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Background: The traditional clinical trial data collection process requires a clinical research coordinator who is authorized by the investigators to read from the hospital's electronic medical record. Using electronic source data opens a new path to extract patients' data from electronic health records (EHRs) and transfer them directly to an electronic data capture (EDC) system; this method is often referred to as eSource. eSource technology in a clinical trial data flow can improve data quality without compromising timeliness. At the same time, improved data collection efficiency reduces clinical trial costs., Objective: This study aims to explore how to extract clinical trial-related data from hospital EHR systems, transform the data into a format required by the EDC system, and transfer it into sponsors' environments, and to evaluate the transferred data sets to validate the availability, completeness, and accuracy of building an eSource dataflow., Methods: A prospective clinical trial study registered on the Drug Clinical Trial Registration and Information Disclosure Platform was selected, and the following data modules were extracted from the structured data of 4 case report forms: demographics, vital signs, local laboratory data, and concomitant medications. The extracted data was mapped and transformed, deidentified, and transferred to the sponsor's environment. Data validation was performed based on availability, completeness, and accuracy., Results: In a secure and controlled data environment, clinical trial data was successfully transferred from a hospital EHR to the sponsor's environment with 100% transcriptional accuracy, but the availability and completeness of the data could be improved., Conclusions: Data availability was low due to some required fields in the EDC system not being available directly in the EHR. Some data is also still in an unstructured or paper-based format. The top-level design of the eSource technology and the construction of hospital electronic data standards should help lay a foundation for a full electronic data flow from EHRs to EDC systems in the future., (© Yannan Yuan, Yun Mei, Shuhua Zhao, Shenglong Dai, Xiaohong Liu, Xiaojing Sun, Zhiying Fu, Liheng Zhou, Jie Ai, Liheng Ma, Min Jiang. Originally published in JMIR Medical Informatics (https://medinform.jmir.org).)

An infrared squaraine dye was utilized to detect Cu 2+ in solvents based on H-aggregates of squaraine dye. H-aggregates are a type of aggregation with enhanced photophysical properties compared to monomers. In the presence of a Ca 2+ solution, F-Cl offers exceptional H-aggregators that can be transformed into monomers by adding Cu 2+ . Furthermore, this mode successfully demonstrated fluorescence changes in HeLa cells cultured in vitro after the addition of Ca 2+ or Cu 2+ . A highly specific detection of Cu 2+ was achieved using this transformation mode., Competing Interests: Declaration of Conflicting InterestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

The herbicide glyphosate, N -(phosphonomethyl)glycine, has been widely used in the past 40 years, and has had many adverse effects on human health. Here, we constructed a convenient "on-off-on" fluorescent platform for detection of glyphosate via Cu 2+ modulated squaraine dye fluorescence quenching. The squaraine dye F-0 exhibited strong fluorescence, which could be quenched by the addition of Cu 2+ . However, the addition of glyphosate restored the fluorescence intensity of F-0 due to the formation of a Cu 2+ -glyphosate complex. F-0 was utilized as a fluorescent probe for the quantitative detection of glyphosate, with the lowest detection limit of 13.16 nmol L -1 . Furthermore, this method demonstrated high selectivity and anti-interference capabilities. The successful monitoring of glyphosate in real samples was achieved using this detection strategy.

Objectives: Our objective was to present the experience on prenatal diagnosis of 1p36 terminal deletion, and further delineated the fetal presentation of the syndrome., Material and Methods: This was a retrospective analysis of three new prenatal cases with pure 1p36 terminal deletion detected by chromosome microarray analysis (CMA) at a single Chinese medical center. We also reviewed 11 published prenatal cases with similar deletion sizes. Clinical data of all cases including indications for invasive testing, sonographic findings, maternal factors, and pregnancy outcomes were reviewed and analyzed., Results: Three new cases with pure 1p36 terminal deletion were prenatal diagnosed by CMA, the sizes of the deletion were 1.3 Mb, 5.0 Mb, and 4.9 Mb respectively. All cases were detected because of abnormal ultrasound findings, including central nervous system (CNS) abnormalities, congenital heart disease (CHD) and fetal growth restriction. Two pregnancies were terminated, and one was live-born but died three months after birth., Conclusions: The 1p36 terminal deletion results in many clinical manifestations, but the specificity of clinical features are not high. Prenatal sonographic findings such as CNS, CHD may act as suggestive signs of 1p36 deletion or other microdeletion/duplication syndromes.

Limited access to embryos has hampered the study of human embryogenesis and disorders that occur during early pregnancy. Human pluripotent stem cells provide an alternative means to study human development in a dish 1-7 . Recent advances in partial embryo models derived from human pluripotent stem cells have enabled human development to be examined at early post-implantation stages 8-14 . However, models of the pre-implantation human blastocyst are lacking. Starting from naive human pluripotent stem cells, here we developed an effective three-dimensional culture strategy with successive lineage differentiation and self-organization to generate blastocyst-like structures in vitro. These structures-which we term 'human blastoids'-resemble human blastocysts in terms of their morphology, size, cell number, and composition and allocation of different cell lineages. Single-cell RNA-sequencing analyses also reveal the transcriptomic similarity of blastoids to blastocysts. Human blastoids are amenable to embryonic and extra-embryonic stem cell derivation and can further develop into peri-implantation embryo-like structures in vitro. Using chemical perturbations, we show that specific isozymes of protein kinase C have a critical function in the formation of the blastoid cavity. Human blastoids provide a readily accessible, scalable, versatile and perturbable alternative to blastocysts for studying early human development, understanding early pregnancy loss and gaining insights into early developmental defects.

MIEF2 (mitochondrial elongation factor 2) is one of the key regulators of mitochondrial fission. Bioinformatics analysis indicated that high expression of MIEF2 predicted a poor prognosis in ovarian cancer patients. However, the relationship between MIEF2 and aberrant lipid metabolism in OC remains elusive. In this study, we demonstrated that MIEF2 significantly promoted lipid synthesis, while has no significant effect on fatty acid uptake and oxidation in OC cells. MIEF2 enhanced de novo fatty acid synthesis through up-regulating the expression of sterol regulatory element binding protein 1 (SREBP1) and its transcriptional target lipogenic genes ACC1, FASN and SCD1. Meanwhile, MIEF2-promoted cholesterol biosynthesis through up-regulating the expression of sterol regulatory element binding protein 2 (SREBP2) and its transcriptional target cholesterol biosynthesis genes HMGCS1 and HMGCR. Mechanistically, increased mitochondrial reactive oxygen species (ROS) production and subsequently activation of AKT/mTOR signaling pathway was found to be involved in the up-regulation of SREBP1 and SREBP2 in OC cells. Moreover, cell growth and metastasis assays indicated that MIEF2-regulated fatty acid synthesis and cholesterol biosynthesis played a critical role in the progression of OC. Taken together, our findings indicate that MIEF2 is a critical regulator of lipid synthesis in OC, which provides a strong line of evidence for this molecule to serve as a drug target in the treatment of this malignancy.

Background: Increasing evidence has revealed the close link between mitochondrial dynamic dysfunction and cancer. MIEF2 (mitochondrial elongation factor 2) is mitochondrial outer membrane protein that functions in the regulation of mitochondrial fission. However, the expression, clinical significance and biological functions of MIEF2 are still largely unclear in human cancers, especially in ovarian cancer (OC)., Methods: The expression and clinical significance of MIEF2 were determined by qRT-PCR, western blot and immunohistochemistry analyses in tissues and cell lines of OC. The biological functions of MIEF2 in OC were determined by in vitro and in vivo cell growth and metastasis assays. Furthermore, the effect of MIEF2 on metabolic reprogramming of OC was determined by metabolomics and glucose metabolism analyses., Results: MIEF2 expression was significantly increased in OC mainly due to the down-regulation of miR-424-5p, which predicts poor survival for patients with OC. Knockdown of MIEF2 significantly suppressed OC cell growth and metastasis both in vitro and in vivo by inhibiting G1-S cell transition, epithelial-to-mesenchymal transition (EMT) and inducing cell apoptosis, while forced expression of MIEF2 had the opposite effects. Mechanistically, mitochondrial fragmentation-suppressed cristae formation and thus glucose metabolism switch from oxidative phosphorylation to glycolysis was found to be involved in the promotion of growth and metastasis by MIEF2 in OC cells., Conclusions: MIEF2 plays a critical role in the progression of OC and may serve as a valuable prognostic biomarker and therapeutic target in the treatment of this malignancy.

Hydrate generation promotion and kinetic models are key issues in the hydrate utilization technology. The formation kinetics of CO 2 hydrates in a graphene oxide (GO) and sodium dodecyl sulfate (SDS) compounding accelerator system was studied experimentally, and the influences of different concentrations on the hydrate formation time and gas consumption were revealed. The results show that with the combination of GO and SDS, the formation rate of CO 2 hydrates was accelerated, the induction time and generation time were shortened, and the gas consumption increased. The optimal compounding concentration was 0.005% GO and 0.2% SDS. Compared with the observations for pure water and a single 0.005% GO system, the hydrate formation time was shortened by 69.7% and 12.2%, respectively, and the gas consumption increased by 11.24% and 3.2%. A chemical affinity model of CO 2 hydrate formation was established for this system. The effects of the GO and SDS compound ratio, temperature and pressure on the chemical affinity model parameters were studied from the model point of view. On using Matlab to program the model and compare it with the experimental results, very good agreement was achieved. Through research, the chemical affinity model can accurately predict the formation of hydrates in complex systems., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

Background: Molecular characteristics of CpG island methylator phenotype (CIMP) in colorectal cancer (CRC) have been well documented in Western, but not in Chinese, populations., Methods: We investigated the incidence of CIMP, BRAF/KRAS mutation, and microsatellite instability (MSI) in a Chinese population with CRC (n = 401) and analysed associations between CIMP status and clinicopathological and molecular features., Results: A total of 41 cases, 310 cases, and 40 cases were classified as CIMP-high, CIMP-low, and CIMP-negative, respectively. We detected a significantly low incidence of BRAF mutation in adenomas (2%) and CRC (0.7%), and a relatively low incidence of KRAS mutation (24.9%) compared with that in other populations. We also detected a relatively low incidence of CIMP-high (10.2%), which was significantly associated with younger age (≤49 years of age), female sex, and proximal tumour location., Conclusions: This study revealed unique characteristics of CIMP in a Chinese population with colorectal cancer. Developing specific CIMP markers based on unique populations or ethnic groups will further help to fully elucidate CIMP pathogenesis.

HER family members are interdependent and functionally compensatory. Simultaneously targeting EGFR/HER2/HER3 by antibody combinations has demonstrated superior treatment efficacy over targeting one HER receptor. However, antibody combinations have their limitations, with high immunogenicity and high cost. In this study, we have developed a three-in-one nucleic acid aptamer-small interfering RNA (siRNA) chimera, which targets EGFR/HER2/HER3 in one molecule. This inhibitory molecule was constructed such that a single EGFR siRNA is positioned between the HER2 and HER3 aptamers to create a HER2 aptamer-EGFR siRNA-HER3 aptamer chimera (H2EH3). EGFR siRNA was delivered into HER2-expressing cells by HER2/HER3 aptamer-induced internalization. HER2/HER3 aptamers act as antagonist molecules for blocking HER2 and HER3 signaling pathways and also as tumor-targeting agents for siRNA delivery. H2EH3 enables down-modulation of the expression of all three receptors, thereby triggering cell apoptosis. In breast cancer xenograft models, H2EH3 is able to bind to breast tumors with high specificity and significantly inhibits tumor growth via either systemic or intratumoral administration. Owing to low immunogenicity, ease of production, and high thermostability, H2EH3 is a promising therapeutic to supplement current single HER inhibitors and may act as a treatment for HER2 + breast cancer with intrinsic or acquired resistance to current drugs., (Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.)

In the synergistic treatment with cytotoxic drug and vascular disrupting agent, the order of drug release shows great importance to enhance the antitumor efficacy. When vascular disrupting agent is firstly administrated, the reduced blood supply and overexpressed hypoxia-inducible factor-1α greatly limit the efficiency of chemotherapy. In this work, an injectable thermo-sensitive polypeptide hydrogel was firstly developed for the locally sequential delivery of hydrophilic doxorubicin (DOX, a cytotoxic agent) and hydrophobic combretastatin A4 (CA4, a vascular disrupting drug). The aqueous solution of polypeptide at low temperature transformed into hydrogel under the body temperature after subcutaneous injection and completely degraded after four weeks with excellent biocompatibility. DOX and CA4 were co-loaded into the hydrogel, and the release of DOX showed much faster than that of CA4 due to their difference in water solubility. The superior inhibition of tumor volume after treatment with DOX and CA4 co-loaded hydrogel occurred in the treatment of grafted mouse U14 cervical tumor compared with both free drugs and single drug-loaded hydrogels. In addition, the co-loaded hydrogel obtained enhanced apoptosis of tumor cells, significant shutdown of blood vessels, and wholly regional tumor apoptosis, which indicated the eradication of solid tumor. Moreover, treatments with the drug-loaded hydrogels showed negligible damage to normal tissues, suggesting their low systemic toxicity. The locally sequential delivery system had great potential for in situ synergistic chemotherapy., Statement of Significance: The release order makes great difference in the synergistic efficacies of cytotoxic drug and vascular disrupting agent. When cytotoxic drug is administrated before vascular disrupting agent, an eradication of tumor might be obtained. On the contrary, the antitumor efficiency will be greatly hindered by limited penetration of later cytotoxic drug and drug resistant induced by vascular disrupting agent. Therefore, the adjustment of the delivery behaviors of such two-pronged agents in one platform was significant for their efficiently synergistic chemotherapy. The present study originally provides a convenient strategy and an advanced sample for sequential administration of cytotoxic drug and vascular disrupting agent in one platform based on their water solubility to achieve upregulated efficacy and safety., (Copyright © 2017 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.)

Epithelial ovarian cancer is the fourth commonest cause of female cancer death, but no proper evidence had proved that surgery could prolong the survival time. Hence, new effective chemotherapy is necessary to improve the survival. Raddeanin A (RA), anoleanane-type triterpenoid sponin, is isolated from Anemone raddeana. Previous study had proved that RA exerted antitumor activity through inhibiting proliferation and promoting apoptosis of some kinds of cancer cell. ROS is a double-edged sword for tumors and might contribute to therapy resistant. In this study, we discuss at the first time whether ROS was involved in the antitumor effect of RA on Skov3 cells, and analysis the mechanism. The results showed that after be treated by RA, the proliferation of Skov3 was inhibited, and this effect can be enhanced by ROS inhibitor NAC. Pretreated with NAC can enhance the cell cycle block but not apoptosis induced by RA. Moreover, as a by-production of RA, ROS induced autophagy can attenuate RA's antitumor activity, and autophagy inhibitor 3-MA could recover RA's antitumor effect. These results demonstrated that ROS and autophagy could be considered as two pro-tumor factors in some conditions. The combination of RA and ROS inhibitor or autophagy inhibitor or both of them may be the novel strategies at least in ovarian cancer therapy., Competing Interests: None., (IJCEP Copyright © 2017.)

The objective of this study was to explore the expression of EpCAM and EGFR in human epithelial ovarian cancer (EOC) and their correlation with clinicopathological parameters. The protein expression levels of epithelial cell adhesion molecule (EpCAM) and epidermal growth factor receptor (EGFR) were evaluated by immunohistochemistry in formalin-fixed paraffin-embedded specimens from 30 patients with epithelial ovarian carcinoma and 15 normal ovary tissues. Clinicopathological characteristics were gathered by retrospective review of the patients' files. The correlation between EpCAM and EGFR expression, as well as their association with clinical pathological parameters were investigated. The SPSS 17.0 package was used to perform statistical analyses. The positive expression rates of EpCAM and EGFR were significantly elevated in epithelial ovarian cancer tissues than in normal ovary tissues. The positive expressions of EpCAM and EGFR in EOC were associated with International Federation of Gynecology and Obstetrics (FIGO) stage and tumor differentiation, lymph node metastasis. Spearman correlation analysis demonstrated a significant positive association between EpCAM and EGFR expression in EOC. The co-expression of EpCAM and EGFR may play an important role in the carcinogenesis of EOC and might provide a promising molecular therapeutic target., Competing Interests: Conflict of interests: No authors report any conflict of interest.

More and more evidence has confirmed that dysregulation of microRNAs (miRNAs) can conduce to the progression of human cancers. Previous studied have shown that dysregulation of miR-135b is in varieties of tumors. However, the roles of miR-135b in cervical cancer remain unknown. Therefore, our aim of this study was to explore the biological function and molecular mechanism of miR-135b in cervical cancer cell lines, discussing whether it could be a therapeutic biomarker of cervical cancer in the future. The MTT assay and ELISA-Brdu assay were used to assess cell proliferation. Cell cycle was detected by flow cytometry. Real-time quantitative polymerase chain reaction (PCR) and Western blot analyses were used to detect expressions of cyclin D1, p21, p27 and FOXO1. In our study, we found that miR-135b is up-regulated in cervical cancer cell lines. Down-regulation of miR-135b evidently inhibited proliferation and arrested cell cycle in cervical cancer cells. Bioinformatics analysis predicted that the FOXO1 was a potential target gene of miR-135b. Besides, miR-135b inhibition significantly increased expressions of the cyclin-dependent kinase inhibitors, p21(/CIP1) and p27(/KIP1), and decreased expression of cyclin D1. However, the high level of miR-135b was associated with increased expression of FOXO1 in cervical cancer cells. Further study by luciferase reporter assay demonstrated that miR-135b could directly target FOXO1. Down-regulation of FOXO1 in cervical cancer cells transfected with miR-135b inhibitor partially reversed its inhibitory effects. In conclusion, down-regulation of miR-135b inhibited cell growth in cervical cancer cells by up-regulation of FOXO1.

Aim: AQP4 in the brain is involved in the occurrence and development of a variety of encephalopathy. AQPs family changes in kidney were accompanied by altered UTs family. The aim of this study was to observe AQP4 and UT-A3 expression in CNS and to explore their role in the pathogenesis of endotoxemia encephalopathy following peripheral LPS injection in mice., Methods: Endotoxemia was induced in C57Bl/6 mice by intraperitoneal injection of LPS. The expression of UT-A3 and AQP4 in brain were detected by Western blot and immunohistochemistry, the level of cytokines were detected by ELISA, and the content of LDH, AST/ALT, BUN and CREA were detected by colorimetric method., Results: As compared with the control group, in model group, the brain weight/ body weight ratio increased by 13%. Meanwhile, a 2.5 fold increase in LDH and a 1.2 fold increase in AST/ALT were found in peripheral serum (P < 0.05), and also, BUN and CREA increased 2.5 fold (P < 0.01). In addition to severe CNS injury in response to lipopolysaccharide, the contents of cytokines and the expression of AQP4 protein in hippocampal is increased (P < 0.05), while the expression of UT-A3 protein in the hippocampus and cortical astrocytes decreased (P < 0.05). And, in part, Dexa pretreatment attenuated those effects., Conclusions: In endotoxemia encephalopathy, AQPs and UTs which regulate the functions of cell membrane are both altered. We suggested that the molecular mechanisms of regulation in endotoxemia may provide a new strategy for clinical treatment of the disease and drug binding sites.

The environmental persistence and bioaccumulation of herbicide atrazine may pose a significant threat to human health. In this experiment, Wistar rats were treated by 5, 25 and 125 mg·kg(-1) atrazine respectively for 28 days, and the oxidative stress responses as well as the activations of Nrf2 signaling pathway in ovarian tissues induced by atrazine were observed. The results showed that after be treated by atrazine, the proportion of atretic follicles in the rat ovary were increased, the contents of NO and MDA in the tissue homogenates were increased, the over-expressed Nrf2 transferred into the nuclei and played an antioxidant role by up-regulated the expression of II phase detoxifying enzymes such as HO1 and NQO1 and the expression of antioxidant enzymes such as CAT, SOD and GSH-PX.

Objective: To investigate the mechanism of genetic toxicity of gaseous benzene to mouse bone marrow cells and to provide an experimental basis for the discovery of early biomarkers among benzene-exposed population., Methods: Male mice were randomly divided into control group and three benzene-exposed groups (6 mice per group). The control group was exposed to ambient air, and the three benzene-exposed groups were exposed to different concentrations of benzene (400, 800, and 1 600 mg/m(3)) for 15 days, 2 hours per day, in static inhalation chambers. At the end of the 15-day experimental period, the mice were killed. Bone marrow cells were separated from sacrificed mice, and superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, myeloperoxidase (MPO) activity, and malondialdehyde (MDA) content were determined by biochemical methods. DNA damage was evaluated by micronucleus assay and single cell gel electrophoresis (SCGE). The expression of MPO protein was determined by immunocytochemistry., Results: The SOD activities in different dose groups (88.67 ± 13.58, 73.64 ± 4.50, and 67.63 ± 5.42 U/mg prot) were significantly decreased as compared with the control group (119.98±9.42 U/mg prot) (P<0.01). Moreover, the SOD activities in medium- and high-dose groups were significantly lower than that of the low-dose group (P < 0.05). The GSH-Px activities in medium- and high-dose groups (705.07 ± 93.75 and 674.77 ± 86.80 U/mg prot) were significantly decreased as compared with that of the control group (940.25 ± 82.63 U/mg prot) (P < 0.01), and the high-dose group had a significantly lower GSH-Px activity than the low-dose group (674.77 ± 86.80 U/mg prot vs 833.98 ± 130.64 U/mg prot, P < 0.05). The MDA content of low-, medium-, and high-dose groups (22.42±2.67, 22.38±3.02, and 27.66±2.89 nmol/mg prot) were significantly higher than that of the control group (12.35±1.58 nmol/mg prot) (P < 0.01), and MDA content was significantly higher in the high-dose group than in the medium- and low-dose groups (P < 0.05). The micronucleus assay showed that the micronucleus rates in different dose groups (4.67±0.82‰, 5.00±0.89‰, and 5.33±1.03‰) were significantly higher than that of the control group (2.50±0.55‰) (P < 0.01). The SCGE demonstrated that the DNA damage rates of medium- and high-dose groups (22.08% and 25.68%) were significantly higher than that of the control group (7.00%) (P < 0.01), and the DNA damage rate of high-dose group was significantly higher than that of the low-dose group (11.24%) (P < 0.05). MPO activity increased with the dose of benzene in all three benzene-treated groups (16.79±2.16, 19.46±2.28, and 22.53±2.76 U/g prot) and was significantly higher than that of the control group (12.89±0.74 U/g prot) (P < 0.01). The positive rates of MPO protein expression in low-, medium-, and high-dose groups (13.20±2.28%, 30.80±3.35%, and 40.20±1.92%) were significantly higher than that of the control group (6.60±1.14%) (P < 0.01). The MPO activity in high-dose group and the positive rates of MPO protein expression in medium- and high-dose groups were all significantly higher than those of the low-dose group (P < 0.01)., Conclusion: Gaseous benzene exposure has toxic effect on genetics of mouse bone marrow cells. It leads to chromosome breakage and DNA damage, enhances the activity and protein expression of MPO, and induces lipid peroxidation. Lipid peroxidation damage is a potential mechanism by which gaseous benzene exerts toxic effect on mouse bone marrow cells.

Atrazine (ATR), one of the most widely used herbicides worldwide, has caused a series of toxicological and environmental problems. This study sought to investigate the effects of ATR on the immune system of mice. Four-week-old female C57B l/6 mice were treated with 5, 25, and 125 mg/kg ATR for 28 days. On day 29, blood was collected and the spleen was harvested to detect lymphocyte transformation, natural killer (NK) cell activity, cellular phenotypes, and cytokines. Results indicated that the thymus and spleen weights decreased after ATR treatment, and the spleen was found to be more sensitive to ATR than the thymus. Decreases in lymphocyte transformation and NK cell activity were also observed in mice treated with 25 mg/kg ATR and 125 mg/kg ATR compared to the control group. In addition, there were also alterations of lymphocyte phenotypes in the spleen, and the percentages of CD3+ and CD4+ cells decreased in mice treated with 25 mg/kg ATR and 125 mg/kg ATR compared to the control group. Moreover, serum interleukin-4 level decreased significantly after treatment with 25 mg/kg and 125 mg/kg ATR, but ATR did not affect the expression of interleukin-2, interferon-γ, and tumor necrosis factor-α. These results suggest that ATR may have induced damage in spleen cells. As ATR is an environmental contaminant, its immunosuppressive action raises concerns that it may potentiate clinical conditions such as tumors, inflammation, and infections. Thus, it needs to be carefully monitored and studied.

In this study, we aimed to evaluate the effect of α- cyperone on S. aureus. We used a hemolysin test to examine the hemolytic activity in supernatants of S. aureus cultured with increasing concentrations of α- cyperone. In addition, we evaluated the production of α- hemolysin (Hla) by Western blotting. Real-time RT-PCR was performed to test the expression of hla (the gene encoding Hla) and agr (accessory gene regulator). Furthermore, we investigated the protective effect of α- cyperone on Hla-induced injury of A549 lung cells by live/ dead and cytotoxicity assays. We showed that in the presence of subinhibitory concentrations of α-cyperone, Hla production was markedly inhibited. Moreover, α- cyperone protected lung cells from Hla-induced injury. These findings indicate that α-cyperone is a promising inhibitor of Hla production by S. aureus and protects lung cells from this bacterium. Thus, α-cyperone may provide the basis for a new strategy to combat S. aureus pneumonia.