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Assisted hatching
Published in David K. Gardner, Ariel Weissman, Colin M. Howles, Zeev Shoham, Textbook of Assisted Reproductive Techniques, 2017
Three distinct glycoproteins have been described both in mice and in humans (ZP1, ZP2, and ZP3) (2). Acrosome-reacted spermatozoa bind to ZP receptors, and biochemical changes have been observed after fertilization (3) that are responsible for the prevention of polyspermic fertilization.
Oocyte maturation arrest produced by TUBB8 mutations: impact of genetic disorders in infertility treatment
Published in Gynecological Endocrinology, 2020
María C. Lanuza-López, Sandra G. Martínez-Garza, Jesús F. Solórzano-Vázquez, Daniela Paz-Cervantes, Claudia González-Ortega, Israel Maldonado-Rosas, Gerardo Villegas-Moreno, Lina G. Villar-Muñoz, Francisco A. Arroyo-Méndez, Antonio M. Gutiérrez-Gutiérrez, Raul E. Piña-Aguilar
Factors related to ovarian superovulation are mainly considered as the etiology, including unproper administration of hCG by the patient or untimed oocyte triggering. In 2014, a genetic etiology for oocyte maturation arrest was described for the first time [4]. Currently, oocyte maturation defects of genetic etiology comprise a group of six different Mendelian disorders: oocyte maturation defect type 1 caused by mutations in ZP1 gene [4] (OMIM 195000), type 2 produced by mutations in TUBB8 gene [5] (OMIM 616768), type 3 related to ZP3 gene [6] (OMIM 182889), type 4 by mutations in PATL2 gene [7,8] (OMIM 614661), type 5 related with WEE2 gene [9] (OMIM 614084) and type 6 produced by mutations in ZP2 gene [10] (OMIM 182888). From a clinical and laboratory point of view, some of these disorders are potentially diagnosed by the abnormal morphology of oocytes when defects affect the structure of zona pellucida but in the others the only visible abnormality is that oocytes are at MI after oocyte capture and IVF or ICSI complicating an accurate clinical diagnosis.
Disposition and measured toxicity of zinc oxide nanoparticles and zinc ions against keratinocytes in cell culture and viable human epidermis
Published in Nanotoxicology, 2020
Amy M. Holmes, Lorraine Mackenzie, Michael S. Roberts
Figure 1(a) shows the differential cytotoxicity of ZnO NP and zinc ions against HaCaT cells in DMEM media. It is apparent that ZnO NP appeared to be more toxic at lower equivalent zinc concentrations than the ZnSO4 in this media. Figure 1(b) shows the HaCaT cell images observed in the DMEM media corresponding to the two survival curves. They show an intense increase in intracellular ZP1 fluorescence and thus increase in intracellular Zn2+ with increasing ZnO NP addition. At a concentration of ZnO NP >1 mM the SHG signal of the ZnO NP can be observed as large aggregates (shown in pink in Figure 1(b) after 24 h of incubation. At high concentrations of ZnO NP (>1 mM) in the complete DMEM, the ZP1 signal increased throughout the whole cell, the cell morphology became rounded and the cells were no longer adherent or viable. For ZnSO4, the ZP1 fluorescence became intense throughout the whole cell at a concentration of ≥488 µM and the HaCaT cells became rounded and lost adherence, suggesting cell death (Figure 1(a,b)).