Publications by authors named "Qiaoyun Xia"

Article Synopsis
  • Non-alcoholic fatty liver disease (NAFLD) is the most common liver problem around the world, and it might be affected by tiny organisms in our gut and something they make called TMAO.
  • A study found that higher levels of TMAO in poop are connected to worse NAFLD, and TMAO can make liver cells store more fat and harm rats with liver issues.
  • TMAO also damages the gut's protective barrier and changes how the liver and certain immune cells work, suggesting that targeting TMAO might help treat NAFLD.
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Gastric cancer (GC) treatment regimens are still unsatisfactory. Recently, Urolithin A (UroA) has gained tremendous momentum due to its anti-tumor properties. However, the therapeutic effect and underlying mechanisms of UroA in GC are unclear.

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Ubiquitous presence of the extremely persistent pollutants, per- and polyfluoroalkyl substances, is drawing ever-increasing concerns for their high eco-environmental risks which, however, are insufficiently considered based on the assembly characteristics of those amphiphilic molecules in environment. This study investigated the re-organization and self-assembly of perfluorooctane sulfonate (PFOS) and macronutrient molecules from rhizospheric organic (RhO) matter induced with a common operation of aeration. Atomic force microscopy (AFM) with infrared spectroscopy (IR)-mapping clearly showed that, after aeration and stabilization, RhO nanocapsules (∼ 1000 nm or smaller) with a core of PFOS-protein complexes coated by "lipid-carbohydrate" layers were observed whereas the capsule structure with a lipid core surrounded by "protein-carbohydrate-protein" multilayers was obtained in the absence of PFOS.

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Hepatic immunity is one of the driving forces for the development of nonalcoholic steatohepatitis (NASH), and targeting gut microbiota is believed to affect the hepatic immune constitution. Here, we aimed to investigate the hepatic immunological state in NASH, with a specific emphasis on natural killer (NK) cells. In addition, we aimed to identify the contributing species that target hepatic immunity to provide new directions and support the feasibility of immunotherapy for NASH.

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Purpose: To determine the population attributable fraction (PAF) of fatty liver disease (FLD) for type 2 diabetes mellitus (T2DM) and compare it to the PAFs of other metabolic abnormalities.

Methods: We conducted a 10-year retrospective cohort study of 33,346 individuals in Karamay Central Hospital of Xinjiang. Individuals were followed up for T2DM occurrence based on FBS.

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N6-methyladenosine (mA) serves a critical role in regulating gene expression and has been associated with various diseases; however, its role in the differentiation of endothelial progenitor cells (EPCs) remains unclear. The present study used liquid chromatography with tandem mass spectrometry and immunofluorescence assays to quantify the levels of mA in human peripheral blood-derived EPCs (HPB-EPCs) before and after differentiation into mature cells. The present study performed Cell Counting Kit 8, Transwell, and tube formation assays to determine the effects of overexpression and knockdown of Wilms' tumor 1-associated protein (WTAP) on HPB-EPCs.

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Background And Aims: Non-alcoholic fatty liver disease (NAFLD) is closely associated with gut microbiota and has become the most common chronic liver disease worldwide, but the relationship between specific strains and NAFLD has not been fully elucidated. We aimed to investigate whether and could prevent NAFLD, the effects of their action alone or in combination, possible mechanisms, and modulation of the gut microbiota.

Methods: Mice were fed with high-fat diets (HFD) for 20 weeks, in which experimental groups were pretreated with quadruple antibiotics and then given the corresponding bacterial solution or PBS.

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The frequent occurrence of epidemics around the world gives rise to increasing concerns of the pollution of pathogens and antibiotic resistant bacteria in water. This study investigated the impacts of virulence factors (VFs) on the removal of antibiotic resistant and pathogenic bacteria from municipal wastewater by ozone-free or ozone-encapsulated Fe(III)-coagulant-modified colloidal microbubbles (O_free-CCMBs or O-CCMBs). The highly interface-dependent process was initiated with cell-capture on the microbubble surface where the as-collected cells could be further inactivated with the bubble-released ozone and oxidative species if O-CCMBs were used.

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Non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease worldwide but still lacks specific treatment modalities. The gut microbiota and its metabolites have been shown to be intimately involved in NAFLD development, participating in and regulating disease progression. Trimethylamine N-oxide (TMAO), a metabolite highly dependent on the gut microbiota, has been shown to play deleterious regulatory roles in cardiovascular disease, but the relationship between it and NAFLD lacks validation from basic experiments.

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Background: ENO3 expression is upregulated in Non-alcoholic fatty liver disease (NAFLD) patient tissues, demonstrated that ENO3 might play crucial roles in NAFLD. However, the mechanism of ENO3 in NAFLD remains unclear. Therefore, this study aimed to investigate the regulatory mechanism of ENO3 in the progression of non-alcoholic steatohepatitis (NASH) and NASH model.

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Effective therapies for non-alcoholic steatohepatitis (NASH) are urgently needed. We investigated the effect of human mesenchymal stem cells (hMSCs) on the intestinal flora in NASH treatment. We isolated the hMSCs from the umbilical cords and divided male C57BL/6 mice into three groups, namely, chow, methionine-choline-deficient (MCD), and MCD+hMSCs.

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Colorectal cancer (CRC) is one of the most pressing health issues in today's society. As such, it is imperative that the scientific community devise effective methods to inhibit the proliferation and metastasis of CRC cells. Ferroptosis is a recently discovered regulatory cell death mode mainly manifested by dysregulation of cellular iron metabolism and mitochondrial lipid peroxidation.

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