Facilely Prepared Carbon Dots as Effective Anode Modifier for Enhanced Performance of Microbial Fuel Cells.

Microbial fuel cells (MFCs) are a promising technology for obtaining energy in wastewater. Effective extracellular electron transfer is one of the key factors for its practical application. In this work, carbon dots (CDs) enriched with oxygen-containing groups on the surface were synthesized as an efficient anode modifier using a simple hydrothermal method and common reactants. The experimental findings indicated that anodes modified with CDs exhibited increased electrical conductivity and greater hydrophilicity. These modifications facilitated increased microorganism loading and contributed to enhancing electrochemical processes within the anode biofilm. The CD-modified MFCs exhibited higher maximum power density (661.1 ± 42.6 mW·m-2) and open-circuit voltage (534.50 ± 6.4 mV), which were significantly better than those of the blank group MFCs (484.1 ± 14.1 mW·m-2 and 447.50 ± 12.1 mV). The use of simple carbon materials to improve the microbial loading on the MFCs anode and the electron transfer between the microbial-electrode may provide a new idea for the design of efficient MFCs.

Automatic recording of rare behaviors of wild animals using video bio-loggers with on-board light-weight outlier detector.

Rare behaviors displayed by wild animals can generate new hypotheses; however, observing such behaviors may be challenging. While recent technological advancements, such as bio-loggers, may assist in documenting rare behaviors, the limited running time of battery-powered bio-loggers is insufficient to record rare behaviors when employing high-cost sensors (e.g. video cameras). In this study, we propose an artificial intelligence (AI)-enabled bio-logger that automatically detects outlier readings from always-on low-cost sensors, e.g. accelerometers, indicative of rare behaviors in target animals, without supervision by researchers, subsequently activating high-cost sensors to record only these behaviors. We implemented an on-board outlier detector via knowledge distillation by building a lightweight outlier classifier supervised by a high-cost outlier behavior detector trained in an unsupervised manner. The efficacy of AI bio-loggers has been demonstrated on seabirds, where videos and sensor data captured by the bio-loggers have enabled the identification of some rare behaviors, facilitating analyses of their frequency, and potential factors underlying these behaviors. This approach offers a means of documenting previously overlooked rare behaviors, augmenting our understanding of animal behavior.

Long non-coding RNA NEAT1 promotes colorectal cancer progression by regulating miR-205-5p/VEGFA axis.

Long non-coding RNAs (lncRNAs) play key roles in tumorigenesis. It has been reported that the lncRNA nuclear-enriched abundant transcript 1 (NEAT1) may act as an oncogenic regulator in several cancers. However, the biological mechanism of action of NEAT1, particularly the miRNA sponge role in colorectal cancer (CRC), has not been fully elucidated. In our study, the expression of NEAT1, miR-205-5p, and vascular endothelial growth factor A (VEGFA) in CRC cell lines were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were examined by wound healing and transwell assays, respectively. RNA-binding protein immunoprecipitation (RIP), and dual-luciferase and RNA pull-down assays were conducted to determine the correlation between miR-205-5p and NEAT1 or VEGFA. VEGFA, matrix metalloproteinase (MMP)2, and MMP9 protein and mRNA expression were measured by western blotting and RT-qPCR analysis, respectively. Our results demonstrated high expression of NEAT1 and VEGFA and low expression of miR-205-5p in CRC cell lines. The RIP and dual-luciferase assays confirmed miR-205-5p as a target of NEAT1. In addition, VEGFA was identified as a direct target of miR-205-5p. Inhibition of NEAT1 or overexpression of miR-205-5p was able to repress VEGFA expression. Moreover, downregulation of NEAT1 and VEGFA inhibited cell proliferation, migration, and invasion. NEAT1 overexpression facilitated tumor growth by modulating miR-205-5p. Taken together, lncRNA NEAT1 was found to be upregulated in CRC cell lines, promoting CRC cell proliferation, migration, and invasion through regulating the miR-205-5p/VEGFA signaling pathway. These findings suggest that NEAT1 may be a promising biomarker in CRC diagnosis and treatment.

Apatinib as an optional treatment in metastatic colorectal cancer.

Antiangiogenic therapy has shown clinical benefit in metastatic colorectal cancer (mCRC). We aimed to evaluate the efficacy and safety of apatinib in patients who failed standard treatment and to explore potential factors related to its efficacy.A total of 47 patients were enrolled in this retrospective study. Patients who received apatinib therapy after failure of standard therapy from December 2014 and February 2018 were included. Progression-free survival (PFS), overall survival (OS), objective response rate (ORR), and treatment-related adverse events were recorded and evaluated.The median PFS was 3.717 months (95% confidence interval [CI], 3.198-4.235), and the median OS was 7.335 months (95% CI, 6.738-7.932). The disease control rate was 72.34%, and the ORR was 8.51%. The most common grade 3 to 4 adverse reactions were hypertension, proteinuria, hand-foot syndrome, and diarrhea. Multivariate analysis indicated previous antiangiogenic therapy and baseline elevated neutrophil-to-lymphocyte ratio (NLR) as independent prognostic factors.Apatinib might be a reasonable treatment option with a controlled safety profile for patients with mCRC who have failed standard therapy. Patients who previously received antiangiogenic therapy and who have baseline elevated NLR are more likely to benefit from apatinib.

miR­1273g­3p promotes proliferation, migration and invasion of LoVo cells via cannabinoid receptor 1 through activation of ERBB4/PIK3R3/mTOR/S6K2 signaling pathway.

MicroRNAs (miR) are important in various crucial cell processes including proliferation, migration and invasion. Dysregulation of miRNAs have been increasingly reported to contribute to colorectal cancer. However, the detailed biological function and potential mechanisms of miR­1273g­3p in colorectal cancer remain poorly understood. The expression levels of miR­1273g­3p in human colorectal cancer LoVo cell lines were detected via reverse transcription­quantitative polymerase chain reaction (RT­qPCR). The target genes of miR­1273g­3p were predicted by bioinformatics and verified by a luciferase reporter assay, RT­qPCR and western blotting. The MTT, wound­healing and Transwell assays were used to examine the biological functions of miR­1273g­3p in LoVo cells. The potential molecular mechanisms of miR­1273g­3p on LoVo cell proliferation, migration and invasion was detected by western blotting. The results of the present study demonstrated that miR­1273g­3p expression was extensively upregulated in LoVo cells compared with the normal colon epithelial NCM460 cell line. Further studies indicated that miR­1273g­3p inhibitor significantly suppressed LoVo cell proliferation, migration and invasion compared with inhibitor control. Following this, the cannabinoid receptor 1 (CNR1) was identified as a direct target gene of miR­1273g­3p. Knockdown of CNR1 restored the phenotypes of LoVo cells transfected with miR­1273g­3p inhibitor. Furthermore, the potential molecular mechanism of miR­1273g­3p on LoVo cell proliferation, migration and invasion may be mediated by activating the Erb­B2 receptor tyrosine kinase 4 (ERBB4)/phosphoinositide­3­kinase regulatory subunit 3 (PIK3R3)/mechanistic target of rapamycin (mTOR)/S6 kinase 2 (S6K2) signaling pathway. These observations indicated that miR­1273g­3p promoted the proliferation, migration and invasion of LoVo cells via CNR1, and this may have occurred through activation of the ERBB4/PIK3R3/mTOR/S6K2 signaling pathway, suggesting that miR­1273g­3p may serve as a novel therapeutic target for the effective treatment of colorectal cancer.