摘要:

AbstractA fetus spontaneously aborted in the 4th month of gestation is described. The fetus displayed nonsymmetrical syndactyly of both hands and partial amputation of fingers in one hand caused by a dense tissue microscopically found to be composed of multiple folds of amnion. The placenta was examined, and showed severe pathology: multiple hematomas, infarctions, and fibrosis. The possible mode of formation of amniogenic bands is discussed and correlated with the clinical history and pathology of the placenta and membranes.

ISSN:0040-3709    

DOI:10.1002/tera.1420090202

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractA syndrome with cleft palate and unusual facies is described in which cleft palate with or without lateral synechia is associated with a beaked nose, short philtrum, maxillary hypoplasia, downturned mouth with a “pouty” lower lip, broad cheeks, and a short or retroplaced chin. Evidence from a previously reported family suggests autosomal dominant inheritance with variable expressivity. Study of further cases will be needed to determine the range of expression of the syndr

ISSN:0040-3709    

DOI:10.1002/tera.1420090203

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractCardiovascular malformations were produced in 17% of A/J and C57BL/6 mice using isogeneic antiheart antibody (RAMHS) and in 22% of C57BL/6 mice using allogeneic RAMHS by injecting on four consecutive days of gestation (days 8–11 or 12–15). The antiheart antibody was raised in rabbits and adsorbed against mouse kidney and liver to yield an antiserum with high antiheart activity and low activity against other organs, demonstrably kidney. Cardiovascular maldevelopment occurred in 9% of mice injected with antikidney antibody (RAMKS), 7% receiving normal rabbit serum, and 1% receiving normal saline. A highly significant (P<.001) difference between all of the RAMHS and the normal saline groups demonstrated that antiheart antibody is teratogenic to the developing heart; and a significant difference (P<.05) between allogenic RAMHS and RAMKS antibody in the frequency of induction of cardiovascular anomalies suggests that there is organ‐specific activity to antiheart antibody. The type of cardiovascular anomalies caused in the mice studied were the same (VSD in C57BL and ASD in A/J) as those that occur spontaneously or are produced by other teratogens such as dextroamphetamine. Antiheart antibody thus did not appear to produce a specific type of maldevelopment but rather made manifest the malformation to which there appears to be a hereditary predisposition (genetic‐environmental inter

ISSN:0040-3709    

DOI:10.1002/tera.1420090204

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractWhen pregnant A/J mice were deprived of drinking water and exposed to circulating dehumidified (dry) air for 72 h starting at gestation day 12, 39% of fetuses alive on day 17 had isolated cleft palate (CP), whereas treatment begun at day 11 gave 23% CP and at day 13 6% CP. A 48‐h exposure to dry air with deprivation of drinking water gave 7% CP. Deprivation of water alone for 72 h resulted in 12% CP and for 48 h gave 2% CP, not significantly above the 1% CP in controls. All treatments increased the fetal death rate but there was no evidence of an effect on the rate of cleft lip with or without cleft palate, a spontaneous defect in A/J mice. Extraembryonic membranes of day‐17 fetuses, after treatment from days 12–15, frequently showed strongly benzidine‐positivt pigment in the yolk‐sac cavity alongside the vitelline vessels. Only rarely vere small amounts of pigment observed in controls. It was thought to be old fetal blood. Fetal red cell and serum loss are discussed in relation to CP resulting from water deprivation and other teratogenic t

ISSN:0040-3709    

DOI:10.1002/tera.1420090205

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractThe folic acid analogue methotrexate (MTX) was evaluated for its embryotoxic potential in ICR mice on day 10 (stage 18) of gestation. No malformations were produced at doses shown to be embryotoxic in humans, rats, rhesus monkeys, and rabbits (0.3–10 mg/kg), although a significant increase in resorption rate was observed in litters treated with 10 mg/kg. Doses between the LD10and the LD50(25 and 50 mg/kg) produced a parallel increase in intrauterine death and congenital defect

ISSN:0040-3709    

DOI:10.1002/tera.1420090206

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractA diet supplemented with freeze‐dried blighted potatoes fed to rats had no teratogenic or embryolethal effects. Separate experiments with α‐solanine, scopoletin, cytochalasin B, indoleacetic acid, and α‐chaconine, intubated orally during organogenesis, gave no evidence of teratogenicity attributable to the test co

ISSN:0040-3709    

DOI:10.1002/tera.1420090207

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractThis study examined the effects of hadacidin, an analogue of L‐aspartic acid, on epithelial fusion, breakdown, and mesenchymal contact in explants of fetal mouse palatal shelves. Shelves from 14‐day C57BL/6Js were explanted to agar‐solidified Eagle's basal medium. Control palates grown in this medium mimicked normal closure; i.e., an epithelial seam formed, broke down, and mesenchymal contact occurred in vitro. Experimental palates were grown in this medium supplemented with 1 or 2 mg/ml hadacidin or with concentrations of L‐aspartic acid equal to or in excess of that of hadacidin. Histological observations of explants exposed to 2 mg of hadacidin for 2 days indicated that cells of the marginal epithelia became adherent to form epithelial bands, but that subsequent epithelial breakdown and mesenchymal contact did not occur. The presence of mi to tic figures in the epithelial bands and in the mesenchyme of treated explants indicated that hadacidin inhibited breakdown, and, in addition, that it did not severely suppress or debilitate all cellular activity. This observation supports the fact that explants treated with hadacidin for 2 days, when moved to control medium for an additional 2 days, were able to undergo epithelial‐band breakdown and mesenchymal penetration. Preliminary data from explants treated with hadacidin and L‐aspartic acid indicated that competitive reversal by the amino acid did not occur consistently in vitro at concentrations of the amino acid 3 times that o

ISSN:0040-3709    

DOI:10.1002/tera.1420090208

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractPregnant Wistar rats were injected ip with a teratogenic dose (100 mg/kg) of 2‐amino‐l,3,4‐thiadiazole hydro‐chloride (ATDA) on day 11 of gestation (sperm day = day 0). Pregnancy was terminated at various intervals following drug injection. At autopsy some embryos were dead, some severely affected, and others only mildly affected by the treatment. The neural tube was more sensitive to ATDA than was any other tissue. The first histologically observable effect of maternal ATDA treatment was embryonic cell death in the caudal end of the neural tube, 12 h after treatment. During the next 24 h additional cells in the neural tube died, as well as cells in associated ganglia and in areas of condensing mesenchyme and somites. The tissues of the tail were especially sensitive to ATDA treatment. Forty‐eight hours after treatment repair and regeneration of neural tissue was evident. At day 20, spinal cords of affected fetuses had excrescences growing from the luminal wall, rosettes, duplication of the central canal, premature termination, and disruption of normal cellular patterns. Fetuses with myelodysplasia also had short or absent tails. It is postulated that malformations resulting from maternal ATDA treatment are due to cell death caused by ATDA acting directly on embryonic cells, with the ultimate outcome depending on the number of mitotically active cells that survive treatment to continue the process of orga

ISSN:0040-3709    

DOI:10.1002/tera.1420090209

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractThe role of mandible growth in normal palate closure and the effects on the mandible of three teratogens‐—cortisone, 6‐aminonicotinamide (6‐AN), and hypervitaminosis A — during palate closure in A/J (susceptible to cleft palate induction by these teratogens) and in C57BL (resistant) inbred strains of mice were investigated. The rate of mandible growth in the control embryos of the two strains was similar during the period of palate closure. Mandible length in A/Js was greater than that in C57BLs at the initial stage of palate closure and this remained true when it was adjusted for palate stage and for body weight. The mandibles were not shortened at the beginning of palate closure by any of the teratogens in either strain. In the cortisone‐treated groups the mandibles of C57BL embryos were consistently longer than those of controls whereas the mandibles of A/J embryos did not differ from those of control embryos at comparable body weights. It is concluded that cortisone, 6‐aminonicotinamide, and hypervitaminosis‐A do not cause cleft palate by reducing the length of the mandible at pala

ISSN:0040-3709    

DOI:10.1002/tera.1420090210

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractSingle doses of epinephrine (5 μg) administered to 83 groups of chick embryos (24–190 h) at 2‐h intervals, produced a spectrum of aortic arch anomalies. The epinephrine was placed on the surface, of the extra embryonic membrane over the developing embryo in ovo, at a time when aortic arch morphogenesis is occurring. The peak incidence of anomalies (94%) occurred after treatment during day 5 of incubation (108–112 h). The anomalies involved the 3rd, 4th, and 6th pairs of aortic arches; those involving the right 4th arch (arcus aortae) were consistently associated with ventricular septal d

ISSN:0040-3709    

DOI:10.1002/tera.1420090211

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY