Search

Green financial markets and products play an essential role in financial support for high-quality development and the construction of ecological civilization as practical subjects for realizing a green economy. This paper selects Guangdong Province as the research object, and based on a total of 120 data on various indicators of green finance and digital inclusive finance in Guangdong Province from 2011 to 2020, it firstly establishes green finance and digital inclusive finance indicator system, and combines the neural network technology based on multi-layer perceptron (MLP) to build a prediction model of the impact of digital inclusive finance on green finance in Guangdong Province. After the model training and measurement, eight important diagrams of independent variables were finally obtained to illustrate the impact of digital inclusive finance on green finance respectively. This provides a theoretical reference for the government to introduce relevant policies to support the development of digital inclusive finance and green finance.

This file contains additional figures related to findings from the described subcutaneous xenograft experiments, the primary murine NSCLC experiments and the metastatic breast cancer xenograft experiments. In addition, it contains a table listing the oligonucleotide sequences utilized in our genetic studies.

The enzyme glucose-6-phosphate dehydrogenase (G6PD) is a major contributor to NADPH production and redox homeostasis and its expression is upregulated and correlated with negative patient outcomes in multiple human cancer types. Despite these associations, whether G6PD is essential for tumor initiation, growth, or metastasis remains unclear. Here, we employ modern genetic tools to evaluate the role of G6PD in lung, breast, and colon cancer driven by oncogenic K-Ras. Human HCT116 colorectal cancer cells lacking G6PD exhibited metabolic indicators of oxidative stress, but developed into subcutaneous xenografts with growth comparable with that of wild-type controls. In a genetically engineered mouse model of non–small cell lung cancer driven by K-Ras G12D and p53 deficiency, G6PD knockout did not block formation or proliferation of primary lung tumors. In MDA-MB-231–derived human triple-negative breast cancer cells implanted as orthotopic xenografts, loss of G6PD modestly decreased primary site growth without ablating spontaneous metastasis to the lung and moderately impaired the ability of breast cancer cells to colonize the lung when delivered via tail vein injection. Thus, in the studied K-Ras tumor models, G6PD was not strictly essential for tumorigenesis and at most modestly promoted disease progression.Significance:K-Ras–driven tumors can grow and metastasize even in the absence of the oxidative pentose pathway, a main NADPH production route.

Deep learning algorithms are facing the limitation in virtual reality application due to the cost of memory, computation, and real-time computation problem. Models with rigorous performance might suffer from enormous parameters and large-scale structure, and it would be hard to replant them onto embedded devices. In this paper, with the inspiration of GhostNet, we proposed an efficient structure ShuffleGhost to make use of the redundancy in feature maps to alleviate the cost of computations, as well as tackling some drawbacks of GhostNet. Since GhostNet suffers from high computation of convolution in Ghost module and shortcut, the restriction of downsampling would make it more difficult to apply Ghost module and Ghost bottleneck to other backbone. This paper proposes three new kinds of ShuffleGhost structure to tackle the drawbacks of GhostNet. The ShuffleGhost module and ShuffleGhost bottlenecks are utilized by the shuffle layer and group convolution from ShuffleNet, and they are designed to redistribute the feature maps concatenated from Ghost Feature Map and Primary Feature Map. Besides, they eliminate the gap of them and extract the features. Then, SENet layer is adopted to reduce the computation cost of group convolution, as well as evaluating the importance of the feature maps which concatenated from Ghost Feature Maps and Primary Feature Maps and giving proper weights for the feature maps. This paper conducted some experiments and proved that the ShuffleGhostV3 has smaller trainable parameters and FLOPs with the ensurance of accuracy. And with proper design, it could be more efficient in both GPU and CPU side.

Background CKD induces loss of muscle proteins partly by suppressing muscle protein synthesis. Muscles of mice with CKD have increased expression of nucleolar protein 66 (NO66), as do muscle biopsy specimens from patients with CKD or those undergoing hemodialysis. Inflammation stimulates NO66 expression and changes in NF-κB mediate the response. Methods Subtotal nephrectomy created a mouse model of CKD with BUN >80 mg/dl. Crossing NO66flox/flox with MCK-Cre mice bred muscle-specific NO66 (MCK-NO66) knockout mice. Experiments assessed the effect of removing NO66. Results Muscle-specific NO66 knockout in mice blocks CKD-induced loss of muscle mass and improves protein synthesis. NO66 suppression of ribosomal biogenesis via demethylase activity is the mechanism behind these responses. In muscle cells, expression of NO66, but not of demethylase-dead mutant NO66, decreased H3K4me3 and H3K36me3 and suppressed pre-rRNA expression. Knocking out NO66 increased the enrichment of H3K4me3 and H3K36me3 on ribosomal DNA. In primary muscle cells and in muscles of mice without NO66, ribosomal RNA, pre-rRNA, and protein synthesis all increased. Conclusions CKD suppresses muscle protein synthesis via epigenetic mechanisms that NO66 mediates. Blocking NO66 could suggest strategies that counter CKD-induced abnormal muscle protein catabolism.

The phylogeny and systematics of cordycipitoid fungi have been extensively studied in the last two decades. However, systematic positions of some taxa in the family Cordycipitaceae have not yet been thoroughly resolved. In this study, a new phylogenetic framework of Cordycipitaceae is reconstructed using multigene (nrSSU, nrLSU, tef-1α, rpb1 and rpb2) sequence data with large-scale taxon sampling. In addition, ITS sequence data of species belonging to the Lecanicillium lineage in the family Cordycipitaceae are used to further determine their phylogenetic placements. Based on molecular phylogenetic data together with morphological evidence, two new genera (Flavocillium and Liangia), 16 new species and four new combinations are introduced. In the new genus Flavocillium, one new species F. bifurcatum and three new combinations previously described as Lecanicillium, namely F. acerosium, F. primulinium and F. subprimulinium, are proposed. The genus Liangia is built by the new species Lia. sinensis with Lecanicillium-like asexual morph, isolated from an entomopathogenic fungus Beauveria yunnanensis. Due to the absence of Paecilomyces hepiali, an economically and medically significant fungus, in the earlier phylogenetic analyses, its systematic position has been puzzling in both business and academic communities for a long time. Here, P. hepiali is recharacterized using the holotype material along with seven additional samples. It is assigned to the genus Samsoniella (Cordycipitaceae, Hypocreales) possessing Cordyceps-like sexual morph and Isaria-like asexual morph, and thus a new combination, namely S. hepiali is proposed. An additional nine new species in Samsoniella are described: S. alpina, S. antleroides, S. cardinalis, S. cristata, S. lanmaoa, S. kunmingensis, S. ramosa, S. tortricidae and S. yunnanensis. Four new species in Cordyceps are described: C. chaetoclavata, C. cocoonihabita, C. shuifuensis and C. subtenuipes. Simplicillium yunnanense, isolated from synnemata of Akanthomyces waltergamsii, is described as a new species.

The fungus Ophiocordyceps sinensis is endemic to the vast region of the Qinghai-Tibetan plateau (QTP). The unique and complex geographical environmental conditions have led to the “sky island” distribution structure of O. sinensis. Due to limited and unbalanced sample collections, the previous data on O. sinensis regarding its genetic diversity and spatial structure have been deemed insufficient. In this study, we analyzed the diversity and phylogeographic structures of O. sinensis using internally transcribed spacer region (ITS) and 5-locus datasets by a large-scale sampling. A total of 111 haplotypes of ITS sequences were identified from 948 samples data of the fungus O. sinensis, with representing high genetic diversity, and 8 phylogenetic clades were recognized in O. sinensis. Both the southeastern Tibet and the northwestern Yunnan were the centers of genetic diversity and genetic differentiation of the fungus, and they were inferred as the glacial refugia in the Quaternary. Three distribution patterns were identified to correspond to the 8 clades, including but not limited to the coexistence of widely and specific local distributive structures. It also revealed that the differentiation pattern of O. sinensis did not fit for the isolation-by-distance model. The differentiation into the 8 clades occurred between 1.56 Myr and 6.62 Myr. The ancestor of O. sinensis most likely originated in the late Miocene (6.62 Myr) in the northwestern Yunnan, and the Scene A–C of the Qinghai–Tibetan movements may have played an important role in the differentiation of O. sinensis during the late Miocene–Pliocene periods. Our current results provide a much clearer and detailed understanding of the genetic diversity and geographical spatial distribution of the endemic alpine fungus O. sinensis. It also revealed that the geochronology resulting from paleogeology could be cross-examined with biomolecular clock at a finer scale. Keywords: Large-scale sampling, Phylogeographic structure, Molecular clock, Correlation, Qinghai–Tibetan plateau

Chest X-ray has become one of the most common ways in diagnostic radiology exams, and this technology assists expert radiologists with finding the patients at potential risk of cardiopathy and lung diseases. However, it is still a challenge for expert radiologists to assess thousands of cases in a short period so that deep learning methods are introduced to tackle this problem. Since the diseases have correlations with each other and have hierarchical features, the traditional classification scheme could not achieve a good performance. In order to extract the correlation features among the diseases, some GCN-based models are introduced to combine the features extracted from the images to make prediction. This scheme can work well with the high quality of image features, so backbone with high computation cost plays a vital role in this scheme. However, a fast prediction in diagnostic radiology is also needed especially in case of emergency or region with low computation facilities, so we proposed an efficient convolutional neural network with GCN, which is named SGGCN, to meet the need of efficient computation and considerable accuracy. SGGCN used SGNet-101 as backbone, which is built by ShuffleGhost Block (Huang et al., 2021) to extract features with a low computation cost. In order to make sufficient usage of the information in GCN, a new GCN architecture is designed to combine information from different layers together in GCNM module so that we can utilize various hierarchical features and meanwhile make the GCN scheme faster. The experiment on CheXPert datasets illustrated that SGGCN achieves a considerable performance. Compared with GCN and ResNet-101 (He et al., 2015) backbone (test AUC 0.8080, parameters 4.7M and FLOPs 16.0B), the SGGCN achieves 0.7831 (−3.08%) test AUC with parameters 1.2M (−73.73%) and FLOPs 3.1B (−80.82%), where GCN with MobileNet (Sandler and Howard, 2018) backbone achieves 0.7531 (−6.79%) test AUC with parameters 0.5M (−88.46%) and FLOPs 0.66B (−95.88%).

The environmental pressures of major wastes in the circular economies can be abated leveraging the complementarity and optimal conditions of their co-combustion. The oxy-fuel co-combustion of phytoremediation biomass of Sedum alfredii Hance (SAH) and textile dyeing sludge (TDS) may be a promising choice for sustainable CO

Description, In Nrf2-activated tumors, G6pd inhibition depletes TCA intermediates and suppresses tumor growth., The KEAP1/NRF2 pathway promotes metabolic rewiring to support redox homeostasis. Activation of NRF2 occurs in many cancers, often due to KEAP1 mutations, and is associated with more aggressive disease and treatment resistance. To identify metabolic dependencies in cancers with NRF2 activation, we performed a metabolism-focused CRISPR screen. Glucose-6-phosphate dehydrogenase (G6PD), which was recently shown to be dispensable in Ras-driven tumors, was a top dependency. G6PD catalyzes the committed step of the oxidative pentose phosphate pathway that produces NADPH and nucleotide precursors, but neither antioxidants nor nucleosides rescued. Instead, G6PD loss triggered tricarboxylic acid (TCA) intermediate depletion because of up-regulation of the alternative NADPH-producing enzymes malic enzyme and isocitrate dehydrogenase. In vivo, G6PD impairment markedly suppressed KEAP1 mutant tumor growth, and this suppression was further augmented by TCA depletion by glutaminase inhibition. Thus, G6PD inhibition–induced TCA depletion is a therapeutic vulnerability of NRF2-activated cancer.

Given the globally abundant availability of waste plastics and the negative environmental impacts of textile dyeing sludge (TDS), their co-combustion can effectively enhance the circular economies, energy recovery, and environmental pollution control. The (co-)combustion performances, gas emissions, and ashes of TDS and two plastics of polypropylene (PP) and polyethylene (PE) were quantified and characterized. The increased blend ratio of PP and PE improved the ignition, burnout, and comprehensive combustion indices. The two plastics interacted with TDS significantly in the range of 200-600 ℃. TDS pre-ignited the combustion of the plastics which in turn promoted the combustion of TDS. The co-combustions released more CO

To examine the association between the hospitalization time and fall incidence.A secondary analysis using the Dryad Digital Repository public database.Data were extracted from the Fukushima Medical University Hospital cohort study between August 2008 and September 2009. The final analytic sample included 8,598 participants, 156 of who fell. The risk of fall incidents according to hospitalization time was estimated using logistic proportional hazards models, and restricted cubic splines with four knots model were developed.The median hospitalization time was 9.00 (4.00, 17.00) days. The incidence of falls was 1.81% (N = 156). A U-shaped association between the hospitalization time and fall incidence, with an inflextion point of 8 days. We found a decreasing fall incidence as the hospitalization time increased from 0 to 8 days (OR 0.72 [0.62 ~ 0.83], p .001); beyond 8 days, the fall incidence increased as the hospitalization time increased (OR 1.06 [1.04 ~ 1.09]).

Long non-coding RNAs (lncRNAs) have been elucidated to play vital roles in the phenotype of trophoblast cells. Nevertheless, the effect of SNHG1 has not been investigated on trophoblast cells in recurrent spontaneous abortion (RSA). We aim to investigate the effect of SNHG1 on the phenotype of trophoblast cells during RSA. The RSA mice were established by mating female CBA/J mice with male DBA/2 mice. Microarray analysis was applied in RSA mice, and SNHG1 was identified as a significantly downregulated lncRNA. SNHG1 improved pregnancy outcome and reduced embryo resorption in RSA mice. Trophoblast cell proliferation, apoptosis, migration, and invasion were investigated by CCK8, EdU, TUNEL, wound healing, and Transwell assays. SNHG1 promoted proliferation, migration, and invasion of trophoblast cells, and reduced apoptosis. Mechanistically, SNHG1 bound to miR-183-5p in trophoblast cells. Moreover, miR-183-5p directly targeted ZEB2. Rescue experiment showed that ZEB2 silencing reversed the ameliorative effect of SNHG1 on pregnancy outcome and the promotion of trophoblast activity in RSA mice by impaired the Wnt/β-catenin pathway. In conclusion, we found that SNHG1 plays a critical role in the progression of RSA via miR-183-5p/ZEB2 and Wnt/β-catenin signaling. It has potential to be a therapeutic marker of RSA.

The finite-time peak-to-peak filtering problem is studied for a class of linear dynamic systems. By reconstructing the system, the dynamic filtering error system is obtained. Our aim is to design a peak-to-peak filter such that the induced L∞ gain from the unknown disturbance to the estimated errors is minimized with respect to the finite-time interval. By using a proper Lyapunov function, sufficient conditions are established on the existence of peak-to-peak filter which also guarantees the finite-time boundedness of the filtering error dynamic systems. The design criteria are presented in the form of linear matrix inequalities and then described as an optimization problem. Simulation results are given to illustrate the validity of the proposed approaches.

Zinc fingers are among the most abundant protein motifs and play a pivotal role in cell proliferation, migration, and differentiation. Emerging studies have focused on the zinc finger transcription factors role in related diseases and discovered they are involved in activating oncogenic transcription, HIV reverse transcription, and bacterium infection. Hence, it is important to investigate and understand how zinc finger transcription factors can be selectively inhibited. The aim of this minireview is to describe how Zn Finger inhibition occurs within both a chemical and biological framework. Complexes Synthesis, inhibition mechanism, and selectivity are comprehensively reviewed. Cells utilize phosphorylation and acetylation to self-inhibit the zinc finger transcription factors by adjusting spatial structure and chemical properties. Also, we propose potential regulation sites of post transcription modification, therapeutic treatments and concerns over animal trials.

The carbon footprint of the cold chain logistics system refers to the greenhouse gas emissions directly or indirectly caused in each link of the cold chain logistics activities. Because cold chain logistics is the main carbon emitter in the field of logistics, research on how to reduce carbon emissions in the field of cold chain logistics plays an important role in energy conservation and emission reduction. Based on the in-depth analysis of the carbon footprint of cold chain logistics, this paper introduces the distance coefficient and freshness parameters into the optimization model innovatively and uses the life cycle assessment method and input-output method to determine the calculation range of the carbon footprint of fresh products of each link in the cold chain logistics. The system calculates the carbon emissions generated by the production and operation activities of each place of origin, distribution center, retailer, and waste disposal during the circulation of fresh products. This paper establishes a carbon footprint optimization model to discuss how to balance carbon constraints and minimized costs. Through the analysis of the simulation results, from the perspective of the government and enterprises, corresponding countermeasures are put forward to more effectively achieve the goal of energy conservation and emission reduction and guide the cold chain logistics industry to sustainable development.

In this study, the detoxification mechanisms of water-soluble fluorine in the bottom ash and the distribution of fluorine during the spent potlining (SPL) incineration were characterized in response to four calcium compounds using an experimental tube furnace. CaSiO3, CaO, Ca(OH)2, and CaCO3-assisted SPL incineration converted NaF to low toxicity compounds in the bottom ash yielding a conversion range of 54.24–99.45% relative to the individual SPL incineration. The two main mechanisms of the fluorine transformation were the formations of CaF2 and Ca4Si2O7F2. The fluorine transformation efficiency was greater with CaSiO3 than CaO, Ca(OH)2, and CaCO3. Our simulations demonstrated that SiO2 enhanced the conversion of NaF. The fluorine leaching content of the bottom ash was estimated at 13.71 mg⋅L−1 after the SPL co-incineration with CaSiO3 (Ca:F = 1.2:1). The acid-alkali solutions had no significant effect on the fluorine leaching content of the bottom ash when 3 ≤ pH ≤ 12. Fluorine during the SPL co-incineration with CaSiO3 (Ca:F = 1.2:1) at 850 °C for 60 min was partitioned into 83.37, 13.90, and 2.72% in the bottom ash, fly ash, and flue gas, respectively. The transformation and detoxification mechanisms of water-soluble fluorine provide new insights into controls on fluorine emission from the SPL incineration.

Objective:Nasopharyngeal carcinoma is highly endemic in Southeast China. Circulating tumor cell is an important biomarker in the prognosis of variety kinds of cancers. Overexpression of fibronectin 1 was observed in variety kinds of malignancies and may contribute to progress and metastasis of the cancers. The current study was aimed to investigate phenotypes of circulating tumor cell in nasopharyngeal carcinoma blood and fibronectin 1 expression in the circulating tumor cell, and their clinical application in predicting nasopharyngeal carcinoma prognosis.Methods:Blood samples were obtained from nasopharyngeal carcinoma patients before and after treatment. CanPatrol circulating tumor cell enrichment and RNA in situ hybridization were applied to identify circulating tumor cell and its phenotypes. Fibronectin 1 messenger RNA expression in the cells of circulating tumors was examined by messenger RNA-in situ hybridization.Results:Circulating tumor cell was not associated with tumor characteristics or lymph node metastasis. Patients with >9 circulating tumor cells or >5 mesenchymal phenotype circulating tumor cell per 5-mL blood had poorer progression-free survival ( P < .05). Multivariable analysis demonstrated that 2 or more mesenchymal phenotype circulating tumor cells with high fibronectin 1 messenger RNA expression predicted shorter progression-free survival ( P < .05).Conclusions:Circulating tumor cells with high-level fibronectin 1 expression was associated with poor survival in patients with nasopharyngeal carcinoma and could be an independent prognostic factor for nasopharyngeal carcinoma.

Cellular mechanisms causing insulin resistance (IR) in chronic kidney disease (CKD) are poorly understood. One potential mechanism is that CKD-induced inflammation activates the signal transducer and activator of transcription 3 (Stat3) in muscle. We uncovered increased p-Stat3 in muscles of mice with CKD or mice fed high-fat diet (HFD). Activated Stat3 stimulates the expression of Fbxo40, a muscle-specific E3 ubiquitin ligase that stimulates ubiquitin conjugation leading to degradation of insulin receptor substrate 1 (IRS1). Evidence that Stat3 activates Fbxo40 includes 1) potential Stat3 binding sites in Fbxo40 promoters; 2) Stat3 binding to the Fbxo40 promoter; and 3) constitutively active Stat3 stimulating both Fbxo40 expression and its promoter activity. We found that IL-6 activates Stat3 in myotubes, increasing Fbxo40 expression with reduced IRS1 and p-Akt. Knockdown Fbxo40 using siRNA from myotubes results in higher levels of IRS1 and p-Akt despite the presence of IL-6. We treated mice with a small-molecule inhibitor of Stat3 (TTI-101) and found improved glucose tolerance and insulin signaling in skeletal muscles of mice with CKD or fed an HFD. Finally, we uncovered improved glucose tolerance in mice with muscle-specific Stat3 KO versus results in Stat3f/fmice in response to the HFD. Thus Stat3 activation in muscle increases IR in mice. Inhibition of Stat3 by TTI-101 could be developed into clinical strategies to improve muscle insulin signaling in inflammation and other catabolic diseases.

NADH provides electrons for aerobic ATP production. In cells deprived of oxygen or with impaired electron transport chain activity, NADH accumulation can be toxic. To minimize such toxicity, elevated NADH inhibits the classical NADH producing pathways: glucose, glutamine, and fat oxidation. Here, through deuterium tracing studies in cultured cells and mice, we show that folate-dependent serine catabolism also produces substantial NADH. Strikingly, when respiration is impaired, serine catabolism through methylene tetrahydrofolate dehydrogenase (MTHFD2) becomes a major NADH source. In cells whose respiration is slowed by hypoxia, metformin, or genetic lesions, mitochondrial serine catabolism inhibition partially normalizes NADH levels and facilitates cell growth. In mice with engineered mitochondrial complex I deficiency (NDUSF4-/-), serine’s contribution to NADH is elevated and progression of spasticity is modestly slowed by pharmacological blockade of serine degradation. Thus, when respiration is impaired, serine catabolism contributes to toxic NADH accumulation.

The aim of the present study was to investigate whether niclosamide could sensitize the nasopharyngeal carcinoma cells to radiation and further explore the underlying mechanisms. CCK-8 assay was used to determine the effect of niclosamide on the proliferation of NPC cells. Colony formation assay was used to evaluate the radiosensitizing effect of niclosamide on NPC cells. Flow cytometry analysis was used to determine the apoptosis of NPC cells induced by niclosamide. Immunofluorescent staining was used to detect the formation of γ-H2AX foci and the localization of Ku70/80 proteins in NPC cells. Real-time PCR quantification analysis was used to examine the level of Ku70/80 mRNA. DNA damage repair-related proteins were detected by western blot analysis. Our results showed that niclosamide markedly suppressed the proliferation of NPC cells. Niclosamide pretreatment followed by irradiation reduced the colony forming ability of NPC cells. Niclosamide in combination with irradiation significantly increased the apoptotic rate of NPC cells. Niclosamide significantly reduced the transcriptional level of K70/80 but not the translocation of Ku70/80 protein induced by irradiation. In conclusion, our study demonstrated that niclosamide could inhibit the growth of NPC cells and sensitize the NPC cells to radiation via suppressing the transcription of Ku70/80.

In fog weather, aiming at the poor performance of fog removal based on the conventional polarization defogging algorithm, a dense fog removal algorithm based on the polarization principle of dark channel priori and guided filtering is proposed. The polarization information is combined with the primal theory of dark primary for the purpose of combining the polarization information with the defogging model. Then the dark channel principle of the image is obtained using atmospheric scattering model. Finally, the atmosphere is corrected by the guidance filtering algorithm. The experimental results show that the standard deviation, entropy and average gradient of the defogged image are much higher than those of the existing polarization defogging technology. This method can effectively enhance the overall contrast of the image under foggy weather and improve the target recognition ability of polarized images.

The eco-friendly disposal choices of phytoremediation biomass still remain to be explored. This study characterized the combustions of Sedum alfredii Hance (SAH) in response to its aboveground (SAH-A) and belowground (SAH-B) parts, the oxy-fuel (CO2/O2) and air (N2/O2) atmospheres, temperature, and heating rate. The decomposition behaviors, gas-to-ash characteristics, thermo-kinetic parameters, and mineral transformations were quantified. In both atmospheres, the combustion performances were better for SAH-A than SAH-B at the same heating rate. In the range of 400.0–598.8 °C, the maximum mass loss rate of both samples obviously decreased and delayed with CO2 replacing N2 at the same oxygen concentration. The SAH-A and SAH-B combustions in both atmospheres emitted C- (CO2, CO, CH4, and small molecular organic substances) and N-containing (HCN and NH3) gases. In both atmospheres, the temperature dependency of the gas emissions remained the same. Both empirical indices and ternary phase diagrams indicated that both samples had a high deposition risk. Thermochemical equilibrium simulations were used to predict the slagging risk in response to ash mineral transformations. Our findings can provide new insights into the combustion dynamics of phytoremediation biomass and its effect on CO2 capture, utilization, and storage in mitigating climate change.

In response to the global initiative for greenhouse gas emission reduction, the co-combustion of coal and spent pot lining (SPL) may cost-effectively minimize waste streams and environmental risks. This study aimed to quantify the emission-to-ash detoxification mechanisms of the co-combustion of SPL and pulverized coal (PC) and their kinetics, gas emission, fluorine-leaching toxicity, mineral phases, and migrations. The main reaction covered the ranges of 335–540 °C and 540–870 °C while the interactions occurred at 360–780 °C. The apparent activation energy minimized (66.99 kJ/mol) with 90% PC addition. The rising PC fraction weakened the peak intensity of NaF and strengthened that of Ca2F, NaAlSiO4, and NaAlSi2O6. The addition of PC enhanced the combustion efficiency of SPL and raised the melting temperature by capturing Na. PC exhibited a positive effect on solidifying water-soluble fluorine and stabilizing alkali and alkaline earth metals. The leaching fluorine concentrations of the co-combustion ashes were lower than did SPL mono-combustion. The main gases emitted were HF, NH3, NOx, CO, and CO2. HF was largely released at above 800 °C. Multivariate Gaussian process model-based optimization of the operational conditions also verified the gas emissions results. Our study synchronizes the utilization and detoxification of SPL though co-combustion and provides insights into an eco-friendlier life-cycle control on the waste-to-energy conversion.

Lung cancer is one of the leading causes of cancer-associated mortality, worldwide. The overall survival rate remains low, but progress has been made in improving the diagnosis and treatment of lung cancer over the past decades. Niclosamide, a salicylanilide derivative used for the treatment of tapeworm infections, is safe, well tolerated, inexpensive and readily available. Previous studies have identified niclosamide as a potential anticancer agent. The present study demonstrated that niclosamide enhanced the effect of irradiation by inhibiting the hypoxia-inducible factor-1α/vascular endothelial growth factor signaling pathway. These findings suggest that niclosamide may be a promising candidate for clinical evaluation as part of a combined regimen for the treatment of non-small cell lung cancer.

Fibrosis in skeletal muscle develops after injury or in response to chronic kidney disease (CKD) but the origin of cells becoming fibrous tissue and the initiating and sustaining mechanisms causing muscle fibrosis are unclear. We have identified muscle fibro/adipogenic progenitor cells (FAPs) that potentially differentiate into adipose tissues or fibrosis. We also demonstrated that CKD stimulates myostatin production in muscle. Therefore, we tested whether CKD induces myostatin which stimulates fibrotic differentiation of FAPs leading to fibrosis in skeletal muscles. We isolated FAPs from mouse muscles and found that myostatin stimulates their proliferation and conversion into fibrocytes. In vivo, FAPs isolated from EGFP-transgenic mice (FAPs-EGFP) were transplanted into muscles of mice with CKD or into mouse muscles that were treated with myostatin. CKD or myostatin stimulated FAPs-EGFP proliferation in muscle and increased α-smooth muscle actin expression in FAP-EGFP cells. When myostatin was inhibited with a neutralizing peptibody (a chimeric peptide-Fc fusion protein), the FAP proliferation and muscle fibrosis induced by CKD were both suppressed. Knocking down Smad3 in cultured FAPs interrupted their conversion into fibrocytes indicating that myostatin directly converts FAPs into fibrocytes. Thus, counteracting myostatin may be a strategy for preventing the development of fibrosis in skeletal muscles of patients with CKD.