Embryology with precision: effective quality control in the in vitro fertilization laboratory.

The purpose of this review is to address the critical need for standardization and clarity in the use of key performance indicators (KPIs) within the realm of in vitro fertilization (IVF), particularly emphasizing the integration of preimplantation genetic testing (PGT) processes. This review is timely and relevant given the persistently modest success rates of IVF treatments, which stand at approximately 30%, and the growing complexity of IVF procedures, including PGT practices. The review synthesizes recent findings across studies focusing on technical and clinical KPIs in embryology and genetic laboratories, identifying gaps in current research and practice, particularly the lack of standardized KPIs and terminology. Recent findings highlighted include the critical evaluation of technical KPIs such as Intracytoplasmic Sperm Injection (ICSI) fertilization rates, embryo development rates, and laboratory performance metrics, alongside clinical KPIs like the proportion of mature oocytes and clinical pregnancy rates. Notably, the review uncovers a significant gap in integrating and standardizing KPIs for PGT applications, which is essential for improving IVF outcomes and genetic diagnostic accuracy. The implications of these findings are profound for both clinical practice and research. For clinical practice, establishing a standardized set of KPIs, especially for PGT, could significantly enhance the success rates of IVF treatments by providing clearer benchmarks for quality and performance. For research, this review underscores the necessity for further studies to close the identified gaps, promoting a more integrated and standardized approach to KPIs in IVF and PGT processes. This comprehensive approach will not only aid in improving clinical outcomes but also in advancing the field of reproductive medicine.

High NaCl Concentrations in Water Are Associated with Developmental Abnormalities and Altered Gene Expression in Zebrafish.

Salt is frequently introduced in ecosystems, where it acts as a pollutant. This study examined how changes in salinity affect the survival and development of zebrafish from the two-cell to the blastocyst stage and from the blastocyst to the larval stage. Control zebrafish embryos were cultured in E3 medium containing 5 mM Sodium Chloride (NaCl), 0.17 mM Potassium Chloride (KCL), 0.33 mM Calcium Chloride (CaCl2), and 0.33 mM Magnesium Sulfade (MgSO4). Experiments were conducted using increasing concentrations of each individual salt at 5×, 10×, 50×, and 100× the concentration found in E3 medium. KCL, CaCl2, and MgSO4 did not result in lethal abnormalities and did not affect early embryo growth at any of the concentrations tested. Concentrations of 50× and 100× NaCl caused embryonic death in both stages of development. Concentrations of 5× and 10× NaCl resulted in uninflated swim bladders in 12% and 65% of larvae, compared to 4.2% of controls, and caused 1654 and 2628 genes to be differentially expressed in blastocysts, respectively. The ATM signaling pathway was affected, and the Sonic Hedgehog pathway genes Shh and Ptc1 implicated in swim bladder development were downregulated. Our findings suggest that increased NaCl concentrations may alter gene expression and cause developmental abnormalities in animals found in affected ecosystems.

Mitochondrial Unfolded Protein Response Gene Clpp Is Required for Oocyte Function and Female Fertility.

Mitochondrial unfolded protein stress response (mtUPR) plays a critical role in regulating cellular and metabolic stress response and helps maintain protein homeostasis. Caseinolytic peptidase P (CLPP) is one of the key regulators of mtUPR and promotes unfolded protein degradation. Previous studies demonstrated that global deletion of Clpp resulted in female infertility, whereas no impairment was found in the mouse model with targeted deletion of Clpp in cumulus/granulosa cells. These results suggest the need to delineate the function of Clpp in oocytes. In this study, we aimed to further explore the role of mtUPR in female reproductive competence and senescence using a mouse model. Oocyte-specific targeted deletion of Clpp in mice resulted in female subfertility associated with metabolic and functional abnormalities in oocytes, thus highlighting the importance of CLPP-mediated protein homeostasis in oocyte competence and reproductive function.

Disruption of mitochondrial unfolded protein response results in telomere shortening in mouse oocytes and somatic cells.

Caseinolytic peptidase P (CLPP) plays a central role in mitochondrial unfolded protein response (mtUPR) by promoting the breakdown of misfolded proteins and setting in motion a cascade of reactions to re-establish protein homeostasis. Global germline deletion of Clpp in mice results in female infertility and accelerated follicular depletion. Telomeres are tandem repeats of 5'-TTAGGG-3' sequences found at the ends of the chromosomes. Telomeres are essential for maintaining chromosome stability during somatic cell division and their shortening is associated with cellular senescence and aging. In this study, we asked whether the infertility and ovarian aging phenotype caused by global germline deletion of Clpp is associated with somatic aging, and tested telomere length in tissues of young and aging mice. We found that impaired mtUPR caused by the lack of CLPP is associated with accelerated telomere shortening in both oocytes and somatic cells of aging mice. In addition, expression of several genes that maintain telomere integrity was decreased, and double-strand DNA breaks were increased in telomeric regions. Our results highlight how impaired mtUPR can affect telomere integrity and demonstrate a link between loss of mitochondrial protein hemostasis, infertility, and somatic aging.