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Reactions of Cu(II) or Co(II) salts and 2-(4-carboxyphenoxy)terephthalic acid (H3cpota) with N-heterocyclic donors (1,10-phenanthroline (phen) or 4,4′-bipyridine (4,4′-bpy)) formed two multidimensi...

Anti-Müllerian hormone (AMH) downregulates the level of stem cell factor (SCF) via the cAMP/PKA signaling pathway in human granulosa cells (GCs). Little information is available on the molecular mechanism underlying the interaction. This study is aimed at determining whether AMH regulates expression of SCF via the cAMP-PKA-CREB signaling pathway in human GCs. In the present study, we verified the binding of cAMP-response element-binding protein (CREB) to promoter of SCF in human GCs. Furthermore, the effect of CREB was tested on the SCF promoter, and the site of CREB binding to SCF promoter was identified using truncations as well as assays of SCF-promoted mutation and CREB mutation. To investigate the correlation among AMH, SCF promoter, and CREB, pGL-Basic-SCF+CREB was transfected into overexpressed AMH GCs (AMH-high GCs), low expressed AMH GCs (AMH-low GCs), and normal GCs (GCs), respectively. Finally, immunofluorescence, double immunostaining, and Western blot were carried out in AMH-high and AMH-low GCs to confirm the AMH-mediated regulation of SCF expression by inhibiting the phosphorylation of CREB (pCREB) in GCs. Results indicated CREB interacted with SCF promoter and significantly enhanced the transcription level of SCF. The CREB binding site was localized at 318-321 bp of SCF gene promote. AMH inhibits the expression of SCF by phosphorylation of CREB via the PKA signaling pathway in GCs. These findings provide an in-depth understanding of the molecular mechanism underlying AMH suppressing the follicle growth, which would aid in the development of a novel therapy.

The sperm quality of some males is in a critical state, making it hard for clinicians to choose the suitable fertilisation methods. This study aimed to develop an intelligent nomogram for predicting fertilisation rate of infertile males with borderline semen. 160 males underwent in vitro fertilisation (IVF), 58 of whom received rescue ICSI (R‐ICSI) due to fertilisation failure (fertilisation rate of IVF ≤30%). A least absolute shrinkage and selection operator (LASSO) regression analysis identified sperm concentration, progressively motile spermatozoa (PMS), seminal plasma anti‐Müllerian hormone (spAMH), seminal plasma inhibin (spINHB), serum AMH (serAMH) and serum INHB (serINHB) as significant predictors. The nomogram was plotted by multivariable logistic regression. This nomogram‐illustrated model showed good discrimination, calibration and clinical value. The area under the receiver operating characteristic curve (AUC) of the nomogram was 0.762 (p

Objective We aimed to identify the factors that influence serum anti-Müllerian hormone (AMH) concentration measurements. Methods We collected serum samples between May and September 2018 and compared the effect on AMH concentration measured by ELISA of conditions including venepuncture, storage time, storage temperature, locations of the reaction microplate, and the use of the oral contraceptive pill and gonadotrophin-releasing hormone (GnRH). Results AMH concentration was not affected by food intake but was affected by haemolysis. It was also much higher in samples on the edge of the ELISA microtitre plate. AMH concentration increased after incubation at room temperature for 1 day, 4°C for 3 days, −20°C for 1 month and −40°C for 4 months, but no change occurred during storage at −80°C for 9 months. AMH concentration was high in patients following GnRH agonist treatment but was not affected by oral contraceptives. Conclusions No fasting is required prior to AMH measurement. Placement of serum samples on the edge of microtitre plates affects the results of the AMH ELISA. If serum samples cannot be assayed immediately, it is best to store them at −80°C. Basal AMH concentration cannot be used as a measure of ovarian reserve after GnRH agonist treatment.

Repeated implantation failure (RIF) is a common endocrine disease that causes female infertility and the etiology is unknown. The abnormal expression of key proteins and hormones at the maternal-fetal interface affected the maternal-fetal communication and leads to adverse pregnancy outcomes. The expression of anti-Mullerian hormone (AMH) and AMH receptor II (AMHRII) was observed in the endometrium. This study aimed to investigate the expression of AMH and AMHRII at the human endometrium, decidual tissue, and blastocyst. Furthermore, the expression of AMH and AMHRII were examined in the RIF patients using immunohistochemistry and quantitative real-time PCR to test the AMHRII expression. The results demonstrated that AMH and AMHRII were present in healthy endometrium and AMHRII was highly expressed in mid-luteal phase. In addition, AMHRII expression was detected throughout the pregnancy and AMHRII's highest expression was in the second trimester. AMHRII was expressed in the blastocysts; however, AMH was not observed. The positive expression rate for AMHRII was significantly higher in the endometrium from RIF. Estrogen receptor (ER), insulin-like growth factor binding protein 1(IGFBP1), and prolactin (PRL) were significantly less expressed in RIF with high expression of AMHRII. The apoptosis was significantly higher in patients with high expression of AMHRII than in patients with normal expression of AMHRII. Our data suggests that AMHRII had an effect on RIF via the AMH and AMHRII signaling pathway. It participated in the development of RIF by interfering with endometrial decidualization and apoptosis.

The objective of the study was to investigate whether genetic polymorphisms of the anti-Mullerian hormone (AMH) and its specific receptor anti-Mullerian hormone type II receptor (AMHRII) were associated with the hormone disorder and phenotype of polycystic ovary syndrome (PCOS). This case-control study included 141 PCOS patients and 123 normal women. Two polymorphisms of AMH and AMHRII and the clinical characteristics of participants such as body mass index (BMI), serum luteinizing hormone (LH), estradiol levels (E2), total testosterone levels (T), and homeostasis model assessment of insulin resistance (HOMA-IR) were analyzed with the case-control sample. Gene–gene interactions of AMH and AMHRII genes were analyzed based multifactor-dimensionality reduction method. A significant difference of AMH gene polymorphisms were observed in IR-PCOS women and controls. The AMH and AMHRII gene polymorphisms were not found a significant difference in non-IR-PCOS and normal groups. To IR-PCOS women, genotypes of AMH were closely related to the serum levels of LH (P = 0.000), testosterone (P = 0.000) and HOMA-IR (P = 0.038), while in the non-IR-PCOS and normal groups, no relationship was found. No impact of AMH and AMHRII gene–gene interactions was demonstrated. Our research suggests that the diversity of AMH genotypes in the AMH signal pathway may be connected with the susceptibility and phenotype of PCOS with insulin resistance.

To analyze the correlations of seminal plasma (sp) anti-Müllerian hormone (spAMH) and inhibin B (spINHB) and serum INHB (serINHB) with semen parameters in oligoasthenospermia patients and explore their value in predicting the outcome of routine in vitro fertilization (IVF).We obtained the levels of spAMH, spINHB and serINHB as well as semen parameters from 88 infertile males undergoing IVF due to oligoasthenospermia or female uterine tubal factors from August 2016 to February 2017. Using the ROC curve and Pearson's correlation analysis, we examined the effects of the obtained parameters on the fertilization rate and assessed the correlation of the levels of spAMH, spINHB and serINHB with the semen parameters of the patients.Concerning the predictive value for the outcome of IVF, Pearson's correlation analysis showed that the area under the ROC curve (AUC) of spAMH was 0.807 (sensitivity = 84.6%, specificity = 76%, cut-off point = 3.529, P0.001) and that of spINHB was 0.768 (sensitivity = 84.6%, specificity = 88.7%, cut-off point = 31.117, P = 0.002). The serINHB level was found positively correlated with sperm concentration (r = 0.346, P = 0.001), total sperm count (r = 0.378, P0.001), sperm motility (r = 0.521, P0.001), and the percentage of progressively motile sperm (r = 0.343, P = 0.001).The levels of spAMH and spINHB can be used as laboratory indexes to predict the fertilization rate of routine IVF and are correlated with semen parameters in oligoasthenospermia patients, while that of serINHB has a positive correlation with the semen parameters of the patients.目的: 分析精浆AMH、INHB及血清INHB与少弱精子症患者精液参数之间的相关性，同时探讨对其常规体外受精（IVF）结局的预测价值及影响。方法: 收集2016年8月至2017年2月因男方少弱精子症或女方输卵管因素就诊于宁夏医科大学总医院生殖中心行IVF助孕的88例不孕夫妇的临床资料，检测精浆AMH、INHB、血清INHB及精液参数（精子活动率、浓度、总数、前向运动精子百分率及正常形态精子百分率），采用受试者工作特征曲线（ROC）分析精浆AMH、INHB、血清INHB及精液参数对其受精率的预测能力；Pearson 相关分析检验精浆 AMH、INHB及血清INHB 与精液参数之间的关系，均设定 P0.05 为有统计学差异。结果： 精浆AMH：AUC=0.807（敏感度84.6%，特异度76.0%，截断点3.529，P=0.000），精浆INHB：AUC=0.768（敏感度84.6%，特异度88.7%，截断点31.117，P=0.002）；血清INHB与精子浓度（r=0.346，P=0.001）、精子总数（r=0.378，P=0.000）、精子活动率（r=0.521，P=0.000）、前向运动（r=0.343，P=0.001）。结论： 精浆AMH、INHB可作为预测少弱精子症患者受精率的实验室指标；血清INHB与少弱精子症精液参数（精子浓度、精子总数、活动率及前向运动精子百分率）呈显著正相关。.

The aim of the present study was to investigate the effects of recombinant human anti-mullerian hormone (rhAMH) on Stem Cell Factor (SCF) expression in human granulosa cells (GCs). GCs were obtained from infertile patients undergoing IVF-ET cycles and cultured with 20 ng/ml of rhAMH. The levels of SCF mRNA and protein were detected in both matched and experimental group by real-time PCR, immunofluorescence, and ELISA, respectively, on day 4 of culture. We found that human GCs expressed SCF mRNA and protein, and SCF expression in the experimental group was significantly lower than that in the matched group (p < 0.05). We further showed that rhAMH inhibited SCF expression at mRNA and protein levels.

Objective To determine whether there is a correlation between antimullerian hormone (AMH) and stem cell factor (SCF) in serum, follicular fluid (FF), and granulosa cells (GCs), and to investigate a possible regulatory mechanism of AMH on SCF in human granulosa cells. Design Prospective clinical and experimental study. Setting Academic center. Patient(s) 163 women undergoing IVF. Intervention(s) Serum, FF, and GCs obtained in all women, primary cultures of human GCs. Main Outcome Measure(s) AMH and SCF were analyzed in serum, FF, and GCs, using enzyme-linked immunosorbent assay, reverse-transcription polymerase chain reaction, and immunoblotting. Result(s) There was a significant negative correlation between AMH and SCF protein level in FF, and in the mRNA expression of AMH and SCF in GCs. Conversely, there was no correlation between AMH and SCF levels in serum. In primary cultures of human GCs, SCF was down-regulated by treatment with recombinant human AMH and was increased by cyclic adenosine 3′:5′ monophosphate (cAMP) in a dose-dependent manner. A protein kinase A (PKA) inhibitor (H89) significantly reversed the effects of recombinant human AMH and cAMP on SCF mRNA and protein expression. Conclusion(s) This is the first report on a modulatory role for AMH as an ovarian/follicular autocrine/paracrine factor controlling SCF expression via the cAMP/PKA pathway.