ABSTRACT
Objective:To analyze the serum anti-Müllerian hormone (AMH) levels in women of childbearing age in different age groups in Henan, and establish the medical reference intervals based on measurement results from this population.Methods:From January to June 2017, 620 healthy women of childbearing age (20-34 years old), who underwent pre-pregnancy eugenics and pre-marital checkups in 13 project sites in Henan, were included in this study. Participants were divided into 3 age groups: 20-24 years group ( n=210), 25-29 years group ( n=207), and 30-34 years group ( n=203). Spearman correlation coefficient was used to evaluate the correlation between serum AMH level and age; Kruskal-Wallis H test was used to compare the serum AMH levels of different age groups; Wilcoxon test was used for comparison between pairs; the percentile method ( P2.5, P97.5) was used to establish medical reference interval of serum AMH in women of childbearing age for the whole population and different age groups, respectively. Results:The correlation coefficient between serum AMH and age in women of childbearing age (20-34 years old) is -0.17 ( P<0.001). There was a statistically significant difference in the overall frequency distribution of serum AMH levels among the three different age groups ( H=21.978, P<0.05). Among them, there is a statistically significant difference between the 20-24 years group and the 30-34 years group ( Z=4.292, P<0.05). There is a statistically significant difference between the 25-29 years group and the 30-34 years group ( Z=3.803, P<0.05). The reference range of serum AMH is 0.281-9.693 μg/L in this cohort; the reference range of serum AMH is 0.524-10.760, 0.229-9.200, 0.115-8.200 μg/L for women of childbearing age at 20-24, 25-29 and 30-34 years, respectively. Conclusion:The serum AMH level of women of childbearing age (20-34 years old) decreases with age. It is of great significance to establish the serum AMH reference interval for women of childbearing age in different age groups in Henan.
ABSTRACT
OBJECTIVE@#To evaluate the efficacy of rapmycin for treatment of experimental autoimmune encephalomyelitis (EAE) in mice and explore the underlying mechanism.@*METHODS@#An EAE model was established in C57BL/6 mice. After immunization, the mice were divided into model group and rapamycin groups treated daily with low-dose (0.3 mg/kg) or high-dose (1 mg/kg) rapamycin. The clinical scores of the mice were observed using Knoz score, the infiltration of IL-17 cells in the central nervous system (CNS) was determined using immunohistochemistry; the differentiation of peripheral Treg cells was analyzed using flow cytometry, and the changes in the levels of cytokines were detected with ELISA; the changes in the expressions of p-Smad2 and p- smad3 were investigated using Western blotting.@*RESULTS@#High-dose rapamycin significantly improved the neurological deficits scores of EAE mice. In high-dose rapamycin group, the scores in the onset stage, peak stage and remission stage were 0.14±0.38, 0.43±1.13 and 0.14±0.37, respectively, as compared with 1.14±0.69, 2.14±1.06 and 2.2±0.75 in the model group. The infiltration of inflammatory IL-17 cells was significantly lower in high-dose rapamycin group than in the model group (43±1.83 153.5±7.02). High-dose rapamycin obviously inhibited the production of IL-12, IFN-γ, IL-17 and IL-23 and induced the anti-inflammatory cytokines IL-10 and TGF-β. The percentage of Treg in CD4+ T cells was significantly higher in high- dose rapamycin group than in the model group (10.17 ± 0.68 3.52 ± 0.32). In the experiment, combined treatments of the lymphocytes isolated from the mice with rapamycin and TGF-β induced a significant increase in the number of Treg cells (13.66±1.89) compared with the treatment with rapamycin (6.23±0.80) or TGF-β (4.87±0.85) alone. Rapamycin also obviously up-regulated the expression of p-Smad2 and p-Smad3 in the lymphocytes.@*CONCLUSIONS@#Rapamycin can promote the differentiation of Treg cells by up-regulating the expression of p-Smad2 and p-smad3 to improve neurological deficits in mice with EAE.