11 research outputs found

    Three-Dimensional Stochastic Distribution Characteristics of Void Fraction in Longwall Mining-Disturbed Overburden of Inclined Coal Seam

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    AbstractFractures in the overburden induced by mining disturbances provide a channel for fluid flow between the surface and the underground. Mining-induced strata movement and fracture distribution are influenced by the gravity and dip angles of rock seams. In this paper, a new three-dimensional theoretical distribution model for void fraction in each partition of overlying rock strata disturbed by inclined coal seam mining was constructed. Based on the theoretical determination model, the three-dimensional random distribution characteristics for void fraction were obtained by combining the random distribution law of void fraction obtained by similar physical simulation experiments and image processing techniques. Theoretical deterministic models, stochastic theoretical models, and similar physical simulations all show that void fraction distribution in the tendency direction of the coal seam shows a bimodal asymmetric distribution with high and low peaks and a symmetric distribution in the strike direction. The void fraction of the overburden in the central part of the mining area is smaller than that of the surrounding area. The results of the theoretically determined model and stochastic model of the void fraction for the strata with different mining lengths and different coal seam inclinations were compared with the results of similar simulation experiments, respectively. The results are in agreement, further verifying the practicality of the model

    The molecular mechanism for inhibiting the growth of nasopharyngeal carcinoma cells using polymethoxyflavonoids purified from pericarp of Citrus reticulata ‘Chachi’ via HSCCC

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    Polymethoxyflavonoids (PMFs), the main bioactive compounds naturally occurring in the pericarp of Citrus reticulata ‘Chachi’ (CRCP), possess significant antitumor action. However, the action of PMFs in nasopharyngeal carcinoma (NPC) is currently unknown. The present research study was conducted to investigate the inhibitory mechanisms of PMFs from CRCP on NPC growth in vivo and in vitro. In our research, we used high-speed counter-current chromatography (HSCCC) to separate four PMFs (nobiletin (NOB), 3,5,6,7,8,3′,4′-heptamethoxyflavone (HMF), tangeretin (TGN), and 5-hydroxy-6,7,8,3′,4′-pentamethoxyflavone (5-HPMF)) from CRCP. CCK-8 assay was used to preliminarily screen cell viability following exposure to the four PMFs. Colony formation, Hoechst-33258 staining, transwell, and wound scratch assays were performed to assess the anti-proliferation, invasion, migration, and apoptosis-inducing effects of HMF on NPC cells. NPC tumors in xenograft tumor transplantation experiments were also established to explore the effect of HMF (100 and 150 mg/kg/day) on NPC. The histopathological changes in the treated rats were observed by H&E staining and Ki-67 detection by immunohistochemical techniques. The expressions of P70S6K, p-P70S6K, S6, p-S6, COX-2, p53, and p-p53 were measured by Western blot. The four PMFs were obtained with high purity (>95.0%). The results of the preliminary screening by CCK-8 assay suggested that HMF had the strongest inhibitory effect on NPC cell growth. The results of the colony formation, Hoechst-33258 staining, transwell, and wound scratch assays indicated that HMF had significant anti-proliferation, invasion, migration, and apoptosis-inducing ability in NPC cells. Moreover, HMF suppressed NPC tumor growth in xenograft tumor transplantation experiments. Further investigation suggested that HMF regulated NPC cells proliferation, apoptosis, migration, and invasion by activating AMPK-dependent signaling pathways. In conclusion, HMF-induced AMPK activation inhibited NPC cell growth, invasion, and metastatic potency by downregulating the activation of the mTOR signaling pathway and COX-2 protein levels, as well as enhancing the p53 phosphorylation level. Our study provides a crucial experimental basis for the clinical treatment of NPC, as well as the development and utilization of PMFs from CRCP

    Numerical study on thermal-hydro coupling characteristics of underground coal combustion under heterogeneous void fraction

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    Coal seam mining will lead to the movement and fissures of the overlying strata, which makes a complex void condition between the mining area and the ground surface. The void condition plays a key role in the occurrence and expansion of underground coal fires. In this study, the void rate model and the coupled thermal-hydro model of the underground coal fire were constructed. The COMSOL Multiphysics was used to study the coupling law of the temperature field and gas flow field of coal seam spontaneous combustion. By setting different oxygen content and inlet gas velocity, the influence of the external environmental parameters on the expansion law of underground coal fire is analyzed. The results show that the void characteristics of the mining area and the overlying strata have an obvious influence on the expansion of underground coal fire, and there is also a two-way coupling effect of the temperature field and gas flow field. The analyses of the influencing parameters show that reducing the oxygen content or increasing the inlet gas velocity will have a certain inhibitory effect on the expansion of underground coal fires, which can reduce the risk of spontaneous combustion

    Colorimetric Visualization of Glucose at the Submicromole Level in Serum by a Homogenous Silver Nanoprism–Glucose Oxidase System

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    In this study, we design a homogeneous system consisting of Ag nanoprisms and glucose oxidase (GOx) for simple, sensitive, and low-cost colorimetric sensing of glucose in serum. The unmodified Ag nanoprisms and GOx are first mixed with each other. Glucose is then added in the homogeneous mixture. Finally, the nanoplates are etched from triangle to round by H<sub>2</sub>O<sub>2</sub> produced by the enzymatic oxidation, which leads to a more than 120 nm blue shift of the surface plasmon resonance (SPR) absorption band of the Ag nanoplates. This large wavelength shift can be used not only for visual detection (from blue to mauve) of glucose by naked eyes but for reliable and convenient glucose quantification in the range from 2.0 × 10<sup>–7</sup> to 1.0 × 10<sup>–4</sup> M. The detection limit is as low as 2.0 × 10<sup>–7</sup> M, because the used Ag nanoprisms possess (1) highly reactive edges/tips and (2) strongly tip sharpness and aspect ratio dependent SPR absorption. Owing to ultrahigh sensitivity, only 10–20 μL of serum is enough for a one-time determination. The proposed glucose sensor has great potential in the applications of point-of-care diagnostics, especially for third-world countries where high-tech diagnostics aids are inaccessible to the bulk of the population

    SEC23A confers ER stress resistance in gastric cancer by forming the ER stress-SEC23A-autophagy negative feedback loop

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    Abstract Background Sec23 homolog A (SEC23A), a core component of coat protein complex II (COPII), has been reported to be involved in several cancers. However, the role of SEC23A in gastric cancer remains unclear. Methods The expression of SEC23A in gastric cancer was analyzed by using qRT-PCR, western blotting and IHC staining. The role of SEC23A in ER stress resistance was explored by functional experiments in vitro and vivo. The occupation of STAT3 on the SEC23A promoter region was verified by luciferase reporter plasmids and CHIP assay. The interaction between SEC23A and ANXA2 was identified by Co-IP and mass spectrometry analysis. Results We demonstrated that SEC23A was upregulated in gastric cancer and predicted poor prognosis in patients with gastric cancer. Mechanistically, SEC23A was transcriptional upregulated by ER stress-induced pY705-STAT3. Highly expressed SEC23A promoted autophagy by regulating the cellular localization of ANXA2. The SEC23A-ANXA2-autophay axis, in turn, protected gastric cancer cells from ER stress-induced apoptosis. Furthermore, we identified SEC23A attenuated 5-FU therapeutic effectiveness in gastric cancer cells through autophagy-mediated ER stress relief. Conclusion We reveal an ER stress-SEC23A-autophagy negative feedback loop that enhances the ability of gastric cancer cells to resist the adverse survival environments. These results identify SEC23A as a promising molecular target for potential therapeutic intervention and prognostic prediction in patients with gastric cancer

    Cancer associated fibroblasts-derived SULF1 promotes gastric cancer metastasis and CDDP resistance through the TGFBR3-mediated TGF-β signaling pathway

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    Abstract SULF1 has been implicated in a number of malignancies. The function of SULF1 in gastric cancer is disputed. The objective of this study was to examine the role and underlying molecular mechanisms of SULF1 in the context of gastric cancer. We found that the expression of SULF1 was increased in gastric cancer, especially in cancer-associated fibroblasts. The overexpression of SULF1 was found to be significantly correlated with unfavorable prognosis among individuals diagnosed with gastric cancer. Functionally, cancer-associated fibroblasts-derived SULF1 served as a oncogenic molecule which facilitated gastric cancer cells metastasis and CDDP resistance. Mechanistically, SULF1 regulated the communication between gastric cancer cells and cancer-associated fibroblasts in tumor microenvironment as a signaling molecule. Cancer-associated fibroblasts-secreted SULF1 interfered with the interaction between TGF-β1 and TGFBR3 by combining with TGFBR3 on gastric cancer cell membrane, subsequently activated TGF-β signaling pathway. In conclusion, our findings have presented novel approaches for potential treatment and prognosis prediction in individuals diagnosed with gastric cancer through the targeting of the CAFs-SULF1-TGFBR3-TGF-β1 signaling axis

    Structural setting of the Narusongduo Pb-Zn ore deposit in the Gangdese belt, central Tibet

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    The Narusongduo Pb-Zn deposit is located at the northern boundary of the Luobadui-Milashan fault zone (LMF) in central Tibet and is spatially associated with the Linzizong volcanic succession (LVS). Our study indicates that the regional structural setting was formed by two-stage tectonic events. The first stage, spanning from the late Mesozoic to early Paleocene, is characterized by significant N-S crustal shortening associated with the Cordilleran-type orogeny along the Gangdese arc. The region's Paleozoic-Mesozoic metasedimentary rocks were penetratively strained. Locally deformation was largely partitioned along the LMF. During the second stage (ca. 66-55 Ma), the area was affected by extensive multi-stage Linzizong volcanism, including caldera formation, as well as a coaxial N-S propagative deformation with a distinctive lower shortening rate. We recognized two types of mineralization, both were formed during the second stage. The first type of mineralization (orebody III) is governed by fractures within the extensively deformed Paleozoic carbonate rocks at the LMF's footwall. The overlying LVS, however, includes discrete but numerous mineralized sections. The terminal splays of the ore shoots typify the products of hydraulic fracturing. We propose that the propagative compressive deformation drained fluid reservoirs at depth to higher levels via the "Fault valve" effect. Episodic fluid influxes and mineral deposition formed the time-integrated mineralization. The second type of mineralization (orebody I) is hosted in the LVS in a number of breccia pipes and dykes that were controlled by the structural weaknesses generated by the intersection of the radial and ring fractures. Mineralization occurs as veinlets in the matrix and clasts inside the breccias, which are characterized by multi-stage brittle cracking, fluid injection and mineral precipitation. It is interpreted that the multi-stage magmatism (ca. 66-55 Ma) triggered repeated hydrothermal activities and incremental mineralization within the ore-bearing breccia bodies

    ACLY promotes gastric tumorigenesis and accelerates peritoneal metastasis of gastric cancer regulated by HIF-1A

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    Mounting evidence indicates the potential involvement of ATP-citrate lyase (ACLY) in the modulation of various cancer types. Nevertheless, the precise biological significance of ACLY in gastric cancer (GC) remains elusive. This study sought to elucidate the biological function of ACLY and uncover its influence on peritoneal metastasis in GC. The expression of ACLY was assessed using both real-time quantitative PCR and western blot techniques. To investigate the impact of ACLY on the proliferation of gastric cancer (GC) cells, colony formation and 5-ethynyl-2’-deoxyuridine (EdU) assays were performed. The migratory and invasive abilities of GC were evaluated using wound healing and transwell assays. Additionally, a bioinformatics analysis was employed to predict the correlation between ACLY and HIF-1A. This interaction was subsequently confirmed through a chromatin immunoprecipitation (ChIP) assay. ACLY exhibited upregulation in gastric cancer (GC) as well as in peritoneal metastasis. Its overexpression was found to facilitate the proliferation and metastasis of GC cells in both in vitro and in vivo experiments. Moreover, ACLY was observed to play a role in promoting angiogenesis and epithelial-mesenchymal transition (EMT). Notably, under hypoxic conditions, HIF-1A levels were elevated, thereby acting as a transcription factor to upregulate ACLY expression. Under the regulatory influence of HIF-1A, ACLY exerts a significant impact on the progression of gastric cancer, thereby facilitating peritoneal metastasis.</p
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