CdTe quantum dots coated with a molecularly imprinted polymer for fluorometric determination of norfloxacin in seawater.

A fluorescent nanoprobe consisting of CdTe quantum dots (QDs) and coated with molecularly imprinted layers was prepared and successfully applied to the determination of norfloxacin (NOR) in seawater and wastewater samples. The 3-mercaptopropionic acid capped QDs were prepared and then covered with a protective silica shell. A molecularly imprinted layer was finally synthesized around the silanized QDs using 3-aminopropyltriethoxysilane as functional monomer and norfloxacin as the template. Compared with the non-imprinted polymer, the fluorescence of the nanoprobe with imprinted polymer (measured at excitation/emission wavelengths of 300/596 nm) is strongly reduced in the presence of NOR, and the imprinting factor is 8.8. Under the optimal experimental conditions, the detection limit of the nanoprobe is 0.18 µM, and response is linear between 0.5 - 28 µM of NOR. The relative standard deviation of the detection of NOR is <7.2%. In order to evaluate the practicality of the probe, wastewater and seawater samples spiked with norfloxacin were analyzed by this method, and recoveries ranged from 96.2 - 106.0%. Graphical abstract Schematic presentation and fluorescence spectrum of fluorescent nanoprobe with selectivity for norfloxacin (NOR). CdTe quantum dots (QDs) are used as fluorescent carriers, 3-aminopropyltriethoxysilane (APTES) as template molecules, tetraethyl orthosilicate (TEOS) as crosslinking agent, and aqueous ammonia as initiator.

FinaleMe: Predicting DNA methylation by the fragmentation patterns of plasma cell-free DNA.

Analysis of DNA methylation in cell-free DNA (cfDNA) reveals clinically relevant biomarkers but requires specialized protocols and sufficient input material that limits its applicability. Millions of cfDNA samples have been profiled by genomic sequencing. To maximize the gene regulation information from the existing dataset, we developed FinaleMe, a non-homogeneous Hidden Markov Model (HMM), to predict DNA methylation of cfDNA and, therefore, tissues-of-origin directly from plasma whole-genome sequencing (WGS). We validated the performance with 80 pairs of deep and shallow-coverage WGS and whole-genome bisulfite sequencing (WGBS) data.

FinaleMe: Predicting DNA methylation by the fragmentation patterns of plasma cell-free DNA.

Analysis of DNA methylation in cell-free DNA reveals clinically relevant biomarkers but requires specialized protocols such as whole-genome bisulfite sequencing. Meanwhile, millions of cell-free DNA samples are being profiled by whole-genome sequencing. Here, we develop FinaleMe, a non-homogeneous Hidden Markov Model, to predict DNA methylation of cell-free DNA and, therefore, tissues-of-origin, directly from plasma whole-genome sequencing. We validate the performance with 80 pairs of deep and shallow-coverage whole-genome sequencing and whole-genome bisulfite sequencing data.

NOMe-HiC: joint profiling of genetic variant, DNA methylation, chromatin accessibility, and 3D genome in the same DNA molecule.

Cis-regulatory elements are coordinated to regulate the expression of their targeted genes. However, the joint measurement of cis-regulatory elements' activities and their interactions in spatial proximity is limited by the current sequencing approaches. We describe a method, NOMe-HiC, which simultaneously captures single-nucleotide polymorphisms, DNA methylation, chromatin accessibility (GpC methyltransferase footprints), and chromosome conformation changes from the same DNA molecule, together with the transcriptome, in a single assay. NOMe-HiC shows high concordance with state-of-the-art mono-omic assays across different molecular measurements and reveals coordinated chromatin accessibility at distal genomic segments in spatial proximity and novel types of long-range allele-specific chromatin accessibility.

Insights into the Role of Na+ on the Transformation of Gypsum into α-Hemihydrate Whiskers in Alcohol-Water Systems.

Alcohol-water solution-mediated transformation of gypsum into α-hemihydrate (α-HH) whiskers provides a green alternative for the high-value-added recycling of flue gas desulfurization (FGD) gypsum. However, the role of non-lattice cations during the transformation is still unclear. We report an evolution from "boosting-retarding" to "boosting-retarding-boosting" and finally to "boosting only" effect of non-lattice Na+ functioned by the concentration of ethylene glycol (EG) in water solutions. The driving force increased almost linearly upon the introduction of Na+ through the formation of ion pairs, and a higher slope was obtained at a higher EG concentration. Adsorption of Na+ ions and solidification of eugsterite on gypsum surfaces blocked the nucleation sites of α-HH. The retarding effect first rapidly increased and gradually approached a limit, following a parabolic trend after Na+ ions were introduced. Pentasalt, with a structure similar to that of α-HH, precipitated on the gypsum surface at higher c(Na+). The interaction of the driving force and the structural evolution of calcium sulfate ionic clusters accounts for the evolution of transformation kinetics. The retardation zone was compressed with the increase in EG volume ratios, and a monotonic boosting effect upon Na+ was observed at a 35.0 vol % of EG. Nucleation kinetics dominates the aspect ratio of α-HH whiskers. This study may provide a significant guidance for the utilization of FGD gypsum.

Construction of Low-Carbon Ferry-A Case of Jingning, China.

As the Chinese government has pledged to reach its carbon peak by 2030 and carbon neutrality by 2060, it is necessary to investigate how regional sustainable development can be achieved. This paper used a 'bottom-up' model to calculate the ferry carbon emissions in Jingning, China, and proposed four measures to reduce carbon emissions, including renewing ferryboats, planting water-level-fluctuating zones, greening the ferries, and installing solar energy. Quantitative analyses were conducted to calculate the possible emissions reduction from 2021 to 2025, with the results indicating that the total emissions could be reduced by 392.67 t. Finally, a new low-carbon ferry concept is proposed, based on simultaneous carbon emission reduction and carbon sink enhancement. This study provided a theoretical and decision-making reference for the operation of green, beautiful, and low-carbon ferries.

CRAG: de novo characterization of cell-free DNA fragmentation hotspots in plasma whole-genome sequencing.

The fine-scale cell-free DNA fragmentation patterns in early-stage cancers are poorly understood. We developed a de novo approach to characterize the cell-free DNA fragmentation hotspots from plasma whole-genome sequencing. Hotspots are enriched in open chromatin regions, and, interestingly, 3'end of transposons. Hotspots showed global hypo-fragmentation in early-stage liver cancers and are associated with genes involved in the initiation of hepatocellular carcinoma and associated with cancer stem cells. The hotspots varied across multiple early-stage cancers and demonstrated high performance for the diagnosis and identification of tissue-of-origin in early-stage cancers. We further validated the performance with a small number of independent case-control-matched early-stage cancer samples.

Functionalizing biochar by Co-pyrolysis shaddock peel with red mud for removing acid orange 7 from water.

Biochar modification by metal/metal oxide is promising for improving its adsorption capability for contaminants, especially the anions. However, conventional chemical modifications are complicated and costly. In this study, novel Fe/Fe oxide loaded biochars (RMBCs) were synthesized from a one-step co-pyrolysis of red mud (RM) and shaddock peel (SP), and their potential application for removing anionic azo dye (acid orange 7, AO7) from the aqueous environment was evaluated. Fe from red mud was successfully loaded onto biochars pyrolyzed at 300-800 °C, which presented from oxidation form (Fe2O3) to the reduction forms (FeO and Fe0) with increasing pyrolysis temperature. The RMBC produced at 800 °C with RM:SP mass ratio of 1:1 (RMBC8001:1) exhibited the best capability for AO7 removal (∼32 mg/g), attributed to both adsorption and degradation. The higher surface area of RMBC8001:1 and its greater affinity for AO7 led to the higher adsorption. In addition, RMBC8001:1-induced degradation of AO7 was another key mechanism for AO7 removal. The reduction forms of Fe (FeO or Fe0) in RMBC8001:1 may provide electrons for breaking down the azo bond in AO7 molecules and result in degradation, which is further enhanced in acid conditions due to the participation of readily release of Fe2+ and the available H+ in AO7 degradation. Furthermore, RMBC8001:1 can be easily separated from the treated water by using magnetic field, which significantly benefits its separation in wastewater treatment.

Nogo-B receptor is required for stabilizing TGF-ß type I receptor and promotes the TGF-ß1-induced epithelial-to-mesenchymal transition of non-small cell lung cancer.

Background and Objective: Metastasis is the leading cause of death in patients with advanced non-small cell lung cancer (NSCLC), and epithelial-mesenchymal transition (EMT) is a crucial event in the metastasis of NSCLC. Our previous works demonstrated that NgBR promoted EMT in NSCLC. However, the molecular mechanism was unclear. Methods: TGF-ß1 was used to induce EMT process of NSCLC cells. The biological functions of NgBR in promoting TGF-ß1-induced NSCLC metastasis were studied by gain- and loss-of-function assays both in vitro and in vivo. The underlying mechanisms were studied using molecular biology assays. Results: We found that knockdown of NgBR inhibited TGF-ß1-induced cell migration and invasion in NSCLC cells. In contrast, NgBR overexpression promoted TGF-ß1-induced EMT of A549 cells. Mechanically, we found that knockdown of NgBR facilitated ubiquitination and degradation of TßRI, leading to downregulation of TßRI expression in NSCLC cells. Moreover, we confirmed a positive correlation between NgBR and TßRI in NSCLC tissues. Conclusions: Our findings provide a novel role of NgBR in modulating TGF-ß1-induced EMT and propose NgBR as a new therapeutic target for treating NSCLC patients.

Ammonium removal using a calcined natural zeolite modified with sodium nitrate.

Ammonium is one of the key factors responsible for the eutrophication of water bodies. The purpose of this study was to remove ammonium from water using a natural zeolite (NZ) modified with sodium nitrate (NaNO3) by impregnation and calcination. The ability of the NZ to remove ammonium from water was determined by single calcination; however, its efficiency was significantly enhanced by impregnation with a NaNO3 solution. Zeolite modified with 3.00 M NaNO3 and calcination at 673 K yielded the best ammonium removal efficiency, which was 39.88 % higher than the NZ alone. The zeolites that were regenerated over six times maintained a removal rate of 79.35-84.79 % by mixing 25.0 mg of the NZ into 50 mL of a 5.0 mg/L ammonium solution. The improved performance of the modified zeolite (qm, 16.96 mg/g) was mainly attributed to its relatively elevated mesopore volumes and higher ion-exchange capacity that results from nitrate decomposition, oxygen release, and sodium-ion exchange. The adsorption kinetics and isotherms are best described by the pseudo-first-order (PFO) and Freundlich model, respectively, and the process was endothermic. The effects of other factors, including coexisting ions, pH, and dosage, on ammonium adsorption were also determined.

Application of molecular imprinting polymer anchored on CdTe quantum dots for the detection of sulfadiazine in seawater.

A molecularly imprinted polymer (MIP) anchored on the surface of CdTe quantum dots (QDs) was fabricated and used as a fluorescent probe for sulfadiazine (SDZ) detection in seawater. CdTe QDs was used as photoluminescent material, SDZ as the template, 3-aminopropyltriethoxysilane (APTES) as the functional monomer and tetraethyl orthosilicate (TEOS) as the cross-linking agent. Characterizations of MIP-QDs were analyzed by Fourier transform infrared (FT-IR), Transmission electron microscopy (TEM) and Scanning electron microscope (SEM). The conditions were optimized for the detection of MIP-QDs to SDZ. The mechanism of fluorescence quenching was studied by UV-Vis absorption spectroscopy and fluorescence spectroscopy. Under optimal conditions, the fluorescence intensity of MIP-QDs decreased linearly between 4- and 20 µM SDZ with a good correlation coefficient of 0.995. The limit of detection is 0.67 µM and the recovery is between 91.8 and 109.4% with RSD lower than 3.9%. These results indicated that MIP-QDs for SDZ detection in seawater was developed successfully.

PDIA6 modulates apoptosis and autophagy of non-small cell lung cancer cells via the MAP4K1/JNK signaling pathway.

BACKGROUND: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with a poor prognosis. We previously found that protein disulfide isomerase family 6 (PDIA6) is upregulated in lung squamous cell carcinoma (LSCC). This study aimed to elucidate the clinical relevance, biological functions, and molecular mechanisms of PDIA6 in NSCLC. METHODS: The expression of PDIA6 in NSCLC was assessed using the TCGA database, western blotting, and immunohistochemistry. Correlations of PDIA6 expression with clinicopathological and survival features were evaluated. The functions of PDIA6 in regulating NSCLC cell growth, apoptosis, and autophagy were investigated using gain-and loss-of-function strategies in vitro or in vivo. The underlying molecular mechanisms of PDIA6 function were examined by human phospho-kinase array and co-immunoprecipitation. FINDINGS: PDIA6 expression was upregulated in NSCLC compared with adjacent normal tissues, and the higher PDIA6 expression was correlated with poor prognosis. PDIA6 knockdown decreased NSCLC cell proliferation and increased cisplatin-induced intrinsic apoptosis, while PDIA6 overexpression had the opposite effects. In addition, PDIA6 regulated cisplatin-induced autophagy, and this contributed to PDIA6-mediated apoptosis in NSCLC cells. Mechanistically, PDIA6 reduced the phosphorylation levels of JNK and c-Jun. Moreover, PDIA6 interacted with MAP4K1 and inhibited its phosphorylation, ultimately inhibiting the JNK/c-Jun signaling pathway. INTERPRETATION: PDIA6 is overexpressed in NSCLC and inhibits cisplatin-induced NSCLC cell apoptosis and autophagy via the MAP4K1/JNK/c-Jun signaling pathway, suggesting that PDIA6 may serve as a biomarker and therapeutic target for NSCLC patients. FUND: National Natural Science Foundation of China and Institutions of higher learning of innovation team from Liaoning province.

Nogo-B receptor promotes epithelial-mesenchymal transition in non-small cell lung cancer cells through the Ras/ERK/Snail1 pathway.

Nogo-B receptor (NgBR) is a specific receptor of Nogo-B that regulates vascular remodeling and angiogenesis. Previously, we found that NgBR promotes the membrane translocation and activation of Ras in breast cancer cells and enhances the chemoresistance of hepatocellular carcinoma cells to 5-fluorouracil. However, the role of NgBR in lung cancer has not yet been elucidated. In the present study, we found that NgBR knockdown inhibited epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC) cells in vitro and metastasis of NSCLC cells in vivo. In contrast, NgBR overexpression promoted EMT in and lung metastasis of NSCLC cells. At the molecular level, NgBR modulated the expression of EMT-related proteins and enhanced the protein expression of Snail1, a crucial transcription factor that represses epithelial cell protein marker E-cadherin. Moreover, we found that NgBR overexpression promoted the membrane localization of Ras and activation of downstream MEK/ERK signaling pathway and that NgBR knockdown by using a specific shRNA inversely affected the expression of EMT-related proteins in NSCLC cells. Thus, our results provide novel insights on the regulatory role of NgBR in the metastasis of NSCLC that should be investigated further for developing a therapeutic strategy for treating patients with NSCLC.

Aldolase A promotes proliferation and G1/S transition via the EGFR/MAPK pathway in non-small cell lung cancer.

BACKGROUND: Our previous study demonstrated that aldolase A (ALDOA) is overexpressed in clinical human lung squamous cell carcinoma and that ALDOA promotes epithelial-mesenchymal transition and tumorigenesis. The present study aimed to explore the function of ALDOA in the modulation of non-small cell lung cancer (NSCLC) proliferation and cell cycle progression and the potential mechanism. METHODS: ALDOA was knocked down by short hairpin RNA in H520 and H1299 cells. ALDOA was overexpressed with vectors carrying the full-length ALDOA sequence in H1299 and H157 cells. The proliferation capacities were assessed with immunohistochemical staining, Cell Counting Kit-8 and colony formation assays. The cell cycle distribution was examined by flow cytometry, and molecular alterations were determined by western blotting. Cell synchronization was induced with nocodazole. The stability of cyclin D1 mRNA was tested. The pyruvate kinase M2 and ALDOA protein distributions were examined. Aerobic glycolysis was evaluated with Cell Titer-Glo assay, glucose colorimetric assay and lactate colorimetric assay. RESULTS: ALDOA knockdown inhibited the proliferation and G1/S transition in H520 cells. Conversely, ALDOA overexpression promoted the proliferation and G1/S transition in H157 cells. The cell cycle synchronization assay showed that ALDOA expression increased in the G1 phase and G1/S transition. Furthermore, ALDOA knockdown reduced cyclin D1 expression by regulating epidermal growth factor receptor/mitogen-activated protein kinase (EGFR/MAPK) pathway. Similar results were found in H1299 and H157 cells. The inhibition of mitogen-activated protein kinase kinase 1/2 prompted the nuclear distribution of ALDOA. Additionally, ALDOA knockdown reduced nuclear distribution of PKM2, the extracellular lactate and intracellular adenosine triphosphate concentrations and elevated the extracellular glucose concentration. CONCLUSIONS: ALDOA contributed to activation of the EGFR/MAPK pathway, thus promoting cyclin D1 expression and enhancing proliferation and G1/S transition in NSCLC. Additionally, ALDOA facilitated NSCLC aerobic glycolysis.

PDIA6 promotes the proliferation of HeLa cells through activating the Wnt/ß-catenin signaling pathway.

Protein disulfide isomerase family 6 (PDIA6) belongs to the protein disulfide isomerase (PDI) family, which function as isomerases and molecular chaperones. PDIA6 has recently been shown to promote the proliferation and growth of various types of human cancer cells; however the underlying molecular mechanism remains elusive. Here, we report that PDIA6 enhances the proliferation of HeLa cells through activation of the Wnt/ß-catenin signaling pathway. Ectopic overexpression of PDIA6 in HeLa cells led to increased cell proliferation accompanied with accelerated cell cycle progression. Further mechanistic investigation demonstrated that overexpression of PDIA6 resulted in decreased phosphorylation of ß-catenin at Ser45 and Ser33/Ser37/Thr41, while increased ß-catenin nuclear accumulation, and upregulation of Wnt/ ß-catenin signaling target genes cyclinD1 and c-myc, which was abolished by ubiquitin-proteasome inhibitor MG132. These results demonstrated that PDIA6 overexpression promoted the proliferation of HeLa cells by suppressing the phosphorylation of ß-catenin, thereby inhibiting the degradation of ß-catenin through the ubiquitin-proteasome pathway.

Improvement of activated sludge dewaterability by mild thermal treatment in CaCl2 solution.

Activated sludge dewatering is of great importance in sludge treatment and disposal. To enhance the dewaterability, a novel method was performed by treating the sludge under mild temperature (50-90 °C) in CaCl(2) solution (3.7-1110.0 mg/g dry sludge). The capillary suction time, zeta potential, Fourier-transformed infrared spectra, concentration of soluble protein and carbohydrates were employed to characterize the dewaterability and influencing mechanism. The sludge dewaterability was deteriorated with single thermal treatment, but significantly promoted in CaCl(2) solution and advanced further together with thermal treatment. An increasing CaCl(2) dosage reduced the surface charge remarkably, and a higher temperature could strengthen this impact. The spectra indicate that Ca(2+) could interact with the protein, phenols and O-H functional group in the flocs. The thermal treatment could cause the solubilization of protein and carbohydrates, providing more binding sites for Ca(2+) to establish a strong bridging among the flocs. As CaCl(2) dosage elevated, the soluble carbohydrates showed a reduction trend, while the soluble protein lowered firstly and then bounced back except that remained unchanged at room temperature. A bridging equilibrium is presumed to exist between Ca(2+) and the soluble protein. And the bridging between Ca(2+) and the soluble carbohydrates plays a more important role in the dewatering. The sludge dewaterability was successfully and economically improved by thermal treatment in CaCl(2) solution.