The Mortality of Human Xo Embryos

Santesson, Berta; Böök, J. A.; Kjessler, B.

doi:10.1530/jrf.0.0340051

Cited by 2 publications

(3 citation statements)

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“…This is similar to man where a large percentage of surviving Turner's syndrome patients are mosaic with a clone of XX cells (Polani, 1961;Sohval, 1965;Bornstein, 1967;Carr, 1969;Hecht, e t a / . , 1969;Stempfel, 1969;Santesson, et a/., 1973). It is not known to what extent mosaicism differed in various tissues of this mare.…”

Section: Discussionmentioning

confidence: 95%

“…(Sharma, A. K. and Sharma, A., 1972). A number of reports in man on phenotypic females with an abnormal sex complement, usually a chromosome number of 45 and an XO sex chromosome constitution (Bornstein, 1967;Hecht and MacFarlane, 1969;Polani, 1961 ;Santesson, Book and Kjessler, 1973;Sohval, 1965;Stempfel, 1969). Sohval (1965) divided these individuals into three groups.…”

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confidence: 99%

“…Individuals with vestigial streak gonads are infertile due to the absence of germ cell elements in this non-functioning remnant. Although infertility has been associated with other syndromes, having abnormalities in sex chromosome complement (Polani, 1961 ;Sohval, 1965;Bornstein, 1967;Stempfel, 1969;Hecht, et a/., 1969;Santesson, et a/., 1973), XO mice are viable, fertile and phenotypically normal (Morris, 1968).…”

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XO—Gonadal Dysgenesis in the Mare

Hughes

Kennedy

Benirschke

1975

Equine Veterinary Journal

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SUMMARY Two cases of XO‐gonadal dysgenesis in the mare are presented. Case No. 1 was a pure 63, XO, while Case No. 2 was a mosaic with a preponderance of XX cells. The clinical picture was one of phenotypically normal female mares with small uteri and infantile ovaries. The ovaries lacked germ cells, and consisted of stroma only. This study emphasizes the importance of chromosome analysis in providing information concerning the mechanisms involved in some cases of equine infertility. RÉSUMÉ Deux cas d'anomalie de ce type sont présentés. Le cas No. 1 est un pur X O, le cas No. 2 est du type en mosaique avec prépondérance de cellules XX. Cliniquement il s'agissait de femelles normales avec de petits utérus et des ovaires infantiles. Les ovaires étaient dépourvus de cellules germinatives. Cette étude souligne l'importance des analyses chromosomiques dans l'interprétation de certaines infertilités. ZUSAMMENFASSUNG Zwei Fälle von XO‐Gonaden‐Dysgenese bei der Stute werden vorgestellt. Beim ersten Fall handelte es sich um ein reines Auftreten von 63,XO, beim zweiten um ein Mosaik mit Vorherrschen von XX‐Zellen. Klinisch zeigten die Stuten einen normalen Phänotyp mit kleinen Uteri und infantilen Ovarien. Die Ovarien bestanden nur aus Stroma, Keimzellen liessen sich nicht finden. Die Studie unterstreicht die Bedeutung der Chromosomenanalyse für die Abklärung bestimmter Fälle von Unfruchtbarkeit.

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Section: Discussionmentioning

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XO—Gonadal Dysgenesis in the Mare

Hughes

Kennedy

Benirschke

1975

Equine Veterinary Journal

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Turner syndrome and female sex chromosome aberrations: deduction of the principal factors involved in the development of clinical features

1995

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Although clinical features in Turner syndrome have been well defined, underlying genetic factors have not been clarified. To deduce the factors leading to the development of clinical features, we took the following four steps: (1) assessment of clinical features in classic 45,X Turner syndrome; (2) review of clinical features in various female sex chromosome aberrations (karyotype-phenotype correlations); (3) assessment of factors that could lead to Turner features; and (4) correlation of the clinical features with the effects of specific factors. The results indicate that the clinical features in 45,X and in other female sex chromosome aberrations may primarily be determined by: (1) degree of global non-specific developmental defects caused by quantitative alteration of a euchromatic or non-inactivated region; (2) dosage effect of a pseudoautosomal growth gene(s), a Y-specific growth gene(s), and an Xp-Yp homologous lymphogenic gene(s); and (3) degree of chromosome pairing failure in meiocytes that are destined to develop as oocytes in the absence of SRY. 1991; Grumbach and Conte 1992). However, the pertinent factors have not been determined to date. The method to clarify the factors responsible for the development of the Turner phenotype can be broken down into the following steps: (1) assessment of clinical features in classic 45,X Turner syndrome; (2) review of clinical features in various female sex chromosome aberrations (karyotype-phenotype correlations); (3) assessment of factors that could lead to Turner features; and (4) correlation of the clinical features with the effects of specific factors. If the clinical features in 45,X and in other female sex chromosome aberrations are explained by the effects of specific factors, it can be said that such factors contribute to the development of Turner features. In this paper, we take each of the above steps, and propose the principal factors involved in the development of clinical features in Turner syndrome.

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The Mortality of Human Xo Embryos

Cited by 2 publications

References 11 publications

XO—Gonadal Dysgenesis in the Mare

XO—Gonadal Dysgenesis in the Mare

Turner syndrome and female sex chromosome aberrations: deduction of the principal factors involved in the development of clinical features

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