ISSN:0040-3709    

DOI:10.1002/tera.1420090312

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

年代:1974

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420090302

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

年代:1974

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420090303

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

年代:1974

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420090304

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

年代:1974

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420090305

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

年代:1974

数据来源: WILEY

摘要:

AbstractThe etiology of micromelia of chick limb caused by the effect of insulin on development in vivo was investigated with reference to patterns of cell death and chondrogenesis in the femur/tibia/fibula region. Insulin (3 IU) was injected into the sub‐blastodermic fluid of 3½‐day chick embryos. Acid phosphatase staining indicated that insulin had no effect in extending the naturally occurring area of cell death in the “opaque patch” region during stages 24–5 (4½–5 days). Autoradiographic study of35SO4incorporation into chondroitin sulfate was carried out by administration of a 2‐h pulse of 40 μCi of35S‐labeled sulfate to the chorioallantoic membrane of 7‐day chick embryos. The autoradiographs showed that insulin suppressed chondrogenesis (i) in the centers of the heads of tibia and femur and (ii) in the joint region. Cell death was found at the center of these regions of suppressed chondrogenesis which may overlap. It is suggested that insulin interferes in vivo with the nutrition of the cartilage and joint regions, possibly through hypoglycemia. These results conflict with Zwilling's ('59) interpretation that in vivo insulin causes extension of the area of the “opaque patch” region of degeneration and its persistence for a

ISSN:0040-3709    

DOI:10.1002/tera.1420090306

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

年代:1974

数据来源: WILEY

摘要:

AbstractSprague‐Dawley rats were treated sc with 100–400 mg/kg/day 5‐iododeoxyuridine (IUDR) for 5 days beginning at 1, 5, or 10 days of age. Hair and somatic growth were markedly reduced in rats given 400 mk/kg beginning at 1 day of age. Animals were examined histologically at 10 or 20 days of age. Cerebellar cortical lesions were evident after the highest dosage in animals killed at 10 days of age, but lesions were of lesser magnitude in all series killed at 20 days of age. Retinal dysplasia was observed in rats treated beginning at 1 day of age. Lesions were characterized by thinning of the retina, undulations, and rosette formation in outer retinal layers. Foci of renal dysplasia were evident in rats treated beginning at 1 day of age. Poorly differentiated glomeruli and tubules together with nests of primordial epithelial cells, indicative of impaired nephrogenesis, were located in the superficial cortex. It is known that developmental defects can occur in the cerebellum, retina, and kidney of animals infected perinatally with certain cytolytic viruses. However, these appear to be the first studies demonstrating that a halogenated uridine given to newborn animals may result in obvious renal cortical and retinal dysp

ISSN:0040-3709    

DOI:10.1002/tera.1420090307

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

年代:1974

数据来源: WILEY

摘要:

AbstractSingle umbilical artery associated with multiple anomalies is described in three stillborn human fetuses. Detailed study of the abdominopelvic arteries showed replacement of the abdominal aorta below the origin of the superior mesenteric artery by the umbilical artery in all three specimens. This finding greatly helps in solving the age‐old riddle of the cause‐effect relation between the umbilical anomaly and its associated defects. Single umbilical artery can give rise to the developmental anomalies in three ways. First by replacing the greater part of the abdominal aorta and disturbing the blood supply of the caudal half of the body during early embryogenesis it can give rise to the developmental anomalies of the cloaca, the genitourinary, gastrointestinal, and central nervous systems, and of the lower limbs; second by impairing the growth of the umbilical mesoderm it can disturb the formation of the infraumbilical portion of anterior abdominal wall and its correlates; and third by disturbing the hemodynamics of the embryo it can give rise to cardiovascular anomalies and possibly also to defects toward the cephalic half of the body. Although single umbilical artery and the associated developmental defects may both be secondary to another regionally operative teratogenic influence the extreme vascular reduction caudal to the aorticoumbilical junction and the concentration of malformations in the caudal half of the body greatly support the angiogenic the

ISSN:0040-3709    

DOI:10.1002/tera.1420090308

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

年代:1974

数据来源: WILEY

摘要:

AbstractEwes were exposed to 44oC for 9 h daily during the last two‐thirds or last third of gestation. The body weights of lambs were significantly reduced and cavitations of the cerebral white matter were found in 75% and micrencephaly in 44% of lamb

ISSN:0040-3709    

DOI:10.1002/tera.1420090309

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

年代:1974

数据来源: WILEY

摘要:

AbstractWistar rats were injected iv with ethlnitrosourea (ENU) between days 14 and 21 of gestation and the offspring killed 0, 3, 6, 10, 15, 21, and 75 days after birth. The brains obtained from these animals, on macroscopic examination, revealed that ENU produced micrencephaly of variable degrees reflected predominantly in the reduced dimensions of the cerebrum and cerebellum, inversely proportional in severity to the gestational age at which ENU was administered. The degrees of micrencephaly were first evident in 15‐day‐old animals and persisted throughout adulth

ISSN:0040-3709    

DOI:10.1002/tera.1420090310

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

年代:1974

数据来源: WILEY