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● It is necessary to address the N flows and their impacts on environment in China for sustainable N management. ● Barriers include better understanding of N cycle mechanisms and improving low cost abatement technologies are needed to overcome. ● Integrated measures and policies are crucial for the abatement of adverse impacts of N. The impacts of nitrogen on environmental quality, greenhouse gas balances, ecosystem and biodiversity in China are of great concern given the magnitude of demand for food and energy. Comprehensive summaries of historic N flows and their critical threats and sustainable management are urgently needed. This paper initially reviews the historical trends of N flows in China and identifies the critical threats of N loss. Subsequently, it describes some recent success stories of N management, and finally indicates barriers to N pollution control. This review highlights three key points. Firstly, a steady increase of N input in China has led to a series of environmental problems via leaching and runoff, ammonia emissions and denitrification. Secondly, although great efforts to improve N management and N safety in China, further quantifications of N flows and analysis of their underlying mechanisms are needed to improve the understanding of the N cycle and pollution control. Finally, it proposes that the best available technologies combined with regulatory plans, laws, projects and policies should be implemented to overcome current barriers in N control and achieve a balance between the sustainable use of N resources and environmental conservation in China.

The reaction of reducing end groups in cellulose nanocrystals with dodecylamine was examined. Using a direct-dissolution solution-state NMR protocol, the regioselective formation of glucosylamines was shown. This provides an elegant approach to sustainably functionalize these bio-based nanomaterials, that may not require further reduction to more stable secondary amines. [ABSTRACT FROM AUTHOR]

Background: Nontuberculous mycobacterial (NTM) pulmonary disease (PD) has rapidly increased globally. The characteristics and comparison of rapidly growing mycobacteria PD (RGM-PD) and slowly growing mycobacteria PD (SGM-PD) are still unclear. Methods: Our study enrolled 31 NTM-PD patients. Clinical data, including baseline, symptoms, underlying disease, laboratory tests, metagenomic next-generation sequencing (mNGS) results, radiological images, treatment, and outcome were recorded and analyzed. Results: Of the 31 patients with NTM-PD, 22 patients were female and 9 were male. It included 11 RGM-PD and 20 SGM-PD. There was no difference in age (P = 0.425) and body mass index (P = 0.152) between the two groups. The common respiratory diseases in prevalence included bronchiectasis and chronic obstructive pulmonary disease. Three patients had positive results of T-SPOT tuberculosis (TB), and none had positive Xpert-Mycobacterium tuberculosis/rifampin results. On admission, patients were symptomatic and included cough/sputum production, fever, weight loss, fatigue, and hemoptysis. In comparison to RGM-PD, patients with SGM-PD had a greater chance of experiencing fatigue (P = 0.012). No significance was found in serum biomarkers between RGM and SGM-PD, including CD4/CD8 ratio, white blood cells, neutrophils, lymphocytes, procalcitonin, ferritin, C-reactive protein, and erythrocyte sedimentation rate. No liver or kidney impairment was found. Patients with RGM-PD were more likely to have right lower lobe (RLL) impairment (P = 0.021) and a cavity characteristic (P = 0.012). All 31 cases had positive mNGS results. The duration of mNGS was shorter than conventional methods (3.4 ± 0.7 vs. 26.4 ± 20.9, P < 0.001). Conclusions: Patients with SGM-PD were more likely to experience fatigue. The cavity and RLL involvement were more frequent in the RGM-PD. mNGS increases the identification of NTM specimens and complements the capabilities of conventional methods. [ABSTRACT FROM AUTHOR]

Background: As a member of the Ephrin protein family that elicits short distance cell‐cell signaling, EphrinA3 has been shown to promote or inhibit tumorigenesis depending on tumor types, but its roles and the underlying mechanisms in lung adenocarcinoma (LUAD) have not been reported. Materials and Methods: The TCGA database and Kaplan‐Meier Plotter database were used to analyze the differential expression of EphrinA3 between LUAD and para‐carcinoma tissues, and its effect on overall survival of LUAD patients. CCK‐8 assay, Edu assay, and flow cytometry were used to probe the effect of EphrinA3 on the proliferation of LUAD cells, and transwell assay was employed to examine its effect on migration and invasion. In addition, the effect of EphrinA3 on the growth of LUAD was further evaluated using a xenograft tumor model. Results: EphrinA3 was expressed highly in LUAD, and its expression level was negatively correlated with the prognosis of LUAD patients. In addition, EphrinA3 promoted proliferation, migration, and invasion of LUAD cells, and accelerated tumor growth in a xenograft LUAD model. The reported EphrinA3 receptors, EphA1 and EphA10, were expressed in clinical LUAD tissues and co‐localized with EphrinA3 in LUAD cells. Mechanistically, EphrinA3/Eph signaling activated AKT, ERK, and p38MAPK, induced epithelial‐mesenchymal transition (EMT), and upregulated matrix metalloproteases‐2 and ‐9 (MMP‐2/−9). Conclusion: EphrinA3 expression was negatively correlated with prognosis of patients with LUAD. EphrinA3 promoted proliferation, migration, and invasion of LUAD cells. EphrinA3 enhanced the phosphorylation of ERK and AKT, and potentiates EMT and MMP expression in LUAD cells. [ABSTRACT FROM AUTHOR]

Background: To reveal the function of protein tyrosine phosphatase‐L1 (PTPL1) in lung adenocarcinoma. Methods: Lung cancer cell lines were transfected with short hairpin RNA against PTPL1 (shPTPL1 group) or negative control (shmock group). Quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blotting were used to verify the transfection efficacy. Cell proliferation was analyzed by ethynyldeoxyuridine (EdU), Cell counting kit 8 (CCK8), and colony formation assay after PTPL1 or PTPL1 and yes‐associated protein (YAP1) knockdown. The effect of PTPL1 on tumor growth was examined in a xenograft lung cancer model. Results: PTPL1 was downregulated in various types of lung cancer cell lines. The EdU, CCK8, colony formation assays and investigation using a xenograft lung cancer model indicated that PTPL1 knockdown increased the proliferation of lung cancer cells. Mechanistically, PTPL1 knockdown induced the activation of the Proto‐oncogene tyrosine‐protein kinase SRC (Src)/Extracellular regulated MAP kinase (ERK) pathway and thereby promoted yes‐associated protein (YAP1) nuclear translocation and activation. Conclusions: In our study, PTPL1 played a crucial suppressive role in the pathogenesis of lung cancer potentially through counteracting the Src/ERK/YAP1 pathway. [ABSTRACT FROM AUTHOR]

Abstract Background Delayed neutrophil apoptosis may be an important factor in the persistent inflammation associated with chronic obstructive pulmonary disease (COPD). Bcl-2 family proteins are important regulators of neutrophil apoptosis. We determined the mRNA levels of pro-apoptotic Bak and anti-aptototic Bcl-xl and Mcl-1 members of the Bcl-2 family in unstimulated peripheral blood neutrophils from patients with mild to moderate COPD and compared these to neutrophils from healthy controls. Methods Neutrophils were isolated from peripheral blood samples of 47 COPD patients (smokers: N = 24) and 47 healthy controls (smokers: N = 24). Percentages of apoptotic cells were determined at 4, 24, and 36 h for unstimulated neutrophils cultured in vitro. Neutrophil mRNA expression of Bak, Bcl-xl, and Mcl-1 was determined by real-time polymerase chain reaction (PCR). FEV1 (% predicted) and FVC were determined by spirometry and correlations between mRNA levels and lung function parameters were determined. Results The percentages of apoptotic cells among unstimulated neutrophils from COPD patients were significantly lower compared to cells from controls after 4, 24, and 36 h in culture; smoking history had only a minimal effect on these differences. Unstimulated neutrophils from COPD patients had significantly lower Bak mRNA expression and higher expressions of Bcl-xl and Mcl-1 mRNA than cells from healthy controls. Again, smoking history had only a minimal effect on these trends. Bak mRNA expression was significantly positively correlated with both % predicted FEV1 and the FEV1/FVC ratio, while Bcl-xl and Mcl-1 mRNA expressions were significantly negatively correlated with %predicted FEV1 and the FEV1/FVC ratio. Conclusions The genes for pro-apoptotic Bak, and anti-apoptotic Bcl-xl and Mcl-1 may be important in regulating the delayed neutrophil apoptosis observed in COPD, which may contribute to COPD pathogenesis. Virtual Slides The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1605269445677066

TUG1 has been reported to play an important role in various cancer types. However, the study about the function of lncRNA TUG1 in myocardial infarction is limited. This study was aimed to investigate the role of TUG1 in H9c2 cell injury induced by hypoxia and explore its possible molecular mechanism. The proliferation assay, migration assay, invasion assay, and apoptosis assay were performed. RT-PCR was used to determine the relative RNA expression of TUG1, miR-124 and Hic-5. Western blotting was used to detect the expression levels of apoptotic proteins, Hic-5, Sp1, and Survivin. Hypoxia could significantly decrease cell proliferation, migration and invasion and increase H9c2 cell apoptosis. Knock-down of TUG1 promoted the cell damage induced by hypoxia. miR-124 was the direct target of TUG1 and down-regulated by TUG1. TUG1 silence aggravated hypoxia injury by up-regulating miR-124. In addition, Hic-5 was the target of miR-124 and negatively regulated by miR-124. Our findings showed that Hic-5 over-expression could significantly induce increases in cell viability, migration and invasion, and induce decrease in cell apoptosis after hypoxia damage. Over-expression of Hic-5 could increase the expression of Sp1 and Survivin, which inhibited the cell apoptosis, thereby reducing the cell damage induced by hypoxia. [ABSTRACT FROM AUTHOR]