ZnO/Carbon Shell/Carbon Cloth as a Stable Host for High Li-Content Anodes

Among all energy storage systems, lithium metal batteries (LMBs) show great advantages in terms of energy density. Nevertheless, the challenges of lithium metal anodes, namely, dendrite formation and low Coulombic efficiency, hinder the practical application of LMBs. In this work, we used the ZnO/carbon shell/carbon cloth as a host for the lithium metal anode. The introduction of ZnO sites reduces the nucleation barrier of lithium deposition, and the existence of a 3D current collector alleviates the volume change during lithium plating/stripping. In addition, the combination of ZnO/C and 3D carbon cloth decreases the local current density and contributes to uniform lithium plating/stripping. The half cells assembled with modified carbon cloth electrodes cycle for more than 125 cycles with a high Coulombic efficiency of 99.34%, even under a high areal capacity of 6 mA h cm–2. By and large, our work provides a simple and effective strategy to modify the current collector for high Li-content anodes

Silencing of C9orf86 induces G1 arrest and apoptosis in breast cancer cells.

<p>(A) Cell cycle distribution was analyzed by flow cytometry 72 h after transfection. Bars are shown as the mean ± SD of cells in G1 phase of the cell cycle. (B) Apoptosis was determined by flow cytometric detection of Annexin-V-FITC-positive/PI-negative cells 72 h after infection. Bars are shown as the mean ± SD of cells with Annexin-V-FITC-positive and PI-negative. All data are shown as mean ± SD of two or three independent experiments, *P<0.05. NC, negative control.</p

C9orf86 expression in breast cancer cells and tissues.

<p>Expression of C9orf86 was quantified in human breast cancer (lanes 2–6), and normal (lane 1) breast epithelial cells by Western blot (A) and qRT-PCR (B). (C) QRT-PCR shows that expression of C9orf86 is increased in invasive BC tissues compared with NATs (P<0.05). Western blotting and RT-PCR were performed using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a control.</p

DataSheet_2_LRRC3B and its promoter hypomethylation status predicts response to anti-PD-1 based immunotherapy.xlsx

BackgroundThe leucine rich repeat containing 3B (LRRC3B) gene is a tumor suppressor gene involved in the anti-tumor immune microenvironment. Expression of LRRC3B and DNA methylation at the LRRC3B promoter region may serve as a useful marker to predict response to anti-PD-1 therapy. However, no studies have yet systematically explored the protective role of LRRC3B methylation in tumor progression and immunity.MethodsExpression of LRRC3B of 33 cancer types in The Cancer Genome Atlas (TCGA) was downloaded from UCSC Xena (http://xena.ucsc.edu/). And, we evaluated the differential expression of LRRC3B according to tumor stage, overall survival, and characteristics of the tumor microenvironment. The immunotherapeutic cohorts included IMvigor21, GSE119144, and GSE72308 which were obtained from the Gene Expression Omnibus database. We conducted pearson correlation analysis of LRRC3B and tumor microenvironment (TME) in pan-cancer. Also, six immune cell types (B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells) and tumor purity were analyzed using the Tumor IMmune Estimation Resource (TIMER1.0) (Tumor IMmune Estimation Resource (TIMER2.0). And, a “silencing score” model base on LRRC3B promoter methylation to predict overall survival (OS) by multivariate Cox regression analysis was constructed. Finally, the model was applied to predict anti-PD-1 therapy in non-small cell lung cancer (NSCLC) and breast cancer (BRCA).ResultsLRRC3B expression associated with less tumor invasion, less severe tumor stage, and decreased metastasis. The inactivation of LRRC3B promoted the enrichment of immuneosuppressive cells, including myeloid-derived suppressor cells (MDSCs), cancer-associated fibroblasts (CAFs), M2 subtype of tumor-associated macrophages (M2-TAMs), M1 subtype of tumor-associated macrophages (M1-TAMs), and regulatory T (Treg) cells. A high silencing score was significantly associated with immune inhibition, low expression of LRRC3B, poor patient survival, and activation of cancer-related pathways.ConclusionOur comprehensive analysis demonstrated the potential role of LRRC3B in the anti-tumor microenvironment, clinicopathological features of cancer, and disease prognosis. It suggested that LRRC3B methylation could be used as a powerful biomarker to predict immunotherapy responses in NSCLC and BRCA.</p

DataSheet_1_LRRC3B and its promoter hypomethylation status predicts response to anti-PD-1 based immunotherapy.docx

BackgroundThe leucine rich repeat containing 3B (LRRC3B) gene is a tumor suppressor gene involved in the anti-tumor immune microenvironment. Expression of LRRC3B and DNA methylation at the LRRC3B promoter region may serve as a useful marker to predict response to anti-PD-1 therapy. However, no studies have yet systematically explored the protective role of LRRC3B methylation in tumor progression and immunity.MethodsExpression of LRRC3B of 33 cancer types in The Cancer Genome Atlas (TCGA) was downloaded from UCSC Xena (http://xena.ucsc.edu/). And, we evaluated the differential expression of LRRC3B according to tumor stage, overall survival, and characteristics of the tumor microenvironment. The immunotherapeutic cohorts included IMvigor21, GSE119144, and GSE72308 which were obtained from the Gene Expression Omnibus database. We conducted pearson correlation analysis of LRRC3B and tumor microenvironment (TME) in pan-cancer. Also, six immune cell types (B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells) and tumor purity were analyzed using the Tumor IMmune Estimation Resource (TIMER1.0) (Tumor IMmune Estimation Resource (TIMER2.0). And, a “silencing score” model base on LRRC3B promoter methylation to predict overall survival (OS) by multivariate Cox regression analysis was constructed. Finally, the model was applied to predict anti-PD-1 therapy in non-small cell lung cancer (NSCLC) and breast cancer (BRCA).ResultsLRRC3B expression associated with less tumor invasion, less severe tumor stage, and decreased metastasis. The inactivation of LRRC3B promoted the enrichment of immuneosuppressive cells, including myeloid-derived suppressor cells (MDSCs), cancer-associated fibroblasts (CAFs), M2 subtype of tumor-associated macrophages (M2-TAMs), M1 subtype of tumor-associated macrophages (M1-TAMs), and regulatory T (Treg) cells. A high silencing score was significantly associated with immune inhibition, low expression of LRRC3B, poor patient survival, and activation of cancer-related pathways.ConclusionOur comprehensive analysis demonstrated the potential role of LRRC3B in the anti-tumor microenvironment, clinicopathological features of cancer, and disease prognosis. It suggested that LRRC3B methylation could be used as a powerful biomarker to predict immunotherapy responses in NSCLC and BRCA.</p

Silencing of C9orf86 expression inhibits invasion ability of MCF-7 cells and SK-BR-3 cells.

<p>Cell invasion was assayed in a transwell coated with Matrigel. Cells that crossed the Matrigel-coated filter were fixed, stained, and counted. Six random microscopic fields were counted for each group. The results presented are an average of six random microscopic fields from three independent experiments. Significant reduction of invasion was observed after silencing C9orf86 expression in MCF-7 cells and SK-BR-3 cells. *P<0.05. NC, negative control.</p

C9orf86 expression and survival in breast cancer patients.

<p>(A) and (B) Representative staining of C9orf86 in the cytoplasm of breast cancer cells, by IHC staining at 40× and 200× magnifications. (C) Kaplan-Meier estimates of overall survival curves for different C9orf86 expression levels in breast cancer patients, stratified by clinical stage.</p

Relationship between C9orf86 expression level and clinicopathological variables of BC patients.

<p>Abbreviations: BC, breast cancer; AJCC, American Joint Committee on Cancer.</p

Effect of C9orf86 knockdown on MCF-7 and SK-BR-3 cell growth in nude mice.

<p>(A) Photographs of nude mice and tumors extracted from C9orf86 knockdown and NC groups (MCF-7 and SK-BR-3). (B) Tumors were weighed after animals were killed 7 weeks post-tumor cell injection. There was a decreasing trend in both the number of cells and size of tumors in the C9orf86 knockdown and NC group of mice for MCF-7 (P<0.01) and SK-BR-3 (P = 0.261) cells. (C) Growth curves for tumors in MCF-7-C9orf86-siRNA-treated group (n = 6) <i>versus</i> the MCF-7-NC-treated group (n = 8) (all P values <0.01) and growth curves for tumors in SK-BR-3-C9orf86-siRNA-treated group (n = 2) <i>versus</i> SK-BR-3-NC-treated group (n = 7) (all P values >0.05). (D) The level of C9orf86 mRNA from the tumor 7 weeks after the injection in NC-group was higher than C9orf86-siRNA group (MCF-7 and SK-BR-3, all P values <0.05). Data are shown as the mean ± SD. *P<0.05. NC, negative control.</p

Additional file 1 of Effects of uric acid-lowering therapy (ULT) on renal outcomes in CKD patients with asymptomatic hyperuricemia: a systematic review and meta-analysis

Additional file 1: Supplementary Figure 1. Assessment of the methodological quality of the included studies. (A) Risk of Bias (B) Risk of Bias Summary