A Triazine Membrane for Sustainable Acquisition of Au(III) from Wastewater.

The recovery of Au(III) from solution using adsorbents in the form of granules or powders is challenging due to issues such as instability during the recovery process or mass loss caused by small particle size. This study introduces a PEI-TCT/PVDF composite membrane designed to intercept and capture Au(III) in wastewater. Experimental results demonstrated that the PEI-TCT/PVDF membrane exhibits a broad pH range (1-8) and a high retention efficiency for Au(III) of 97.8%, with a maximum adsorption capacity of 294.5 mg/g. The mechanism of Au(III) adsorption on the PEI-TCT/PVDF membrane was mainly through electrostatic adsorption, which caused AuCl4- to aggregate on the surface of the membrane and gradually reduced to Au0 and Au+. Furthermore, the membrane can be entirely regenerated within 20 min and maintains its performance in subsequent adsorption cycles. This study highlights the potential of PEI-TCT/PVDF membranes for the recovery of precious Au(III).

Thyrotropin receptor autoantibody (TRAb) enhance the expression of thyrotropin receptor on mouse brain vascular endothelial cells: in vivo and in vitro.

The possibility that thyrotropin receptor (TSHR) expression in non-thyroid tissue is well-documented. However, there is insufficient data on the expression of TSHR in medulla oblongata regions, particularly when focusing on the background of encephalopathy associated with hyperthyroidism. In this study, we explored the expression of the functional TSHR in Graves' disease (GD) mouse cerebral vascular endothelial cells and the effects of thyrotropin receptor autoantibody (TRAb) on its expression. A mouse model of GD was constructed with an adenovirus overexpressing TSHR289. The location and expression of the TSHR gene and protein in vivo were determined via RT-qPCR, Western blot, and immunofluorescence techniques. The effect of TRAb on the expression of functional TSHR in vitro was investigated using bEnd.3 cells. Our results show that medulla oblongata vascular endothelial cells from GD mice expressed higher levels of TSHR compared to control mice. In an in vitro experiment, novel results demonstrated that after treatment with a monoclonal TSHR-specific agonistic antibody (M22), the expression of TSHR on the bEnd.3 cells increased at both the protein and mRNA levels. Furthermore, compared with bEnd.3 cells were treated with IBMX only, those treated with M22 showed increased cAMP production. This study suggested that TSHR is expressed and functionally active in the mouse medulla oblongata and in vitro-cultured bEnd.3 cells and TRAb (M22) increased the expression of TSHR on bEnd.3 cells.

Separable alginate gel spheres encapsulated with La-Fe modified biochar for efficient adsorption of Sb(III) with high capacity.

Sb and its compounds have been widely used in various industrial applications. Therefore, the preparation of Sb adsorbents with easy recovery and excellent adsorption levels is an urgent problem that must be resolved. By calcining and treating La/Fe metal-organic frameworks (MOF) biochar as a precursor, a loaded La-Fe-modified water hyacinth biochar was synthesised and used as a filler to synthesise iron alginate composite gel spheres, MBC/algFe. Through a series of static adsorption experiments, the effects of different filler addition ratios, solution pH, reaction time, coexisting ions, and other factors on the adsorption of Sb(III) were investigated. According to the Langmuir model, the maximum adsorption capacity of MBC/algFe at 25 â„ƒ was 277.8 mg·g-1. The adsorption mechanism mainly involved hydrogen bonding and metal-organic complexation interactions.

MIL-161 Metal-Organic Framework for Efficient Au(III) Recovery from Secondary Resources: Performance, Mechanism, and DFT Calculations.

The recovery of precious metals from secondary resources is significant economically and environmentally. However, their separation is still challenging because they often occur in complex metal ion mixtures. The poor selectivity of adsorbents for gold in complicated solutions prevents further application of adsorption technology. In this study, a Zr-based MOF adsorbent, MIL-161, was synthesized using s-tetrazine dicarboxylic acid (H2STz) as an organic ligand. MIL-161 demonstrated a high adsorption capacity of up to 446.49 mg/g and outstanding selectivity for gold(III) in a simulated electronic waste solution as a result of the presence of sulfur- and nitrogen-containing groups. In addition, the MIL-161 adsorbents were characterized using Fourier transform infrared (FT-IR), field emission scanning electron microscopy (FESEM), thermogravimetric analysis (TG), Brunner-Emment-Teller (BET), and X-ray photoelectron spectroscopy (XPS). Additionally, the adsorption kinetics, isotherms, and thermodynamics of the MOF adsorbents were also thoroughly examined. More importantly, the experimental results and DFT calculations indicate that chelation and electrostatic interactions are the main adsorption mechanisms.

MoS2 nanosheets grown on bowl-shaped hollow carbon spheres as an efficient electrochemical sensor for ultrasensitive determination of nephrotoxic aristolochic acids in Chinese traditional herbs.

Aristolochic acid, a substance in herbs, is highly nephrotoxic, so it is crucial to develop an assay that can rapidly and accurately analyze its content. In this study, bowl-shaped hollow carbon spheres (BHCs) were synthesized using a complex template method, and a MoS2 layer was grown in situ on their surface using a hydrothermal method. The synthesized MoS2-BHCs were used to fabricate an electrochemical sensor for the ultrasensitive and highly selective detection of aristolochic acids (AAs). The optimal conditions for AA detection were determined by tailoring the amount of MoS2 used to modify the BHCs and the pH of the electrolyte. Under optimal conditions, the MoS2-BHC-based sensor presented excellent AA detection performance. The linear concentration ranges of the MoS2-BHC-based sensor for the detection of AA were 0.05-10 µmol L-1 and 10-80 µmol L-1, and the limit of detection of the sensor was 14.3 nmol L-1. Moreover, the MoS2-BHC-based sensor detected AA in Aristolochia and Asarum sieboldii samples. The results were consistent with high-performance liquid chromatography data, demonstrating the satisfactory recovery and accuracy of the sensor. Therefore, we believe that MoS2-BHC-based sensors can be used as effective platforms for detecting AA in traditional Chinese herbs.

Selective Adsorption Behavior and Mechanism for Cd(II) in Aqueous Solution with a Recoverable Magnetie-Surface Ion-Imprinted Polymer.

A novel recoverable magnetic Cd(II) ion-imprinted polymer was synthesized on the surface of silica-coated Fe3O4 particles via the surface imprinting technique and chemical grafting method. The resulting polymer was used as a highly efficient adsorbent for the removal of Cd(II) ions from aqueous solutions. The adsorption experiments revealed that Fe3O4@SiO2@IIP had a maximum adsorption capacity of up to 29.82 mg·g-1 for Cd(II) at an optimal pH of 6, with the adsorption equilibrium achieved within 20 min. The adsorption process followed the pseudo-second-order kinetic model and the Langmuir isotherm adsorption model. Thermodynamic studies showed that the adsorption of Cd(II) on the imprinted polymer was spontaneous and entropy-increasing. Furthermore, the Fe3O4@SiO2@IIP could rapidly achieve solid-liquid separation in the presence of an external magnetic field. More importantly, despite the poor affinity of the functional groups constructed on the polymer surface for Cd(II), we improved the specific selectivity of the imprinted adsorbent for Cd(II) through surface imprinting technology. The selective adsorption mechanism was verified by XPS and DFT theoretical calculations.

Selective removal and recovery of Ni(ii) using a sulfonic acid-based magnetic rattle-type ion-imprinted polymer: adsorption performance and mechanisms.

It is significant to selectively remove Ni(ii) ions from wastewater. A novel sulfonic acid-based magnetic rattle-type ion-imprinted polymer (Fe3O4@void@IIP-Ni(ii)) was designed by taking advantage of the strong interaction between Ni(ii) and sulfonic acid groups. Green polymerization was used to synthesize Fe3O4@void@IIP-Ni(ii), which was then investigated using SEM, TEM, FT-IR, VSM, TGA, EDS, and XPS. The adsorption results indicated that the prepared imprinted material had a short adsorption equilibrium time (10 min), good magnetic responsiveness (about 5 seconds) and high adsorption capacity (44.64 mg g-1) for Ni(ii) at the optimal pH of 6.0. The removal rate of Ni(ii) was up to 99.97%, and the adsorption process was spontaneous and endothermic, following the pseudo-secondary kinetic model and Langmuir model. The selectivity coefficients of the imprinted material were 4.67, 4.62, 8.94 and 9.69 for Ni(ii)/Co(ii), Ni(ii)/Cu(ii), Ni(ii)/Pb(ii) and Ni(ii)/Zn(ii), respectively. The regeneration and application of the imprinted material in actual water samples have been verified. Moreover, the mechanism of selective adsorption for Ni(ii) was investigated by FTIR, XPS and density functional theory (DFT) calculation. The results showed that the imprinted sorbent has a strong binding ability with Ni(ii), and the adsorption of Ni(ii) on Fe3O4@void@IIP-Ni(ii) was the result of the co-coordination of O atoms of the sulfonic acid groups and N atoms of -N-C[double bond, length as m-dash]O groups in AMPS with Ni(ii).

Expression of functional thyroid-stimulating hormone receptor in microglia.

OBJECTIVE: The purpose of the present study was to clarify the expression of thyroid-stimulating hormone receptor (TSHR) in microglial cells, and to explore its function. MATERIALS AND METHODS: Expression of TSHR in microglia was determined by Western blot, immunocytofluorescence and double immunohistofluorescence. Cyclic adenosine 3',5'-monophosphate (cAMP) production was measured after thyrotropin receptor stimulating antibody (TSAb) treatment. RESULTS: Results showed that TSHR protein was expressed and mainly located in the mouse microglia membrane. Moreover, TSAb stimulated cAMP production in mouse microglia (P<0.05). CONCLUSIONS: This study demonstrated the presence of TSHR in microglial cells. Brain TSHR was able to respond specifically to TSAb stimulation, suggesting that TSHR expression is functional. As microglia are innate immune cells that maintain environmental stability in the central nervous system and play a key role in many neuroimmune diseases, expression of functional TSHR in microglia has important pathophysiological implications.

Salubrinal Regulates the Apoptosis of Adrenocortical Carcinoma Cells via the PERK/eIF2α/ATF4 Signaling Pathway.

The protein-kinase-R- (PKR-) like endoplasmic reticulum kinase (PERK) signaling pathway is a well-known promoter of cell apoptosis. In this study, we aimed to determine whether salubrinal (Sal), a selective activator of eukaryotic translation initiation factor 2 (eIF2α), can induce apoptosis of human adrenocortical carcinoma (ACC) cell via activating the PERK/eIF2α/ATF4 signaling pathway, and the potential mechanisms of this action were explored. The ACC cell lines, including SW-13 and NCI-H295 R, were used. 3-(4,5)-Dimethylthiazol(-z-y1)-3,5-di-phenytetrazoliumromide (MTT) assay, cell scratch experiments, flow cytometry, and JC-1 staining assays were performed to detect the cell viability, cell migration, and cell apoptosis. The expression of PERK/eIF2α/ATF4 signaling-pathway-related proteins and apoptosis-related proteins was detected by western blot (WB). Intracellular Ca2+ ion concentration was determined by a confocal laser scanning microscope. The results showed that Sal inhibited the migration and proliferation of ACC cells. Sal remarkably increased the influx of Ca2+ ion and the apoptosis rate of ACC cells in vitro. Furthermore, the expression levels of PERK/eIF2α/ATF4 signaling-related proteins and apoptosis-related proteins were upregulated in the treatment of Sal. The research demonstrated that Sal reduces the cell viability, increases the intracellular calcium concentration, and promotes the apoptosis of ACC cells in vitro through increasing the phosphorylation level of eIF2α and activating the PERK/eIF2α/ATF4 signaling. PERK/eIF2α/ATF4 is expected to act as a potential therapeutic target for the treatment of adrenocortical carcinoma.

Curcumin induces apoptosis and inhibits the growth of adrenocortical carcinoma: Identification of potential candidate genes and pathways by transcriptome analysis.

Adrenocortical carcinoma (ACC) is an endocrine tumour with high malignancy, high invasiveness and poor prognosis. Curcumin, a major component in turmeric, has been reported to have good efficacy and biological safety in treating cancer. However, the role and mechanism of curcumin in ACC have not yet been fully investigated and were thus the focus of this study. In vitro, ACC SW-13 and NCI-H295R cells were treated with curcumin and their viability, migration and invasion were assessed by CCK-8 and Transwell assays. Apoptosis was detected via flow cytometry and western blotting. High-throughput sequencing and comprehensive bioinformatics analyses were performed to elucidate the molecular processes underlying curcumin activity. In vivo, SW-13 cells were injected into nude mice, and the tumour volumes and weights were observed after 2 weeks of curcumin treatment. Organelle changes were observed by electron microscopy, and potential candidate genes and pathways were analysed by RT-qPCR and western blotting. The role of the CHOP target gene in curcumin-induced ACC cell apoptosis was verified via lentiviral transfection experiments. Curcumin inhibited the viability, migration and invasion, and induced the apoptosis of ACC cells. Transcriptome sequencing analysis showed that curcumin treatment markedly changed the gene expression levels. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses showed that the MAPK and endoplasmic reticulum (ER) stress pathways were the predominant pathways associated with curcumin-induced apoptosis of ACC cells. Subsequent in vivo and in vitro results demonstrated that the JNK, p38 MAPK and ER stress pathways were activated in curcumin-treated ACC cells, and that C/EBP homologous protein induction was responsible for curcumin-induced apoptosis of ACC cells. In summary, curcumin induced ACC cell apoptosis and inhibited tumour growth by activating the JNK, p38 MAPK and ER stress pathways. Thus, curcumin may be a potential therapeutic drug for ACC.

Nicotinamide mononucleotide (NMN) protects bEnd.3 cells against H2 O2 -induced damage via NAMPT and the NF-κB p65 signalling pathway.

An increasing number of studies have shown that nicotinamide mononucleotide (NMN) can inhibit not only ageing but also oxidative stress and inflammatory reactions by improving energy metabolism. However, the role of NMN in regulating the anti-apoptotic, antioxidative stress and inflammatory responses of brain microvascular endothelial cells is still unknown. Therefore, here we studied the effects of NMN on H2 O2 -induced oxidative damage of bEnd.3 cells. In this study, we found that NMN could inhibit the NF-κBp65 inflammatory signalling pathway and increase the expression of the enzymes NAMPT, VEGF and eNOS, alleviating H2 O2 -induced apoptosis in bEnd.3 cells. Taken together, these results suggest that NMN reduces H2 O2 -induced oxidative stress and apoptosis and improves cell functions by inhibiting the NF-κBp65 inflammatory pathway and increasing NAMPT expression.

Tauroursodeoxycholic acid mediates endoplasmic reticulum stress and autophagy in adrenocortical carcinoma cells.

Adrenocortical carcinoma (ACC) is an invasive tumor that occurs in the endocrine system. Increasing evidence has shown that endoplasmic reticulum (ER) stress and autophagy play an important role in tumor formation. Tauroursodeoxycholic acid (TUDCA) is an ER chemical chaperone that can alleviate ER stress. In the present study, TUDCA promoted the proliferation, migration and invasion of ACC SW-13 and NCI-H295R cells. Reverse transcription-quantitative PCR and western blot analysis showed that the expression of glucose-regulated protein 78, a promoter of ER stress, was decreased. The expression levels of protein kinase R (PKR)-like ER kinase and activating transcription factor 6 were correspondingly decreased, and the downstream proteins, C/EBP homologous protein and JNK, were also decreased. The expression levels of the autophagy factor microtubule-associated protein light chain 3-II/I and the anti-apoptotic factor Bcl-2 increased following TUDCA treatment, while the expression of the pro-apoptotic factor Bax decreased. TUDCA alleviated ER stress in ACC SW-13 and NCI-H295R cells and induced autophagy, thereby inhibiting ACC cell apoptosis. ER stress- and autophagy-related signaling pathways are involved in the occurrence of ACC, which may provide potential therapeutic targets for ACC treatment.

Thapsigargin induces apoptosis in adrenocortical carcinoma by activating endoplasmic reticulum stress and the JNK signaling pathway: an in vitro and in vivo study.

OBJECTIVE: Thapsigargin (TG) is a natural product that exists in most parts of the plant Thapsia garganica L. and possesses potential anticancer activities against variety tumor cell lines. TG induces endoplasmic reticulum (ER) stress and apoptosis by inhibiting cancer growth. However, the antineoplastic effect of TG in human adrenocortical carcinoma (ACC) cells is still unknown. METHODS: In this study, two human ACC cell lines including SW-13 and NCI-H295R were employed to explore the potential role of TG in ACC. A mouse xenograft model of SW-13 cells was established to verify the role of TG in vivo. The cell viability was tested using Cell Counting Kit-8 and Transwell assays. Flow cytometry and Hoechst 33,258 staining were employed to analyze cell apoptosis. RT-qPCR and Western blot (WB) were performed to explore the underlying mechanism of TG-induced apoptosis in ACC cells. RESULTS: The results indicated that TG dose-dependently inhibited proliferation, migration and invasion in human ACC cells. TG significantly increased the mitochondrial rate of apoptosis and ER stress activity in ACC cells and suppressed ACC xenograft growth in vivo. In addition, the expression of Jun N-terminal kinase (JNK) signaling-related genes and proteins was upregulated by the treatment with TG. CONCLUSION: Our findings suggest that TG inhibits the viability of ACC cells by inducing apoptosis through the activation of JNK signaling. Thus, TG is expected to be a potential candidate for the treatment of ACC.