1
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Neural tube defects and uterus development in human fetuses

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          One of the most common malformations of the central nervous system is related to embryonic neural tube alterations. We hypothesized that anencephaly affects the development of the uterus during the human second trimester of pregnancy. The objective of this study was to study the biometric parameters of the uterus in fetuses with anencephaly and compare them with normocephalic fetuses at that important. In our study, 34 female fetuses were analyzed, 22 normal and 12 anencephalic, aged between 12 and 22 weeks post-conception (WPC). After dissection of the pelvis and individualization of the genital tract, we evaluated the length and width of the uterus using the Image J software. We compared the means statistically using the Wilcoxon-Mann–Whitney test and performed linear regression. We identify significant differences between the uterus length (mm)/weight (g) × 100 (p = 0.0046) and uterus width (mm)/weight (g) × 100 (p = 0.0013) when we compared the control with the anencephalic group. The linear regression analysis indicated that 80% significance was found in the correlations in normocephalic fetuses (12.9 to 22.6 WPC) and 40% significance in anencephalic fetuses (12.3 to 18.6 WPC). The measurements of the uterus were greater in anencephalic group but there are no difference in the uterine width and length growth curves during the period studied. Further studies are required to support the hypothesis suggesting that anencephaly may affect uterine development during the human fetal period.

          Related collections

          Most cited references31

          • Record: found
          • Abstract: found
          • Article: not found

          Why boys will be boys: two pathways of fetal testicular androgen biosynthesis are needed for male sexual differentiation.

          Human sexual determination is initiated by a cascade of genes that lead to the development of the fetal gonad. Whereas development of the female external genitalia does not require fetal ovarian hormones, male genital development requires the action of testicular testosterone and its more potent derivative dihydrotestosterone (DHT). The "classic" biosynthetic pathway from cholesterol to testosterone in the testis and the subsequent conversion of testosterone to DHT in genital skin is well established. Recently, an alternative pathway leading to DHT has been described in marsupials, but its potential importance to human development is unclear. AKR1C2 is an enzyme that participates in the alternative but not the classic pathway. Using a candidate gene approach, we identified AKR1C2 mutations with sex-limited recessive inheritance in four 46,XY individuals with disordered sexual development (DSD). Analysis of the inheritance of microsatellite markers excluded other candidate loci. Affected individuals had moderate to severe undervirilization at birth; when recreated by site-directed mutagenesis and expressed in bacteria, the mutant AKR1C2 had diminished but not absent catalytic activities. The 46,XY DSD individuals also carry a mutation causing aberrant splicing in AKR1C4, which encodes an enzyme with similar activity. This suggests a mode of inheritance where the severity of the developmental defect depends on the number of mutations in the two genes. An unrelated 46,XY DSD patient carried AKR1C2 mutations on both alleles, confirming the essential role of AKR1C2 and corroborating the hypothesis that both the classic and alternative pathways of testicular androgen biosynthesis are needed for normal human male sexual differentiation. Copyright © 2011 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Postnatal developmental changes in the pituitary-ovarian axis in preterm and term infant girls.

            Postnatal pituitary-testicular activation in infant boys is well characterized. However, the ovarian response to pituitary activation in infancy is less well understood. The aim of the study was to compare postnatal developmental changes in the pituitary-ovarian axis in preterm and term infant girls. Sixty-three infant girls, divided into three groups according to gestational age (GA) [i.e. full term (FT; n = 29; GA, 37-42 wk), near term (NT; n = 17; GA, 34-37 wk), and preterm (PT; n = 17; GA, 24-34 wk)] were examined monthly from 1 wk (D7) to 6 months (M1-M6) of age and reexamined at the corrected age of 14 months (cM14). We performed a longitudinal follow-up of urinary FSH and serum anti-Müllerian hormone (AMH) levels and the number of follicles in transabdominal ovarian ultrasonography. The postnatal FSH surge was stronger and more prolonged in NT and PT girls than in FT girls (P ≤ 0.001). Increased folliculogenesis and a rise in AMH levels were observed in all three groups after the FSH surge. In NT and PT girls, follicular development was delayed in comparison with FT girls, and a decrease in high FSH levels around the 40th postmenstrual week was temporally associated with the appearance of antral follicles in ultrasonography and an increase in AMH levels. The postnatal FSH surge results in transient ovarian stimulation in term and preterm girls. A delay in ovarian folliculogenesis shown in ovarian ultrasonography and by low serum AMH levels may provide an explanation for the exaggerated FSH surge in NT and PT girls.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Müllerian duct anomalies: embryological development, classification, and MRI assessment.

              Müllerian duct anomalies (MDA) occur due to abnormal development of the uterus, cervix, and vagina, many times affecting a woman's ability to conceive and carry a pregnancy to term. The spectrum of possible abnormalities are related to the development of two separate Müllerian systems, which then fuse and subsequently undergo degeneration of the fused segments. This multiphasic development explains the multiple variations within the scheme of MDA classification. The purpose of this article is to review the embryologic development of the Müllerian ducts, relate the development to the most commonly used classification system, and review the magnetic resonance imaging (MRI) assessment of Müllerian duct anomalies. A brief review of the treatment options, as they relate to the imaging diagnosis, will be provided as well.
                Bookmark

                Author and article information

                Contributors
                lufavorito@yahoo.com.br
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                18 August 2022
                18 August 2022
                2022
                : 12
                : 14051
                Affiliations
                GRID grid.412211.5, ISNI 0000 0004 4687 5267, Urogenital Research Unit, , State University of Rio de Janeiro, ; Rua Professor Gabizo, 104/201, Tijuca, Rio de Janeiro, RJ CEP 20271-320 Brazil
                Article
                18431
                10.1038/s41598-022-18431-1
                9388483
                35982132
                cb4953a5-8663-4bf9-870b-92caf62df483
                © The Author(s) 2022

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 10 May 2022
                : 11 August 2022
                Categories
                Article
                Custom metadata
                © The Author(s) 2022

                Uncategorized
                anatomy,urology
                Uncategorized
                anatomy, urology

                Comments

                Comment on this article