Understanding the Spatial and Temporal Patterns of Copper In-Use Stocks in China

Two approaches are adopted to characterize the comprehensive pattern of the copper in-use stocks in China. The top-down results indicate that both the total amount and the per capita quantity of the stocks have exhibited a significant and increasing trend for the past 60 years, especially since 2000. The top-down results show that the copper stocks increased from a negligible level of less than 1 kg/capita in 1952 to 44 kg/capita in 2012. The total stocks in 2012 are estimated to be 60 Mt by a top-down approach or 48 Mt by a bottom-up calculation. The bottom-up method determines that the largest reservoir is the infrastructure sector, which accounts for approximately 58% of the total stocks. The spatial pattern indicates that the copper in-use stocks are predominately spatially distributed in the eastern regions of China, a feature that is obviously different from the geographical distribution of the primary resources. Analysis on the prospects of stocks shows both the total magnitude and per capita value will continuously increase in the following decade, and enter a relatively stable stage in around 2030, with a maximum value of 106 kg/capita. The results improve the knowledge about closing copper cycles

Fas signaling promotes AGS cell metastasis <i>in vivo</i> through STAT3/Fascin pathway.

<p>2 × 10⁶ AGS tumor cells pre-stimulated with anti-Fas or ISO for 2 h were intravenously injected nude mice. (A) The number of lung tumor foci was counted (n = 5). (B) The expression of Fascin in tumor tissues from lung was detected by immunohistochemistry. 2 × 10⁶ AGS tumor cells were intravenously injected into nude mice and 24 h later, the mice received intravenous injection of S3I-201 at 5 mg/kg every 2 days for total 3 times. (C) The number of lung tumor foci was counted (n = 5). (D) The expression of Fascin in tumor tissues from lung was detected by immunohistochemistry (magnification: ×100). Data are representative of two independent experiments. (*p <0.05, ***p <0.001)</p

Activation of Fas signaling promotes the migration of GC cells.

<p>(A) The Fas expression in AGS and MNK-45 cells were detected by real-time PCR (upper) and Western blot (down). (B) Susceptibility of AGS and MNK-45 cells to Fas-induced apoptosis was measured by staining with Annexin V and PI after both cells were stimulated with anti-Fas or ISO at the indicated concentrations for 24 h (left) and the apoptotic cells were statistically analyzed (right) (n = 3). (C) After stimulated with 5 μg/ml anti-Fas or ISO for 2 h, the AGS cells were collected and seeded into the top chamber. Forty-eight hours later, the number of cells on the bottom of the Transwell filter was imaged (left) and quantified (right) (n = 5). Magnification: 200×. (D) The proliferation of AGS cells was measured by CCK8 assay after stimulation with 5 μg/ml of anti-Fas or ISO in the indicated timepoint. Data are representative of three independent experiments. (*p <0.05, ***p <0.001)</p

Activation of Fas signaling upregulated Fascin expression in AGS cells through activation of STAT3.

<p>The AGS cells were stimulated with 5 μg/ml of anti-Fas in the indicated times. (A) The phosphorylated STAT3 was detected by Western blot. (B) The expression of Fascin mRNA was assayed by real-time PCR. (C) After stimulation with 5 μg/ml anti-Fas for 24 h, the protein level of phosphorylated STAT3 and Fascin in AGS cells was detected by Western blot. (D) The AGS cells were pre-treated with 10 μM of Stattic for 2 h and followed by 5 μg/ml of anti-Fas stimulation for 24 h; the protein level of phosphorylated STAT3 and Fascin was detected by Western blot. After transfection with STAT3 siRNA or NC siRNA for 36 h, (E) the STAT3 expression in the AGS cells was detected by Western blot; (F) the AGS cells were then stimulated with 5 μg/ml of anti-Fas for 2 h, and the Fascin expression in the cells was detected by Western blot. Data are representative of three independent experiments.</p

Patient characteristics.

<p>NOTE: Data are mean ± standard deviation.</p><p>*According to American Joint Committee on Cancer.</p><p>Abbreviation: ECOG PS, Eastern Cooperative Oncology Group Performance Status.</p><p>Patient characteristics.</p

Fas signaling promoted AGS cell migration dependent on STAT3/Fascin pathway.

<p>(A) AGS cells were transfected with Fascin siRNA or NC siRNA for 36 h, and Fascin expression in the cells was detected by Western blot. After (B) inhibition of Fascin expression by siRNA; or (C) treated with 10 μM Stattic for 2 h; or (D) inhibition of STAT3 expression by siRNA, and stimulated with 5 μg/ml of anti-Fas for 2 h, the number of AGS cells which migrated to the bottom of the Transwell filter was quantified (n = 5). Data are representative of three independent experiments. (**p <0.01)</p

Correlation of the mRNA levels of Fas and Fascin in tumor tissues from GC patients.

<p>Fas and Fascin mRNA expression was measured by real-time PCR and normalized to β-actin mRNA (n = 23). Positive correlation was obtained by Spearman correlation analysis.</p

DataSheet_1_Comprehensive analysis to identify the influences of SARS-CoV-2 infections to inflammatory bowel disease.docx

BackgroundCoronavirus disease 2019 (COVID-19) and inflammatory bowel disease (IBD) are both caused by a disordered immune response and have direct and profound impacts on health care services. In this study, we implemented transcriptomic and single-cell analysis to detect common molecular and cellular intersections between COVID-19 and IBD that help understand the linkage of COVID-19 to the IBD patients.MethodsFour RNA-sequencing datasets (GSE147507, GSE126124, GSE9686 and GSE36807) from Gene Expression Omnibus (GEO) database are extracted to detect mutual differentially expressed genes (DEGs) for IBD patients with the infection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to find shared pathways, candidate drugs, hub genes and regulatory networks. Two single-cell RNA sequencing (scRNA-eq) datasets (GSE150728, PRJCA003980) are used to analyze the immune characteristics of hub genes and the proportion of immune cell types, so as to find common immune responses between COVID-19 and IBD.ResultsA total of 121 common DEGs were identified among four RNA-seq datasets, and were all involved in the functional enrichment analysis related to inflammation and immune response. Transcription factors-DEGs interactions, miRNAs-DEGs coregulatory networks, and protein-drug interactions were identified based on these datasets. Protein-protein interactions (PPIs) was built and 59 hub genes were identified. Moreover, scRNA-seq of peripheral blood monocyte cells (PBMCs) from COVID-19 patients revealed a significant increase in the proportion of CD14+ monocytes, in which 38 of 59 hub genes were highly enriched. These genes, encoding inflammatory cytokines, were also highly expressed in inflammatory macrophages (IMacrophage) of intestinal tissues of IBD patients.ConclusionsWe conclude that COVID-19 may promote the progression of IBD through cytokine storms. The candidate drugs and DEGs-regulated networks may suggest effective therapeutic methods for both COVID-19 and IBD.</p

Additional file 1 of α-Synuclein-containing erythrocytic extracellular vesicles: essential contributors to hyperactivation of monocytes in Parkinson’s disease

Additional file 1. Additional figures

IL4I1 Is a Novel Regulator of M2 Macrophage Polarization That Can Inhibit T Cell Activation via L-Tryptophan and Arginine Depletion and IL-10 Production

<div><p>Interleukin 4-induced gene-1 (IL4I1) was initially described as an early IL-4-inducible gene in B cells. IL4I1 protein can inhibit T cell proliferation by releasing its enzymatic catabolite, H₂O₂, and this effect is associated with transient down-regulation of T cell CD3 receptor-zeta (TCRζ) expression. Herein, we show that IL4I1 contributes to the regulation of macrophage programming. We found that expression of IL4I1 increased during bone marrow-derived macrophage (BMDM) differentiation, expression of IL4I1 is much higher in primary macrophages than monocytes, and IL4I1 expression in BMDMs could be induced by Th1 and Th2 cytokines in two different patterns. Gene expression analysis revealed that overexpression of IL4I1 drove the expression of M2 markers (Fizz1, Arg1, YM-1, MR) and inhibited the expression of M1-associated cytokines. Conversely, knockdown of IL4I1 by siRNA resulted in opposite effects, and also attenuated STAT-3 and STAT-6 phosphorylation. Furthermore, IL4I1 produced by macrophages catalyzed L-tryptophan degradation, while <i>levo</i>-1-methyl-tryptophan (L-1-MT), but not <i>dextro</i>-1-methyl-tryptophan, partially rescued IL4I1-dependent inhibition of T cell activation. Other inhibitors, such as diphenylene iodonium (DPI), an anti-IL-10Rα blocking antibody, and a nitric oxide synthase inhibitor, NG-monomethyl-L-arginine, also had this effect. Overall, our findings indicate that IL4I1 promotes an enhanced M2 functional phenotype, which is most likely associated with the phosphorylation of STAT-6 and STAT-3. Moreover, DPI, L-1-MT, NG-monomethyl-L-arginine, and anti-IL-10Rα blocking antibody were all found to be effective IL4I1 inhibitors <i>in vitro</i>.</p></div