The microbiome compositional and functional differences between rectal mucosa and feces.

In recent years, most studies on the gut microbiome have primarily focused on feces samples, leaving the microbial communities in the intestinal mucosa relatively unexplored. To address this gap, our study employed shotgun metagenomics to analyze the microbial compositions in normal rectal mucosa and matched feces from 20 patients with colonic polyps. Our findings revealed a pronounced distinction of the microbial communities between these two sample sets. Compared with feces, the mucosal microbiome contains fewer genera, with Burkholderia being the most discriminating genus between feces and mucosa, highlighting its significant influence on the mucosa. Furthermore, based on the microbial classification and KEGG Orthology (KO) annotation results, we explored the association between rectal mucosal microbiota and factors such as age, gender, BMI, and polyp risk level. Notably, we identified novel biomarkers for these phenotypes, such as Clostridium ramosum and Enterobacter cloacae in age. The mucosal microbiota showed an enrichment of KO pathways related to sugar transport and short chain fatty acid metabolism. Our comprehensive approach not only bridges the knowledge gap regarding the microbial community in the rectal mucosa but also underscores the complexity and specificity of microbial interactions within the human gut, particularly in the Chinese population. IMPORTANCE: This study presents a system-level map of the differences between feces and rectal mucosal microbial communities in samples with colorectal cancer risk. It reveals the unique microecological characteristics of rectal mucosa and its potential influence on health. Additionally, it provides novel insights into the role of the gut microbiome in the pathogenesis of colorectal cancer and paves the way for the development of new prevention and treatment strategies.

Green and facile fabrication of porous titanium dioxide as efficient sulfur host for advanced lithium-sulfur batteries: An air oxidation strategy.

Lithium-sulfur (Li-S) battery has been considered a promising next-generation electrochemical energy storage device due to its high theoretical capacity and high energy density. However, the dissolution and shuttling problems of lithium polysulfides (LiPSs) are major obstacles hindering the performance and application of Li-S batteries. To address these issues, we report the rapid preparation of porous TiO2 nanoparticles (p-TiO2-NPs) as an effective sulfur host for Li-S batteries using a facile, scalable, and green one-step air oxidation strategy. Experimental results reveal that the p-TiO2-NPs have a mesopores-rich structure and strong chemical adsorption capability against LiPSs, which effectively mitigates the dissolution and shuttling of LiPSs by way of physical and chemical adsorptions. Incorporating highly conductive multi-wall carbon nanotubes to interconnect with the active materials, the p-TiO2-NPs-based cathode delivers a high discharge capacity of 1276 mAh g-1 at 0.2 C and stable cycling performance with an ultralow capacity decay rate of 0.0526% per cycle at 1 C over 1200 cycles. This green and facile fabrication strategy can also be extended to other metal carbides to endow an environmentally friendly route for the sustainable development of high-performance Li-S batteries.

Silicon-nanoparticle-based composites for advanced lithium-ion battery anodes.

Lithium-ion batteries (LIBs) play an important role in modern society. The low capacity of graphite cannot meet the demands of LIBs calling for high power and energy densities. Silicon (Si) is one of the most promising materials instead of graphite, because of its high theoretical capacity, low discharge voltage, low cost, etc. However, Si shows low conductivity of both ions and electrons and exhibits a severe volume change during cycles. Fabricating nano-sized Si and Si-based composites is an effective method to enhance the electrochemical performance of LIB anodes. Using a small size of Si nanoparticles (SiNPs) is likely to avoid the cracking of this material. One critical issue is to disclose different types and electrochemical effects of various coupled materials in the Si-based composites for anode fabrication and optimization. Hence, this paper reviews diverse SiNP-based composites for advanced LIBs from the perspective of composition and electrochemical effects. Almost all kinds of materials that have been coupled with SiNPs for LIB applications are summarized, along with their electrochemical influences on the composites. The integrated materials, including carbon materials, metals, metal oxides, polymers, Si-based materials, transition metal nitrides, carbides, dichalcogenides, alloys, and metal-organic frameworks (MOFs), are comprehensively presented.

Effect of salvianolic acid A on the proliferation and apoptosis in esophageal cancer cells and the underlying mechanisms. / ä¸¹é šé ¸Aå¯¹é£Ÿç®¡ç™Œç»†èƒžå¢žæ®–ä¸Žå‡‹äº¡çš„å½±å“åŠå ¶æœºåˆ¶.

OBJECTIVES: To explore the effect of salvianolic acid A (SalA) on the proliferation and apoptosis in esophageal cancer cell line KYSE-150 and the possible mechanisms. METHODS: The esophageal cancer cells were randomly divided into 4 groups: a control group, a 10 µmol/L SalA group, a 25 µmol/L SalA group, and a 50 µmol/L SalA group. Cell counting kit-8 (CCK-8) was used to detect the cell proliferation activity. Flow cytometry was used to detect cell cycle distribution and cell apoptosis rate. Western blotting was used to detect the protein expression of cell proliferation maker Ki-67, cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6, B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X (Bax), cleaved-caspase-9, cleaved-caspase-3, phosphatidylinositol 3-kinase (PI3K), phosphorylated protein kinase B (p-Akt) and mechanistic target of rapamycin (mTOR). RESULTS: Compared with the control group, the cell proliferation activity was significantly reduced (P<0.01); the cells in the G1 phase were significantly increased, and the S phase cells were significantly reduced (both P<0.01); the cell apoptosis rate was significantly increased (P<0.01) in the SalA groups at different concentration; the expression levels of Ki-67, cyclin D1, CDK4, CDK6, Bcl-2, PI3K, p-Akt and mTOR were decreased significantly, but the expression levels of p21, Bax, cl-caspase-9 and cl-caspase-3 were increased significantly in the SalA groups at different concentration (all P<0.01). CONCLUSIONS: SalA can inhibit the proliferation and induce G1 phase arrest and apoptosis in the esophageal cancer cell line KYSE-150, which may be related to the activation of PI3K/Akt/mTOR signal pathway.

Weighted gene co-expression network analysis and connectivity map identifies lovastatin as a treatment option of gastric cancer by inhibiting HDAC2.

OBJECTIVE: This study aimed to identifying and validating therapeutic compounds which might have positive effects on patients with gastric cancer (GC) based on weighted gene co-expression network analysis (WGCNA) and connectivity map (CMap). METHODS: We performed WGCNA to gain insights into the molecular aspects of GC. Raw microarray datasets (including 132 samples) were downloaded from the Gene Expression Omnibus (GEO) website. We utilized the WGCNA to identify the coexpressed genes (modules) and modular hub genes after non-specific filtering. Furthermore, these differentially expressed genes were submitted to CMap analysis to identify candidate therapeutic compounds for GC. In experimental part, cell growth inhibition was evaluated by Cell Counting Kit-8 (CCK-8) and colony formation assays. Tumor growth was assessed using nude mice with xenografts established in vivo. QRT-PCR and western blot were used for determination of HDAC2 expression level and immunohistochemistry was performed to quantify HDAC2 in gastric tumor samples. RESULTS: Through WGCNA and CMap analysis, we found two potential therapeutic compounds, the valproic acid (VPA), which is the histone deacetylase (HDAC) inhibitor and lovastatin. HDAC2 was overexpressed in gastric cancer cell lines including AGS, BGC-823, NCI-N87 and MKN28. Dose-dependent inhibition of gastric cancer cells by VPA and lovastatin was verified in vitro. Apoptosis of GC cells was induced after treatment with VPA and lovastatin through suppressing HDAC2 expression. Furthermore, the inhibition of VPA with cisplatin and lovastatin with cisplatin were also dose-dependent and cisplatin exhibited synergistic effects. In the xenografts, similar results were found. CONCLUSION: WGCNA was able to identify significant groups of genes associated with cancer prognosis. Moreover, analysis of gene expression signature using CMap is a powerful way to explore potential therapeutics for human diseases. For treating GC, lovastatin may be a potential drug.

LncRNA CASC11 promoted gastric cancer cell proliferation, migration and invasion in vitro by regulating cell cycle pathway.

In this study, we aimed to investigate the effects of lncRNA CASC11 on gastric cancer (GC) cell progression through regulating miR-340-5p and cell cycle pathway. Expressions of lncRNA CASC11 in gastric cancer tissues and cell lines were determined by qRT-PCR. Differentially expressed lncRNAs, mRNAs and miRNAs were screened through microarray analysis. The relationship among CASC11, CDK1 and miR-340-5p was predicted by TargetScan and validated through dual luciferase reporter assay. Western blot assay examined the protein level of CDK1 and several cell cycle regulatory proteins. GO functional analysis and KEGG pathway analysis were used to predict the association between functions and related pathways. Cell proliferation was determined by CCK-8 assays. Cell apoptosis and cell cycle were detected by flow cytometry assay. CASC11 was highly expressed in GC tissues and cell lines. Knockdown of CASC11 inhibited GC cell proliferation, promoted cell apoptosis and blocked cell cycle. KEGG further indicated an enriched cell cycle pathway involving CDK1. QRT-PCR showed that miR-340-5p was down-regulated in GC cells tissues, while CDK1 was up-regulated. Furthermore, CASC11 acted as a sponge of miR-340-5p which directly targeted CDK1. Meanwhile, miR-340-5p overexpression promoted GC cell apoptosis and induced cell cycle arrest, while CDK1 overexpression inhibited cell apoptosis and accelerated cell cycle. Our study revealed the mechanism of CASC11/miR-340-5p/CDK1 network in GC cell line, and suggested that CASC11 was a novel facilitator that exerted a biological effect by activating the cell cycle signaling pathway. This finding provides a potential therapeutic target for GC.