ABSTRACT Exposure of developing chick embryos to non-thermogenic dose of 428 MHz radio frequency (RF) have been reported to cause embryo lethality, teratogenicity and delayed hatching (Saito et al., 1991). To elucidate the mechanisms of such adverse biological effects, developing chick embryos were exposed to 428 MHz RF at 5.5 mW/ cm2 for the first 48 hrs of incubation. Ten fertilized eggs were used in each experiment; exposure and sham-exposure were alternatively repeated 10 times. Embryos were examined on viability, then excised, fixed in alcohol and examined morphologically on the developing status. Some embryos were subjected to histological study. In the exposed group, embryos were alive but the development was severely delayed. The average num- ber of somites was 10.522.8 SD in the exposed group and 13.1 r2.3 in the control, respectively. Embryos with less than 10 somites were about 27% in the exposed group. The minimum number of somites was 3 in the exposed group and 7 in the control. Developmental delay was about 6 to 16 hrs in terms of Hamburger-Hamilton stage. Two cases of duplication anomalies were detected at positions 3 (specific absorption rate, SAR: 47.1 mWkg) and 10 (8.6 mW/kg). The positions in the incubator with severely affected corresponded to those with high embryo lethality in our previous study. Histological observations suggested developmental delay might not be due to direct cytotoxicity but to the slower cell proliferation and/or to disturbances of cell-cell interaction, migration and orientation. The possibility that non-thermogenic RF electromagnetic field may affect ear- ly embryogenesis indirectly through physico-chemical modifications of metal-containing proteins are discussed.
ABSTRACT Marshall-Smith syndrome is a rare disorder characterized by accelerated skeletal maturation, bullet-shaped proximal and middle phalanges, dysmorphic facial fea- tures, and failure to thrive, and is often associated with mental retardation of variable degree. We describe an 8-month-old female with this syndrome, who has a hypoplastic corpus callosum and extreme upper airway obstruction requiring tracheostomy. Also, we review the previous reports of this syndrome since 1971 (Marshall et al., 1971).
ABSTRACT NC-eob mice are mutants having open eyelids at birth with complete pene- trance. The present study was aimed at investigating the possible effects of cortisone acetate (CA) on the eyelid closure of NC-eob mice. For comparison, fusion of pinnae to the scalp was also investigated. NC strain mice were used as a control. Females were given daily subcutaneous doses of 0, 20, 40 or 80 mg/kg of CA on days 13 to 15 of gestation. Live fetuses were removed from the uteri on day 16 or 18 of gestation. Day-18 fetuses were weighed along with the placenta and examined for external abnormalities. Day-16 fetuses were fixed in Bouin’s fluid and examined for the developmental stages of eyelid closure and pinnal fusion. In day-18 NC and NC-eob fetuses, decreases in body weight and placental weight and an increase in the incidence of cleft palate were observed in a dose-related manner. However, no eyelid closure occurred in any NC-eob fetuses. In day-16 NC-eob fetuses, although slight enhancement of the eyelid growth and epidermal differentiation was seen, eyelid openings remained wide. Clear accelerating effects of CA treatment were noted for the pinnal fusion. In CA treated NC fetuses, both eyelid closure and pinnal fusion were clearly accelerated. These results indicate that the effects of CA on the eyelid development in NC-eob fetuses are insufficient for closing eyelids.
ABSTRACT A wild-derived strain of Japanese house mice, Mus rnusculus rnolossinus (MSM), was compared with laboratory mice (DBA/2N, C57BW6, C3H/He, BDF1, and ICR) for the susceptibility to teratogenic effect of ethylnitrosourea (ENU). ENU was applied i.p. to mice in each strain on day 7 of gestation. On day 18 of gestation, uterine contents were examined and viable fetuses were inspected for external and skeletal mal- formations. The dose (mg/kg) required to induce 25% embryonic lethality (LD25) was 46 in MSM and 28-54 in the laboratory mice. The frequencies of external and of skeletal malformations at LD25 were, respectively, 8 and 47% in MSM, 29-97% and 65-95% in the laboratory mice. Thus, MSM was less susceptible to ENU teratogenesis compared to any of the laboratory mice used and the difference in the susceptibility between MSM and the laboratory mice was more marked for external malformations than for skeletal mal- formations. These results are compatible with the hypothesis that laboratory mice may have genetic traits that facilitate teratological assays of drugs.