Publications by authors named "Linying Cao"

In recent years, low-dimensional organic-inorganic hybrid metal halides have garnered significant attention for optoelectronic applications due to their exceptional photophysical properties, despite their persistent challenge of low stability. Addressing this challenge, our study introduces 1-[5-(trifluoromethyl)pyridin-2-yl]piperazinium (TFPP) as a cation, harvesting a novel one-dimensional hybrid cadmium-based halide semiconductor (TFPP)CdCl, which exhibits intense blue-light emission upon UV excitation. Additionally, (TFPP)CdCl demonstrates a high scintillation performance under X-ray excitation, producing 16600 ± 500 photons MeV and achieving a low detection limit of 0.

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Triclocarban (TCC) and triclosan (TCS) have been detected ubiquitously in human body and evoked increasing concerns. This study aimed to reveal the induction risks of TCC and TCS on triple negative breast cancer through non-genomic GPER-mediated signaling pathways. Molecular simulation indicated that TCC exhibited higher GPER binding affinity than TCS theoretically.

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Article Synopsis
  • Previous studies indicated that the antimicrobial agents triclocarban (TCC) and triclosan (TCS) disrupt lipid metabolism, but research on their effects specifically on adipose (fat) tissue is limited.
  • This study found that TCC promotes the differentiation of preadipocytes into mature adipocytes more than TCS, activating multiple peroxisome proliferator-activated receptors (PPARs), while TCS mainly activates one type of PPAR.
  • In in vivo experiments, TCC increased fat accumulation and body weight in mice, with male mice showing greater susceptibility to TCC's obesogenic effects.
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Background: Tibiotalocalcaneal arthrodesis is an established surgical procedure for treating patients with end-stage ankle joint arthritis and subtalar joint arthritis. Although it greatly relives pain, a major drawback is loss of range of motion. Although it is known to restrict an additional subtalar joint compared to tibiotalar arthrodesis, there is a lack of gait analysis studies comparing the two methods.

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Triclosan (TCS) and triclocarban (TCC) have become ubiquitous pollutants detected in human body with concentrations up to hundreds of nanomolar levels. Previous studies about the hepatic lipid accumulation induced by TCS and TCC were focused on pollutant itself, which showed weak or no effects. High-fat diet (HFD), as a known environmental factor contributing to lipid metabolism-related disorders, its synergistic action with environmental pollutants deserves concern.

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  • - Neonicotinoid insecticides (NIs) are prevalent in the environment and human bodies, showing concentrations that could potentially affect health, but their mechanisms regarding toxicity, especially in relation to breast cancer, remain unclear.
  • - Research focused on the G protein-coupled estrogen receptor (GPER) found that certain NIs, particularly acetamiprid (ACE), significantly activated GPER, leading to increased migration and proliferation of breast cancer cells.
  • - ACE was shown to promote breast cancer growth and lung metastasis in mouse models via the GPER mechanism, suggesting that NIs could potentially exacerbate breast cancer progression at levels encountered in human exposure.
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  • Benzotriazole ultraviolet stabilizers (BUVs) are emerging environmental pollutants that may disrupt hormone functions by interacting with estrogen-related receptors α and γ (ERRα and ERRγ).
  • The study found that BUVs bind effectively to ERRγ, promoting its transcriptional activity at low concentrations relevant to human exposure.
  • Molecular analyses indicate that factors like molecular polarizability and electron-donating ability significantly influence how BUVs bind to ERRγ, highlighting their potential estrogenic effects.
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Niclosamide (NIC), a helminthic drug used widely for controlling schistosomiasis, can reportedly disrupt the endocrine system. However, its underlying mechanisms are still unclear. In this study, we revealed the potential endocrine disruption mechanism of NIC by activating estrogen receptors (ERs) and estrogen-related receptors (ERRs).

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A bacterial consortium for efficient decontamination of high-concentration Fe-Mn acid mine drainage (AMD) was successfully isolated. The removal efficiencies of Fe and Mn were effective, reaching 99.8 % and 98.

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The potential causal relationship between exposure to environmental contaminants and diabetes is troubling. Exposure of perfluoroalkyl substances (PFASs) is found to be associated with hyperinsulinemia and the enhancement of insulin secretion by islet β cells in humans, but the underlying mechanism is still unclear. Here, by combining studies with both wild type and gene knockout mice and studies with mouse islet β cells (β-TC-6), we demonstrated clearly that 1 h exposure of perfluorooctanesulfonate (PFOS) stimulated insulin secretion and intracellular calcium level by activating G protein-coupled receptor 40 (GPR40), a vital free fatty acid regulated membrane receptor on islet β cells.

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Hydroxyl radical (OH)- and sulfate radical ()-based advanced oxidation technologies (AOTs) have been proven an effective method to remove antibiotics in wastewater treatment plants (WWTPs). This study aims to gain insights into kinetics and mechanisms of neutral sulfamethoxazole (SMX) degradation, a representative antibiotic, by OH and using an experimental and theoretical approach. First, the second-order rate constants (k) of SMX with OH and were determined to be (7.

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Airborne lower-chlorinated PCBs are vulnerable to metabolization to PCB sulfates through further sulfation of the hydroxylated metabolites (OH-PCBs). However, studies on the toxic effects and mechanisms of PCB sulfates are still very limited. Here, we investigated for the first time the potential endocrine disruption effects of PCB sulfates through estrogen-related receptor γ (ERRγ) in comparison with their OH-PCBs precursors and PCB parent compounds.

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Previously, perfluoroalkyl substances (PFASs) have been found to be associated with many adverse effects mediated by the peroxisome proliferator-activated receptor α (PPARα) and PPARγ. Here, we found another subtype of the peroxisome proliferator-activated receptors (PPARs); the PPARβ/δ mediated pathway might also be a potential adverse outcome pathway for PFASs. We investigated the direct binding and transcriptional activity of PFASs toward human PPARβ/δ, and further revealed the structure-binding and structure-activity relationship between PFASs and PPARβ/δ.

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Estrogen-related receptor γ (ERRγ) is an orphan nuclear receptor having functional cross-talk with classical estrogen receptors. Here, we investigated whether ERRγ is a potential target of polybrominated diphenyl ethers (PBDEs) and their hydroxylated metabolites (OH-PBDEs). By using a fluorescence competitive binding method established in our laboratory, the binding potencies of 30 PBDEs/OH-PBDEs with ERRγ were determined for the first time.

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Background: Numerous studies have indicated the estrogenic effects of polybrominated diphenyl ethers (PBDEs) and hydroxylated PBDEs (OH-PBDEs). However, the previous mechanistic studies focused on their estrogenic effects through genomic transcriptional activation of estrogen receptors.

Objective: The present study aimed to investigate the estrogenic effects of PBDEs and OH-PBDEs via nongenomic G protein-coupled estrogen receptor (GPER) pathways.

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Chlorinated polyfluorinated ether sulfonates (Cl-PFAESs) are the alternative products of perfluorooctanesulfonate (PFOS) in the metal plating industry in China. The similarity in chemical structures between Cl-PFAESs and PFOS makes it reasonable to assume they possess similar biological activities. In the present study, we investigated whether Cl-PFAESs could induce cellular effects through peroxisome proliferator-activated receptors (PPARs) signaling pathways like PFOS.

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Numerous studies have indicated estrogenic disruption effects of bisphenol A (BPA) analogues. Previous mechanistic studies were mainly focused on their genomic activities on nuclear estrogen receptor pathway. However, their nongenomic effects through G protein-coupled estrogen receptor (GPER) pathway remain poorly understood.

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Perfluoroalkyl substances (PFASs) have been shown to cause abnormal levels of thyroid hormones (THs) in experimental animals, but the molecular mechanism is poorly understood. Here, a fluorescence displacement assay was used to determine the binding affinities of 16 PFASs with two major TH transport proteins, transthyretin (TTR) and thyroxine-binding globulin (TBG). Most of the tested PFASs bound TTR with relative potency (RP) values of 3×10(-4) to 0.

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Previous animal experiments have implied that organophosphate esters (OPEs) have a disruption effect on the thyroid endocrine system. However, knowledge of the toxicological mechanism remains limited. In this study, the activities of four OPEs have been characterized against the thyroid hormone (TH) nuclear receptor (TR) using two in vitro models, with the aim of evaluating their toxicity mechanisms towards the TR.

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Human G protein-coupled receptor 40 (hGPR40), with medium- and long-chain free fatty acids (FFAs) as its natural ligands, plays an important role in the enhancement of glucose-dependent insulin secretion. To date, information about the direct binding of FFAs to hGPR40 is very limited, and how carbon-chain length affects the activities of FFAs on hGPR40 is not yet understood. In this study, a fluorescein-fasiglifam analogue (F-TAK-875A) conjugate was designed and synthesized as a site-specific fluorescence probe to study the interaction of FFAs with hGPR40.

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A rhodamine nitroxide probe was designed to detect the hydroxyl radical (·OH), which presented high selectivity for ·OH over other reactive oxygen species (ROS) and linear fluorescence response to ·OH produced by Fenton reaction. The product was detected by HPLC-MS, indicating that the main product of the reaction was O-methylhydroxylamine and the product peak areas measured by HPLC-UV/vis and HPLC-FLD both enhanced proportionally with the increase of ·OH concentration. The application of the probe in biological system was explored to trace the production of ·OH in cells under oxidative stress condition induced by rotenone which can inhibit the mitochondria respiratory chain complex I and we found that appropriate rotenone may induce the normal human liver cells (L02) and human hepatoma cells (HepG2) to produce ·OH at different degrees.

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