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  1. Rachagan SP, Kutty K, Govindan KS
    Med J Malaysia, 1997 Sep;52(3):293-4.
    PMID: 10968101
    A case of persistent trophoblastic tissue on the pelvic peritoneum is presented. While most cases are secondary to conservative surgery for tubal ectopic pregnancy, primary implantation can also occur as highlighted by this case. A brief pathophysiology of the condition is presented. The importance of monitoring the serum for beta subunit human chorionic gonadotrophin (HCG) is emphasised.
    Matched MeSH terms: Trophoblasts/pathology*
  2. Goh JYL, Rachagan SP, Low EC
    Med J Malaysia, 1987 Mar;42(1):70-1.
    PMID: 3431507
    A case of an ovarian ectopic pregnancy is
    presented. The diagnosis was made at laparotomy.
    Histology of the surgical specimen confirmed a
    primary ovarian pregnancy. The aetiologic factors
    and diagnostic criteria are discussed.
    Matched MeSH terms: Trophoblasts/pathology
  3. Hayati AR, Cheah FC, Tan AE, Tan GC
    Early Hum Dev, 2007 Jan;83(1):41-6.
    PMID: 16750336 DOI: 10.1016/j.earlhumdev.2006.04.002
    BACKGROUND: Septal hypertrophic cardiomyopathy (sHCM) is a characteristic anomaly of the infant of diabetic mother (IDM). Insulin-like growth factor-1 (IGF-1) has been identified as a mediator of tissue overgrowth and we have previously shown that maternal IGF-1 levels were significantly elevated among neonates with asymmetrical sHCM. IGF-1 does not cross the placenta; it exerts physiologic action through binding to the IGF-1 receptor (IGF-1R). Localisation and expression of IGF-1R in term diabetic pregnancies are largely unclear. We have studied IGF-1R in the placentae of diabetic and normal pregnancies and this receptor expression in association with neonates with sHCM.
    METHODS: IGF-1R localization and expression in the placentae of six diabetic pregnancies associated with neonatal sHCM were compared with six each of randomly selected diabetic and normal pregnancies without neonatal sHCM by immunohistochemistry. The staining for IGF-1R in the deciduas, cytotrophoblasts, syncytiotrophoblasts and villous endothelium for these 18 samples were assessed and scored by two pathologists who were blinded to the respective diagnoses.
    RESULTS: Placental IGF-1R staining was negative in the villous endothelium for all three groups. IGF-1R staining was present in deciduas, cytotrophoblasts and syncytiotrophoblasts but the staining was weaker in the entire group of infants with sHCM compared to those without sHCM.
    CONCLUSIONS: IGF-1R is localized in all cell types of the placenta except in villous endothelium. Weaker placental IGF-1R staining in the placentae of diabetic pregnancies associated with sHCM suggests reduced expression of IGF-1R. This may be a down-regulatory response to elevated maternal IGF with neonatal sHCM outcome.
    Matched MeSH terms: Trophoblasts/pathology
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