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MicroRNAs (miRNAs) are small noncoding RNAs (ncRNAs) that play their roles in the regulation of physiological and pathological processes. Originally, it was assumed that miRNAs only modulate gene expression posttranscriptionally in the cytoplasm by inducing target mRNA degradation. However, with further research, evidence shows that mature miRNAs also exist in the cell nucleus, where they can impact gene transcription and ncRNA maturation in several ways. This review provides an overview of novel models of nuclear miRNA functions. Some of the models remain to be verified by experimental evidence, and more details of the miRNA regulation network remain to be discovered in the future.

Purpose: The crosstalk between hepatocellular carcinoma (HCC) cells and hepatic stellate cells (HSCs) is one of the important mechanisms of liver cancer metastasis. The relationship between liver cancer metastasis and glycolysis has been extensively studied recently. However, the role of von Willebrand factor (vWF) mediated glycolysis mechanism in liver cancer metastasis is currently unknown. Methods: Western blot was used to verify the expression of vWF in HCC cells. PAS staining, glycogen and L-lactate content assays were used to reflect cellular glycolysis levels. The ability of cell migration was explored by Wound-healing and Transwell assays. Besides, the effect of vWF on the progression of HCC in vivo was also studied using subcutaneous xenograft model. Results: vWF derived from HCC cells promoted tumor migration by mediating glycolysis. Besides, vWF participated in the crosstalk between HCC cells and HSCs. HCC cells activated HSCs through vWF-mediated TGFB1 expression and secretion, and activated HSCs upregulated vWF expression in HCC cells through IL-6 secretion feedback. Further, in vitro and in vivo experiments also confirmed the importance of the JAK1/vWF/TGFB1 axis in regulating HSCs-derived IL-6 mediated HCC migration and growth. Conclusion: In summary, this article demonstrated that IL-6 released from hepatic stellate cells enhanced glycolysis and migration ability of liver cancer cells by activating JAK1/vWF/TGFB1 axis which may also be a potential target for inhibiting liver cancer metastasis. [ABSTRACT FROM AUTHOR]

This study explores the efficiency of using carbon dioxide (CO2) to extract shale gas, highlighting its potential to enhance extraction while mitigating environmental CO2 pollution. Given the intricate microstructure of shale, CO2 injection inevitably induces deformation within the shale reservoir's internal microstructure, thereby impacting gas displacement efficiency. The organic matter (kerogen) network and fracture network in shale, serving as primary spaces for gas adsorption and migration, exhibit complex microstructural characteristics. Thus, we developed a dynamic coupled hydro-mechanics permeability model for binary gas displacement, and three novel, interdisciplinary fractal power-law parameters are proposed to represent the distribution of shale fractures, considering the adsorption–desorption strength of the kerogen network. Numerical simulations analyzed the changes in gas seepage, diffusion, shale stress, permeability, and factors influencing displacement efficiency during the CO2–EGR (enhanced gas recovery) projects. Key findings include (1) CO2 injection leads to a nonlinear increase in the number of shale fracture networks, thereby enhancing the CH4 output efficiency. (2) Compared to traditional fractal theory, the proposed power-law model is applicable to a wider range of reservoir fracture distributions and effectively characterizes the density (by α), size (by r), and complexity (by n) of the fracture network during the CO2–EGR process. (3) Changes in the proposed interdisciplinary power-law parameters significantly alter CO2 and CH4 adsorption capacities and, in turn, significantly affects displacement efficiency and shale deformation. According to calculations, these parameters have the greatest impact on the CO2–EGR process, ranging from 16.3% to 68.1%. [ABSTRACT FROM AUTHOR]

The formation and evolution of the foreland basin in the south of the Dabie Orogen are both closely related to the uplift of the orogenic belt. However, the Late Triassic paleoenvironment and the provenance of the sediments in the foreland basin remain controversial. Nine samples from the Upper Triassic Puqi Group of the foreland basin were analysed for whole‐rock major and trace elements and three sandstone samples were selected for zircon dating by U–Pb laser ablation inductively coupled plasma mass spectrometry. The concentrations of some major (e.g., CaO and Na2O) and trace (e.g., Rb, Sr and Ba) elements varied over a large range and showed different degrees of depletion. A series of major and trace element indicators, as well as the patterns of the rare earth elements, suggested derivation from felsic igneous rocks. The Late Triassic experienced fluctuations between cold warm climates, as indicated by the chemical weathering index ranging from 51.33 to 88.65. The CaO/(FeO + CaO), Rb/Sr and Ba/K ratios indicated that the paleosalinity changed from high to low. The Fe2O3/FeO, U/Th, V/Cr and Ni/Co ratios indicated an oxidizing sedimentary environment. The cathodoluminescence images, Th/U ratios and rare earth elements patterns of the detrital zircons all indicated a magmatic origin. Three samples showed significant peak ages of 224, 440, 748, 1870 and 2492 Ma, corresponding to the development of the Dabie Orogen. Our comprehensive analyses suggest that the Upper Triassic Puqi Group was formed by deposition during continental–continental collision. The Dabie Orogen was exhumed in the Late Triassic and supplied detrital sediments to the foreland basin. [ABSTRACT FROM AUTHOR]

The therapeutic effects of pharmaceuticals depend on their drug concentrations in the cochlea. Efficient drug delivery from the systemic circulation into the inner ear is limited by the blood‐labyrinth‐barrier (BLB). This study investigated a novel noninvasive sound conditioning (SC) strategy (90 dB SPL, 8–16 kHz, 2 h sound exposure) to temporally enhance BLB permeability in a controllable way, contributing to maximizing the penetration of pharmaceuticals from blood circulation into the cochlea. Trafficking of Fluorescein Isothiocyanate conjugated dextran and bovine serum albumin (FITC‐dextran and FITC‐BSA) demonstrated that paracellular leakage of BLB sustained for 6 h after SC, providing a controllable time window for systemic administration. Cochlear concentrations of dexamethasone (DEX) and dexamethasone phosphate (DEX‐P), respectively transported by transcellular and paracellular pathways, showed a higher content of the latter one after SC, further confirming the key role of paracellular pathway in the SC‐induced hyperpermeability. Results of high‐throughput RNA‐sequencing identified a series of tight junction (TJ)‐associated genes after SC. The expressions of TJ (ZO‐1) were reduced and irregular rearrangements of the junction were observed by transmission electron microscopy after SC. We further determined the inhibiting role of Rab13 in the recruitment of ZO‐1 and later in the regulation of cellular permeability. Meanwhile, no significant change in the quantifications of endothelial caveolae vesicles after SC indicated that cellular transcytosis accounted little for the temporary hyperpermeability after SC. Based on these results, SC enhances the BLB permeability within 6 h and allows systemically applied drugs which tend to be transported by paracellular pathway to readily enter the inner ear, contributing to guiding the clinical medications on hearing loss. [ABSTRACT FROM AUTHOR]