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Cholangiocarcinoma (CCA) has accounted for a high rate of mortality and morbidity in the recent years. Long non-coding RNAs (lncRNAs) play an important role in different cellular environments, including cancer. As such, they have been used as potential targets during CCA therapy. The objective of this study was to investigate the effects of lncRNA PVT1 on CCA and its mechanisms behind lncRNA PVT1 regulation. The interactions among SOX2, lncRNA PVT1, miR-186 and SEMA4D were verified by chromatin immunoprecipitation, RNA immunoprecipitation and dual luciferase reporter gene assay. Gain- and loss-of-function experiments were conducted to explore the modulatory effects of SOX2, lncRNA PVT1, miR-186 and SEMA4D on cell viability, migration and invasion of CCA by CCK-8 and Transwell assays. In vivo effects of lncRNA PVT1 or SEMA4D were studied in a nude mouse model. MiR-186 was poorly expressed while SOX2, lncRNA PVT1 and SEMA4D were highly expressed in CCA cells. SOX2 induced the transcriptional activation of lncRNA PVT1 expression to promote proliferation, migration and invasion of CCA cells. LncRNA PVT1 bound to miR-186 and miR-186 was found to target SEMA4D. Sapanisertib The overexpression of lncRNA PVT1 and SEMA4D, as well as the inhibition of miR-186 led to elevated CCA cell proliferation, migration and invasion. In vivo experiments confirmed the inhibitory role of lncRNA PVT1 knockdown or SEMA4D knockdown in CCA. All in all, SOX2 down-regulated miR-186 through the transcriptional activation of lncRNA PVT1, whereas elevating SEMA4D expression, thus promoting the progression of CCA. Cardiac fibrosis after myocardial infarction (MI) is a major cause of heart deterioration. Recently, the roles of microRNAs (miRNAs) in various cardiovascular diseases associated with cardiac fibrosis have been extensively investigated. The present study aimed to investigate the role and mechanism of miR-29b-3p in cardiac fibrosis after MI. miR-29b-3p expression in TGF-β1-activated cardiac fibroblasts (CFs) was detected by qRT-PCR. Cell Counting Kit-8 (CCK-8) and Trans-well assays were performed to evaluate CFs proliferation and migration ability, respectively. Protein expressions of α-SMA, collagen I, collagen III, MMP2, and MMP9 were examined by Western blot assay. Bioinformatics, luciferase, and RNA immunoprecipitation (RIP) assays were carried out to determine whether FOS was targeted by miR-29b-3p. TGF-β1 treatment dose-dependently curbed miR-29b-3p expression in CFs. miR-29b-3p restrained the promotive impacts of TGF-β1 on CFs proliferation, migration, and differentiation. FOS was affirmed to be a target of miR-29b-3p, elevated expression of FOS reversed the inhibitory effects of miR-29b-3p on cell proliferation, migration, and differentiation in TGF-β1-activated CFs. miR-29b-3p degraded the pro-fibrosis effect induced by TGF-β1 via targeting FOS, providing a prospective therapeutic avenue for cardiac fibrosis after MI. miR-29b-3p degraded the pro-fibrosis effect induced by TGF-β1 via targeting FOS, providing a prospective therapeutic avenue for cardiac fibrosis after MI.Inflammatory bowel diseases (IBDs) are highly heterogeneous in disease phenotype, behavior, and response to therapy. Diagnostic and therapeutic decisions in IBD are based primarily on clinical and endoscopic severity and histopathologic analysis of intestinal biopsies. With this approach, however, only a minority of patients experience durable remission. This may be due to substantial heterogeneity in disease pathogenicity that is not accounted for by current classification systems. Patients can present with similar clinical and endoscopic severity and receive similar therapy but show divergent response ranging from mucosal/transmural healing to nonresponse. Using mucosal biopsy samples that are already obtained as part of the clinical practice to support the diagnosis and state-of-the-art high throughput sequencing approaches can detect the widest range in host gene expression in the actual lining of the affected gut. These analyses can better dissect disease heterogeneity and guide potential treatment response. Here we review studies that use gut tissue-based gene expression profiles to predict disease outcome in IBD.Chronic obstructive pulmonary disease (COPD) is a type of respiratory disease. The dysregulation of long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) has been reported in diverse diseases. This study aimed to explore the functions and mechanism of TUG1 in COPD. The levels of TUG1 and BRD4 were significantly up-regulated, and the level of miR-34c was apparently down-regulated in COPD patients or CSE-treated BEAS-2B cells. TUG1 was verified to sponge to miR-34c, and BRD4 was validated as a target of miR-34c. TUG1 depletion or miR-34c overexpression promoted cell proliferation but restrained apoptosis, inflammatory response in CSE-treated BEAS-2B cells. MiR-34c inhibitor mitigated the inhibitory effect on cell proliferation and the promotion effects on cell apoptosis, inflammatory response in CSE-treated BEAS-2B cells induced by TUG1 silencing. Mechanistically, TUG1 modulated BRD4 expression in CSE-treated BEAS-2B cells by sponging miR-34c. TUG1 modulated BRD4 to regulate cell proliferation, cell apoptosis and inflammatory response in CSE-treated BEAS-2B cells by sponging miR-34c. Plants depend fundamentally on establishment from seed. However, protocols in trait-based ecology currently estimate seed size but not seed number. This can be rectified. For annuals, seed number should simply be a positive function of vegetative biomass and a negative function of seed size. Using published values of comparative seed number as the 'gold standard' and a large functional database, comparative seed yield and number per plant and per m2 were predicted by multiple regression. Subsequently, ecological variation in each was explored for English and Spanish habitats, newly calculated C-S-R strategies and changed abundance in the British flora. As predicted, comparative seed mass yield per plant was consistently a positive function of plant size and competitive ability, and largely independent of seed size. Regressions estimating comparative seed number included, additionally, seed size as a negative function. Relationships differed numerically between regions, habitats and C-S-R strategies. Moreover, some species differed in life history over their geographical range.