and newborn sera was investigated using double diffusion in agar gel. Levels of C3 activator and C7 were measured by the single radial diffusion method, using a minor modification of the technique described by Kohler and MullerEberhard (1967). Levels of C7 were also estimated with the agarose plate technique (Lachman, Hobart and Aston, 1973) using guinea pig red cells and C56 euglobulin prepared from sera collected from normal women after childbirth. Concentrations of C9 were estimated by comparing the patterns of precipitations of serial dilutions of a normal adult serum with those of fetal and newborn samples.In the present paper the amount of C3 activator is expressed in mg/100 ml, using a standard serum provided by Behringwerke (Marburg, Germany), and levels of C7 and C9 in fetal and newborn sera are expressed as a percentage of the amount detected in adult samples.

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The role that genetic and environmental factors play in triggering neural tube defects in the mouse mutant curly‐tail (ct) were investigated by transplanting curly‐tail blastocysts into the uterus of either curly‐tail females or females of an unrelated A strain with a low natural incidence of abnormalities of the neural tube. The percentages of fetuses with neural tube defects were found to be similar in both groups. These results show that in curly‐tail mice exencephaly and spina bifida are manifested independently of the maternal environment.

The levels of beta-trace protein and lysozyme were estimated in amniotic fluids from normal fetuses and from fetuses with neuraltube defects. The values of these proteins in normal amniotic fluids were found to be similar to those detected in fetuses with anencephaly and spina bifida. The levels of lysozyme were shown to be correlated with gestational age.