official journal of Congeital Anomalies Research Association of Japan
Online ISSN : 2433-1503
Print ISSN : 0037-2285
Volume 18 , Issue 1
Showing 1-15 articles out of 15 articles from the selected issue
  • Type: Cover
    1978 Volume 18 Issue 1 Pages Cover1-
    Published: March 31, 1978
    Released: February 01, 2019
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  • Type: Appendix
    1978 Volume 18 Issue 1 Pages App1-
    Published: March 31, 1978
    Released: February 01, 2019
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  • Type: Index
    1978 Volume 18 Issue 1 Pages Toc1-
    Published: March 31, 1978
    Released: February 01, 2019
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  • Hiroaki SOMA
    Type: Article
    1978 Volume 18 Issue 1 Pages 1-10
    Published: March 31, 1978
    Released: February 01, 2019
    JOURNAL FREE ACCESS
    The placenta is a vital organ for fetal development in utero. Placental abnormalities, therefore, might be reflected in the production of fetal abnormalities. In general, the formation of the placental circulation can be correlated with the organogenetic period of the embryo. If a circulatory disturbance occurs between the fetus and placenta at this period, fetal abnormalities may appear. There is, however, some doubt whether as to a causal relationship to fetal malformations should be ascribed to the placenta. To imply that the placenta itself is concerned in the production of congenital anomalies would require more proof, because of experimental difficulties and a paucity of available retrospective data. In order to define the possible relationship between congenital malformations and the placenta more precisely, the placenta must be examined carefully and recorded. As a result of such detailed examinations, the relationships between placental pathology and fetal anomalies are summarized as follows; 1) chromosomal anomalies (trisomy, triploidy), 2) fetal storage disease (1-cell disease), 3) intrauterine infection (virus, bacteria, protozoa), 4) placental tumor (chorangioma) and fetal congenital tumor (sacral teratoma), 5) fetoplacental function (low estriol secretion, placental sulfatase deficiency), 6) amniotic band syndrome and amnion nodosum, 7) single umbilical artery and abnormal insertion of the cord, and 8) twin placentation. Anastcmosis in twin.
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  • SHOJI TERAMOTO, Akiko SHINGU, Masahiro KANEDA, Rikiko SAITO
    Type: Article
    1978 Volume 18 Issue 1 Pages 11-17
    Published: March 31, 1978
    Released: February 01, 2019
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    Teratogenic potentials of ethylenethiourea were investigated in three different species of animals. Pregnant Wistar-Imamichi rats, JCL-ICR mice, and syrian golden hamsters were administered 10-50, 200-800, and 90-810 mg/kg of ETU in daily oral doses on days 6-15, 7-15, and 6-13 of pregnancy, respectively. In rats, fetuses were significantly reduced in size at a dose of 30 mg/kg or more of ETU without any increase of the mortality. Gross external malformations observed were cranial meningocele, micrognathia, short or kinky tail, digital defects in the fore and hind limbs, and anal atresia. Skeletal defects were seen in the clavicles, ribs, sternebrae, and vertebral column. In rats the brain appeared to be the most commonly affected organ. Even the lowest dose, 10 mg/kg, resulted in dilatation of the lateral ventricles without any other defects. In hamsters, fetal survival was affected after treatment with 810 mg/kg of ETU. Doses of 270 mg/kg or more significantly reduced fetal weights and induced cleft palate, kinky tail, oligodactyly in the fore limbs, and anal atresia. Skeletal defects were frequently observed in the ribs and vertebral column. However, defects in the brain were not so prominently induced as in rats even after the highest dose. In mice, on the other hand, neither the survival nor growth of the fetuses was affected and no malformations were induced at any dose tested.
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  • Hiroshi NAGAI, Kimiko KAMBARA, Hiroko SUDO, Setsuya YOKOYAMA, Tamio KA ...
    Type: Article
    1978 Volume 18 Issue 1 Pages 19-23
    Published: March 31, 1978
    Released: February 01, 2019
    JOURNAL FREE ACCESS
    L-azetidine-2-carboxylic acid was administered to pregnant rats and their fetuses were examined for developmental abnormalities. In the two groups that received the daily doses of 100 mg/kg for 3 days from day 8 to 10 and those from day 11 to 13 of pregnancy, no significant change in the rate of mortality, body weight, and frequency of malformations was observed. In the group that received a single dose of 300 mg/kg on day 8 of pregnancy, a higher mortality was observed. In that group, skeletal malformations, skeletal variations, delayed ossification and growth retardation were observed. The skeletal malformations were fusion of the cervical vertebral arches and of thoracic vertebral bodies, defect of the cervical vertebral body, fusion of the cervical vertebral arch and the exoccipital bone. The results suggested that L-azetidine had an influence on the skeletal development in the rat fetus when administered in the early period of organogenesis.
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  • Hiroshi NAGAI, Hiroko SUDO, Kimiko KAMBARA, Shun KIHARA, Noriyuki NAGA ...
    Type: Article
    1978 Volume 18 Issue 1 Pages 25-31
    Published: March 31, 1978
    Released: February 01, 2019
    JOURNAL FREE ACCESS
    The effects of L-azetidine-2-carboxylic acid, a proline analogue, on the matrix formation and mineralization of the incisal dentine were examined histologically and microradiographically in rats and mice. After a single administration of 300 mg/kg of L-azetidine, disturbance of dentine formation was discernible from the appearance of hypomineralization and hypermineralization lines in both rats and mice. The disturbance of mineralization was observed in both rodents as radiopaque lines, which were found to be negative to collagen staining and positive to neutral polysaccharides and to acid mucopolysaccharides stainings. These histochemical changes in the matrix formation were temporary.
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  • Jack CHAMBERLAIN.G
    Type: Article
    1978 Volume 18 Issue 1 Pages 33-40
    Published: March 31, 1978
    Released: February 01, 2019
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    Gross and light microscopic craniofacial features of a severely malformed, day 21 rat fetus are described. The holoprosencephalic-type of anomaly illustrated resulted from a single maternal injection of the niacin anti-metabolite, 6-aminonicotinamide (6-AN), on day 9 of gestation. Twenty-four hours later a countertherapy injection of nicotinamide (NAM) was similarly given. The markedly defective fetus had primarily right-sided anomalies of the face, eye and brain combined with pituitary agenesis. Proposed fetal hemorrhage and neural crest cell damage are discussed.
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  • Yujiroh KAMIGUCHI, Kenji FUNAKI, Kazuya MIKAMO
    Type: Article
    1978 Volume 18 Issue 1 Pages 41-48
    Published: March 31, 1978
    Released: February 01, 2019
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  • Type: Bibliography
    1978 Volume 18 Issue 1 Pages 49-59
    Published: March 31, 1978
    Released: February 01, 2019
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  • Type: Appendix
    1978 Volume 18 Issue 1 Pages 60-61
    Published: March 31, 1978
    Released: February 01, 2019
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  • Type: Bibliography
    1978 Volume 18 Issue 1 Pages 62-
    Published: March 31, 1978
    Released: February 01, 2019
    JOURNAL FREE ACCESS
    Download PDF (72K)
  • Type: Appendix
    1978 Volume 18 Issue 1 Pages App2-
    Published: March 31, 1978
    Released: February 01, 2019
    JOURNAL FREE ACCESS
    Download PDF (362K)
  • Type: Cover
    1978 Volume 18 Issue 1 Pages Cover2-
    Published: March 31, 1978
    Released: February 01, 2019
    JOURNAL FREE ACCESS
    Download PDF (35K)
  • Type: Cover
    1978 Volume 18 Issue 1 Pages Cover3-
    Published: March 31, 1978
    Released: February 01, 2019
    JOURNAL FREE ACCESS
    Download PDF (35K)
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