Unrecognized extensive charge of microbial gas in the Junggar basin.

Different from the Qaidam basin with about 320 billion m3 microbial gas, only limited microbial gases were found from the Junggar basin with similarly abundant type III kerogen. To determine whether microbial gases have not yet identified, natural gas samples from the Carboniferous to Cretaceous in the Junggar basin have been analyzed for chemical and stable isotope compositions. The results reveal some of the gases from the Mahu sag, Zhongguai, Luliang and Wu-Xia areas in the basin may have mixed with microbial gas leading to straight ethane to butane trends with a "dogleg" light methane in the Chung's plot. Primary microbial gas from degradation of immature sedimentary organic matter is found to occur in the Mahu sag and secondary microbial gas from biodegradation of oils and propane occurred in the Zhongguai, Luliang and Beisantai areas where the associated oils were biodegraded to produce calcites with δ13C values from + 22.10‰ to + 22.16‰ or propane was biodegraded leading to its 13C enrichment. Microbial CH4 in the Mahu sag is most likely to have migrated up from the Lower Wuerhe Formation coal-bearing strata by the end of the Triassic, and secondary microbial gas in Zhongguai and Beisantan uplifts may have generated after the reservoirs were uplifted during the period of the Middle and Late Jurassic. This study suggests widespread distribution of microbial gas and shows the potential to find large microbial gas accumulation in the basin.

Aggregating fine hydrophilic materials in froth flotation to improve separation efficiency through a homo-aggregation flotation process.

As a versatile separation technology, froth flotation has gained extensive applications in both primary resource recovery and secondary resource recycling. It exploits differences in the water-wettability of solid surfaces to separate value components from wastes. Hydrophobic (water-repelling) particles attach to gas bubbles, float away from hydrophilic (water-loving) particles and become froth products. However, flotation separation deteriorates with low efficiency and low selectivity when treating fine (< circa 20 µm) and ultrafine (< circa 5 µm) particles. Particularly, fine hydrophilic particles affect value mineral recovery and froth product grade by attaching indiscriminately to value minerals, increasing pulp viscosity, and entering froth products by entrainment. Many mitigation measures have been proposed in the literature to target the fine hydrophilic particles in the flotation process, mainly from physical/mechanical perspective. Notably, recent investigations suggest that selectively aggregating fine hydrophilic particles could reduce their entrainment to froth products and increase froth product grade. In this review, we first analyze the adverse effects of fine hydrophilic particles on froth flotation and summarize current mitigation methods. Following the review, a homo-aggregation flotation (HAF) concept different from conventional approaches is proposed to improve the separation efficiency of fine particles in froth flotation. We present case studies highlighting the necessity of aggregating fine hydrophilic materials to improve separation efficiency in froth flotation, noting that hydrophobic aggregation is a natural process in water.

Selective Separation of Chalcopyrite from Pyrite Using Sodium Humate: Flotation Behavior and Adsorption Mechanism.

Flotation separation of chalcopyrite from pyrite using lime or cyanides as depressants results in serious problems, such as the blockage of pipelines and environmental pollution. Eco-friendly organics are a future trend for beneficiation plants. In this research, the eco-friendly organic depressant sodium humate (SH) was chosen as a depressant to separate chalcopyrite from pyrite by flotation. The results indicated that SH could selectively depress pyrite owing to the oxidation species (FeOOH, Fe2(SO4)3) on its surface. The oxidation species were the adsorption sites for the COO- in the SH structure and impeded the subsequent collector potassium ethyl xanthate (KEX) adsorption. However, chalcopyrite was slightly oxidized with fewer oxidation species for SH adsorption, and KEX could be adsorbed and functioned effectively. This research suggested that SH could be an effective and eco-friendly depressant in chalcopyrite-pyrite flotation separation, which had potential use in the industry.

Utilization and Mechanisms of Tannic Acid as a Depressant for Chalcopyrite and Pyrite Separation.

Current flotation practices using lime or cyanide as depressants in chalcopyrite and pyrite separation have significant disadvantages, such as substantial reagent consumption, high slurry pH, and environmental hazards. This work aimed to explore the utilization and mechanisms of tannic acid (TA) as an eco-friendly alternative to lime or cyanide in chalcopyrite-pyrite separation. Flotation results showed that TA selectively depressed pyrite yet allowed chalcopyrite to float at neutral or alkaline pH. Adsorption density and zeta potential results indicated that TA adsorbed intensely on pyrite but minorly on chalcopyrite. Besides, potassium ethyl xanthate was still largely adsorbed on chalcopyrite but not on pyrite after TA adsorption. Surface analysis by Fourier transform infrared spectroscopy and X-ray photoelectron spectroscopy further showed that the oxidation species of FeOOH and Fe2 (SO4)3, particularly FeOOH were the main active sites for TA chemical adsorption. Owing to the greater and faster oxidation of pyrite, more FeOOH and Fe2 (SO4)3 were generated on the pyrite surface, and the chemical adsorption of TA was more pronounced on the pyrite surface than on the chalcopyrite surface.

A review of the roles of constituent minerals and residual bitumen in the solid-liquid separation of oil sands tailings.

The efficient dewatering of fluid fine tailings (FFT) generated from warm-water extraction of Canadian oil sands is a major challenge that has limited the timely reclamation of the tailings. It is generally recognized that both chemical amendments and physical/mechanical solid-liquid separation treatments are required to speed up FFT dewatering. Significant efforts have been made to enhance the rate of solid-liquid separation of FFT in the past several decades. The fact that these efforts have met with limited successes calls for a better fundamental understanding of the solid-liquid separation process. In this work, we reviewed and critically analyzed the factors that contribute to the difficult dewatering of FFT, including the role of constituent minerals and residual bitumen. In particular, the effects of mineralogical composition, mineral particle size, and the role of residual bitumen on settling rate, hydraulic conductivity, and filtration rate are reviewed and discussed. This review also points out directions to accelerate the dewatering of FFT, such as reducing the effective volume fraction of swelling clays and releasing bitumen coating from clay surfaces, that may significantly increase the filtration rate of oil sands tailings.

Anlotinib Induces a T Cell-Inflamed Tumor Microenvironment by Facilitating Vessel Normalization and Enhances the Efficacy of PD-1 Checkpoint Blockade in Neuroblastoma.

PURPOSE: Anlotinib has achieved good results in clinical trials of a variety of cancers. However, the effects of anlotinib on the tumor microenvironment (TME) and systemic immunity have not been reported. There is an urgent need to identify the underlying mechanism to reveal new opportunities for its application in neuroblastoma (NB) and other cancers. Understanding the mechanism will hopefully achieve the goal of using the same method to treat different cancers. EXPERIMENTAL DESIGN: This study used bioinformatics, NB syngeneic mouse models, flow cytometry, RNA-seq, and immunofluorescence staining to explore the mechanisms of anlotinib on the TME, and further explored anlotinib-containing combination treatment strategies. RESULTS: We proved that anlotinib facilitates tumor vessel normalization at least partially through CD4+ T cells, reprograms the immunosuppressive TME into an immunostimulatory TME, significantly inhibits tumor growth, and effectively prevents systemic immunosuppression. Moreover, the combination of anlotinib with a PD-1 checkpoint inhibitor counteracts the immunosuppression caused by the upregulation of PD-L1 after monotherapy, extends the period of vascular normalization, and finally induces NB regression. CONCLUSIONS: To our knowledge, this study is the first to dynamically evaluate the effect of a multitarget antiangiogenic tyrosine kinase inhibitor on the TME. These findings have very important clinical value in guiding the testing of related drugs in NB and other cancers. Based on these findings, we are conducting a phase II clinical study (NCT04842526) on the efficacy and safety of anlotinib, irinotecan, and temozolomide in the treatment of refractory or relapsed NB, and hopefully we will observe patient benefit.

Sound Velocities, Elasticity, and Mechanical Properties of Stoichiometric Submicron Polycrystalline δ-MoN at High Pressure.

Acoustic velocities and elasticity of stoichiometric submicron polycrystalline δ-MoN have been reported at high pressure using ultrasonic measurements and first-principles calculations. Using the finite-strain equation-of-state approach, the bulk modulus and shear rigidity, as well as their pressure derivatives, are derived from the current experimental data, yielding BS0 = 360.0(8) GPa, G0 = 190.0(5) GPa, ∂BS/∂P = 3.4(2), and ∂G/∂P = 1.4(1). Based on our experimental data and the velocity-elasticity correlated models, the mechanical/thermal properties (i.e., hardness, fracture toughness, Grüneisen parameter, Debye temperature, Poisson's ratio) are also derived. Interestingly, we find that hexagonal δ-MoN is almost as incompressible as superhard cubic boron nitride (cBN) (∼384 GPa) and its hexagonal ε-NbN (∼373 GPa) counterpart, and its shear rigidity (G = 190 GPa) is comparable to that of the superhard diamond composite (G = 204 GPa). Moreover, the fracture toughness of submicron δ-MoN polycrystals is achieved up to ∼4.3 MPa·m1/2, which is comparable to superhard diamond (4-7 MPa·m1/2) and cBN (2-5 MPa·m1/2). The Vickers hardness of submicron δ-MoN is estimated to be Hv ≈ 17.4 GPa using Chen's model, which is found to be almost as hard as hexagonal ε-NbN and δ-WN, and may be very important for its applications in extreme environments.

Polo-like kinase 4 mediates epithelial-mesenchymal transition in neuroblastoma via PI3K/Akt signaling pathway.

Neuroblastoma (NB) is the most common malignant tumor in infancy and most common extracranial solid tumor in childhood. With the improvement of diagnosis and treatment, the survival rate of patients with low-risk and intermediate-risk NB can reach up to 90%. In contrast, for high-risk NBs, the long-term survival rate is still <40% because of heterogeneity of this tumor. The pathogenesis of NB is still not explicit, therefore it is of great significance to explore the mechanism of NB tumorigenesis and discover new therapeutic targets for NB. Polo-like kinase 4 (PLK4), one of the polo-like kinase family members, is an important regulator of centriole replication. The aberrant expression of PLK4 was found in several cancers and a recent study has unraveled a novel function of PLK4 as a mediator of invasion and metastasis in Hela and U2OS cells. However, the function of PLK4 in NB development and progression remains to be elucidated. The study showed the expression level of PLK4 in NB tissues was remarkably upregulated and high expression of PLK4 was negatively correlated with clinical features and survival, which suggested that PLK4 could be a potential tumor-promoting factor of NB. Functional studies indicated downregulation of PLK4 suppressed migration and invasion and promoted apoptosis in NB cells. Further experiments showed that downregulation of PLK4 in NB cells inhibited EMT through the PI3K/Akt signaling pathway. Animal experiments demonstrated that the downregulation of PLK4 in SK-N-BE(2) cells dramatically suppressed tumorigenesis and metastasis. PLK4 may be a promising therapeutic target for NB.

Clinical evaluation of integrated panel testing by next-generation sequencing for somatic mutations in neuroblastomas with MYCN unamplification.

Neuroblastomas (NBs) exhibit heterogeneity and show clinically significant prognosis classified by genetic alterations. Among prognostic genes or genome factors, MYCN amplification (MNA) is the most established genomic marker of poor prognosis in patients with NB. However, the prognostic classification of more than 60% of patients without MNA has yet to be clarified. In this study, the application of target next-generation sequencing (NGS) was extended on the basis of a comprehensive panel of regions where copy number variations (CNVs) or point mutations occurred to improve the prognostic evaluation of these patients and obtain the sequence of 33 patients without MNA. A mean coverage depth of 887× was determined in the target regions in all of the samples, and the mapped read percentage was more than 99%. Somatic mutations in patients without MNA could be precisely defined on the basis of these findings, and 17 unique somatic aberrations, including 14 genes, were identified in 11 patients. Among these variations, most were CNVs with a number of 13. The 3-year event-free survival (EFS) of CNV(-) patients was 60.0% compared with the EFS (16.7%) of CNV(+) patients (P = 0.015, HR = 0.1344, 95%, CI = 0.027 to 0.678). CNVs were also associated with unfavorable histological characteristics (P = 0.003) and likely to occur in stage 4 (P = 0.041). These results might further indicate the role of CNVs in NB chemotherapy resistance (P = 0.059) and show CNVs as a therapeutic target. In multivariate analysis, the presence of CNVs was a clinically negative prognostic marker that impaired the outcome of patients without MNA and associated with poor prognosis in this tumor subset. Comprehensive genetic/genomic profiling instead of focusing on single genetic marker should be performed through in-depth NGS that could reveal prognostic information, improve NB target therapy, and provide a basis for investigations on NB pathogenesis.

Strain induced topological phase transitions in monolayer honeycomb structures of group-V binary compounds.

We present first-principles calculations of electronic structures of a class of two-dimensional (2D) honeycomb structures of group-V binary compounds. Our results show these new 2D materials are stable semiconductors with direct or indirect band gaps. The band gap can be tuned by applying lattice strain. During their stretchable regime, they all exhibit metal-indirect gap semiconductor-direct gap semiconductor-topological insulator (TI) transitions with increasing strain from negative (compressive) to positive (tensile) values. The topological phase transition results from the band inversion at the Γ point which is due to the evolution of bonding and anti-bonding states under lattice strain.

Functional MUC4 suppress epithelial-mesenchymal transition in lung adenocarcinoma metastasis.

The mucin MUC4 is a high molecular weight membrane-bound transmembrane glycoprotein that is frequently detected in invasive and metastatic cancer. The overexpression of MUC4 is associated with increased risks for several types of cancer. However, the functional role of MUC4 is poorly understood in lung adenocarcinoma. Using antisense-MUC4-RNA transfected adenocarcinoma cells, we discovered that the loss of MUC4 expression results in epithelial-mesenchymal transition (EMT). We found morphological alterations and the repression of the epithelial marker E-cadherin in transfected cells. Additionally, the loss of MUC4 caused the upregulation of the mesenchymal marker vimentin compared to control cells. Using a MUC4-knockdown versus control LTEP xenograft mice model (129/sv mice), we also found that EMT happened in lung tissues of MUC4-knockdown-LTEP xenograft mice. Moreover, antisense-MUC4-RNA transfected cells had a significantly increased cellular migration ability in vitro. The loss of MUC4 also occurred in lung adenocarcinoma patients with lymph node metastases. We further investigated MUC4 and found that it plays a critical role in regulating EMT by modulating ß-catenin. Taken together, our study reveals a novel role for MUC4 in suppressing EMT and suggests that the assessment of MUC4 may function as a prognostic biomarker and could be a potential therapeutic target for lung adenocarcinoma metastasis.

Succinate dehydrogenase 5 (SDH5) regulates glycogen synthase kinase 3ß-ß-catenin-mediated lung cancer metastasis.

We demonstrate that loss of succinate dehydrogenase 5 (SDH5) expression initiates epithelial-mesenchymal transition (EMT), which is visualized by the repression of E-cadherin and up-regulation of vimentin in lung cancer cell lines and clinical lung cancer specimens. In SDH5 knock-out mice, lung epithelial cells exhibited elevated mesenchymal markers, which is characteristic of EMT. Using a human lung xenograft-mouse model, we observed that knocking down endogenous SDH5 in human carcinoma cells leads to the development of multiple lymph node metastases. Moreover, our data indicate that SDH5 functions as a critical protein in regulating EMT by modulating the glycogen synthase kinase (GSK)-3ß-ß-catenin signaling pathway. These results reveal a critical role for SDH5 in EMT and suggest that SDH5 may be a prognostic biomarker and potential therapeutic target for lung cancer metastasis.

Clinical significance of E-cadherin, ß-catenin, vimentin and S100A4 expression in completely resected squamous cell lung carcinoma.

OBJECTIVE: The aim of this study was to evaluate the prognostic value of E-cadherin, ß-catenin, vimentin and S100A4 expression in a cohort of squamous cell lung carcinoma (SqCC) patients. METHODS: Tumours from 204 patients with surgically resected SqCC were used for the immunohistochemical analyses of E-cadherin, ß-catenin, vimentin and S100A4 expression. Correlations between the expression of these markers and clinicopathological parameters were analysed using the χ(2) test. The prognostic value of these markers was evaluated using univariate Kaplan-Meier survival analyses and multivariate Cox proportional hazards model analyses. RESULTS: Significant associations between E-cadherin expression and T stage (p=0.040), histological differentiation (p=0.005), lymph node metastasis (p<0.001), and recurrence (p<0.001) were identified. Decreased ß-catenin expression was significantly correlated with T stage (p=0.003) and lymph node metastasis (p=0.010). Vimentin expression was associated with histological differentiation (p=0.017) and lymph node metastasis (p=0.001). Moreover, significant correlations were observed between S100A4 expression and lymph node metastasis (p=0.020) and recurrence (p<0.001). In the univariate analyses, high E-cadherin expression was a positive indicator for overall survival (OS) (p<0.001) and disease-free survival (DFS) (p<0.001), whereas high S100A4 or vimentin expression were negative indicators for OS (p<0.001 and p=0.010, respectively) and DFS (p<0.001 and p=0.006, respectively). In the multivariate analyses, E-cadherin and S100A4 expression were independent prognostic factors for OS (HR 0.697, 95% CI 0.524 to 0.926, p=0.013, and HR 1.508, 95% CI 1.122 to 2.027, p=0.007, respectively) and DFS (HR 0.634, 95% CI 0.471 to 0.852, p=0.003, and HR 1.490, 95% CI 1.101 to 2.015, p=0.010, respectively). CONCLUSIONS: Effective analysis of E-cadherin and S100A4 expression may allow for the identification of patients who are at a high risk of recurrence and poor prognosis in SqCC.