Objective:To identify the best predictor of late-onset severe ovarian hyperstimulation syndrome (OHSS) in ≤35 years old women undergoing ovarian stimulation.Methods:In this retrospective cohort study, the data from 1138 in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) cycles at the Third Affiliated Hospital of Guangzhou Medical University from December 2017 to December 2018 were analyzed. The pregnancy cycles were compared between OHSS group and non-OHSS group. The differences were calculated for two groups using one-way ANOVA and chi-squared test. Factors were identified to predict late onset OHSS using multivariable logistic regression. Receiver operating characteristic (ROC) curves were used to evaluate the predictors of OHSS. Results:Antral follicle count (AFC) ( P=0.009), estradiol levels on human chorionic gonadotropin (hCG) injection day ( P<0.001), the number of oocytes retrieved ( P=0.001), available embryos ( P=0.016) and high-quality embryos ( P=0.007) were higher, whereas, priming dosage of exogenous follicle-stimulating hormone (FSH) ( P=0.002), total dosage of gonadotropin (Gn) used ( P<0.001) and stimulation duration ( P=0.034) were lower in OHSS group than in non-OHSS group. The number of gestational sacs was higher in OHSS group than in non-OHSS group ( P<0.001). The number of gestational sacs ( OR=2.408, 95% CI=1.529-3.793, P<0.001) was found to be independent predictive factors of late onset OHSS in ≤35 years old women. Linear predictor (lp)=number of gestational sacs ×0.879-3.946. The risk ratio of OHSS was 2.25 for patients with the number of gestational sacs ≥2 compared with those with 1 gestational sacs. Conclusion:In ≤35 years old women, the number of gestational sacs was the independent predictive factor of late-onset severe OHSS, which was higher when ≥2 gestational sacs occurred.

Objective:To identify the best predictor of late-onset severe ovarian hyperstimulation syndrome (OHSS) in ≤35 years old women undergoing ovarian stimulation.Methods:In this retrospective cohort study, the data from 1138 in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) cycles at the Third Affiliated Hospital of Guangzhou Medical University from December 2017 to December 2018 were analyzed. The pregnancy cycles were compared between OHSS group and non-OHSS group. The differences were calculated for two groups using one-way ANOVA and chi-squared test. Factors were identified to predict late onset OHSS using multivariable logistic regression. Receiver operating characteristic (ROC) curves were used to evaluate the predictors of OHSS. Results:Antral follicle count (AFC) ( P=0.009), estradiol levels on human chorionic gonadotropin (hCG) injection day ( P<0.001), the number of oocytes retrieved ( P=0.001), available embryos ( P=0.016) and high-quality embryos ( P=0.007) were higher, whereas, priming dosage of exogenous follicle-stimulating hormone (FSH) ( P=0.002), total dosage of gonadotropin (Gn) used ( P<0.001) and stimulation duration ( P=0.034) were lower in OHSS group than in non-OHSS group. The number of gestational sacs was higher in OHSS group than in non-OHSS group ( P<0.001). The number of gestational sacs ( OR=2.408, 95% CI=1.529-3.793, P<0.001) was found to be independent predictive factors of late onset OHSS in ≤35 years old women. Linear predictor (lp)=number of gestational sacs ×0.879-3.946. The risk ratio of OHSS was 2.25 for patients with the number of gestational sacs ≥2 compared with those with 1 gestational sacs. Conclusion:In ≤35 years old women, the number of gestational sacs was the independent predictive factor of late-onset severe OHSS, which was higher when ≥2 gestational sacs occurred.

OBJECTIVETo investigate the histomorphology and the expressions of the proliferation marker Ki-67 and estrogen receptor in the uterus of mice with autoimmune premature ovarian failure (POF) induced by zona pellucida 3 peptide (pZP3).

METHODSAutoimmune POP models were established in 20 female BALB/c mice (7-8 weeks old) by immunization with pZP3 and another 20 mice served as the control group. The POP models were verified by vaginal cytology, serum sex hormones, ovary histomorphology and ZP3 antibody immunohistochemistry. The histomorphology and expressions of Ki-67, estrogen receptor α and estrogen receptor β in the uterus of the mice were detected.

RESULTSAutoimmune POP models were established successfully in 80% of the mice at 8 weeks after the immunization. Compared with those in the control group, the mice in the model group showed a smaller volume of the uterus, thinner endometrium and a reduced number of glands. The luminal epithelial cells, glandular epithelial cells and stromal cells in the uterus of the model mice all presented with a lower expression of Ki-67 than those in the control group, and Ki-67 translocation from the nuclei to the cytoplasm was found in the model group. The luminal epithelial cells, glandular epithelial cells and stromal cells showed positive ERα immunoreactivity in the model group but not in the control group. No obvious ERβ expression was found in the uterus in either of the groups.

CONCLUSIONpZP3 can induce autoimmune POP, cause suppressed proliferation of the endometrial epithelial cells and stromal cells, and reduce the cellular expression of ERα in the uterus of mice.

Animals ; Autoimmune Diseases ; metabolism ; Cell Nucleus ; Egg Proteins ; Endometrium ; Epithelial Cells ; Estrogen Receptor alpha ; metabolism ; Estrogen Receptor beta ; metabolism ; Female ; Immunohistochemistry ; Ki-67 Antigen ; metabolism ; Membrane Glycoproteins ; Mice ; Mice, Inbred BALB C ; Primary Ovarian Insufficiency ; metabolism ; Receptors, Cell Surface ; Stromal Cells ; Uterus ; metabolism ; Zona Pellucida Glycoproteins

Objective To investigate the histomorphology and the expressions of the proliferation marker Ki-67 and estrogen receptor in the uterus of mice with autoimmune premature ovarian failure (POF) induced by zona pellucida 3 peptide (pZP3). Methods Autoimmune POP models were established in 20 female BALB/c mice (7-8 weeks old) by immunization with pZP3 and another 20 mice served as the control group. The POP models were verified by vaginal cytology, serum sex hormones, ovary histomorphology and ZP3 antibody immunohistochemistry. The histomorphology and expressions of Ki-67, estrogen receptorαand estrogen receptorβin the uterus of the mice were detected. Results Autoimmune POP models were estblished successfully in 80%of the mice at 8 weeks after the immunization. Compared with those in the control group, the mice in the model group showed a smaller volume of the uterus, thinner endometrium and a reduced number of glands. The luminal epithelial cells, glandular epithelial cells and stromal cells in the uterus of the model mice all presented with a lower expression of Ki-67 than those in the control group, and Ki-67 translocation from the nuclei to the cytoplasm was found in the model group. The luminal epithelial cells, glandular epithelial cells and stromal cells showed positive ERαimmunoreactivity in the model group but not in the control group. No obvious ERβexpression was found in the uterus in either of the groups. Conclusion pZP3 can induce autoimmune POP, cause suppressed proliferation of the endometrial epithelial cells and stromal cells, and reduce the cellular expression of ERαin the uterus of mice.

Objective To investigate the histomorphology and the expressions of the proliferation marker Ki-67 and estrogen receptor in the uterus of mice with autoimmune premature ovarian failure (POF) induced by zona pellucida 3 peptide (pZP3). Methods Autoimmune POP models were established in 20 female BALB/c mice (7-8 weeks old) by immunization with pZP3 and another 20 mice served as the control group. The POP models were verified by vaginal cytology, serum sex hormones, ovary histomorphology and ZP3 antibody immunohistochemistry. The histomorphology and expressions of Ki-67, estrogen receptorαand estrogen receptorβin the uterus of the mice were detected. Results Autoimmune POP models were estblished successfully in 80%of the mice at 8 weeks after the immunization. Compared with those in the control group, the mice in the model group showed a smaller volume of the uterus, thinner endometrium and a reduced number of glands. The luminal epithelial cells, glandular epithelial cells and stromal cells in the uterus of the model mice all presented with a lower expression of Ki-67 than those in the control group, and Ki-67 translocation from the nuclei to the cytoplasm was found in the model group. The luminal epithelial cells, glandular epithelial cells and stromal cells showed positive ERαimmunoreactivity in the model group but not in the control group. No obvious ERβexpression was found in the uterus in either of the groups. Conclusion pZP3 can induce autoimmune POP, cause suppressed proliferation of the endometrial epithelial cells and stromal cells, and reduce the cellular expression of ERαin the uterus of mice.