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Microlens arrays (MLAs), as the important optical devices, are easily polluted by the water droplets or power‐like‐contaminates in the air. Endowing the artificial MLAs with anti‐water and self‐cleaning abilities remains great challenge. In this paper, the authors report a novel method for fabricating superhydrophobic polydimethylsiloxane (PDMS) MLAs by the combination of femtosecond laser wet etching and femtosecond laser direct writing methods. The resultant surface is composed of a convex MLA and the surrounding rough micro/nanoscale hierarchical structures. Water droplet on the surface of the as‐prepared MLA shows a contact angle of 162° and can easily roll away when the substrate is slightly tilted 0.5°. In addition to their excellent imaging performance, such ultralow adhesive and ultrahigh superhydrophobicity also endows the as‐prepared MLA with excellent anti‐water ability as well as the self‐cleaning function relative to the normal MLA. The authors believe that the anti‐water and self‐cleaning MLAs will potentially have many important applications in solar cells, medical endoscopes, and other optical systems that are often used in the humid environment or outdoors. A superhydrophobic PDMS microlens array with great water repellence and imaging ability is prepared by the combination of femtosecond laser wet etching and femtosecond laser direct writing methods. The superhydrophobic PDMS MLA consist of a convex MLA and the rest laser‐induced rough micro/nanoscale hierarchical structures. The as‐prepared MLA shows superhydrophobicity and ultralow adhesion, besides its inherent great imaging performance. [ABSTRACT FROM AUTHOR]

Leukemia stem cells (LSC) require frequent adaptation to maintain their self-renewal ability in the face of longer exposure to cell-intrinsic and cell-extrinsic stresses. However, the mechanisms by which LSC maintain their leukemogenic activities, and how individual LSC respond to stress, remain poorly understood. Here, we found that DNAJC10, a member of HSP40 family, was frequently up-regulated in various types of acute myeloid leukemia (AML) and in LSC-enriched cells. Deficiency of DNAJC10 leads to a dramatic increase in the apoptosis of both human leukemia cell lines and LSC-enriched populations. Although DNAJC10 is not required for normal hematopoiesis, deficiency of Dnajc10 significantly abrogated AML development and suppressed self-renewal of LSC in the MLL-AF9-induced murine leukemia model. Mechanistically, inhibition of DNAJC10 specifically induces endoplasmic reticulum stress and promotes activation of PERK-EIF2α-ATF4 branch of unfolded protein response (UPR). Blocking PERK by GSK2606414 (PERKi) or shRNA rescued the loss of function of DNAJC10 both in vitro and in vivo. Importantly, deficiency of DNAJC10 increased sensitivity of AML cells to daunorubicin (DNR) and cytarabine (Ara-C). These data revealed that DNAJC10 functions as an oncogene in MLL-AF9-induced AML via regulation of the PERK branch of the UPR. DNAJC10 may be an ideal therapeutic target for eliminating LSC, and improving the effectiveness of DNR and Ara-C.

The topic of cardiovascular hazards from multiple metal (loid)s exposures has attracted widespread attention. Here, we measured concentrations of twenty-three urinary metal (loid)s and mean platelet volume (MPV), an early cardiovascular damage biomarker, for 3396 Chinese adults. We aimed to comprehensively assess the associations of single metal (loid) and multiple metal (loid)s (as a mixture) with MPV by combined use of five statistical methods, including general linear models, Bayesian kernel machine regression (BKMR), weight quartile sum (WQS) regression, quantile g-computation (QGC), and adaptive elastic network regression (AENR). And based on that, we hope to provide insight into assessing the health effect of multipollutant exposure. After adjustment for potential covariates, at least three methods jointly suggested that of twenty-three metal (loid)s, iron, arsenic, and antimony were positively while aluminum, tungsten, and thallium were inversely associated with MPV. The environmental risk score of metal (loid)s construed by AENR was significantly positively associated with MPV, while the association between overall twenty-three metal (loid)s mixture and MPV was neutralized to be insignificant in QGC and BKMR. Conclusively, single metal (loid) may be inversely (iron, arsenic, and antimony) and positively (aluminum, tungsten, and thallium) associated with early cardiovascular damage, while the association of overall twenty-three metal (loid)s mixture with MPV was insignificant when concurrent exposures exist. It is crucial to select appropriate statistical methods based on study purpose and principles/characteristics of statistical methods, and combined employment of multimethod is insightfully suggested when assessing health effects of multipollutant exposure., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Polychlorinated biphenyls (PCBs) exposure has been related to the abnormal glucose metabolism and the risk of diabetes. However, the joint effects of various PCBs are uncertain and the potential mechanisms remain unclear. Our objectives were to evaluate the associations of serum PCBs with fasting plasma glucose (FPG) and the risk of diabetes among a general Chinese population, and to estimate the mediating effects of oxidative stress in the above associations. Serum levels of seven indicator-PCBs (PCB-28, 52, 101, 118, 138, 153, and 180) and FPG values were determined among 4498 subjects from the Wuhan-Zhuhai cohort. Oxidative DNA damage biomarker (urinary 8-hydroxy-2'-deoxyguanosine, 8-OHdG) and lipid peroxidation biomarker (urinary 8-isoprostane, 8-iso-PGF 2α ) were also measured. Positive relationships of serum PCBs with FPG values as well as the risk of diabetes were observed. With each 1% increment in the natural log-transformed values of wet weight serum PCBs, FPG levels increased a 0.125% for PCB-52, 0.168% for PCB-118, 0.221% for PCB-138, 0.273% for PCB-153, and 0.379% for ΣPCB (the sum of seven PCBs). The adjusted odds ratios of diabetes associated with wet weight PCBs were 1.186 for PCB-52, 1.373 for PCB-118, 1.635 for PCB-153, and 1.456 for ΣPCB. The seven serum PCBs showed positive overall effect on the risk of diabetes. Elevated PCB-28, PCB-52, PCB-118, PCB-138, PCB-153, and ΣPCB were associated with the increased urinary 8-iso-PGF 2α , which was positively related with FPG values. Furthermore, urinary 8-iso-PGF 2α partially mediated the positive associations between PCBs and FPG values, with the mediated proportions ranged from 3.20 to 12.93%. In conclusion, our results suggested that serum PCBs were positively related with increased oxidative stress, FPG values, and the risk of diabetes among a general Chinese population. Serum PCBs mixture had positive overall effect on the risk of diabetes. Lipid peroxidation partly mediated the FPG elevation induced by PCB exposure., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Environmental risk factors have been implicated in adverse health effects. Previous epidemiological studies on environmental risk factors mainly analyzed the impact of single pollutant exposure on health, while in fact, humans are constantly exposed to a complex mixture consisted of multiple pollutants/chemicals. In recent years, environmental epidemiologists have sought to assess adverse health effects of exposure to multi-pollutant mixtures based on the diversity of real-world environmental pollutants. However, the statistical challenges are considerable, for instance, multicollinearity and interaction among components of the mixture complicate the statistical analysis. There is currently no consensus on appropriate statistical methods. Here we summarized the practical statistical methods used in environmental epidemiology to estimate health effects of exposure to multi-pollutant mixture, such as Bayesian kernel machine regression (BKMR), weighted quantile sum (WQS) regressions, shrinkage methods (least absolute shrinkage and selection operator, elastic network model, adaptive elastic-net model, and principal component analysis), environment-wide association study (EWAS), etc. We sought to review these statistical methods and determine the application conditions, strengths, weaknesses, and result interpretability of each method, providing crucial insight and assistance for addressing epidemiological statistical issues regarding health effects from multi-pollutant mixture., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Emerging evidence has shown that long non-coding RNAs (lncRNAs) play an important role in inhibiting tumor cell proliferation and inducing differentiation. In this study, integrative analysis of whole transcriptome sequencing data demonstrated that lncRNA-Gm31932 is significantly decreased in all-trans retinoic acid (ATRA)-induced and sodium 4-phenylbutanoate (PB-4)-induced mouse melanoma B16 cells. Silencing lncRNA-Gm31932 could inhibit B16 cell proliferation, with cell cycle arrest at the G0/G1 phase and obvious differentiation characteristics, e.g., increased cell volume, melanin content and tyrosinase (Tyr) activity. Furthermore, a series of experiments (luciferase reporter assay, RNA pull-down assay, and western blotting) showed that lncRNA-Gm3932 down-regulated Prc1 and Nuf2 by competitively sponging miR-344d-3-5p, which subsequently reduced the expression of cell cycle-related proteins CDK2, CDC2, and Cyclin B1, and increased the expression of P21 and P27. Moreover, silencing lncRNA-Gm31932 could significantly inhibit tumor growth in B16 melanoma-bearing mice. Taken together, these results indicate that as a possible signaling pathway for ATRA and PB-4, lncRNA-Gm31932 can induce cell cycle arrest and differentiation via miR-344d-3-5p/Prc1 (and Nuf2) axis., (© 2022. The Author(s).)

We expected to explore the associations of hearing loss and hearing thresholds at different frequencies with total and cause-specific mortality. In this study, 11,732 individuals derived from the National Health and Nutrition Examination Survey (NHANES) 1999-2012 were included. Data of death was extracted from the NHANES Public-Use Linked Mortality File through December 31, 2015. Cox proportional hazards models were used to explore the associations between hearing loss, hearing thresholds at different frequencies, and total or cause-specific mortality. A total of 1,253 deaths occurred with a median follow-up of 12.15 years. A significant positive dose-response relationship between hearing loss in speech frequency and total mortality was observed, and the HRs and 95% CIs were 1.16 (0.91, 1.47), 1.54 (1.19, 2.00), and 1.85 (1.36, 2.50), respectively, for mild, moderate, and severe speech-frequency hearing loss (SFHL) with a P trend of 0.0003. In addition, moderate (HR: 1.90, 95% CI: 1.20-3.00) and greater (3.50, 1.38-8.86) SFHL significantly elevated risk of heart disease mortality. Moreover, hearing thresholds of >25 dB at 500, 1000, or 2000 Hz were significantly associated with elevated mortality from all causes (1.40, 1.17-1.68; 1.44, 1.20-1.73; and 1.33, 1.10-1.62, respectively) and heart disease (1.89, 1.08-3.34; 1.95, 1.21-3.16; and 1.89, 1.16-3.09, respectively). Hearing loss is associated with increased risks of total mortality and heart disease mortality, especially for hearing loss at speech frequency. Preventing or inhibiting the pathogenic factors of hearing loss is important for reducing the risk of death., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The application of photodynamic therapy (PDT) for the treatment of skin diseases has been receiving much attention. Here, we examined the anti-tumor effect of a novel porphyrin-based photosensitizer TBPoS-2OH in the malignant melanoma A375 and B16 cells. TBPoS-2OH has obvious cell photo-cytotoxicity, but it has low cell dark-cytotoxicity. Further research showed that TBPoS-2OH is enriched in lysosomes after being taken up by cells. Subsequently, the apoptotic rates were significantly increased in TBPoS-2OH-treated A375 and B16 cells. The specific mechanism may be that after receiving light stimulation, TBPoS-2OH could effectively increase the level of intracellular reactive oxygen species (ROS), thereby activating mitochondrial apoptosis pathway-related proteins in A375 and B16 cells. We found an increase in the content of cytochrome C in the cytoplasm, and the levels of related proteins, such as cleaved caspase-3, cleaved caspase-9, and cleaved PARP1, were significantly increased in TBPoS-2OH-treated cells. These results indicated that the new compound TBPoS-2OH could be developed and become an alternative drug for the treatment of melanoma. Some reference ideas for the development of new photosensitizers are also provided., (Copyright © 2020 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.)

Photodynamic therapy (PDT) is an emerging alternative cancer treatment modality that utilizes photo-sensitivity to cause cell death upon photo-irradiation. However, PDT efficiency has been hampered by tumor hypoxia, blue-shifted excitation wavelengths, and the high dark toxicity of photo-sensitizers. We designed and synthesized two novel porphycene-based photosensitizers (TBPoS-OH and TBPoS-2OH) with potent photo-cytotoxicity and a LD 50 in the nM range under both normoxic and hypoxic conditions in a variety of cell types after photo-irradiation (λ = 640 ± 15 nm). Further studies showed fast-cellular uptake for TBPoS-OH that localized lysosomes and subsequently induced cell apoptosis via the lysosomal-mitochondrial pathway. Moreover, TBPoS-OH significantly reduced tumor growth in two xenografted mouse models bearing melanoma A375 and B16 cells. Finally, TBPoS-OH exhibited no obvious immunogenicity and toxicity to blood cells and major organs in mice. These data demonstrated that these two porphycene-based photosensitizers, especially TBPoS-OH, could be developed as a potential PDT modality., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Masson SAS. All rights reserved.)

Emerging evidence suggests that cinobufagin, an active ingredient in Venenum Bufonis, inhibits cell proliferation in several tumor cells. However, the anti-tumor effect of cinobufagin on nasopharyngeal carcinoma and the underlying molecular mechanisms are still unclear. In this study, we found that cinobufagin significantly inhibits the proliferation of nasopharyngeal carcinoma HK-1 cells. Further analyses demonstrated that cinobufagin induces cell cycle arrest at the S phase in HK-1 cells through downregulating the levels of CDK2 and cyclin E. Moreover, cinobufagin significantly downregulates the protein level of Bcl-2 and upregulates the levels of Bax, subsequently increasing the levels of cytoplasmic cytochrome c, Apaf-1, cleaved PARP1, cleaved caspase-3, and cleaved caspase-9, leading to HK-1 apoptosis. Furthermore, we found that cinobufagin significantly increases ROS levels and decreases the mitochondrial membrane potential in HK-1 cells. Collectively, these data imply that cinobufagin induces cell cycle arrest at the S phase and induces apoptosis through increasing ROS levels, thereby inhibiting cell proliferation in HK-1 cells. Therefore, cinobufagin is a promising bioactive agent that may contribute to the development of treatment strategies of nasopharyngeal carcinoma., (Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Our previous studies have indicated that human umbilical vein endothelial cell (HUVEC) vaccination appears to be a potentially promising anti-angiogenesis therapy, but the modest therapeutic anti-tumour efficiency limits its clinical use. This highlights the importance of identifying more potent therapeutic HUVEC vaccine strategies for clinical testing. In the present study, the immune-modulating doses of docetaxel (DOC) was combined with 1 × 10 6 viable HUVECs as a means to enhance the therapeutic anti-tumour efficiency of the HUVEC vaccine. Our results demonstrated that 5 mg/kg DOC administrated prior to HUVEC vaccine could most effectively assist HUVEC vaccine to display a remarkable suppression of tumour growth and metastasis as wells as a prolongation of survival time in a therapeutic procedure. CD31 immunohistochemical analysis of the excised tumours confirmed a significant reduction in vessel density after treatment with the HUVEC vaccine with 5 mg/kg DOC. Additionally, an increased HUVEC-specific antibody level, activated CTLs and an elevated IFN-γ level in cultured splenocytes were revealed after treatment with HUVEC vaccine with 5 mg/kg DOC. Finally, 5 mg/kg DOC coupled with the HUVEC vaccine led to induction of significant increases in CD8 + T cells and decrease in Tregs in the tumour microenvironment. Taken together, all the results verified that 5 mg/kg DOC could assist HUVEC vaccine to elicit strong HUVEC specific humoral and cellular responses, which could facilitate the HUVEC vaccine-mediated inhibition of cancer growth and metastasis. These findings provide the immunological rationale for the combined use of immune-modulating doses of DOC and HUVEC vaccines in patients with cancer., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Objective: Hepatocellular carcinoma (HCC) is one of the cancer types with poor prognosis. To effectively treat HCC, new molecular targets and therapeutic approaches must be identified. Alkaline ceramidase 3 (Acer3) hydrolyzed long-chain unsaturated ceramide to produce free fatty acids and sphingosine. However, whether and how Acer3 modulates progression of HCC remains largely unknown., Methods: Acer3 mRNA levels in different types of human HCC samples or normal tissues were determined from Gene Expression across Normal and Tumor tissue (GENT) database. The expression level of Acer3 in human HCC cell lines were examined by western blot. Overall survival and disease-free survival of HCC patients were determined by Kaplan-Meier analysis. Effects of Acer3 knockdown by lentivirus infection were evaluated on cell growth and apoptosis. The mechanisms involved in HCC cells growth and apoptosis were analyzed by western blot., Results: In silico analysis of TCGA databases of HCC patients showed that the expression of Acer3 significantly inversely correlates with the overall and disease-free survival of HCC patients. Knockdown expression of Acer3 resulted in decreased cell growth and increased apoptosis. Notably, inhibition of Acer3 resulted in intracellular exhaustion of Sphingosine-1-phosphate (S1P) and inhibited activation of S1PR2/PI3K/AKT signaling. Finally, knockdown of Acer3 induced up-regulation of Bax and down-regulation of Bcl-2., Conclusions: Our study suggests that Acer3 contributes to HCC propagation, and suggests that inhibition of Acer3 may be novel strategy for treating human HCC., (Copyright © 2018 Elsevier GmbH. All rights reserved.)

Hepatocellular carcinoma (HCC) is one of the most common malignancies and has a poor prognosis. Novel diagnostic or prognostic biomarkers and potential therapeutic targets for HCC are thus urgently needed. CEP55 plays a crucial role in regulating physical cytokinesis. Whether, and how, CEP55 contributes to HCC development remains unclear. Herein, we demonstrate that CEP55 is abnormally upregulated in HCC tissue, and these high levels of CEP55 are closely related to the poor prognosis of HCC patients. Knockdown of CEP55 expression significantly inhibits HCC cell migration and invasion. We also demonstrate that CEP55 physiologically interacts with JAK2 and promotes its phosphorylation; thus, it is a novel regulator of JAK2⁻STAT3 signaling and its target genes MMP2/9. Finally, blocking JAK2 or STAT3 blunts the stimulation of migration and invasion due to CEP55 overexpression. In summary, our results suggest that CEP55, as an oncogene, promotes HCC cell migration and invasion through regulating JAK2⁻STAT3⁻MMPs signaling.

The 78kDa glucose regulated protein (GRP78) is a multifunctional chaperone that is involved in a variety of cellular processes. Insulin like growth factor I receptor (IGF-IR) often aberrant expresses in many types of tumor cells. The IGF-IR signaling plays key roles in carcinogenesis and maintenance of the malignant phenotype. The crosstalk between GRP78 and IGF-IR molecules has not well been illuminated. Here, we demonstrated a reciprocal regulation of GRP78 expression and IGF-IR pathway activation. IGF-I induced GRP78 expression in hepatoma cells. IGF-IR knockdown or IGF-IR inhibitor repressed GRP78 expression. Both phosphatidylinositol 3-kianase (PI3K) and mitogen-activated protein kinase (MAPK) pathways involved in IGF-I induction of GRP78 expression. Interestingly, treatment of hepatoma cells with IGF-I re-distributes GRP78 from endoplasmic reticulum (ER) to cell surface and promotes its physical interaction with IGF-IR. Also, GRP78 promotes IGF-IR phosphorylation and activation. Blocked of GRP78 by small interfering RNA or inhibition of GRP78 function by (-)-epigallocatechin gallate (EGCG) blocks IGF-I induced IGF-IR phosphorylation and its downstream signaling. Further, blocked cell surface GRP78 with antibody inhibits IGF-I stimulated cellular proliferation and migration. These data reveal an essential role for the molecular chaperone GRP78 in IGF-IR signaling and implicate the use of GRP78 inhibitors in blocking IGF-IR signaling in hepatoma cells., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Objective To explore the effect of combined hypoxia and tumor necrosis factor α (TNF-α) on the apoptosis of human pulmonary microvascular endothelial cells (HPMVECs) and the involved signaling pathway mechanism. Methods Some HPMVECs were treated with hypoxia within 6, 12, or 24 hours, and the other cells were treated with TNF-α at the concentrations of 10, 20, 50, or 100 ng/mL. Cell activity was determined by MTT assay in each group to determine the best combined stimulatory conditions. Under the optimal costimulatory condition, the activity of caspase-3 was detected by flow cytometry, annexin V-FITC/PI double staining combined with flow cytometry was used to detect the apoptosis, Western blotting was performed to test the level of phosphorylated signal transducer and activator of transcription 3 (pSTAT3) and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2). Results The cell activity was the lowest in 24-hour hypoxia group and 100 ng/mL TNF-α group. Therefore, we confirmed the combination of hypoxia for 24 hours and 100 ng/mL TNF-α as the costimulatory conditions. The caspase-3 activity and apoptosis rate in the combined treatment group were higher, compared with the other groups. The expression of pSTAT3, rather than pERK1/2, increased in the combined treatment group, compared with the control group. Moreover, the STAT3 inhibitor S3I-201 reduced the apoptosis rate in the combined treatment group. Conclusion Combined hypoxia and TNF-α could promote HPMVEC apoptosis by activating STAT3 rather than ERK1/2.

A highly effective analytical method for multi-residue determination of antibiotics in aquifer sediments was first established in this study. Microwave-assisted solvent extraction (MASE) and solid-phase extraction were used for sample pre-concentration and purification, ultra-high performance liquid chromatography coupled to hybrid quadrupole-high resolution Orbitrap mass spectrometry (UHPLC-Q-Orbitrap) was applied for detection. For high resolution mass spectrometry (HRMS), the target compounds were tentatively identified by retention time and accurate mass which was measured with precursor ions in Target-SIM scan, and then confirmed by the monitoring of daughter ion fragments which were generated in dd-MS(2) scan. The results provided good mass accuracy with mass deviations below 2ppm (except norfloxacin with -2.3ppm) for quantitative analysis of the compounds by HRMS. Reasonable recoveries of all analytes were obtained more than 60% (except doxytetracycline) in fortification samples at concentrations higher than 10μgkg(-1). Relative standard deviations of repeatability and inter-day precision were below 21% and 11%. Limits of detection (LOD) ranged from 0.1 to 3.8μgkg(-1), whereas limits of quantification (LOQ) were established between 0.3-9.0μgkg(-1). The method was applied to analyze real aquifer sediment samples in different aquifer depth of 4.0, 7.5, 13.0 and 18.0m. Chlorotetracycline and ofloxacin were observed at relative high concentrations of 53 and 19μgkg(-1) respectively in 18.0m deepness. The exposure to low doses of these compounds in subsurface environment increases concerns on long-term ecological security of underground system., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Here we evaluate the quantitative relationship between carbon isotopic fractionation and anoxic biodegradation of phthalate esters (PAEs), a kind of endocrine disruptors. The stable carbon isotope delta values (δ(13)C) of 4 PAEs, i.e. di-methyl phthalate (DMP), di-ethyl phthalate (DEP), di-n-butyl phthalate (DBP), and di-iso-butyl phthalate (DiBP), were analyzed during biodegradation by a pure bacteria strain isolated from the shallow aquifer sediment in anoxic condition. Results showed that the carbon isotopic fractionation in the initial degradation of PAEs was well-described by the Rayleigh equation model with R(2) from 0.8885 to 0.9821. The carbon isotopic fractionation (ε) for DMP and DEP were -4.6±0.4‰ and -2.9±0.1‰, respectively, while DBP and DiBP showed limited isotopic fractionation. A linear relationship between ε values and the total carbon atoms present in straight-carbon-chain PAE molecules with R(2) of 0.9918. The apparent kinetic isotope effects (AKIEs) were calculated for proposed 4 initial transformation pathways of PAEs. The high carbon AKIEs of 1.048 and 1.036 were obtained for single enzymatic hydrolysis of DMP and DEP, respectively, and fell in the expected KIE range of 1.03-1.09. However, the intrinsic carbon isotope effects for enzymatic hydrolysis of DBP and DiBP might be masked., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Objective: To investigate the effects of interleukin (IL)-22 and interferon (IFN)-γ on epithelial-mesenchymal transition (EMT) of pleural mesothelial cells, and to explore the relevant signal transduction pathways, in tuberculous pleural effusion., Methods: Twenty-two patients (12 males and 10 females, age range 22-64 years, mean 38.4 years) with tuberculous pleurisy hospitalized in department of respiratory medicine of the First People's Hospital of Foshan were recruited from July 2013 to June 2014. Diagnosis was confirmed by pathology. Freshly isolated pleural mesothelial cells (PMCs) from tuberculous pleural effusion were cultured either in medium alone as control, or stimulated with IL-22 and/or IFN-γ, and the phosphorylated signal transducers and activators of transcription (STAT) signalings in PMCs were determined by flowcytometry. In some experiments, STAT inhibitors were added into coculture with IL-22 and/or IFN-γ, and then morphological changes of PMCs were observed, and the expressions of epithelial markers such as cytokeratin-8 and E-cadherin as well as mesenchymal markers such as vimentin and α-Smooth muscle actin (SMA) were also determined by flow cytometry., Results: As compared with the control group, IFN-γ induced epithelial-mesenchymal transition of PMCs via a STAT1 pathway as evidenced by down-regulation of cytokeratin-8 [(43.8 ± 2.8)% vs (14.3 ± 1.5)%,t=8.1, P<0.05] and E-cadherin [(43.8 ± 1.9)% vs (13.4 ± 1.2)%, t=9.7, P<0.05], and by up-regulation of vimentin [(41.2 ± 2.4)% vs (70.6 ± 3.6)%,t=8.5, P<0.05] and α-SMA [(55.8 ± 2.0)% vs (80.6 ± 2.9)%,t=7.2, P<0.05]. IL-22 not only maintained the epithelial property of PMCs, but also reverted IFN-γ-induced EMT [cytokeratin-8 (62.4 ± 3.1)%, E-cadherin (46.5 ± 3.6)%, vimentin (36.7 ± 2.8)%, and α-SMA (35.2 ± 2.5)% in 'IFN-γ + IL-22' group, all P<0.05 as compared with those of IFN-γ group]. Whereas addition of STAT3 inhibitor significantly abrogated such anti-EMT effect of IL-22 on PMCs [cytokeratin-8 (16.7 ± 0.7)%, E-cadherin (14.4 ± 0.9)%, vimentin (67.9 ± 2.5)%, and α-SMA (79.2 ± 5.7)% in 'IFN-γ + IL-22 + STAT3 inhibitor' group, all P<0.05 as compared with those of 'IFN-γ + IL-22' group]., Conclusion: The IL-22-STAT3 signal pathway could revert IFN-γ-induced EMT of PMCs, and might play a protective role in anti-pleural fibrosis in tuberculous pleurisy.