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Complicated terrains, specific regions, and high wind turbulence intensity frequently trigger shutdown protection of wind turbines due to vibration beyond the designated limit, resulting in serious loss of power generation. This paper aims at reducing the frequency of shutdowns and improving operational stability of wind turbines. Operational characteristics of wind turbines under complicated conditions such as specific regions and strong turbulent wind were analyzed. A fuzzy control approach was proposed based on pertinent theory, to deal with complicated operating conditions at specific sites. This strategy incorporates a vibration recognition algorithm to classify vibration conditions and a fuzzy control algorithm for vibration suppression based on the categorized conditions. Compared with the conventional shutdown or sector-based control methods, the proposed fuzzy control strategy of vibration suppression eliminates the frequent starting and stopping of wind turbines, thus ensuring power generation and improving operational stability. Furthermore, a simulation analysis was performed using Bladed software, taking 3.x MW wind turbines as the research object. Subsequent experimental verification was carried out at a wind farm. In the experiment, the application of the fuzzy vibration suppression control method effectively led to the quick ride-through of the wind turbine amid the complicated operating conditions including the specific region and strong turbulent wind. A 23.87% reduction in the maximum RMS of the front and rear accelerations of the nacelle demonstrated a substantial enhancement in the wind turbine reliability.

With the substantial increase of the installed capacity of wind power, it has brought great challenges to grid stability and safety. In order to improve the grid stability and the anti-interference ability of grid frequency, wind farms urgently need to have frequency regulation function and increase frequency response speed. According to the latest technical requirements such as starting time and adjustment time of grid, this paper analyzes the current mainstream frequency regulation schemes in the market. A frequency regulation scheme combining energy management platform and frequency regulation equipment is proposed, so that the wind turbine receives instructions from the energy management platform and frequency regulation equipment at the same time, and adopts different control strategies for inertia response and primary frequency regulation to adjust the active power of the wind farm to ensure the response speed and stability during frequency regulation.The scheme has been tested for inertia response and primary frequency modulation in a wind farm in Yunnan province. In the test results, the response time of inertia response is less than 1 sec, the control deviation is within ±1% of rated capacity, the starting time of primary frequency modulation is less than 2 sec, the response time is less than 5 sec, the adjustment time is less than 8 sec, and the control deviation of primary frequency regulation is within ±1% of rated capacity. All the technical indexes meet the requirements of Yunnan Grid.

Objective To explore the effect and mechanism of metformin(Metf) on side population(SP) cells of human esophageal squamous cell carcinoma. Methods We detected SP ratio of different esophageal squamous cell lines and sorted of SP cells by flow cytometry. The effects of metformin on the proliferation of SP cells in vitro were detected by CCK-8 method, plate cloning and sphere assay. The effect of Metf on the expression of SP cell-associated gene protein was detected by Western blot. Results The SP ratio of the nine esophageal squamous carcinoma cell lines in this experiment was 0.2%-2%. Metf could reduce the SP ratio of KYSE 150, significantly inhibiting the cell proliferation, the number of clones and the number of spheres of SP cells. The degree of inhibition was positively correlated with Metf concentration and administration time. The difference is statistically significant (P < 0.01). In addition, Metf reduced the expression of the relevant stem genes SOX2 and OCT4 in SP cells to varying degrees. Conclusion Metf could reduce the ratio of SP cells in esophageal squamous cell carcinoma, which may provide a new approach for the treatment and prevention of esophageal cancer.

Ferroptosis is a recently discovered mode of cell death that inhibits tumor growth. Single-cell RNA sequencing (scRNA-seq) is a powerful tool for analyzing tumor heterogeneity and the immune microenvironment at the single-cell level. We used CIBERSORT to identify cellular immune scores and found that monocytes had significantly infiltrated and were correlated with prognosis in cholangiocarcinoma. scRNA-seq data were extracted from the Gene Expression Omnibus database, and the FindCluster() package was used for cell cluster analysis, which obtained 21 cell clusters, and there was increased TNFSF13B-TFRC intercellular communication between monocytes and cholangiocytes. A weighted correlation network analysis was performed with the WGCNA package to obtain monocyte-related gene modules. Univariate and multivariate Cox analyses were then performed to further establish the signature, and the reliability of the signature was assessed by receiver operating characteristic curve and decision curve analysis. A nomogram signature based on the Kaplan-Meier survival analysis was established. We found that the communication between monocytes and malignant cells in cholangiocarcinoma may be a regulatory factor of ferroptosis in cancer cells. The prognostic stratification system of the three-gene signature related to monocytes and ferroptosis can accurately assess the prognostic risk for cholangiocarcinoma., Competing Interests: The authors declare no competing interests., (© 2022 The Author(s).)

Chromosome 2 open reading frame 40 (C2ORF40) plays a significant role in numerous processes, including cell differentiation, senescence, apoptosis, inflammation and neuroendocrine hormone regulation. Moreover, C2ORF40 is a candidate tumor suppressor gene in a variety of tumors, and is closely associated with prognosis. Bioinformatics analysis has indicated that pro-C2ORF40 is a secreted protein with a signal peptide. Secreted C2ORF40 protein (sC2ORF40) exists in cancer cell medium. However, thus far, the exact biological function of sC2ORF40 in carcinogenesis has not been thoroughly researched. In the present study, the signal peptide sequence of the C2ORF40 complementary DNA was initially cut off to produce secreted recombinant human C2ORF40 protein (rhC2ORF40). The soluble rhC2ORF40 was expressed, purified and examined for tumor-suppressing function for the first time. The results revealed that the soluble purified rhC2ORF40 protein was concentrated with a purity of >95%. Furthermore, the rhC2ORF40 inhibited esophageal cancer cell proliferation in vitro (P<0.05) and caused cell cycle G 1 phase block, as determined by flow cytometric analysis (P<0.05). Overall, the soluble rhC2ORF40 protein with high purity and biological activity was obtained, which suppressed esophageal cancer cells proliferation by inducing cell cycle G 1 phase block in vitro . Therefore, the soluble rhC2ORF40 protein could be potential biological therapy drug for esophageal carcinoma.

Objective: To compare the transcriptome of esophageal cancer cells (EC9706), human mesenchymal stem cells (MSCs), and after fusion of esophageal cancer cells with MSCs, and to further study their different expression profiles and the changes of their signaling pathways., Methods: We examined the gene expression profiles of these cells with transcriptome microarray using LIMMA package and several web-based applications, such as DAVID, ToppGene and MSigDB. The resulting sets of differentially expressed genes (DEGs) were comprehensively analyzed to identify the pathways and their changes after the cell fusion., Results: A total of 4 548 significantly DEGs among the three cell lines were found by LIMMA. Three functional annotation web tools predicted that DNA damage repair, cell cycle arrest and apoptosis pathways were enriched. Total DEGs were mapped to the canonic pathways with KEGGanim which depicted that the core genes of DNA damage repair, cell cycle arrest and pro-apoptosis were up-regulated in fusion cells, and they mightbe combined to respond the fusion-induced damage stress. The up-regulation of suppressive factor DUSP6 might feedback inhibit the MAPK signaling pathway in the fusion cells, too., Conclusions: Transcriptome analysis suggests that hMSCs and EC9706 cell fusion may inhibit growth of EC cells by induction of pro-apoptotic signaling and DUSP6 negative feedback inhibition mechanism. In addition, the changes of immune regulation-related and differentiation-related genes indicate that the fusion cells inherited certain immune-suppressive function from the stem cells.

Prior studies on the biology and therapeutic application of human stem cells in human malignancies have reported mixed results. Some evidence shows the use of stem cell transplantation is an important tool in the treatment of several hematologic and non-hematologic malignancies while some others suggest both human stem cells and mature stromal cells can contribute to the development and growth of human malignancies. Aiming to provide more evidence on this controversial issue, we investigated the effect of cell fusion of mesenchymal stem cells with esophageal carcinoma cells on tumorigenesis. Results suggest that artificial fusion of human umbilical cord mesenchymal stem cells with esophageal carcinoma cells resulted in hybrids with declined cell growth, increased apoptosis and suppressed tumorigenicity. The comparison of gene expression profiles of human mesenchymal stem cells, esophageal carcinoma cells and hybrids indicated that fusion induced activation of apoptosis. Furthermore, the expression of DUSP6/MKP3 in MAPK pathway increased strikingly and the exogenous overexpression confirmed the growth suppression. Our results demonstrate fusion of human mesenchymal stem cells with esophageal carcinoma cells induced apoptosis and benign transdifferentiation rather than reprogramming to cancer stem cells.