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Malaria remains a significant public health issue on a global scale. The disease exhibits pronounced sexual dimorphism, with male-infected individuals often presenting more severe symptoms and higher mortality rates compared to females. However, gender factors are frequently overlooked in many experimental studies related to Plasmodium infection. As a primary female sex hormone, estrogen plays a crucial role in regulating immune responses and inflammatory signals, contributing significantly to the gender differences observed in malaria infections. Here, starting from the basic physiological functions and immune regulatory roles of estrogen, review and summarize the epidemiological evidence of gender differences in malaria infection reported in the past, and delve into how estrogen affects malaria infection and its potential roles within the context of the disease. Given the current absence of a comprehensive review on sex differences in malaria in China, we hope that this article will draw researchers' attention to the sexual dimorphism in malaria. Understanding and emphasizing the sexual dimorphism in malaria, as well as the underlying causes, can help us gain a more profound comprehension of the pathology of malaria and the individual immune responses it elicits. This knowledge may provide new insights for related basic research and potentially aid in future malaria prevention and control efforts. [ABSTRACT FROM AUTHOR]

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Condyloma acuminatum (CA) is a sexually transmitted disease characterized by proliferative lesions in the anogenital region, and its pathogenesis is mainly related to HPV infection and disturbed immune responses. Studies have shown that the incidence of CA is higher in women than in men, and the incidence of CA during pregnancy is higher than that during non-pregnancy. Sex hormones may be related to the occurrence and development of CA. This article reviews the association of estrogen and progesterone with CA, and discusses the possible link of estrogen and CA to the balance of Th1/Th2 and Th17/Treg in cellular immunity during HPV infection, in addition to exploration of the role of estrogen and progesterone in the pathogenesis and recurrence of CA, in order to provide new ideas for the clinical diagnosis and treatment of CA.

Objective To investigate the causal association between estrogen and breast cancer incidence and mortality risk. Methods Using summary data from genome 一 wide association studies, with estradiol representing estrogen, genetic variants associated with estradiol were utilized as instrument variables. Employing the univariate Mendelian randomization method, the causal association between estradiol and the risk ofincidence (4 outcomes), as well as the risk of mortality (6 outcomes) of female breast cancer and its subtypes, were assessed by the inverse variance - weighted method. Results The results revealed that elevated levels of estradiol (175 pmol/L) were associated with an increased risk of overall breast cancer (OR 二 1. 43, 95% CI11. 27 - 1. 60?P = 2. 92 x 10 ~9), estrogen receptor 一 negative breast cancer (OR 二 1. 41, 95% CI: L 25 - 1. 60, P = 2. 16 x 10 8), and estrogen receptor 一 positive breast cancer (OR = 1. 49, 95% CI: 1. 29 - 1. 72, P = 6. 92 x 10 8) incidence. However, there was no evidence that elevated levels of estradiol were the risk factors for triple - negative breast cancer incidence. Moreover, overall breast cancer and its subtypes mortality risks were not shown to be causally related to estradiol. Conclusion Elevated estrogen levels (175 pmol/L) are associated with an increased risk of overall breast cancer, estrogen receptor 一 negative breast cancer, and estrogen receptor - positive breast cancer incidence. [ABSTRACT FROM AUTHOR]

Condyloma acuminatum (CA) is a sexually transmitted disease characterized by proliferative lesions in the anogenital region, and its pathogenesis is mainly related to HPV infection and disturbed immune responses. Studies have shown that the incidence of CA is higher in women than in men? and the incidence of CA during pregnancy is higher than that during non-pregnancy. Sex hormones may be related to the occurrence and development of CA. This article reviews the association of estrogen and progesterone with CA, and discusses the possible link of estrogen and CA to the balance of Thl/Th2 and Thl7/Treg in cellular immunity during HPV infection, in addition to exploration of the role of estrogen and progesterone in the pathogenesis and recurrence of CA, in order to provide new ideas for the clinical diagnosis and treatment of CA. [ABSTRACT FROM AUTHOR]

Objective: To investigate the relationship between serum estradiol (E2 ) level in early pregnancy and the risk of hypertensive disorder complicating pregnancy (HDCP). Methods: 100 HDCP patients (HDCP group) who were admitted to our hospital from December 2021 to December 2022 were selected, and 80 healthy pregnant women who underwent prenatal examination during the same period were selected as control group, patients were divided into gestational hypertension group (26 cases), preeclampsia-eclampsia group (35 cases), pregnancy with chronic hypertension group (21 patients), and chronic hypertension with preeclampsia group (18 patients）according to the HDCP classification.Serum E2 levels were detected, and the differences of serum E2 levels in different groups were compared.The risk factors affecting the incidence of HDCP were analyzed by Logistic regression analysis.The value of serum E2 level in predicting HDCP were analyzed by receiver operating characteristic (ROC) curve.Results: The serum E2 level in HDCP group was lower than that in control group (P＜0.05), The serum E2 level of the preeclampsia-eclampsia group was lower than that of the chronic hypertension with preeclampsia group, the pregnancy with chronic hypertension group and the pregnancy with hypertension group (P＜0.05), and the serum E2 level of chronic hypertension with preeclampsia group was lower than that of pregnancy with chronic hypertension group and the pregnancy with hypertension group (P＜0.05). Age≥35 years old, high pre-pregnancy BMI, parity≥2 times, family history of hypertension, and maternal history of HDCP were risk factors for HDCP (P＜0.05), and E2 was a protective factor (P＜0.05). The critical value of E2 in predicting HDCP was 162.35 ng/L, the area under the curve was 0.744, the sensitivity was 79.00%, and the specificity was 76.25%.Conclusion: The level of serum E2 in early pregnancy of HDCP patients was significantly decrease, which is relate to the aggravation of HDCP, the detection of E2 level could predict the risk of HDCP. [ABSTRACT FROM AUTHOR]

Pre -eclampsia (PE) is a pregnancy specific syndrome characterized by hypertension and multiple organ dysfunction. Although the specific pathogenesis is not yet clear, insufficient placental perfusion and persistent hypoxia caused by shallow and limited invasion of trophoblasts during placental formation may be important initial events. As an important steroid hormone secreted by the placenta, estrogen regulates target gene expression levels through genomic or non-genomic effects of estrogen receptor (ER) and estrogen response element (ERE) signaling pathways, leading to changes in biological behaviors such as trophoblast proliferation, apoptosis, invasion, and possibly mediating the loss of endometrial decidualization, thereby participating in placental shallow implantation and the occurrence of insufficient perfusion. Estrogen and its signaling pathways can also regulate the levels of vasoactive factors such as nitric oxide and the activity of related ion channels to regulate the contractile and relaxing ability of uterine artery smooth muscle, and participate in the occurrence and development of highrisk pregnancies such as PE and recurrent spontaneous abortion through various mechanisms. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of estrogen on endometrial epithelialization, endometrial glandular duct density and ovarian blood supply in patients after intrauterine adhesions surgery. Methods A total of 67 patients with moderate and severe intrauterine adhesions admitted to the hospital from June 2019 to September 2021 were retrospectively analyzed. According to different doses of estrogen, they were divided into low-dose group（36 cases of estradiol valerate three mg each time) and high-dose group（31 cases of estradiol valerate eight mg each time). The incidence of adverse reactions and clinical efficiency rate of the two groups were recorded.The degree of endometrial epithelization and the satisfaction of endometrial glandular density after drug treatment were evaluated. The endometrial thickness, uterine volume and ovarian artery blood flow resistance index（RI), maximum systolic velocity(Vmax),end diastolic velocity(Vmin) before operation and after three cycles of medication were observed. Results The total clinical effective rate, overall endometrial epithelialization and satisfaction rate of endometrial glandular density in the high-dose group were significantly higher than those in the low-dose group. The satisfaction rate of endometrial epithelialization and glandular density in patients with severe intrauterine adhesions was significantly higher than that in the low-dose group, and the differences were statistically significant（P＜0.05). The endometrial thickness, uterine volume, Vmax and Vmin levels of the two groups after treatment were significantly higher than those before operation, RI was significantly lower than that before operation, and the endometrial thickness, uterine volume, Vmax and Vmin levels of the high-dose group after treatment were significantly higher than those of the low-dose group, RI was significantly lower than that of the low-dose group, the differences were statistically significant（P＜0.05). There was no significant difference in the incidence of adverse reactions between the two groups（P＞0.05). Conclusion Using high-dose estrogen after intrauterine adhesions surgery can effectively improve the degree of endometrial epithelialization, and the satisfaction of endometrial glandular duct density and improve the ovarian blood supply, which has good effectiveness and safety. [ABSTRACT FROM AUTHOR]

The increased incidence of gout in men and postmenopausal women suggests that gout is closely associated with sex and affected by sex hormones. However， how sex hormones are involved in the onset of gout and the exact relationship between these two are poorly understood. In this article， recent advances in the study of gout were summarized， and the mechanism underlying the role of sex hormones in the pathogenesis of gout was reviewed.

目的　探讨缺氧环境下外源性雌激素对子宫内膜癌细胞上皮间充质转化 (EMT) 的影响及其机制。 方法　选择雌激素受体阳性的子宫内膜癌细胞 Ishikawa, 体外传代培养。取传 3代、对数生长期、生长状态良好的 Ishikawa细胞进行后续实验。取部分Ishikawa细胞, 于0. 5% O2、5% CO2、94. 5% N2环境中缺氧预处理2 h, 随机分为 siRNA-缺氧诱导因子1α (HIF-1α) 组与siRNA-NC组、HIF-1α过表达组与Control组, siRNA-HIF-1α组、siRNA-NC组、 HIF-1α过表达组分别转染siRNA-HIF-1α、siRNA-NC、HA-HIF-1α-pcDNA3, Control组不予转染; 另取部分Ishikawa细 胞, 于0. 5% O2 、5% CO2 、94. 5% N2环境中缺氧预处理2 h后加入0. 01 µmol/L β-雌二醇, 随机分为Estrogen组、Estrogen + siRNA-NC 组、Estrogen + siRNA-HIF-1α 组以及 Control 组、Estrogen + HIF-1α 过表达组, Estrogen + siRNA-NC 组、 Estrogen + siRNA-HIF-1α 组、Estrogen + HIF-1α 过表达组分别转染 siRNA-NC、siRNA-HIF-1α、HA-HIF-1α-pcDNA3。 转 染 24 h, 收 集 各 组 细 胞, 分 别 采 用 实 时 荧 光 定 量 PCR 法、Western blotting 法 检 测 HIF-1α 及 EMT 相 关 基 因 (E-cadherin、N-cadherin、β-catenin、TGF-β1 ) mRNA和蛋白表达。结果　与siRNA-NC组比较, siRNA-HIF-1α组HIF-1α、 N-cadherin、β-catenin、TGF-β1 mRNA 和蛋白相对表达量均降低, E-cadherin mRNA 和蛋白相对表达量均升高 (P 均< 0. 05) ; 与 Control组比较, HIF-1α过表达组 HIF-1α、N-cadherin、β-catenin、TGF-β1 mRNA和蛋白相对表达量均升高, E-cadherin mRNA 和 蛋 白 相 对 表 达 量 均 降 低 (P 均 <0. 05) 。 Estrogen + siRNA-HIF-1α 组 HIF-1α、N-cadherin、 β-catenin、TGF-β1 mRNA和蛋白相对表达量均低于Estrogen + siRNA-NC组和Estrogen组, E-cadherin mRNA和蛋白相 对表达量均高于Estrogen + siRNA-NC组和Estrogen组 (P均<0. 05) ; Estrogen + HIF-1α过表达组HIF-1α、N-cadherin、 β-catenin、TGF-β1 mRNA 和蛋白相对表达量均高于 Estrogen 组和 Control组, E-cadherin mRNA 和蛋白相对表达量均 低于Estrogen组和Control组 (P均<0. 05) 。结论　缺氧环境下外源性雌激素可能通过激活HIF-1α来促进子宫内膜 癌细胞EMT。 [ABSTRACT FROM AUTHOR]

Fecal cortisol, which can measure the stress level of animals, is a good indicator to analyze stress responses and to assess captive animals’ welfare. In order to investigate the stress response of yellow-cheeked gibbons (Nomascus gabriellae) at Chengdu Zoo, we measured fecal cortisol of two gibbons from April 2016 to April 2017, and emphasized on the relationship between cortisol and tourist disturbance, season and estrus. The results showed that there was no significant difference in cortisol levels between holidays and non-holidays in both the female and male gibbon (p=0. 061, 0. 057, and female cortisol was significantly higher than male cortisol during holidays (p<0. 001). In addition, fecal cortisol level in both genders were the highest in winter compared to spring (p<0. 01), summer (p<0. 05） and autumn (p<0. 01). There was a significant positive correlation between cortisol and estrogen for the female (r =0. 790, p=0. 011), but no such correlation for the male (r =0. 027, p=0. 944). Our findings suggested that stress response of the two yellow-cheeked gibbons to tourist disturbance was small, but the female showed higher sensitivity to the disturbance than the male. Moreover, for captive yellow-cheeked gibbons, cortisol level is seasonally regulated, and its significant increase in winter may be related to energy metabolism and immunity. Additionally, cortisol may also be associated with reproductive and physiological needs during breeding season, and therefore a gender difference may exist. [ABSTRACT FROM AUTHOR]

The increased incidence of gout in men and postmenopausal women suggests that gout is closely associated with sex and affected by sex hormones. However, how sex hormones are involved in the onset of gout and the exact relationship between these two are poorly understood. In this article, recent advances in the study of gout were summarized, and the mechanism underlying the role of sex hormones in the pathogenesis of gout was reviewed. [ABSTRACT FROM AUTHOR]

BACKGROUND: In recent years, numerous studies have found that long non-coding RNA is involved in the occurrence and development of osteoporosis. p38MAPK signaling pathway is involved in the differentiation of bone marrow mesenchymal stem cells, osteoblasts and osteoclasts, and participates in the development of osteoporosis. LncRNA can directly or indirectly participate in the occurrence and development of osteoporosis by affecting the p38MAPK signaling pathway. OBJECTIVE: To review the effect of long non-coding RNA directly or indirectly on the progression of osteoporosis through the p38MAPK signaling pathway, and to provide a new idea for long non-coding RNA in the prevention and treatment of osteoporosis. METHODS: PubMed, CNKI, and Wanfang databases were searched with “long non-coding RNA, osteoporosis, mesenchymal stem cells, osteoblasts, osteoclasts, p38 signaling pathway” as the Chinese and English search terms. Old, repeated and low-credibility views were excluded. The retrieved literature was summarized, summed up, and analyzed. Seventy-six representative articles were selected. RESULTS AND CONCLUSION: (1) Long non-coding RNA participates in the prevention and treatment of osteoporosis through a variety of ways, including promoting the osteogenic differentiation of bone marrow mesenchymal stem cells, promoting the differentiation and secretion activity of osteoblasts, inhibiting the proliferation and bone resorption of osteoclasts, and regulating the activation or inhibition of osteoblast-related cellular pathways. Activation of p38MAPK signaling pathway can delay the progression of osteoporosis, and inhibition of p38MAPK signaling pathway can inhibit the absorption of osteoclasts, thereby affecting the occurrence and development of osteoporosis. (2) The overexpression or low expression of the corresponding long non-coding RNA can affect the proliferation or differentiation of osteoblasts and osteoclasts through the p38MAPK signaling pathway, regulate the process of bone remodeling, and then affect the occurrence and development of osteoporosis. A large number of basic research results show that long non-coding RNA and p38MAPK signaling pathway may be potential application and clinical translation value in the treatment of osteoporosis. Moreover, the corresponding long non-coding RNA overexpression or low expression lentivirus, transfection plasmid, and the corresponding p38MAPK signaling pathway inhibitor have been confirmed to have targeted regulatory effects in vitro cell experiments and animal models. (3) Therefore, targeting long non-coding RNA and p38MAPK signaling pathways to regulate the differentiation and function of bone marrow mesenchymal stem cells or inhibiting the proliferation and differentiation of osteoclasts may provide an innovative therapeutic strategy to delay the progression of osteoporosis. [ABSTRACT FROM AUTHOR]

With the aging of the population and the improvement of people′s living standards, the prevalence of pelvic organ prolapse (POP) is increasing year by year. In the diagnosis and treatment of POP patients, it is not difficult to find cases with human papilloma virus (HPV) infection and cervical lesions. This article reviewed the correlation between the changes of vaginal microenvironment and HPV infection in POP patients. The results showed that POP patients were more likely to suffer from vaginitis due to the long-term exposure of prolapsed pelvic floor organs and tissues to the surrounding unclean environment. At the same time, the vaginal microenvironment changed significantly due to the decrease of estrogen level, the decrease of lactobacillus number, the increase of vaginal potential of hydrogen (PH) value, the decrease of systemic immunity and local immunity in the vagina. The combination of these factors may increase the risk of POP patients infected with high-risk HPV. Persistent high-risk HPV infection is a high-risk factor leading to cervical cancer, and cervical cancer is one of the three malignant tumors with the highest mortality rate among women, which seriously threatens the health of women. Therefore, in the clinical treatment of POP patients, attention should be paid to the health management of their vaginal microenvironment to prevent serious consequences caused by HPV infection, and further improve the quality of life of patients. [ABSTRACT FROM AUTHOR]

As an acute cerebrovascular disease, ischemic stroke is one of the leading causes of death and disability worldwide. It involves in fast developing and irreversible brain damage. Effective treatment is an important strategy to save patients' life and maintain their health. G protein-coupled estrogen receptor （GPER） mediates a rapid effect of estrogen, which can protect the nerves after ischemic brain injury. This review aims to summarize the multiple pathophysiological processes and signaling pathways of the involvement of GPER in cerebral ischemia, so as to provide theoretical reference for further study of the pathogenesis of ischemic stroke and new ideas for the development of drug targets. [ABSTRACT FROM AUTHOR]

Oxytocin (OT) regulates parturition and breast milk secretion and holds bone directly by peripheral OT and oxytocin receptor (OTR) rather than central. Bone marrow mesenchymal stem cells, osteoblasts (OB), osteoclasts (OC), osteocytes, chondrocytes, and adipocytes all expressed OT and OTR. OB synthesizes OT under the stimulation of estrogen and becomes a paracrine-autocrine regulator of bone formation. Under the mediation of estrogen, OT/OTR and OB form a feedforward loop. The Osteoclastogenesis inhibitory factor (OPG)/receptor activator of nuclear factor-κB ligand (RANKL) signal pathway is the critical pathway for OT and OTR to exert anti-Osteoporosis (OP) action. OT down-regulates the bone resorption markers by up-regulating bone morphogenetic protein, thus improving the activity of bone marrow mesenchymal stem cells and promoting them to differentiate into OB rather than adipocytes. OT induces OB mineralization by promoting OTR translocation to the nucleus of OB. OT regulates the proportion of OPG/RANKL in OB by triggering the release of cytoplasmic Ca2+ and the synthesis of nitric oxide and has a bidirectional regulatory effect on osteoclasts. In addition, OT can also increase the activity of osteocytes and chondrocytes and plays a vital role in increasing bone mass and improving bone microstructure. Based on the fact that OT and OTR have sound anti-OP effects, this article reviews the research on the regulation of bone metabolism by OT and OTR in recent years, in order to provide reference for their clinical application and research. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Agro-Environment Science is the property of Journal of Agro-Environment Science Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The clinical application of biochemical indicators of bone metabolism provides molecular biological basis for the diagnosis， differential diagnosis， prediction of fracture risk and evaluation of therapeutic effect of anti-osteoporosis treatment of osteoporosis， and has important significance in the epidemiological study of osteoporosis， pathogenesis， and development and research of osteoporosis drugs. Because of the high specificity and sensitivity of bone metabolism biochemical indicators， its application is increasingly widespread. This paper has searched a large number of Chinese and foreign literatures， compiled and reviewed the Expert Consensus on Clinical Application of Bone Metabolism Biochemical Indicators （2023 Revision）， and discussed the classification of bone metabolism biochemical indicators， the methodology and biological significance of bone metabolism biochemical indicators， and the detection and variation of bone metabolism indicators. [ABSTRACT FROM AUTHOR]

Human papillomavirus (HPV) infection is related to cervical cancer. Estrogen and its receptor combined with HPV oncogene can promote the occurrence of cervical cancer. Moreover, high parity and the use of contraceptives incrcasing the risk of cervical cancer support estrogen and HPV infection synergistically promotes cervical cancer. Estrogen can both combine with HPV responsive elements to change viral gene expression accelerating the process of HPV infection, and develop HPV-positive cervical cancer by exerting immunomodulatory function in tumor microenvironment. Estrogen and its receptor play vital roles in cervical cancer and are expected to be a potential therapeutic target for treatment of cervical cancer.

ObjectiveTo study the relationship between the exposure to two kinds of phthalate esters （PAEs） ［Di-N-butyl phthalate，（DBP） and Di-（2-ethylhexyl）phthalate （DEHP）］ and estrogen homeostasis in pregnant women.MethodsIn 2021， we classified the Jiading District of Shanghai into five geographical areas， east， west， south， north and central. A total of 151 pregnant women from each area were selected for questionnaire survey， with random urine samples during first， second， and third trimesters collected. A DBP metabolite ［Mono-N-butyl phthalate （MBP）］ and two DEHP metabolites ［Mono（2-ethylhexyl） phthalate （MEHP）， Mono（2-ethyl5-oxohexyl） phthalate， （MEOHP）］ and three estrogens ［estrone （E1）， 17β -estradiol （E2）， and estriol （E3）］ in urine were determined by ultra-performance liquid chromatography tandem quadrupole time-of-flight mass spectrometry. After a natural logarithmic transformation of PAEs metabolite levels and estrogen concentration， multivariable linear regression was used to control potential confounders and determine the relationship between PAEs metabolite levels and estrogen concentration.ResultsThe detection rates of three PAEs metabolites in urine of pregnant women were more than 98%. The median corrected concentrations of MBP， MEHP and MEOHP were 5.18， 0.59 and 4.23 mg·kg-1， respectively. During the whole pregnancy， MEOHP was positively correlated with E1 （β=0.450， 95%CI： 0.057‒0.844）， and MBP was positively correlated with E3 （β=0.250， 95%CI： 0.034‒0.465）. Stratified by trimesters， MBP was positively correlated with E3 in the first trimester （β=0.428， 95%CI： 0.103‒0.752）. MEOHP was positively correlated with E1 in the second trimester （β=0.734， 95%CI： 0.130‒0.752）， and had a possitive trend with E1 in the third trimester （β=0.744， 95%CI： -0.140‒1.629）. In addition， MEHP had a negative correlation with E1 in the second trimester （β=-0.498， 95%CI： -1.063‒0.066）. MEOHP had a positive correlation trend with E2 （β=0.628， 95%CI： -0.101‒1.356） in the third trimester.ConclusionPAEs exposure may interfere with estrogen homeostasis during pregnancy and differs by trimesters. Given the cross-sectional nature of this study， it warrants further study to validate the findings.

BACKGROUND: Postmenopausal women are prone to developing osteoporosis and osteoarthritis, and the effect of estrogen replacement therapy combined with treadmill exercise on bone mass and articular cartilage is unclear. OBJECTIVE: To investigate the effects of exogenous estrogen combined with low intensity treadmill exercise on bone mass and articular cartilage in an ovariectomized mouse model. METHODS: Thirty-five C57BL/6 mice were randomly divided into five groups: sham group, sham and low intensity treadmill exercise group (sham-sport group), ovariectomized group, ovariectomized and supplying exogenous estrogen group (estrogen group), ovariectomized and supplying exogenous estrogen combined with low intensity treadmill exercise group (estrogen-sport group). The mice were subjected to bilateral ovariectomy or sham operation. The mice in the estrogen and estrogen-sport groups were injected with estrogen every other day after the operation, and the mice in the sham-sport and estrogen-sport groups ran on a treadmill for 6 weeks. The changes in the number of osteoclasts and bone mass in the metaphysis of the distal femur of the mice were observed. Osteoarthritis Research Society International histopathology was used to evaluate the degeneration of knee joint cartilage in mice. RESULTS AND CONCLUSION: Bone volume per total volume in the estrogen-sport group was significantly higher than that in the ovariectomized group (P < 0.01). There was no statistical difference among the estrogen-sport, sham, sham-sport group, and estrogen groups (P > 0.05). Osteoclast number per bone surface and osteoclast surface per bone surface were significantly decreased in the estrogen-sport group compared with the ovariectomized group (P < 0.01). There was no statistical significance among the estrogen-sport, sham-sport, and estrogen groups (P > 0.05). The knee Osteoarthritis Research Society International histopathology of the estrogen-sport group was significantly higher than that of the other groups (P < 0.01). In conclusion, exogenous estrogen supplementation with low-intensity treadmill exercise can increase bone mass in ovariectomized mice but lead to articular cartilage degeneration. [ABSTRACT FROM AUTHOR]

Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disease, and its incidence shows obvious gender differences. The incidence of IBS in females is higher than that in males, and the clinical characteristics of IBS also show some gender differences. The levels of estrogen and androgen in patients with IBS are significantly different from those in healthy controls, which suggests that gender differences, sex hormone levels and their biological effects between men and women may play an important role in the pathogenesis of IBS. Therefore, the review systematically reviews the correlation between sex hormones and the pathogenesis of IBS, and the research progress of its related mechanism in IBS, in order to provide new ideas for explaining the pathogenesis of IBS and exploring new therapeutic strategies. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of different doses of shikonin on the protein expression of ER, PR and P-ERK in uterine tissue of rats with uterine fibroids established by estrogen plus progesterone loading method. Methods: 60 clean-grade SD female rats were selected and divided into model group, blank control group, positive control group (estradiol group), low-dose shikonin group, middle-dose shikonin group, and high-dose shikonin group groups, 10 rats in each group. Rats in the blank control group and model group were given 10 mL/kg·d normal saline by gavage, the positive control group was given estradiol valerate tablets by gavage at a dose of 50 μg/kg·d, and the low-dose group was given 5 mg by gavage. /kg shikonin, the middle-dose group was given 10 mg/kg shikonin by gavage, and the high-dose group was given 20 mg/kg shikonin by gavage. Record the modeling results of the rats, observe the uterine morphology and uterine histopathology of the rats, and compare the uterine weight, uterine coefficient, the maximum diameter of the uterus, the maximum diameter of the cervix and the thickness of the smooth muscle layer of the rats in each group. Serum P and E2 levels of rats and ER, PR and p-ERK protein contents in uterine tissue of rats in each group. Results: The uterine weight, uterine coefficient, the maximum diameter of the uterus, the maximum diameter of the cervix and the thickness of the smooth muscle layer of the six groups of rats were compared, and the differences were statistically significant (P<0.05). Pairwise comparison of the inflammatory cell infiltration score and the uterine wall smooth muscle thickness score in the six rats (P<0.05); The difference was statistically significant (P<0.05); the ER, PR, p-ERK protein levels in the uterine tissue of the six groups of rats were compared with each other, and the difference was statistically significant (P<0.05). Conclusion: Shikonin has the effect of anti-uterine fibroid activity. With the increase of shikonin dose, the anti-uterine fibroid activity increases obviously, which may be related to the decrease of ER, PR and P-ERK activities and serum P, E2 in uterine tissue. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Agro-Environment Science is the property of Journal of Agro-Environment Science Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Sex hormone receptors are widely distributed in brain neurons. Studies have shown that sex hormones play the important promoting role on learning and memory capacities,moreover their effects have the potential gender divergence. The long-term potentiation is one of the most intensively studied memory cell models,in each link,it shows the sexual bimodal phenomenon of memory encoding. This paper reviews the mechanism causing the difference of learning and memory abilities between sexes from the perspective of sex hormones by comparatively analyzing the action mechanisms of estrogen and androgen respectively in brain neurons,synapses and glial cells [ABSTRACT FROM AUTHOR]

To gain insight into the physicochemical characteristics and molecular structure of G protein-coupled estrogen receptor 1 (GPER1), series of bioinformatics tools were used to analyze human GPRE1, its physical-chemical properties, signal peptide region, transmembrane domains, subcellular localization, phosphorylation sites and glycosylated sites, secondary structure, conserve domain, protein-protein interaction networks and correlation with tumor. GPER1 has a relative molecular weight of 42 247.59 Da, its theoretical isoelectric point is 8.63, molecular formula is C1938H3018N510O509S20, unstable coefficient is 48.12, adipose coefficient is 110.51, the average of hydrophilicity is 0.449. GPER1 is a hydrophobic and unstable protein, with 7 transmembrane domains, localized in the plasma membrane (60.9%), endoplasmic reticulum (13.0%) and vacuolar (17.4%), respectively. The secondary structure mainly involves alpha-helix, 4 N-glycosylation sites and 10 O-glycosylation, 27 phosphorylation sites. The interacting proteins of GPER1 mainly include 10 proteins such as ESR1, DLG4, GNAQ and so on. In addition, GPER1 was lowly expressed in UCEC (uterine corpus endometrial carcinoma) tissues, and GPER1 gene mutation group suggesting that the overall survival of UCEC patients significantly decreased. Human GPER1 could be a key factor in the GPCRs (G protein-coupled receptors) signaling pathway, which provided an important reference for further exploring its roles in the molecular mechanism of tumor. [ABSTRACT FROM AUTHOR]

Crohn's disease (CD) is a subtype of inflammatory bowel diseases and may be resulted from endocrine disorders. Estrogen and its receptors exert an important role in the pathogenesis of CD. Studies have revealed that estrogen can down-regulate the expression of inflammatory mediators while estrogen supplementation helps reduce the severity of inflammatory response. The expression of receptors (GPER, ERα and ERβ) also influence local immune responses, and the imbalance of them mediate intestinal inflammation. Nowadays, estrogen and its receptors are expected to become a new rarget in the research of CD.

Periodontium regeneration and repair is a controversial and difficult point in the treatment of periodontosis. The proliferation, differentiation, migration and adhesion of periodontal ligament cells and the dynamic relationship between periodontal ligament cells and their extracellular matrix proteins are the basis of periodontium morphological reconstruction, functional maintenance and tissue repair. This article reviews the mechanism of estrogen-regulated periodontal membrane fine repair and periodontal tissue reconstruction to provide the basis for follow-up research on the treatment of periodontitis and the promotion of periodontal tissue repair and reconstruction by exogenous estrogen-mediated periodontal membranes. Under the regulation of certain concentrations of estrogen, the proliferation and differentiation ability of periodontal ligament stem cells (PDLSCs) and bone mesenchymal stem cells (BMSCs) to other periodontal ligament cells were enhanced. At the same time, PDLSCs, BMSCs, human periodontal ligament fibroblasts (HPLFSs), osteoblasts and cementoblasts synthesized and secreted collagen I (COLI), osteopontin (OPN), bone sialoprotein (BSP) and osteocalcin (OCN) into the extracellular matrix. They interact with fibronectin (FN) and cementum attachment protein (CAP) in the extracellular matrix to form a variety of chain complexes and regulate each other, thus promoting the growth, migration, adhesion and fibrosis of periodontal ligament cells, repairing the collagen fiber skeleton of the periodontal ligament and adhering the two ends to the new cementum and the inherent alveolar bone.

Copyright of Wool Textile Journal is the property of National Wool Textile Science & Technology Information Center and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

OBJECTIVE: In recent years, the incidence of premature ovarian failure has been on the rise, showing the young trend. Because of the complex etiology of premature ovarian failure and poor clinical outcome, there is an urgent need to find a safe and effective treatment modality. This study systemically assessed the effectivity of stem cell transplantation of premature ovarian failure animal models. METHODS: PubMed, The Cochrane Library, EMbase, CBM, CNKI, Wanfang, and VIP were retrieved before June 10, 2020. A series of studies on the treatment of premature ovarian failure animal models by stem cells were collected. Two evaluators independently screened the literature and extracted the data. The SYRCLE risk of bias assessment scale for animal experiments was used to evaluate the quality of the literature. The primary outcome indicators were analyzed using RevMan 5.3 software for meta-analysis. RESULTS: (1) A total of 13 randomized controlled animal experimental studies were included, with 348 mice, and overall quality was moderate. Stem cell group (n=184) only received stem cell transplantation, and control group (n=164) only received blank control, normal saline or PBS intervention. (2) Meta-analysis results showed that compared with the control group, serum estrogen level (SMD=3.02, 95%CI: 1.87-4.18, P < 0.000 01), serum anti-Müllerian hormone level (ng/mL subgroup: SMD=4.77, 95%CI: 0.95-8.59, P=0.01; pg/mL subgroup: SMD=4.94, 95%CI: 0.91-8.97, P=0.02), serum luteinizing hormone level (SMD=- 1.47, 95%CI: -1.73 to -1.22, P < 0.000 01), the number of follicles at all levels (SMD=1.91, 95%CI: 0.85-2.97, P=0.000 4) and fertility rate increased (RR=2.07, 95%CI: 1.39-3.09, P=0.000 4), but serum follicle-stimulating hormone level decreased (P < 0.000 1) in the stem cell group. The number of follicles at all levels was significantly higher in the stem cell group than that in the control group (P < 0.05). Subgroup analysis showed that with the increase of follow-up time, the number of primordial follicles, primary follicles and secondary follicles was significantly increased (P < 0.05), and the number of atresic follicles was significantly decreased (P < 0.05). Different types of stem cell transplantation could improve the serum estrogen level, and the recovery of serum estrogen level was more significant with the increase of unit dose of stem cell injection (P < 0.05). CONCLUSION: Available evidence from animal studies suggests that stem cell transplantation is effective in treating premature ovarian failure model mice. Stem cell transplantation induces an increase in estrogen levels, a decrease in follicle-stimulating hormone levels, and an improvement in follicle numbers at all levels in premature ovarian failure. Stem cells have some restorative effects on the ovary, but large samples and high quality human trials are still needed to verify clinical application effects. [ABSTRACT FROM AUTHOR]

BACKGROUND: Periodontal tissue regeneration engineering based on stem cells provides a broad prospect for the treatment of periodontal diseases. Estrogenmediated osteogenic differentiation in human periodontal ligament stem cells is closely related to the Wnt signaling pathway OBJECTIVE: To study the regulation of Wnt/β-catenin and Wnt/Ca2+ signaling pathways on estrogen-mediated osteogenic differentiation in human periodontal ligament stem cells, as well as the crosstalk between the two pathways. METHODS: Premolars with healthy periodontal condition were collected to isolate and culture human periodontal ligament stem cells. Surface markers of the cells were detected by flow cytometry. The osteogenic/adipogenic differentiation potential was detected by Alizarin red S and Oil red O staining. The thirdgeneration human periodontal ligament stem cells were randomly divided into blank group, control group, estrogen group, XAV939 (Wnt/β-catenin pathway inhibitor) group, L-690,330 (Wnt/Ca2+ pathway inhibitor) group, and XAV939+L-690,330 group. Except for the blank group, all other groups were cultured for osteogenic induction. qRT-PCR and western blot assay were performed to measure expression of osteogenic markers (Runx2, OCN) and key signal molecules of Wnt/β-catenin and Wnt/Ca2+ pathway. Intracellular Ca2+ concentration was evaluated by Fluo-4 fluorescent probe. Alkaline phosphatase assay was conducted to measure the alkaline phosphatase activity. Osteogenic differentiation potential was detected by Alizarin red S staining. RESULTS AND CONCLUSION: (1) The human periodontal ligament stem cells isolated and purified by collagenase digestion were spindle shaped and polygonal. Flow cytometry proved that human periodontal ligament stem cells were of mesenchymal origin, and they also demonstrated the capacity to differentiate into osteogenic/adipogenic lineages. (2) Estrogen at 10-7 mol/L in the osteogenic medium can upregulate intracellular Ca2+ concentration, CaMKII and NLK gene expression and CaMKII protein expression of human periodontal ligament stem cells. (3) The usage of Wnt/β-catenin and Wnt/Ca2+ signaling pathway inhibitors can minimize osteogenic differentiation. (4) Inhibiting either of the two signaling pathways can increase crucial protein expression of the other pathway, which had no significant effect on the osteogenic differentiation of the cells. (5) In conclusion, estrogen through Wnt/Ca2+ and Wnt/β-catenin signaling pathways induces osteogenic differentiation of human periodontal ligament stem cells. In addition, there is mutual compensation between the two pathways, thus working together to regulate osteogenic differentiation. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of B-ultrasound combined with Jinkui Wenjing Decoction in the treatment of patients with premature ovarian failure and the effects of reproductive function and serum estrogen. Methods: From May 2018 to December 2020, 96 cases of patients with premature ovarian failure who were diagnosed and treated in this hospital were selected as the research objects. All the cases were divided into the study group and the control group with 48 cases each groups accorded to the 1:1 random number table method. The control group were treated with hormone replacement therapy, and the study group were treated with Jinkui Wenjing Decoction on the basis of the treatment of the control group, so the patients underwent B-ultrasound observation before and after treatment. Results: After treatment, the total effective rate of the study group were 97.9 %, which were higher than 85.4 % of the control group (P<0.05). There were no serious adverse reactions in the two groups during the treatment. The serum Follicle-stimulating Hormone (FSH) and Luteinising Hormone (LH) levels after treatment in the two groups were lower than before treatment (P<0.05), and the study group were lower than the control group (P<0.05). The erum estradiol (E2) levels were higher than before treatment, and the study group were higher than the control group (P<0.05). The modified Kupperman scores of the two groups after treatment were lower than those before treatment, and the study group were lower than the control group(P<0.05). The number and size of follicles after treatment in the two groups were higher than before treatment (P<0.05), and the study group were higher than that in the control group (P<0.05). Conclusion: Jinkui Wenjing Decoction can improve the treatment effect of patients with premature ovarian failure, improve the patient's serum estrogen secretion and reproductive function, and also help to inhibit the expression of inflammatory factors. The use of combined with B-ultrasound can reflect the patient's follicular condition, and more Conducive to guiding clinical treatment and prognosis prediction. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Asian Journals of Ecotoxicology is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To explore the effect and mechanism of estrogen on endothelial progenitor cells（EPCs）function in diabetic rats. Methods EPCs were isolated from bone marrow of rats and characterized by fluorescence microscopy and flow cytometry. Rat diabetic model was established via streptozotocin induction. The bone marrow was taken to culture EPCs. EPCs of diabetes were incubated with Estrogen 10 nmol/L for 24h. The functions and proliferation of EPCs in vitro were detected. The levels of MnSOD and NO in EPCs and TSP-1 in supernatant were assayed. Results Compared with control group, EPCs proliferation, adhesion and angiogenesis functions were impaired in diabetic rats. The level of MnSOD and NO in diabetic EPCs were significantly decreased, while TSP-1 protein level in the supernatant increased. The above changes can be reversed with estrogen incubation. Conclusion Estrogen improved the EPCs migration and tubule formation in diabetic rats. The mechanism may be related to the reduction of oxidative stress and downregulation of TSP-1 expression in diabetic EPCs. [ABSTRACT FROM AUTHOR]

Objective To observe the effect of flavored angelica caulis spatholobi decoction on bone mineral density and bone mass in ovariectomized rat models, and to explore the related mechanism and signal pathways. Methods Thirty 3-month-old female rats were randomly divided into Sham group, OVX group, and OVX+T group, with 10 rats in each group. After two weeks of adaptive feeding, ovariectomy for both ovaries was performed for rats in OVX and OVX+T group, while rats were sham operated in Sham group. Rats in OVX+T group received equivalent flavored angelica caulis spatholobi decoction through gavage two months after the operation. After continuous administration for 12 weeks, the serum and femoral tissues of rats in each group were collected for bone mineral density (BMD) test, tissue section test, Western blotting test, and serum index test. Results X-rays and HE sections showed that BMD and bone microparameters in OVX group were lower than those in Sham group, and BMD and bone microparameters in OVX+T group were higher than those in OVX group (P<0.05). Serum indicators show that the level of 17β-E2 in OVX group was lower than that in Sham group, and the content or activity of ALP, CTX-1, and TRAcP-5b were higher than those in Sham group. The level of 17β-E2 in OVX+T group was higher than that in OVX group, and the content or activity of ALP, CTX-1 and TRAcP-5b were lower than those in OVX group (P<0.05). Western blotting results showed that the expression levels of OPG and ERK in OVX group were lower than those in Sham group, and the ratios of RANKL, RANK, and RANKL/OPG were higher than those in Sham group. The expression levels of OPG and ERK in OVX+T group were higher than those in OVX group, and the ratio of RANKL, RANK, and RANKL/OPG was lower than that in OVX group (P<0.05). Conclusion The study shows that flavored angelica caulis spatholobi decoction is most likely to inhibit high bone conversion rate through estrogen-like effect, and to promote bone formation and to inhibit bone absorption through OPG/RANKL/RANK signaling pathway, so as to prevent and treat osteoporosis caused by estrogen deficiency. ERK signaling pathway may be involved in this process. [ABSTRACT FROM AUTHOR]

This study aims to explore the roles of three estrogen receptors (Esr1, Esr2, and Gper1) in early differentiation of embryonic gonads of Trachemys scripta . The expression characteristics of the receptor genes were studied first. The Esr1, Esr2, and Gper1 agonists PPT, WAY 200070, and G-1 were respectively injected into the embryos at the male-producing temperature (MPT) before initiation of gonadal differentiation. The sex reversal of the treated embryonic gonads was analyzed in terms of morphological structure of gonads, distribution pattern of germ cells, and expression of key genes and proteins involved in sex differentiation. The expression level of esr1 during the critical stage of sex differentiation was higher than those of esr2 and gper1 (very low expression) and was particularly high in the gonads at the female-producing temperature (FPT). After treatment with PPT, the MPT gonads presented obviously feminized morphology and structure, with the germ cells exhibiting a female distribution pattern. Furthermore, the mRNA expression levels of the key genes ( dmrt1 , amh , and sox9 ) for male differentiation were down-regulated significantly, while those of the key genes ( foxl2 and cyp19a1 ) for female differentiation were up-regulated observably. The fluorescent signals of Amh and Sox9 expression almost disappeared, while Foxl2 and Arom were activated to express abundantly, which fully demonstrated the sex reversal of the gonads from male to female (sex reversal rate: 70.27%). However, the MPT gonads treated with WAY 200070 and G-1 still differentiated into testes, and the expression patterns of the key genes and proteins were similar to those in male gonads. The above results demonstrate that activation of Esr1 alone can fully initiate the early female differentiation process of gonads, suggesting that estrogen may induce early ovarian differentiation via Esr1 in Trachemys scripta . The findings provide a basis for further revealing the mechanisms of estrogen regulation in sex determination and differentiation of turtles.

BACKGROUND: Orthodontic tooth movement and orthodontic induced root resorption are an important part of orthodontic treatment. Estrogen can regulate the rate of orthodontic tooth movement by influencing the bone remodeling of periodontal tissue, thereby inhibiting orthodontic-induced root resorption. OBJECTIVE: To review the mechanism of estrogen underlying orthodontic tooth movement and orthodontic induction of root resorption. METHODS: The first author searched PubMed, CNKI, and WanFang databases using the keywords of "estrogen; orthodontic tooth movement; orthodontically induced root resorption; osteoclast; osteoblast; bone marrow mesenchymal stem cells; periodontal ligament stem cells" in English and Chinese, respectively. Finally, 53 articles were included for further review. RESULTS AND CONCLUSION: Orthodontic tooth movement is an important part of orthodontic treatment. It can be achieved through bone reconstruction under mechanical force, and alveolar bone reconstruction is the basis of orthodontic tooth movement. Estrogen acts as an important regulator of bone tissue remodeling. Estrogen inhibits osteoclast differentiation, prolongs the life span of osteoclasts, promotes the proliferation, differentiation and function of osteoblasts through a variety of pathways and multiple cytokines, thereby inhibiting bone resorption, promoting bone formation, reducing bone remodeling, and inhibiting orthodontic tooth movement. Estrogen may reduce orthodontics-induced dental root resorption by inhibiting cementoclasts. The differentiation of osteoclasts and odontoclasts is of great significance in the process of tooth movement and root resorption. Recent studies have found that tyrosine kinase acts as an important signal medium for estrogen to inhibit the differentiation, survival and function of human osteoclasts. Although preliminary studies on the role of estrogen in bone remodeling and tooth root resorption have been reported, which mechanism exerts the dominant role has not been elucidated, and most of them are at the stage of basic or animal research. Research on relevant mechanisms and clinical research on this aspect are still needed. [ABSTRACT FROM AUTHOR]

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Objective To explore the recurrence and metastasis and prognosis of Her-2 positive breast cancer patients with different hormones levels.Methods Seventy-eight cases with Her-2 positive breast cancer were selected in the Third Affiliated Hospital of Xinxiang Medical College from February 2015 to February 2017 as the research subjects.All patients received radical surgery and postoperative adjuvant therapy, and they were divided into the HR+/Her-2+ group(43 cases) and the HR-/Her-2+ group(35 cases) according to expression levels of estrogen receptor(ER) and progesterone(PR).The pathological characteristics and related hormones and protein expression were analyzed in the two groups, and the surgical treatment was used as the observation point, and the patients were followed up for 3 years.The survival status of the two groups was statistically analyzed during follow-up, and the recurrence and metastasis were recorded,including local recurrence, first multiple recurrence and metastatic organs.Results In the HR+/Her-2+ group, the proportion of ER+/PR+ double expression accounted for 67.44%, the proportion of tumor diameter>2 cm, the proportion of positive axillary lymph nodes during surgery and Ki-67 high expression rates at postmenopausal state and during diagnosis were 60.47%,53.49%,41.86% and 34.88% respectively, which were lower than 82.86%,77.14%,65.71% and 57.14% in the HR-/Her-2+ group(P <0.05).The 3-year survival rate of patients in the HR+/Her-2+ group was significantly higher than that in the HR-/Her-2+ group(72.09% vs. 48.57%), the difference was statistically significant (P <0.05).The combined bone metastasis rate in the HR+/Her-2+ group was significantly higher than that in the HR-/Her-2+ group(83.33% vs. 38.23%), and the lung metastasis rate was significantly lower than that in the HR-/Her-2+ group (12.50% vs. 37.50%), the differences were statistically significant(P <0.05).Binary logistic regression analysis was conducted with the above factors, and the results showed that tumor diameter >2 cm, positive axillary lymph nodes and positive HR and Ki-67 high expression were all risk factors affecting the prognosis of patients (P <0.05).Conclusion Patients with HR negative Her-2 positive breast cancer often have poor prognosis, and are more likely to have visceral metastasis, and their 3-year survival rate is lower than that of patients with HR positive Her-2 positive breast cancer patients. [ABSTRACT FROM AUTHOR]

Objective To study the serum levels of estrogen and preadipose factor-1 in postmenopausal osteoporotic vertebral compression fracture (OVCF) patients and correlation with bone and bone mineral density. Methods A total of 64 menopausal OVCF patients diagnosed in our hospital from January 2019 to November 2020 were divided into OVCF group and 45 healthy postmenopausal women as control group. The levels of estradiol and Pref-1 were compared. The patients with OVCF were divided into high and low groups, and a series of indexes such as bone metabolism and bone mineral density were compared. The correlations between the levels of estradiol, Pref-1, bone metabolism and mineral were analyzed by Preason. Results The level of estradiol in OVCF was significantly lower than control (t=13.275, P<0.05), while the level of Pref-1 was significantly higher (t=10.360, P<0.05). The levels of 25-(OH) VitD and N-MID in the serum of patients in the lower expression group of estradiol high expression group, as well as lumbar vertebrae density and hip bone density, all increased significantly (t=7.378, 5.472, 10.290, 9.774, P<0.05),The expression level of PINP and β-CTX decreases （t=6.447, 9.103, P<0.05）.The levels of 25- (OH) VitD and N-MID as well as lumbar bone density and hip bone density were significantly decreased in the lower expression group in the high Pref-1 expression group t=8.350, 7.426, 12.376, 10.450, P<0.05),The PINP, β-CTX levels were all significantly increased（t=8.266,11.205, P<0.05）.The serum estradiol in OVCF was positively correlated with 25-(OH) VitD, N-MID and hip bone mineral（r>0, P<0.05）, but negatively correlated with PINP and β-CTX（r＞0,P<0.05）. Pref-1 was inversely associated with 25- (OH) VitD, N-MID levels, and lumbar bone density, and hip bone density（r<0,P<0.05）, Positive correlation was observed with PINP, β-CTX levels（r>0, P<0.05）. Conclusion Serum estrogen level is significantly down-regulated and Pref-1 level is significantly up-regulated in postmenopausal OVCF patients, and they are closely related to bone metabolism and bone mineral density. Medical intervention on the two levels may bring new opportunities for clinical treatment of OVCF. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exogenous hydrogen sulfide has an important effect on the formation and differentiation of osteoblasts, which are important functional cells in the development of osteoporotic disease. The effect of exogenous hydrogen sulfide on osteoporosis levels and related hormones has not been studied. OBJECTIVE: To investigate the correlation between endogenous hydrogen sulfide concentration and osteoporosis, and the effect of exogenous hydrogen sulfide supplementation on the biochemical and hormonal parameters commonly used in the clinical follow-up of bone metabolism. METHODS: Sixty rats were randomly divided into sham-operated group, model group, and exogenous hydrogen sulfide group (n=20 per group). A classical osteoporosis model was established by removing both ovaries of rats in the latter two groups. No ovariectomy was conducted in the sham-operated group. Rats in the sham-operated and model groups were intraperitoneally given 1 mg/kg normal saline, while those in the exogenous hydrogen sulfide group intraperitoneally injected 100 μg/kg GYY4137, a slow-released agent of exogenous hydrogen sulfide. Treatments in each group were conducted twice a day, for 12 weeks. Plasma hydrogen sulfide concentration, blood calcium and phosphorus concentrations, alkaline phosphatase activity, osteocalcin, calcitonin, parathyroid hormone, and leptin laboratory index data of each group were analyzed by quantitative comparison. RESULTS AND CONCLUSION: Bone mineral density of the L5, plasma hydrogen sulfide, calcium, phosphorus, alkaline phosphatase, calcitonin concentrations were significantly lower, and osteocalcin, parathyroid hormone, and leptin levels were significantly higher in the model group compared with the shamoperated group at weeks 8 and 12 (P < 0.05). There were no significant differences between the sham-operated and exogenous hydrogen sulfide groups at weeks 8 and 12 in terms of L5 bone mineral density, plasma hydrogen sulfide, phosphorus, osteocalcin, calcitonin, parathyroid hormone and leptin levels (P > 0.05). Whereas blood calcium concentration and alkaline phosphatase activity were still decreased in the exogenous hydrogen sulfide group compared with the sham-operated group (P < 0.05). Compared with the model group, plasma hydrogen sulfide, blood calcium and phosphorus concentrations were elevated and leptin level was decreased in the exogenous hydrogen sulfide group (P < 0.05), while the differences in L5 bone mineral density, alkaline phosphatase activity, osteocalcin, calcitonin and parathyroid hormone levels at weeks 8 and 12 were not significant between the two groups (P > 0.05). Therefore, in the ovariectomized osteoporotic rat model, endogenous hydrogen sulfide concentration was negatively correlated with the severity of osteoporosis, and exogenous supplementation to increase plasma hydrogen sulfide concentration could improve or reverse plasma calcium, phosphorus and some hormone indexes related to bone metabolism. To conclude, plasma hydrogen sulfide concentration and osteoporosis are correlated, and exogenous hydrogen sulfide supplementation has a potential therapeutic effect on osteoporosis which is caused by estrogen reduction. [ABSTRACT FROM AUTHOR]

Objective To explore the relationships between the estrogen and astrocyte cell proliferation as well as invasion. Methods Astrocyte cell line U-87 was cultured in vitro and treated with 0, 10－12, 10－10, 10－8 and 10－6 mol/L estrogen. The gene and protein expressions were analyzed by qPCR, Western blot, ELISA; and the cell proliferation and invasion was analyzed by CCK-8 kits and transwell experiments. Results Estrogen significantly inhibited IL-1, TNF-α, IL-6 expression and promoted the expression of NGF and PGE2 (P＜0.05). Furthermore, estrogen inhibited aquaporin 2(AQP2) expression (P＜0.05). The proliferation and invasion experiments showed that estrogen promoted the U-87 cell proliferation and invasion (P＜0.05). Conclusions Estrogen down-regulates the expression of inflammatory factors, inhibites the expression of AQP2, promotes the proliferation and invasion of U-87 cells.

Objective: To explore the pathogenic roles of miR-21, estrogen (E2), and estrogen receptor (ER) in adenomyosis., Methods: We examined the expression levels of miR-21 in specimens of adenomyotic tissue and benign cervical lesions using qRT-PCR. In primary cultures of cells isolated from the adenomyosis lesions, the effect of ICI82780 (an ER inhibitor) on miR-21 expression levels prior to E2 activation or after E2 deprivation were examined with qRT-PCR. We further assessed the effects of a miR-21 mimic or an inhibitor on proliferation, apoptosis, migration and autophagy of the cells., Results: The expression level of miR-21 was significantly higher in adenomyosis tissues than in normal myometrium ( P < 0.05). In the cells isolated from adenomyosis lesions, miR-21 expression level was significantly higher in E2 activation group than in ER inhibition + E2 activation group and the control group ( P < 0.05); miR-21 expression level was significantly lower in cells in E2 deprivation+ER inhibition group than in E2 deprivation group and the control group ( P < 0.05). The adenomyosis cells transfected with miR-21 inhibitor showed inhibited proliferation and migration, expansion of mitochondrial endoplasmic reticulum, increased lysosomes, presence of autophagosomes, and increased cell apoptosis, while transfection of the cells with the miR-21 mimic produced the opposite effects., Conclusion: MiR-21 plays an important role in promoting proliferation, migration, and antiapoptosis in adenomyosis cells by altering the cell ultrastructure, which may contribute to early pathogenesis of the disease. In addition to binding with E2, ER can also regulate miR-21 through other pathways to participate in the pathogenesis of adenomyosis, thus having a stronger regulatory effect on miR-21 than E2.

17 β -Estradiol (E2), an important endocrine hormone in the mammalian body, participates in the regulation of the physiological functions of the reproductive system, mammary glands, bone, and cardiovascular system, among others. Paradoxically, despite the physiological actions of endogenous E2 (0.2-1.0 nmol/L), numerous clinical and experimental studies have demonstrated that high-dose E2 treatment can cause tumor regression and exert pro-apoptotic actions in multiple cell types; however, the underlying mechanism remains undescribed. In particular, little information of the cellular processes responding to the lethality of E2 is available. In the present study, we attempted to characterize the cellular processes responding to high-dose (μmol/L) E2 treatment using quantitative phosphoproteomics to obtain a better understanding of the regulatory mechanism of E2-induced cell death. First, the cell phenotype induced by high-dose E2 was determined by performing Cell Counting Kit-8 assay (CCK8), cell cytotoxicity analysis by trypan blue staining, and microscopic imaging on HeLa cells treated with 1-10 μmol/L E2 or dimethyl sulfoxide (DMSO) for 1-3 d. E2 inhibited cell proliferation and induced cell death in a dose- and time-dependent manner. Compared with the DMSO-treated HeLa cells, the cells treated with 5 μmol/L E2 for 2 d demonstrated >74% growth inhibition and approximately 50% cell death. Thus, these cells were used for quantitative phosphoproteomic analysis. Next, a solid-phase extraction (SPE)-based immobilized titanium ion affinity chromatography (Ti 4+ -IMAC) phosphopeptide-enrichment method coupled with data-independent acquisition (DIA)-based quantitative proteomics was employed for the in-depth screening of high-dose E2-regulated phosphorylation sites to investigate the intracellular processes responding to high-dose E2 treatment. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) identified over 10000 phosphorylation sites regulated by E2 and DMSO in HeLa cells. In comparison with the DMSO-treated cells, the cells treated with 5 μmol/L E2 showed 537 upregulated phosphorylation sites and 387 downregulated phosphorylation sites, with a threshold of p <0.01 and |log 2 (fold change)|≥1. A total of 924 phosphorylation sites on 599 proteins were significantly regulated by high-dose E2, and these sites were subjected to enrichment analysis. In addition, 453 differently regulated phosphorylation sites on 325 proteins were identified only in the E2- or DMSO-treated cell samples. These phosphorylation sites may be phosphorylated or dephosphorylated in response to high-dose E2 stimulation and were subjected to parallel enrichment analyses. Taken together, 1218 phosphorylation sites on 741 proteins were significantly regulated by high-dose E2 treatment. The functional phosphoproteins in these two groups were then analyzed using Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) to determine the biological processes in which they participate and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database. Consistent with the cell-phenotype data, cell cycle-related proteins were highly enriched in the two groups of E2-regulated phosphoproteins ( p <0.05), indicating that high-dose E2 treatment can regulate cell proliferation. In addition, E2-regulated phosphoproteins were highly enriched in the cellular processes of ribosome biogenesis, nucleocytoplasmic transport, and messenger ribonucleic acid (mRNA) processing/splicing ( p <0.05), indicating that the activation of these processes may contribute to high-dose E2-induced cell death. These results further confirm that high-dose E2 treatment inhibits protein translation and induces cell death. Furthermore, the significant upregulation of multiple phosphorylation sites associated with epidermal growth factor receptor (EGFR) and mitogen-activated protein kinases (MAPKs) MAPK1, MAPK4, and MAPK14 by high-dose E2 indicates that the EGFR and MAPK signaling pathways are likely involved in the regulation of E2-induced cell death. These phosphorylation sites likely play vital roles in E2-induced cell death in HeLa cells. Overall, our phosphoproteomic data could be a valuable resource for uncovering the regulatory mechanisms of E2 in the micromolar range.

OBJECTIVE: To probe into the efficacy of Anshen Ningxin capsule on the perimenopausal metabolic syndrome, and its effect on estrogen secretion level and metabolism-related indicators. METHODS: Totally 140 patients with perimenopausal metabolic syndrome (liver-depression and spleen-deficiency type) admitted into Xintai Hospital of Traditional Chinese Medicine from 2018 to 2019 were selected and divided into control group and observation group via the random number table, with 70 cases in each group. The control group was given estradiol valerate and dydrogesterone orally, while the observation group was treated with Anshen Ningxin capsule on the basis of control group. The traditional Chinese medicine( TCM) syndrome integral, TCM syndrome efficacy, estrogen secretion level [ estradiol ( E2 ), leuteinizing hormone ( LH) and follicle-stimulating hormone ( FSH ) ], fasting blood glucose, fasting blood lipid [ triglyceride ( TG) and high density lipoprotein-cholesterol ( HDL-C) J, waist circumference (WC), body mass index ( BMI), blood pressure [systolic pressure( SP), diastolic pressure( DP ) J before and after treatment were compared between two groups. RESULTS: After treatment, the TCM syndrome integral of two groups were significantly decreased, the secretion levels of E2, FSH and LH were significantly improved, the fasting blood glucose, TG, BMI, WC, SP and DP levels were significantly decreased, while the HDL-C was significantly increased, with statistically significant differences ( P < 0. 05) ; all the above indicators in observation group were significantly better than those of the control group, with statistically significant differences ( P

Objective To explore the correlation between oxytocin and bone metabolism and bone mineral density of lumbar vertebrae and hip in postmenopausal women. Methods the concentrations of serum oxytocin, leptin, estrogen and bone metabolic markers were measured in 185 cases of normal bone mineral density and 132 cases of osteoporosis. The BMD of lumbar vertebrae and femoral neck were measured by dual energy X-ray absorptiometry. The relationship between oxytocin level and bone mineral density was explored. Results The serum oxytocin concentration in the osteoporotic women was lower than that in the normal bone mineral density women (P<0.05). In osteoporosis group, serum oxytocin concentration was negatively correlated with age, menopausal years, BMI, serum PINP, BLAP and CTX, and positively correlated with leptin and estrogen. In normal bone mineral density group, no significant correlation was found between serum oxytocin concentration and various indexes. After adjusting age and BMI, the BMD of lumbar vertebrae and femoral neck was still negatively correlated with the years of menopause and the concentrations of serum PINP, BLAP and CTX, and positively correlated with the concentrations of estrogen, leptin and oxytocin. After adjusting for age and BMI, multiple regression analysis showed that years of menopause, serum oxytocin, PINP and CTX were significant predictors of bone mineral density of lumbar vertebrae and femoral neck. Conclusion The level of serum oxytocin in postmenopausal women is related to high bone mineral density of lumbar vertebrae and femoral neck. [ABSTRACT FROM AUTHOR]

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Epidemiological data have shown that postmenopausal women have a significantly higher incidence rate of metabolic associated fatty liver disease（ MAFLD） than premenopausal women and men of the same age. Aiming at this phenomenon,this article summarizes the potential influence mechanism of estrogen deficiency on MAFLD in postmenopausal women from the four aspects of insulin resistance,liver lipid metabolism,liver fibrosis,and intestinal flora,so as to provide a reference for the early clinical prevention and treatment of MAFLD in postmenopausal women. [ABSTRACT FROM AUTHOR]

Osteoporosis is a disease that severely damages the elderly. The chlorine channel can drive the mineralization of osteoblasts and regulate bone structure. Some studies have found that estrogen can activate the chlorine channel and participate in bone formation, suggesting that the chlorine channel may be an important target for estrogen to regulate bone formation. The Wnt signaling pathway plays a key role in bone formation. Experiments have shown that estrogen can activate the Wnt signaling pathway. Inhibiting or down-regulating the ClC-3 chlorine channel can block the activation of the Wnt signaling pathway, suggesting that the ClC-3 chlorine channel may mediate estrogen to promote bone formation by regulating Wnt signaling pathway. This paper reviews the relationship between the chlorine channel, estrogen, Wnt signaling pathway and osteoporosis. [ABSTRACT FROM AUTHOR]