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Background. Physical subhealth directly correlates to people’s work effectiveness and quality of life, so subhealth prevention has become an urgent medical problem. Methods. A random sampling method was used to conduct a questionnaire survey of physical examinees from June to September, 2019. In total, 770 people participated in our study. The Pearson correlation and multiple stepwise regression analysis were used to explore the relationship among demographic variables, physical subhealth, and risk perception. Also, this study used a two-way interaction moderated multiple regression approach to examine the moderating effects of demographic variables on physical subhealth and risk perception. Results. The risk perception level was negatively associated with physical health. Age, education level, and subhealth proportion in the work unit all significantly and positively influence physical health, whereas living place, subhealth duration, and marital status negatively influence physical health. Living place, average annual household income, number of employees in the work unit, and subhealth proportion in the work unit significantly and positively influence the risk perception, and only age negatively influences the risk perception. The number of children had a moderating effect on physical subhealth and risk perception (Interaction coefficient α = −0.3, P < 0.05 ). Conclusions. To achieve the overall improvement of public health, relevant management departments can provide targeted interventions for the public with different levels of risk perception. Also, the physical subhealth of the public can be addressed by encouraging the public to attach importance to education, improving the public living environment to build a livable city, strengthening psychological guidance and intervention for couples heading toward divorce to reduce the divorce rate, focusing on the health of work unit employees and regularly organizing employees to attend medical checkups, and actively responding to the national policy of family planning.

Background: Diabetic heart dysfunction is a common complication of diabetes. Cell death is a core event that leads to diabetic heart dysfunction. However, the time sequence of cell death pathways and the precise time to intervene of particular cell death type remain largely unknown in the diabetic heart. This study aims to identify the particular cell death type that is responsible for diabetic heart dysfunction and to propose a promising therapeutic strategy by intervening in the cell death pathway. Methods: Type 2 diabetes models were established using db/db leptin receptor–deficient mice and high-fat diet/streptozotocin–induced mice. The type 1 diabetes model was established in streptozotocin-induced mice. Apoptosis and programmed cell necrosis (necroptosis) were detected in diabetic mouse hearts at different ages. G protein–coupled receptor–targeted drug library was searched to identify potential receptors regulating the key cell death pathway. Pharmacological and genetic approaches that modulate the expression of targets were used. Stable cell lines and a homemade phosphorylation antibody were prepared to conduct mechanistic studies. Results: Necroptosis was activated after apoptosis at later stages of diabetes and was functionally responsible for cardiac dysfunction. Cannabinoid receptor 2 (CB2R) was a key regulator of necroptosis. Mechanically, during normal glucose levels, CB2R inhibited S6 kinase–mediated phosphorylation of BACH2 at serine 520, thereby leading to BACH2 translocation to the nucleus, where BACH2 transcriptionally repressed the necroptosis genes Rip1 , Rip3 , and Mlkl . Under hyperglycemic conditions, high glucose induced CB2R internalization in a β-arrestin 2–dependent manner; thereafter, MLKL (mixed lineage kinase domain-like), but not receptor-interacting protein kinase 1 or 3, phosphorylated CB2R at serine 352 and promoted CB2R degradation by ubiquitin modification. Cardiac re-expression of CB2R rescued diabetes-induced cardiomyocyte necroptosis and heart dysfunction, whereas cardiac knockout of Bach2 diminished CB2R-mediated beneficial effects. In human diabetic hearts, both CB2R and BACH2 were negatively associated with diabetes-induced myocardial injuries. Conclusions: CB2R transcriptionally repressed necroptosis through interaction with BACH2; in turn, MLKL formed a negative feedback to phosphorylate CB2R. Our study provides the integrative view of a novel molecular mechanism loop for regulation of necroptosis centered by CB2R, which represents a promising alternative strategy for controlling diabetic heart dysfunction.

Volume overload (VO) and pressure overload (PO) are two common pathophysiological conditions associated with cardiac disease. VO, in particular, often occurs in a number of diseases, and no clinically meaningful molecular marker has yet been established. We intend to find the main differential gene expression using bioinformatics analysis. GSE97363 and GSE52796 are the two gene expression array datasets related with VO and PO, respectively. The LIMMA algorithm was used to identify differentially expressed genes (DEGs) of VO and PO. The DEGs were divided into three groups and subjected to functional enrichment analysis, which comprised GO analysis, KEGG analysis, and the protein–protein interaction (PPI) network. To validate the sequencing data, cardiomyocytes from AR and TAC mouse models were used to extract RNA for qRT-PCR. The three genes with random absolute values of LogFC and indicators of heart failure (natriuretic peptide B, NPPB) were detected: carboxylesterase 1D (CES1D), whirlin (WHRN), and WNK lysine deficient protein kinase 2 (WNK2). The DEGs in VO and PO were determined to be 2761 and 1093, respectively, in this study. Following the intersection, 305 genes were obtained, 255 of which expressed the opposing regulation and 50 of which expressed the same regulation. According to the GO and pathway enrichment studies, DEGs with opposing regulation are mostly common in fatty acid degradation, propanoate metabolism, and other signaling pathways. Finally, we used Cytoscape’s three techniques to identify six hub genes by intersecting 255 with the opposite expression and constructing a PPI network. Peroxisome proliferator-activated receptor (PPARα), acyl-CoA dehydrogenase medium chain (ACADM), patatin-like phospholipase domain containing 2 (PNPLA2), isocitrate dehydrogenase 3 (IDH3), heat shock protein family D member 1 (HSPD1), and dihydrolipoamide S-acetyltransferase (DLAT) were identified as six potential genes. Furthermore, we predict that the hub genes PPARα, ACADM, and PNPLA2 regulate VO myocardial changes via fatty acid metabolism and acyl-Coa dehydrogenase activity, and that these genes could be employed as basic biomarkers for VO diagnosis and treatment.

With the improvement of medical level and the increase of people's demand for health services, the imbalance of supply and demand between doctors and patients leads to the increase of the number of doctor-patient risk cases. The tense doctor-patient relationship has attracted the attention of various academic circles. Risk perception has an evaluation effect on the occurrence of doctor-patient risk, and it is also the key to the development of doctor-patient risk events. It is of great significance to grasp the research progress of doctor-patient risk perception in real time for improving the tense situation of doctor-patient relationship, perfecting its guidance mechanism and reducing the doctor-patient risk events. This study is based on the theory of risk perception, through literature review, to explore the research progress of doctor-patient risk perception, and provide theoretical basis for doctor-patient risk management.

Purpose: The quality of specimens directly affects the experimental results. The stability and structural integrity of nucleic acids in samples have a decisive influence on high-throughput sequenci...

Honey bees (Apis spp.) are widely used as biological indicators of environmental changes. Recently, bees have been explored by researchers to monitor air contamination by listening to their hive sound. However, no study has determined whether beehive sound reflects the responses of bees to in-hive or out-hive chemicals. In this study, we conducted a feeding experiment to address this. First, we fed colonies with pure syrup (PS), syrup containing acetone (SA) or syrup containing ethyl acetate (SE) to collect beehive sound to establish multiple classifications using machine learning (ML) models. Then, we orderly fed colonies with PS, followed by SE, SA and PS. Next, we fed colonies in PS, SA, SE and PS order. Eventually, we evaluated the recall and precision of the model in detecting each syrup type. The result built on orderly feeding had a recall of 99%, 80%, 30%, 53% in detecting PS, SE, SA, PS, respectively. In the reverse feeding experiment, the ML model has a recall of 99%, 89%, 37% and 44% in detecting PS, SA, SE, and PS, respectively. Because the collected syrup in the two orderly feeding sessions was not removed from the frames during the experiment, the results indicate that beehive sound responds to chemicals in or out of the beehive.

Honey bees (Apis spp.) are often used as biological indicators of environmental changes. Recently, bees have been explored to monitor air contaminants by listening to the beehive sound. The beehive sound is believed to encode information on bee responses to chemicals outside their hives. Here we conducted an experiment to address this. First, we randomly fed colonies with pure syrup (PS), acetone-laced syrup (AS), or ethyl acetate-laced syrup (ES) in front of the beehives and collect the beehive sound. Based on the audio data, we build machine learning (ML) models to identify the types of syrup. The result shows that ML models achieved over 90% accuracy for identifying syrup types, indicating that the bees inside their hives emitted the sound associated with the chemicals outside their hives. Then, we sequentially fed the colonies in the order of PS, ES, and AS (the first session) and again in the reverse order (the second session), but did not remove the accumulated ES or AS in the alternative feeding experiment. Based on the audio data, the identification accuracy of both ES and AS by the ML model built on the randomly feeding experiment was different, indicating that the accumulated chemical residuals could confuse the ML models. Therefore, the beehive sound-based environmental monitoring should simultaneously consider the responses of bees to the chemicals outside their hives and their responses to those accumulated inside their hives, which may act simultaneously.

Background: Secreted frizzled-related protein 2 (sFRP2) plays an important role in metabolic syndrome and cardiovascular diseases (CVDs); However, its relevance with cardiometabolic diseases remains to be elucidated. We aimed to determine the serum levels of sFRP2 in patients at different stages of heart failure (HF) with or without type 2 diabetes mellitus (T2DM), and assess the correlation between circulating sFRP2 levels and cardiometabolic risk factors.Methods: In this study, serum samples from 277 patients visiting Zhongshan Hospital affiliated to Fudan University were collected. These patients were clinically diagnosed and categorized as five groups, including the control group, pre-clinical HF group, pre-clinical HF+T2DM group, HF group and HF+T2DM group. Serum sFRP2 levels were measured with enzyme-linked immunosorbent assay (ELISA) tests and the clinical characteristics of each patient were recorded. Spearman rank correlation analysis and multiple stepwise linear regression analysis were conducted. Univariate and multivariate logistic regression analysis were performed to screen risk factors for HF in patients with CVDs.Results: Serum sFRP2 levels were significantly lower in the HF+T2DM group compared with the other four groups. Spearman rank correlation analysis showed that sFRP2 was negatively correlated with parameters including patients' age, fasting plasma glucose (FPG), glycated hemoglobin A1c (HbA1c), cardiac troponin T (cTNT), N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (hs-CRP), left atrial dimension (LAD) and left ventricular posterior wall (LVPW), and positively correlated with hemoglobin, estimated glomerular filtration rate (eGFR), albumin, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and left ventricular ejection fraction (LVEF). However, in multiple regression analysis, significant associations with ln(sFRP2) were observed only in FPG, hs-CRP and LAD. Higher serum sFRP2 was significantly linked to lower odds of HF in patients with CVDs.Conclusion: sFRP2 progressively decreased when glucose homeostasis and cardiac function deteriorated. sFRP2 acted as a risk factor for HF in patients with CVDs, especially in those with concomitant T2DM.

Background: Physical sub-health is directly related to people's work effectiveness and quality of life. Sub-health prevention has become an urgent medical problem. Current research on sub-health mainly focuses on the diagnosis, influencing factors and treatment. Based on the proposed physical sub-health risk perception scale, we explore the differences in the demographic factors and the mechanism of risk perception level on physical sub-health to provide data support for the management of public physical sub-health.Methods: Clinical and risk perception data were collected from 770 physical examinees, which were analyzed using SPSS 23.0, R, and Python software. Pearson correlation coefficient was used to investigate the correlation and multiple stepwise regression analysis was used to explore the influence of demographic variables on physical sub-health and risk perception. Also, this study used a two-way interaction moderated multiple regression approach to examine the moderating effects of demographic variables on physical sub-health and risk perception.Results: Attribute of living place, sub-health duration, marital status, average annual household income, risk perception level were negatively associated with physical sub-health (r= -0.07 ~ -0.17, P < 0.05). The risk perception level was positively correlated with education, attribute of living place,average annual household income, sub-health duration, number of employees in the unit and sub-health proportion in the unit (r= 0.09 ~0.26, P＜0.05), but negatively correlated with age (r= -0.11, P＜0.05). The number of children had a moderating effect on physical sub-health and risk perception (Interaction coefficient α= -0.3, P＜0.05).Conclusions: The factors directly affecting the physical sub-health included age, education, attribute of living place,sub-health duration and sub-health proportion in the unit, while the risk perception level, marital status and average annual household income were found to be indirect influencing factors. The number of children had a moderating effect on physical sub-health and risk perception. Therefore, we suggest attaching importance to public physical exercise and health checkups, correctly guiding public risk perception, and spreading the national policy of bearing and rearing better children etc. to promote the development of public physical health in China.

This article compared the performance of 18 electrocardiographic (ECG) left ventricular hypertrophic (LVH) criteria and four P-wave indices for the diagnosis of echocardiographic (ECHO) LVH and left atrial enlargement (LAE), including the deepest S-wave amplitude added to the S-wave amplitude of lead V4 (SD +SV4 ) and P-wave terminal force in lead V1 (PTFV1 ). A total of 152 middle-aged hypertensive patients without evident cardiovascular diseases (CVDs) were enrolled. The gold standard for the diagnosis of LVH and LAE was ECHO left ventricular mass index (LVMI) and largest left atrial volume index (LAVI). For the detection of LVH, Sokolow-Lyon voltage, Cornell voltage, Cornell product, SD +SV4 , Manning, and R+S in any precordial lead had relatively higher sensitivity, especially SD +SV4 criteria. Their combination could further increase sensitivity (43% vs 29% [SD +SV4 ], P = 0.016). PTFV1 was the only criterion that had significant diagnostic value for ECHO LAE (AUC, 0.68; 95% CI: 0.54-0.73, P = 0.008). For middle-aged hypertensive patients without evident cardiovascular diseases, SD +SV4 had the highest sensitivity for the diagnosis of LVH and the combination of several ECG LVH criteria might further increase sensitivity. PTFV1 had significant diagnostic value for ECHO LAE.

OBJECTIVE To compare the risk of stroke and coronary heart disease (CHD) among various blood pressure (BP) levels in diabetic and people without diabetes Chinese patients. METHODS This cross-sectional study was part of Prospective Urban Rural Epidemiology China study. Patients aged 35 to70 years were recruited from 12 provinces of China between 2005 and 2009. The participants were classified into three groups: hypertension (HTN), high normal BP, and normal BP, and also into SBP and DBP quintiles. RESULTS A total of 42 959 patients were analyzed with 38 975 (90.7% of total population) people without diabetes and 3984 (9.3% of total population) diabetic patients. Among diabetic patients, the HTN group was associated with an increased risk of stroke (odds ratio, 3.03; 95% confidence interval, 1.47-6.25) and CHD (odds ratio, 2.21; 95% confidence interval, 1.45-3.38), when compared with normal BP group. Similar results were drawn in nondiabetic patients. However, no significant difference in risk of stroke or CHD was found between high normal BP and normal BP groups in either diabetic or nondiabetic patients. Risk of CHD and stroke increased significantly when SBP was above 125 mmHg or DBP above 72 mmHg in people without diabetes, whereas this trend was attenuated in diabetic patients. CONCLUSION HTN was associated with a two-fold increased risk of CHD and a three-fold increased risk of stroke compared with normotension irrespective of diabetes status. For diabetic patients with HTN, a more comprehensive method is essential for assessing cardiovascular risk.

Monogalactosyl diacylglycerol (MGDG), the main component of the plastid membrane, is essential for chloroplast photosynthesis; however, little information is available about the function of MGDG synthases gene (TaMGD) in wheat grain. In this manuscript, three homologous genes were identified in wheat grain, and their functions were investigated by gene silencing and overexpression techniques. Three TaMGD homologous genes, TaMGD-6A, -6B, and -6D, located on chromosome 6A, 6B, and 6D, respectively, were isolated from common wheat. The transcription of TaMGD was detected in stems, roots, leaves and grains, and high levels of gene transcripts were detected in stems and leaves. Silencing of TaMGD in common wheat spikes resulted in a decrease in grain weight and starch content, and proteomic analysis showed that the differentially expressed proteins mainly included carbohydrate metabolism- and nucleic acid-related proteins. In comparison with wild-type, transgenic rice plants overexpressing TaMGD-6A and -6D showed an increase in thousand kernel weight, as well as an increase in the expression level of genes related to starch biosynthesis, whereas transgenic rice plants overexpressing TaMGD-6B showed increased grain yield and grain number per spike. The results of gene silencing and overexpression indicated that TaMGD plays an important role in wheat grain weight, which might be associated with carbohydrate metabolism. Hence, this study provides new insights regarding the role of TaMGD in wheat grain characteristics.

Artificial Bee Colony (ABC) has been wildly used in various global optimization problems. In order to avoid premature convergence, a modified chaotic artificial bee colony algorithm using process solutions (CABC-WTB) is presented. Chaos initialization increases population diversity, chaotic local search helps to get out of local minima, process solutions are used to improve convergence speed. Comparative studies have been performed using 800 randomly generated functions. The proposed algorithm raises the performance of ABC algorithm.

Duck hepatitis A virus type 1 (DHAV-1) causes acute hepatitis with high morbidity and mortality in ducklings of the genera Cairina and Anas and is characterized by ecchymotic haemorrhage and necrosis of the liver surface. Since September 2011, a new subtype of DHAV-1 (named pancreatitis-type DHAV-1) has been isolated. This new subtype is characterized by yellowish or haemorrhagic pancreatitis, but with no significant pathological changes in the liver. To further investigate the difference in pathogenicity between hepatitis-type DHAV-1 and pancreatitis-type DHAV-1, we infected Muscovy ducklings with a hepatitis-type DHAV-1 strain, FZ86, or a pancreatitis-type DHAV-1 strain, MPZJ1206, and then compared the resulting gross lesions, histopathological changes, viral distribution and cellular apoptosis in the liver and pancreas of Muscovy ducklings. The results suggested that FZ86 induced a more efficient viral propagation in the liver than MPZJ1206, and the gross and histopathological lesions were also limited to the liver. However, MPZJ1206 induced more effective viral replication in the pancreas than FZ86. The MPZJ1206-infected Muscovy ducklings showed an obviously yellowed and haemorrhagic pancreas, but with no significant pathological changes in the liver. Furthermore, FZ86 induced notable hepatocyte apoptosis and increased the expression of caspase-3 in the liver, whereas MPZJ1206 caused apoptosis in a large number of acinar epithelial cells and elevated the expression of caspase-3 in the pancreas. Taken together, these results demonstrated that pancreatitis-type DHAV-1 has many new pathogenic features which distinguish it from the hepatitis-type DHAV-1. RESEARCH HIGHLIGHTS Pancreatitis-type DHAV-1 (MPZJ1206) was characterized by pancreatic haemorrhage and yellow discolouration, but with no obvious haemorrhage and necrosis in the liver. Pancreatitis-type DHAV-1 (MPZJ1206) exhibits many new pathogenic features which distinguish it from the hepatitis-type DHAV-1 (FZ86).

Novel flower-like Cu3SnS4 microspheres and a series of Cu3SnS4/reduced graphene oxide composites were synthesized by a simple one-pot solvothermal method. The structure and morphology of samples were characterized by SEM, TEM, XRD, XPS, Raman spectroscopy, and N2 adsorption-desorption isotherms. The flower-like CTS microspheres loaded on the surface of rGO are well-dispersive and smaller than these without graphene oxide, which can provide more photocatalytic active sites. CTS/rGO-30 degraded 97% of methyl orange within 120 min under visible light irradiation, which was nearly 1.2 and 2.4-times higher than the CTS and GO samples. Moreover, CTS/rGO-30 exhibited excellent stability and recoverability. The UV–Vis diffuse reflectance spectra was used to explore the photocatalytic degradation mechanism. The results indicated that CTS/rGO have a narrow band-gap and efficient separation of electron-hole pairs, which can absorb and utilize light energy better.

G protein-coupled estrogen receptor (GPER) is identified as a critical estrogen receptor, in addition to the classical estrogen receptors ERα and ERβ. In ERα-negative ovarian cancer cells, our previous studies have found that estrogen stimulated cell proliferation and metastasis via GPER. However, the ligand-independent function of GPER in ovarian cancer cells is still not clear. Herein, we describe that GPER has a co-expression with ERα and ERβ, which are first determined in SKOV3 ovarian cancer cell line. In the absence of estrogen, GPER depletion by specific siRNA inhibits the proliferation, migration and invasion of SKOV3 cells. Whereas abrogation of ERα or ERβ by specific antagonist MPP and PHTPP has the opposite effects for stimulation of cell growth. Markedly, GPER knockdown attenuates MPP or PHTPP-induced cell proliferation, migration and invasion. Furthermore, GPER modulates protein expression of the cell cycle critical components, c-fos and cyclin D1 and factors for cancer cell invasion and metastasis, matrix metalloproteinase 2 (MMP-2) and MMP-9. These findings establish that GPER ligand-independently stimulates the proliferation, migration and invasion of SKOV3 cells. Knockdown of GPER attenuates the progression of ovarian cancer that caused by functional loss of ERα or ERβ. Targeting GPER provides new aspect as a potential therapeutic strategy in ovarian cancer.

G protein-coupled estrogen receptor (GPER) is recently identified as a membrane-associated estrogen receptor that mediates non-genomic effects of estrogen. Our previous immunohistochemistry study found an association between GPER and the proliferation of epithelial ovarian cancer. However, the contributions and mechanisms of GPER in the proliferation of ovarian cancers are not clear. We have examined the role of GPER in estrogen receptor α (ERα)-negative/GPER positive OVCAR5 ovarian cancer cell line. MTT assay was used to detect cell proliferation. BrdU incorporation assay was used to measure the cells in S-phase. Protein expression of marker genes of proliferation, cell cycle and apoptosis were examined by Western blot. The results showed that 17β-estradiol and selective GPER agonist G-1 stimulated the proliferation of OVCAR5 cells and increased the cells in S-phase. Both ligands upregulated the protein levels of c-fos and cyclin D1. Small interfering RNA targeting GPER or G protein inhibitor pertussin toxin (PTX) inhibited basal cell proliferation and attenuated 17β-estradiol- or G-1-induced cell proliferation. GPER mediated cell growth was also associated with the apoptosis of OVCAR5 cells. These findings suggest that GPER has an important function in the proliferation of ovarian cancer cells lacking ERα. GPER might be a promising therapeutic target in ovarian cancer.

G protein-coupled estrogen receptor (GPER) is identified as a critical estrogen receptor, in addition to the classical estrogen receptors ERα and ERβ. In ERα-negative ovarian cancer cells, our previous studies have found that estrogen stimulated cell proliferation and metastasis via GPER. However, the ligand-independent function of GPER in ovarian cancer cells is still not clear. Herein, we describe that GPER has a co-expression with ERα and ERβ, which are first determined in SKOV3 ovarian cancer cell line. In the absence of estrogen, GPER depletion by specific siRNA inhibits the proliferation, migration and invasion of SKOV3 cells. Whereas abrogation of ERα or ERβ by specific antagonist MPP and PHTPP has the opposite effects for stimulation of cell growth. Markedly, GPER knockdown attenuates MPP or PHTPP-induced cell proliferation, migration and invasion. Furthermore, GPER modulates protein expression of the cell cycle critical components, c-fos and cyclin D1 and factors for cancer cell invasion and metastasis, matrix metalloproteinase 2 (MMP-2) and MMP-9. These findings establish that GPER ligand-independently stimulates the proliferation, migration and invasion of SKOV3 cells. Knockdown of GPER attenuates the progression of ovarian cancer that caused by functional loss of ERα or ERβ. Targeting GPER provides new aspect as a potential therapeutic strategy in ovarian cancer.

G protein-coupled estrogen receptor (GPER) was identified as a new member of the estrogen receptor family in recent years. It has become apparent that GPER mediates the non-genomic signaling of 17β-estradiol (E2) in a variety of estrogen-related cancers. Our previous study has found that GPER was overexpressed in human epithelial ovarian cancer and was positively correlated with the expression of matrix metalloproteinase 9 (MMP-9), which suggested GPER might promote the metastasis of ovarian cancer. However, the mechanisms underlying GPER-dependent metastasis of ovarian cancer are still not clear. In the present study, estrogen receptor α (ERα)-negative/GPER-positive OVCAR5 ovarian cancer cell line was used to investigate the role of GPER in the migration and invasion of ovarian cancer. Wound healing assay and transwell matrigel invasion assay were performed to determine the potentials of cell migration and invasion, respectively. The production and activity of MMP-9 in OVCAR5 cells were examined by Western blot and gelatin zymography analysis. The results showed that E2 and selective GPER agonist G-1 increased cell motility and invasiveness, and upregulated the production and proteolytic activity of MMP-9 in OVCAR5 cells. Small interfering RNA (siRNA) targeting GPER and G protein inhibitor pertussin toxin (PTX) inhibited the migration and invasion of OVCAR5 cells, and also reduced the expression and activity of MMP-9. Our data suggested that GPER promoted the migration and invasion of ovarian cancer cells by increasing the expression and activity of MMP-9. GPER might play an important role in the progression of ovarian cancer.