[Characteristics and drivers of vegetation temporal dynamics in Hunan Province of China during 2002-2020]. / 湖南省2002­2020å¹´æ¤è¢«åŠ¨æ€æ¼”å˜ç‰¹å¾åŠå½±å“å› å­.

Understanding the influences of climate change and human activities on vegetation change is the foundation for effective ecosystem management. Based on the 250 m MODIS-NDVI data from 2002 to 2020, we employed Theil-Sen Median trend analysis and the Mann-Kendall test to quantify vegetation change in Hunan Province. By combining with meteorological, nighttime light index, land cover and other data, residual analysis and correlation analysis, we examined the impacts of human activities and climate change on vegetation dynamics at both the pixel level and the county level. The results showed that the normalized difference vegetation index (NDVI) in Hunan Province exhibited a spatial pattern of "overall improvement with localized degradation" during 2002-2020. Approximately 64.9% of the study area experienced significant vegetation improvement, mainly occurring in the western and central-southern parts of Hunan Province. 1.4% of the study area experienced significant vegetation degradation, mostly in the newly developed urban areas and the farmland in the Dongting Lake Plain. Human activities and climate change jointly promoted vegetation improvement in 67.9% of the study area. Human activities and climate contributed to 96% and 4% of the NDVI change, respectively. At the county level, human activities contributed to over 80% of the NDVI change in each district or county. The impacts of human activities on vegetation change exhibited significant spatial heterogeneity. Urban expansion led to vegetation degradation in the newly developed areas, while vegetation growth appeared in the old developed urban areas. The ecological restoration projects promoted vegetation restoration in the western part of Hunan Province. This study could help us better understand the spatiotemporal variations of vegetation and their responses to climate change and human activities, which would offer scientific basis for effective ecological restoration policy.

Primary Nasopharyngeal Melanoma without invasive and Metastasis: A Rare Case Reports and Literature Reviews.

Objective: Nasopharyngeal melanoma is a rare mucosal malignant melanoma with high recurrence rate, metastasis rate and vascular invasion rate. In this paper, we report a case of primary nasopharyngeal mucosal melanoma. Methods: A case of primary nasopharyngeal mucosal melanoma was reported, and its clinical symptoms, pathological characteristics, treatment and follow-up were described in detail. Results: This report describes a 59-year-old male patient with persistent nasal congestion and suspected malignant nasopharyngeal neoplasm. Patients receive surgical resection and adjuvant radiotherapy after complete resection. Imaging studies showed no tissue invasion or lymph node metastases. The results of immunohistochemistry were Melan-A(+), HMB45(+), and S100(+). The final diagnosis was malignant nasopharyngeal melanoma. After 2 years of follow-up, the prognosis was good, and there was no metastasis or recurrence. Discussion: Nasopharyngeal melanoma is a rare malignancy with a poor prognosis, and surgical resection is the mainstay of treatment. Postoperative adjuvant therapy can improve the rate of local control of lesions. Early diagnosis and thorough examination are extremely important for the patient's prognosis.

Evaluation of ciliary body morphology and position of the implantable collamer lens in low-vault eyes using ultrasound biomicroscopy.

PURPOSE: To investigate the ciliary body anatomy and position of the implantable collamer lens (ICL) in low-vault eyes and analyze factors related to insufficient vault. SETTING: Zhongshan Ophthalmic Center, Guangzhou, China. DESIGN: Retrospective case-control observational study. METHODS: In this study, 73 eyes of 73 patients with an insufficient vault (<250 µm) were matched with 73 eyes with an ideal vault (250 to 750 µm). Ultrasound biomicroscopy was used to determine the ciliary body morphology and ICL position. The biometric parameters acquired by Scheimpflug tomography were compared. The correlation between the vault and these factors was analyzed, and the least absolute shrinkage and selection operator method was used to screen the risk factors for low vault. RESULTS: The low-vault group had a steeper corneal curvature, thicker lens thickness (LT), higher crystalline lens rise, and shorter axial length (AL) (all P < .005). The ciliary process length (CPL) and maximum ciliary body thickness (CBTmax) were significantly smaller, and the trabecular-ciliary angle (TCA), iris-ciliary angle (ICA), and ciliary sulcus width (CSW) were significantly greater in the low-vault eyes (all P < .005). The low-vault group had more ICL haptics below the ciliary process, and TCA, ICA, CPL, CBTmax, CSW, and haptic position were related to the postoperative vault (all P < .05). CPL, AL, and LT were identified as predictors of a low vault. CONCLUSIONS: Malposition of ICL haptics behind the ciliary process is a risk factor for low vault. A shorter CPL, thicker LT, and shorter AL are significant risk factors for the postoperative low vault.

Evaluation of the efficacy and safety of endoscopic injection of polidocanol combined with low-dose tissue glue occlusion in the treatment of F3 type esophageal varices in liver cirrhosis / 中国医师杂志

Objective:To explore the efficacy and safety of endoscopic injection of polidocanol combined with low-dose tissue glue occlusion in the treatment of F3 esophageal varices in liver cirrhosis.Methods:Retrospective analysis was made on 42 patients with cirrhosis type F3 esophageal varices admitted to the Affiliated Hospital of Zunyi Medical University from January 2020 to June 2021. According to different treatment methods, they were divided into the observation group and the control group, with 21 cases in each group. The observation group received endoscopic injection of polidocanol combined with low-dose tissue glue occlusion, while the control group received endoscopic injection of polidocanol. The differences in the effectiveness (remission rate of varices) and safety (incidence of intraoperative bleeding and postoperative rebleeding, incidence of ectopic embolism, incidence of esophageal ulcer, incidence of esophageal perforation, incidence of esophageal stricture) of the two groups of patients were compared.Results:The total effective rate of relieving esophageal varices in the observation group was significantly better than that in the control group [95.2%(20/21) vs 61.9%(13/21), χ 2=6.929, P=0.008]. There were no cases of ectopic embolism in both groups; The intraoperative bleeding rate in the observation group was 4.8% (1/21), significantly lower than the 38.1% (8/21) in the control group (χ 2=6.929, P=0.008); There was no statistically significant difference in postoperative rebleeding rates between the two groups [33.3%(7/21) vs 23.8%(5/21), χ 2=0.467, P=0.495]; The incidence of esophageal ulcers in the observation group was higher than that in the control group [23.8%(5/21) vs 0, χ 2=5.676, P=0.017], mainly caused by glue discharge ulcers; There were no cases of esophageal perforation and esophageal stricture in both groups. Conclusions:Endoscopic injection of polidocanol combined with low-dose tissue glue occlusion for the treatment of F3 esophageal varices in liver cirrhosis is safe, can greatly reduce the occurrence of intraoperative bleeding, and has a better one-time variceal eradication effect.

Construction of competency model for outpatient nurses in pediatrics / 中国实用护理杂志

Objective:To explore the scientific and practical modeling method and construct the post competency model of pediatric outpatient nurses to provide reference for the recruitment, training and selection of pediatric outpatient nurses.Methods:Competency factors were extracted by literature review, behavioral event interview, exploratory common factor molecular method and Delphi method, and the weight of each factor was determined by AHP and expert scoring method.Results:6 items of differential competence were obtained, and the final competency model of pediatric outpatient post was formed, including personal characteristics, professional accomplishment, development ability, professional knowledge, professional technology and management ability. The weight range was 0.107 4-0.210 1, 39 secondary indexes, the weight range was 0.086 4-0.256 5, and the combined weight range was 0.009 9-0.053 9.Conclusion:The modeling method is scientific and reasonable, the model is reliable and practical, which provides the basis for the admission, training and performance appraisal of pediatric outpatient nurses, and has theoretical and practical significance.

Nrf2 modulates immunosuppressive ability and cellular senescence of human umbilical cord mesenchymal stem cells.

In the application of human umbilical cord-derived mesenchymal stem cells (UC-MSCs) as clinical therapeutics, long term cells ex vivo expansion results in decline in their function. It has been widely concerned that cellular senescence is associated with UC-MSCs immunomodulatory ability. In this study, we evaluated the effects of consecutive passages on cellular senescence and the immunomodulatory abilities of UC-MSCs. Long term-cultured UC-MSCs showed decreased proliferation, senescence phenotypes and impaired immunosuppressive effects on PHA induced peripheral blood mononuclear cell (PBMC) proliferation. We found that Nrf2, a transcription factor that responds to oxidative stress, that showed decreased expression in long term-cultured UC-MSCs, and the further knock-down of Nrf2 in UC-MSCs induced premature senescence, decreased proliferation ability and immunosuppressive abilities. Furthermore, the protein expression of IDO-1 were decreased in response to the downregulation of Nrf2 in UC-MSCs, suggesting that Nrf2 regulates the immunosuppressive properties of UC-MSCs via Nrf2-mediated IDO-1 expression. In conclusion, our results demonstrate that Nrf2 plays a key role in the regulation of the immunosuppressive properties of UC-MSCs, and we suggest that these findings might provide a strategy to enhance the functionality of UC-MSCs for use in therapeutic applications.

Secretomic Analysis of Host-Pathogen Interactions Reveals That Elongation Factor-Tu Is a Potential Adherence Factor of Helicobacter pylori during Pathogenesis.

The secreted proteins of bacteria are usually accompanied by virulence factors, which can cause inflammation and damage host cells. Identifying the secretomes arising from the interactions of bacteria and host cells could therefore increase understanding of the mechanisms during initial pathogenesis. The present study used a host-pathogen coculture system of Helicobacter pylori and monocytes (THP-1 cells) to investigate the secreted proteins associated with initial H. pylori pathogenesis. The secreted proteins from the conditioned media from H. pylori, THP-1 cells, and the coculture were collected and analyzed using SDS-PAGE and LC-MS/MS. Results indicated the presence of 15 overexpressed bands in the coculture. Thirty-one proteins were identified-11 were derived from THP-1 cells and 20 were derived from H. pylori. A potential adherence factor from H. pylori, elongation factor-Tu (EF-Tu), was selected for investigation of its biological function. Results from confocal microscopic and flow cytometric analyses indicated the contribution of EF-Tu to the binding ability of H. pylori in THP-1. The data demonstrated that fluorescence of EF-Tu on THP-1 cells increased after the addition of the H. pylori-conditioned medium. This study reports a novel secretory adherence factor in H. pylori, EF-Tu, and further elucidates mechanisms of H. pylori adaptation for host-pathogen interaction during pathogenesis.

Enterovirus 71 virion-associated galectin-1 facilitates viral replication and stability.

Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal brain stem encephalitis complicated with pulmonary edema. Several severe EV71 endemics have occurred in Asia-Pacific region, including Taiwan, and have become a serious threat to children's health. EV71 infection is initiated by the attachment of the virion to the target cell surface. Although this process relies primarily upon interaction between viruses and cell surface receptors, soluble factors may also influence the binding of EV71 to host cells. Galectin-1 has been reported to participate in several virus infections, but is not addressed in EV71. In this study, we found that the serum levels of galectin-1 in EV71-infected children were higher than those in non-infected people. In EV71 infected cells, galectin-1 was found to be associated with the EV71 VP1 and VP3 via carbohydrate residues and subsequently released and bound to another cell surface along with the virus. EV71 propagated from galectin-1 knockdown SK-N-SH cells exhibited lower infectivity in cultured cells and less pathogenicity in mice than the virus propagated from parental cells. In addition, this galectin-1-free EV71 virus was sensitive to high temperature and lost its viability after long-term storage, which could be restored following supplement of recombinant galectin-1. Taken together, our findings uncover a new role of galectin-1 in facilitating EV71 virus infection.

[Regional differences of inputs of organic matter and chemical fertilizer in South Central China].

This article analyzed the inputs of organic matter and chemical fertilizer in the cropland of South Central China, i.e., Hunan, Hubei, Guangdong and Guangxi, and then calculated the budgets of nitrogen (N), phosphorus (P) and potassium (K), based on the data from field investigations and peasant household surveys in the four provinces. The results showed that total amounts of organic matter inputs in the four provinces was ranked as follow: 8993 kg · hm(-2) in Guangxi, 6390 kg · hm(-2) in Hunan, 5012 kg · hm(-2) in Hubei, 4630 kg · hm(-2) in Guangdong, and average NPK inputs in the four provinces were ranked as follow: 777.5 kg · hm(-2) in Guangxi, 501.6 kg · hm(-2) in Hunan, 486.4 kg · hm(-2) in Hubei, 340.4 kg · hm(-2) in Guangdong. The N and P input surpluses were greatest in Guangxi (67.2% and 99.0% as for N and P, respectively) , followed by Hunan (33.2% and 50.8%), Hubei (11.8% and 11.0%), and Guangdong (7.8% and 30.0%). However, K input was deficient in Hunan, Hubei, and Guangdong (6.6%, 18.7% and 12.4%), but surplus in Guangxi (19.5%).

Impact of glycogen synthase kinase-3β (GSK-3β) inhibitor on Wnt and NF-κB signal pathways in a rat model of diabetic nephropathy / 中华病理学杂志

<p><b>OBJECTIVE</b>To explore the impact of glycogen synthase kinase-3β (GSK-3β) on Wnt and NF-κB pathways in a rat model of diabetic nephropathy (DN).</p><p><b>METHODS</b>SD rats were randomly divided into normal control group (NC), DN model group (DM) and GSK-3β inhibitor group (DI). Blood glucose and 24-hour urine protein were monitored in three groups. Renal tissue samples were stained by HE. The expression of GSK-3β and NF-κB proteins was studied by immunohistochemistry. GSK-3β and NF-κB mRNAs were detected by RT-qPCR.</p><p><b>RESULTS</b>Ten weeks after STZ injection, the level of blood glucose increased significantly in DM group [(23.2±5.4) mmol/L] and DI group [(25.0±4.0) mmol/L], compared with NC group, and the level of 24-hour urinary protein increased significantly in DM group [(185.2±35.6) g/24 h] and DI group [(179.6±44.7) g/24 h], compared with NC group. Two weeks after LiCl injection, the level of blood glucose and 24-hour urinary protein decreased in DI group (17.6±2.1) mmol/L, (106.9±30.0) g/24 h], compared with DM Group. Compared with NC group, pathological changes of the kidney of DM group aggravated along with increased mRNA and protein expression of GSK-3β and NF-κB. But the pathological changes of the kidney in DI group alleviated along with declined mRNA and protein expression of GSK-3β and NF-κB as compared with DM group (all P<0.05).</p><p><b>CONCLUSIONS</b>NF-κB protein expression positively correlates with the GSK3β expression. Wnt and NF-κB signal pathways play an important role in the development of diabetic nephropathy.</p>

Dengue virus infection induces autophagy: an in vivo study.

BACKGROUND: We and others have reported that autophagy is induced by dengue viruses (DVs) in various cell lines, and that it plays a supportive role in DV replication. This study intended to clarify whether DV infection could induce autophagy in vivo. Furthermore, the effect of DV induced autophagy on viral replication and DV-related pathogenesis was investigated. RESULTS AND CONCLUSIONS: The physiopathological parameters were evaluated after DV2 was intracranially injected into 6-day-old ICR suckling mice. Autophagy-related markers were monitored by immunohistochemical/immunofluorescent staining and Western blotting. Double-membrane autophagic vesicles were investigated by transmission-electron-microscopy. DV non-structural-protein-1 (NS1) expression (indicating DV infection) was detected in the cerebrum, medulla and midbrain of the infected mice. In these infected tissues, increased LC3 puncta formation, LC3-II expression, double-membrane autophagosome-like vesicles (autophagosome), amphisome, and decreased p62 accumulation were observed, indicating that DV2 induces the autophagic progression in vivo. Amphisome formation was demonstrated by colocalization of DV2-NS1 protein or LC3 puncta and mannose-6-phosphate receptor (MPR, endosome marker) in DV2-infected brain tissues. We further manipulated DV-induced autophagy by the inducer rapamycin and the inhibitor 3-methyladenine (3MA), which accordingly promoted or suppressed the disease symptoms and virus load in the brain of the infected mice.We demonstrated that DV2 infection of the suckling mice induces autophagy, which plays a promoting role in DV replication and pathogenesis.

A microfluidic immunomagnetic bead-based system for the rapid detection of influenza infections: from purified virus particles to clinical specimens.

Seasonal and novel influenza infections have the potential to cause worldwide pandemics. In order to properly treat infected patients and to limit its spread, a rapid, accurate and automatic influenza diagnostic tool needs to be developed. This study therefore presents a new integrated microfluidic system for the rapid detection of influenza infections. It integrated a suction-type, pneumatic-driven microfluidic control module, a magnetic bead-based fluorescent immunoassay (FIA) and an end-point optical detection module. This new system can successfully distinguish between influenza A and B using a single chip test within 15 min automatically, which is faster than existing devices. By utilizing the micromixers to thoroughly wash out the sputum-like mucus, this microfluidic system could be used for the diagnosis of clinical specimens and reduced the required sample volume to 40 µL. Furthermore, the results of diagnostic assays from 86 patient specimens have demonstrated that this system has 84.8 % sensitivity and 75.0 % specificity. This developed system may provide a powerful platform for the fast screening of influenza infections.

Targeting NFKB by autophagy to polarize hepatoma-associated macrophage differentiation.

Tumor-associated macrophages (TAMs) have been linked to promoting tumor progression by stimulating angiogenesis, cell growth and inflammation. NFKB activity in TAMs may mediate inflammation-associated tumor formation. However, most isolated TAMs from established tumors express a M2 phenotype with less NFKB activation and show a strong immunosuppressive phenomenon. How tumors affect the dynamic of NFKB activity in TAMs, and hence maintain their pro-tumor M2 phenotype is still poorly understood. We recently found that hepatoma-derived toll-like receptor 2 (TLR2)-related ligands are capable of stimulating M2 macrophage differentiation via controlling NFKB RELA/p65 protein homeostasis by selective autophagy. TLR2 signal induces NFKB RELA cytosolic ubiquitination and leads to its degradation by SQSTM1/p62-mediated autophagy. Inhibition of autophagy will rescue NFKB activity and shape the phenotype of hepatoma-polarized M2 macrophages. This suggests that autophagy might play a role in manipulating TAM functions and tumor-associated immune responses. Our study also demonstrates that autophagy can directly control a transcriptional factor in addition to its regulatory molecules. This finding uncovers a new role of autophagy in controlling cellular functions.

Autoimmunity in dengue pathogenesis.

Dengue is one of the most important vector-borne viral diseases. With climate change and the convenience of travel, dengue is spreading beyond its usual tropical and subtropical boundaries. Infection with dengue virus (DENV) causes diseases ranging widely in severity, from self-limited dengue fever to life-threatening dengue hemorrhagic fever and dengue shock syndrome. Vascular leakage, thrombocytopenia, and hemorrhage are the major clinical manifestations associated with severe DENV infection, yet the mechanisms remain unclear. Besides the direct effects of the virus, immunopathogenesis is also involved in the development of dengue disease. Antibody-dependent enhancement increases the efficiency of virus infection and may suppress type I interferon-mediated antiviral responses. Aberrant activation of T cells and overproduction of soluble factors cause an increase in vascular permeability. DENV-induced autoantibodies against endothelial cells, platelets, and coagulatory molecules lead to their abnormal activation or dysfunction. Molecular mimicry between DENV proteins and host proteins may explain the cross-reactivity of DENV-induced autoantibodies. Although no licensed dengue vaccine is yet available, several vaccine candidates are under development. For the development of a safe and effective dengue vaccine, the immunopathogenic complications of dengue disease need to be considered.

Factors contributing to the disturbance of coagulation and fibrinolysis in dengue virus infection.

Hemorrhage is one of the hallmarks of dengue hemorrhagic fever. However, the mechanisms that cause hemorrhage are unclear. In this review we focus on the possible factors that may be involved in the disturbance of coagulation and fibrinolysis during dengue virus (DENV) infection. Factors such as autoantibodies and cytokines induced by DENV infection as well as hemostatic molecules expressed on DENV-infected cells, and DENV viral proteins may all contribute to the defect of hemostasis during DENV infection. It is the combination of these viral and host factors that may tilt the balance of coagulation and fibrinolysis toward bleeding in dengue patients.

The serotype-independent but concentration-dependent enhancing antibodies among Thai dengue patients.

Antibody-dependent enhancement of infection (ADE) is central to explaining the development of severe disease at the end of post-dengue virus infection. Non-neutralizing anti-dengue antibodies bound to the dengue virion enhances the virus entrance into the target cells via the Fc receptor. The titer of enhancing antibodies in dengue patients is not determined during dengue virus infection. Sensitive flow cytometry detecting dengue virus-infected K562 cells was used to quantitate enhancing activity among Thai DF and DHF patients against four serotypes and the patient's dengue isolate. The titer was defined as the reciprocal of the final dilution that loses enhancing activity. The serum of Thai patients confirmed to have dengue infection were found to have high titers of enhancing antibodies and increased gradually through the convalescent phase of infection. The enhancing antibody titers were not different among the four serotypes or from the infecting isolate. The anti-dengue antibodies from dengue patients can enhance dengue virus infections in a concentration-dependent, serotype-independent manner.

Cytokine immunopathogenesis of enterovirus 71 brain stem encephalitis.

Enterovirus 71 (EV71) is one of the most important causes of herpangina and hand, foot, and mouth disease. It can also cause severe complications of the central nervous system (CNS). Brain stem encephalitis with pulmonary edema is the severe complication that can lead to death. EV71 replicates in leukocytes, endothelial cells, and dendritic cells resulting in the production of immune and inflammatory mediators that shape innate and acquired immune responses and the complications of disease. Cytokines, as a part of innate immunity, favor the development of antiviral and Th1 immune responses. Cytokines and chemokines play an important role in the pathogenesis EV71 brain stem encephalitis. Both the CNS and the systemic inflammatory responses to infection play important, but distinctly different, roles in the pathogenesis of EV71 pulmonary edema. Administration of intravenous immunoglobulin and milrinone, a phosphodiesterase inhibitor, has been shown to modulate inflammation, to reduce sympathetic overactivity, and to improve survival in patients with EV71 autonomic nervous system dysregulation and pulmonary edema.

The regulatory T cells in anti-influenza antibody response post influenza vaccination.

The efficacy and effectiveness of influenza vaccines depend primarily on the vaccine recipient and the virus similarity to the endemic virus. Regulatory T cells (Tregs) and cytokines are known to restrict immune responses against viral infections. We conducted this study to explore the role of Tregs, cytokines, and antibody production after influenza vaccination. The whole blood was collected from healthy subjects (n = 36) before and two weeks after influenza vaccine immunization for two or three consecutive years. The cell surface markers, intracellular staining of Foxp3(+) Tregs, and Th1/Th2 cytokines were determined. The antibody titer was detected using the hemagglutination inhibition test. The CD3(+), CD127(+), CD4(+)CD25(+) and CD4(+)Foxp3(+) cells were increased significantly post vaccination. The plasma level of the transforming growth factor (TGF-ß), but not interleukin (IL)-2, IL-4, IL-5, IL-10, IFN-γ, TNF-α, was also found to increase significantly after vaccination. We further correlated the cytokine fold-increases with the anti-influenza antibody titer for individual post vaccination. It was found that the IL-10 level after vaccination correlated with the fold-increases of anti-H1N1, anti-H3N2, anti-B/Yamagata, and anti-B/Victoria antibodies. But, a negative relationship occurs between the TGF-ß level and fold-increases of anti-H1N1, anti-H3N2, anti-B/Yamagata, and anti-B/Victoria antibodies post vaccination. Treg cells and TGF-ß seem to participate in the downregulation of the anti-influenza antibody response post influenza vaccination. Alteration of Treg activity might enhance influenza vaccine antibody responses and efficacy.

TBK1-associated protein in endolysosomes (TAPE)/CC2D1A is a key regulator linking RIG-I-like receptors to antiviral immunity.

Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are key RNA viral sensors for triggering antiviral immunity. The underlying mechanisms for RLRs to trigger antiviral immunity have yet to be explored. Here we report the identification of TAPE (TBK1-associated protein in endolysosomes) as a novel regulator of the RLR pathways. TAPE functionally and physically interacts with RIG-I, MDA5, and IPS-1 to activate the IFN-ß promoter. TAPE knockdown impairs IFN-ß activation induced by RLRs but not IPS-1. TAPE-deficient cells are defective in cytokine production upon RLR ligand stimulation. During RNA virus infection, TAPE knockdown or deficiency diminishes cytokine production and antiviral responses. Our data demonstrate a critical role for TAPE in linking RLRs to antiviral immunity.

Macrophage migration inhibitory factor induces autophagy via reactive oxygen species generation.

Autophagy is an evolutionarily conserved catabolic process that maintains cellular homeostasis under stress conditions such as starvation and pathogen infection. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine that plays important roles in inflammation and tumorigenesis. Cytokines such as IL-1ß and TNF-α that are induced by MIF have been shown to be involved in the induction of autophagy. However, the actual role of MIF in autophagy remains unclear. Here, we have demonstrated that incubation of human hepatoma cell line HuH-7 cells with recombinant MIF (rMIF) induced reactive oxygen species (ROS) production and autophagy formation, including LC3-II expression, LC3 punctae formation, autophagic flux, and mitochondria membrane potential loss. The autophagy induced by rMIF was inhibited in the presence of MIF inhibitor, ISO-1 as well as ROS scavenger N-acetyl-L-cysteine (NAC). In addition, serum starvation-induced MIF release and autophagy of HuH-7 cells were partly blocked in the presence of NAC. Moreover, diminished MIF expression by shRNA transfection or inhibition of MIF by ISO-1 decreased serum starvation-induced autophagy of HuH-7 cells. Taken together, these data suggest that cell autophagy was induced by MIF under stress conditions such as inflammation and starvation through ROS generation.