Rescue of follicle development after oocyte-induced ovary dysfunction and infertility in a model of POI.

The mechanisms and aetiology underlying the development of premature ovarian insufficiency (POI) are poorly understood. However, the oocyte clearly has a role as demonstrated by the Double Mutant (DM) mouse model where ovarian dysfunction (6 weeks) is followed by POI (3 months) due to oocyte-specific deletion of complex and hybrid N- and O-glycans. The ovaries of DM mice contain more primary follicles (3a stage) accompanied by fewer developing follicles, indicating a block in follicle development.

Rapid ovarian transcript changes during the onset of premature ovarian insufficiency.

The manuscript has been submitted without altering abstract in line with Reproduction's Flexible Submission Process. The abstract is extended and thus does not fit this space.

Formation of multiple-oocyte follicles in culture.

Basement membranes are found in every organ of the body. They provide structure and a selective filter for molecules. The ovary is no different with the follicular basal lamina (FBL) separating the granulosa and theca cells, facilitating regulation of the changing follicular environment providing appropriate conditions for the developing oocyte.

Analysis of in vitro follicle development during the onset of premature ovarian insufficiency in a mouse model.

Premature ovarian insufficiency (POI) occurs in 1% of women under 40 years of age and is predominantly idiopathic. In a transgenic mouse model of follicular POI, the Double Mutant (DM), female mice are fertile at 6 weeks of age, become infertile by 9 weeks and exhibit POI by 3 months. DM female mice generate oocytes lacking mucin O-glycans and complex N-glycans due to deletion of core 1 synthase, glycoprotein-N-acetylgalactosamine 3-β-galactosyltransferase 1 (C1galt1) and mannoside acetylglucosaminyltransferase 1 (Mgat1) respectively (DM, C1galt1Mgat1:ZP3Cre; Control, C1galt1Mgat1).

Oocyte-derived Smad4 is not required for development of the oocyte or the preimplantation embryo.

Unlabelled: The generation of a competent egg requires complex molecular interactions between the oocyte and the ovary, and transforming growth factor β (TGF-β) is a major signaling pathway. Smad4 is a central regulator of the TGF-β signaling pathway as it mediates gene expression triggered by activation of TGF-β receptors. Deletion of Smad4 in granulosa cells disrupts follicle development; however, the role of Smad4 in the oocyte has not been confirmed.

Maternal-fetal unit interactions and eutherian neocortical development and evolution.

The conserved brain design that primates inherited from early mammals differs from the variable adult brain size and species-specific brain dominances observed across mammals. This variability relies on the emergence of specialized cerebral cortical regions and sub-compartments, triggering an increase in brain size, areal interconnectivity and histological complexity that ultimately lies on the activation of developmental programs. Structural placental features are not well correlated with brain enlargement; however, several endocrine pathways could be tuned with the activation of neuronal progenitors in the proliferative neocortical compartments.

Embryos generated from oocytes lacking complex N- and O-glycans have compromised development and implantation.

Female mice generating oocytes lacking complex N- and O-glycans (double mutants (DM)) produce only one small litter before undergoing premature ovarian failure (POF) by 3 months. Here we investigate the basis of the small litter by evaluating ovulation rate and embryo development in DM (Mgat1(F/F)C1galt1(F/F):ZP3Cre) and Control (Mgat1(F/F)C1galt1(F/F)) females. Surprisingly, DM ovulation rate was normal at 6 weeks, but declined dramatically by 9 weeks.

[Extent of sperm DNA damage in spermatozoa from men examined for infertility. Relationship with oxidative stress].

Background: Cryptorchidism and oligozoospermia are clinical conditions closely associated with impaired fertility. Oxidative stress and related sperm DNA damage have been identified as significant causes of male infertility.

Aim: To determine the extent of sperm nuclear DNA damage in patients affected with idiopathic oligozoospermia or undescended testes and to examine its relationship with oxidative stress.

YqTER deletion causes arrest of spermatogenesis in early puberty.

We report a 12-7/12 year-old male with obesity, eunuchoid proportions, genetic stigmata of Turner's syndrome and mild developmental delay. We investigated whether cytogenetic alterations could be responsible for his phenotype. Conventional karyotype in 70 peripheral blood cells was 45,X(15%)/46,XYqh-(85%).

Absence of Y chromosome microdeletions in patients with cryptorchidism and hypospadias.

Microdeletions of the Y chromosome have been observed in some patients with cryptorchidism and severe defects of spermatogenesis. We investigated whether microdeletions of the Y chromosome may be present in patients with cryptorchidism and hypospadias. Peripheral blood was obtained from 20 male patients 5.