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The dried bark of Ailanthus altissima (Mill.) Swingle (BAA), commonly designated as "Chunpi" in Chinese, is extensively used as a common traditional medicine in China, Korea, and India. It has been used to treat multiple ailments, including asthma, epilepsy, spermatorrhea, bleeding, and ophthalmic diseases, for thousands of years.<br />To present a comprehensive and constructive review on the phytochemistry, pharmacology, pharmacokinetics, traditional uses, quality control, and toxicology of BAA; to aid the assessment of the therapeutic potential of BAA; to guide researchers working on the development of novel therapeutic agents.<br />Information related to BAA (from 1960 to 2020) was retrieved from a wide variety of electronic databases, such as PubMed, Web of Science, China Knowledge Resource Integrated Database, ScienceDirect, SciFinder, and Google Scholar. Additional information and materials were acquired from Chinese Medicine Monographs, the 2020 edition of the Chinese Pharmacopoeia, and several web sourcesrointestinal inflammation. These studies present a wide range of perspectives for the development of new drugs related to BAA. However, only a few traditional uses are associated with the reported pharmacological activities of BAA and have been confirmed by preclinical and clinical studies. Moreover, the pharmacokinetics, toxicology, and quality control of BAA should be considered indispensable research topics.<br />Modern pharmacological studies have revealed that BAA, as a valuable medicinal resource, possesses the potential to treat a wide variety of ailments, especially, cancer and gastrointestinal inflammation. These studies present a wide range of perspectives for the development of new drugs related to BAA. However, only a few traditional uses are associated with the reported pharmacological activities of BAA and have been confirmed by preclinical and clinical studies. Moreover, the pharmacokinetics, toxicology, and quality control of BAA should be considered indispensable research topics.<br />WeiChang'An Pill (WCAP) is used in Traditional Chinese Medicine (TCM) to clinically treat diarrhoea-predominant irritable bowel syndrome (IBS-D); however, the underlying pharmacological mechanisms are unclear to date.<br />To explore the mechanism underlying the therapeutic action of WCAP in IBS-D using a network pharmacology approach and in vivo experiments.<br />The active compounds of WCAP were selected from the TCM Systems Pharmacology Database and TCM Integrated Database, and the potential targets were identified using the Swiss Target Prediction and Similarity Ensemble Approach (SEA) databases. The targets related to IBS-D were mined from the Therapeutic Target Database (TTD), National Center for Biotechnology Information Search database (NCBI), DrugBank database, and DisGeNET database. The intersecting protein-protein interactions (PPIs) of the drug-disease crossover genes were analysed, and the central PPI network was constructed using the String database, version 11.0, and Cytoscape version 3.7.2. Follownt pathways. Subsequent molecular biology experiments revealed that the expression levels of cAMP, phospho-(Ser/Thr) protein kinase A substrates (p-PKA), 5-hydroxytryptamine, and proteins in the cAMP signalling pathway, including G protein-coupled receptor (GPCR), adenylyl cyclase 5 (AC5), and cAMP-response element binding protein (CREB), were significantly upregulated in rat models of IBS-D following treatment with WCAP (P&lt;0.05). However, a reverse trend was observed in the expression of nuclear factor kappa-B (NF-κB) (P&lt;0.05), which could be attributed to the low-grade inflammation that occurs in IBS-D.<br />We demonstrated that WCAP may alleviate the symptoms of diarrhoea and visceral sensitivity in IBS-D by regulating the cAMP signalling pathway.<br />We demonstrated that WCAP may alleviate the symptoms of diarrhoea and visceral sensitivity in IBS-D by regulating the cAMP signalling pathway.The mechanism that mediates the interaction between the contractile ring and the plasma membrane during cytokinesis remains elusive. We previously found that ERM (Ezrin/Radixin/Moesin) proteins, which usually mediate cellular pole contraction, become over-accumulated at the cell equator and support furrow ingression upon the loss of other actin-membrane associated proteins, anillin and supervillin. In this study, we addressed the molecular basis of the exchangeability between ezrin and other actin-membrane associated proteins in mediating cortical contraction during cytokinesis. We found that depletion of anillin and supervillin caused over-accumulation of the membrane-associated FERM domain and actin-binding C-terminal domain (C-term) of ezrin at the cleavage furrow, respectively. This finding suggests that ezrin differentially shares its binding sites with these proteins on the actin cytoskeleton or inner membrane surface. Using chimeric mutants, we found that ezrin C-term, but not the FERM domain, can substitute for the corresponding anillin domains in cytokinesis and cell proliferation. On the other hand, either the membrane-associated or the actin/myosin-binding domains of anillin could not substitute for the corresponding ezrin domains in controlling cortical blebbing at the cell poles. Our results highlight specific designs of actin- or membrane-associated moieties of different actin-membrane associated proteins with limited exchangeability, which enables them to support diverse cortical activities on the shared actin-membrane interface during cytokinesis.Inadequate trophoblast proliferation, shallow invasion and exaggerated rate of trophoblast apoptosis are implicated in early recurrent miscarriage (ERM). However, the mechanistic bases of this association have not been fully established. We aimed at investigating the involvement of fascin, an actin-bundling protein, in trophoblast activities and ERM. We found that fascin was downregulated in the cytotrophoblasts (CTBs) and distal cytotrophoblasts (DCTs) of ERM placentae. Knockdown of fascin altered cellular and nucleolar morphology, and inhibited the proliferation but increased apoptosis of trophoblastic HTR8/SVneo cells. Furthermore, fascin knockdown decreased the expression of transcription factors such as Snail1/2, Twist and Zeb1/2, mesenchymal molecules such as Vimentin and N-cadherin, and the protein expression of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphorylates signal transducer and activator of transcript 3 (STAT3). [https://www.selleckchem.com/products/BafilomycinA1.html Selleckchem Bafilomycin A1] Exposure of HTR-8/SVneo cells to hypoxia reoxygenation (H/R) decreased fascin expression to affect the cells' invasion.