Objective:To investigate the effect of endometrial thickness(EMT) on the clinical outcome of blastocyst hormone replacement freeze-thawed embryo transfer (HRT-FET) on the first progesterone day, and to analyze the threshold and optimal thickness interval corresponding to ideal clinical pregnancy rate by statistical method.Methods:The endometrial preparation protocols of 2 825 blastocyst HRT-FET cycles from January 2013 to December 2016 in Henan Provincial People′s Hospital and the Second Hospital of Hebei Medical University were studied retrospectively. According to EMT on the first progesterone day, they were divided into 5 subgroups: group Q1(EMT: 3.5-7.9 mm), group Q2(EMT: 8.0-8.9 mm), group Q3(EMT: 9.0-9.5 mm), group Q4(EMT: 9.6-10.7 mm), group Q5(EMT: 10.8-21.0 mm). Univariate analysis, classification multivariate Logistic regression analysis, curve fitting and threshold effect analysis were used to investigate the effect of endometrial thickness on clinical outcome of blastocyst HRT-FET.Results:Group Q1 was set as the control group in classification multivariate Logistic regression analysis, after adjusting for confounding factors, the clinical pregnancy rate and live birth rate in other groups were higher than the control group. The clinical pregnancy rate and live birth rate in group Q3 and Q4 were significantly increased and the differences were statistically significant(all P<0.05). The cut-off value of the endometrial thickness was 9.6 mm. When endometrial thickness was less than 9.6 mm, with 1 mm increase of endometrial thickness, the clinical pregnancy rate increased by 23%( OR=1.23, 95% CI=1.11-1.36) and the live birth rate increased by 21%( OR=1.21, 95% CI=1.10-1.33). When the endometrial thickness was thicker than the threshold, the clinical pregnancy rate did not increase significantly( OR=0.92, 95% CI=0.84-1.02), and the live birth rate showed a downward trend( OR=0.88, 95% CI=0.81-0.96). Conclusions:In the blastocyst HRT-FET cycle, endometrial thickness showes a curvilinear relationship with clinical outcome. The optimal endometrial thickness range for ideal clinical outcome is 9.0-11.0 mm.

Zn²⁺ is required for the activity of many mitochondrial proteins, which regulate mitochondrial dynamics, apoptosis and mitophagy. However, it is not understood how the proper mitochondrial Zn²⁺ level is achieved to maintain mitochondrial homeostasis. Using Caenorhabditis elegans, we reveal here that a pair of mitochondrion-localized transporters controls the mitochondrial level of Zn²⁺. We demonstrate that SLC-30A9/ZnT9 is a mitochondrial Zn²⁺ exporter. Loss of SLC-30A9 leads to mitochondrial Zn²⁺ accumulation, which damages mitochondria, impairs animal development and shortens the life span. We further identify SLC-25A25/SCaMC-2 as an important regulator of mitochondrial Zn²⁺ import. Loss of SLC-25A25 suppresses the abnormal mitochondrial Zn²⁺ accumulation and defective mitochondrial structure and functions caused by loss of SLC-30A9. Moreover, we reveal that the endoplasmic reticulum contains the Zn²⁺ pool from which mitochondrial Zn²⁺ is imported. These findings establish the molecular basis for controlling the correct mitochondrial Zn²⁺ levels for normal mitochondrial structure and functions.
Animals ; Caenorhabditis elegans/metabolism* ; Cation Transport Proteins/genetics* ; Homeostasis ; Mitochondria/metabolism* ; Zinc/metabolism*