Characterizing the coefficient of friction between a capsule robot and the colon.

OBJECTIVE: A capsule robot (CR) with an onboard active locomotion mechanism, has been developed as a promising alternative to colonoscopy due to its minimally-invasive advantage. Predicting the traction force and locomotion resistance of the CR, which are both the friction force, is significantly important for the CR development and control. However, a comprehensive study concerning the coefficient of friction (COF) in the colon, which is necessary for prediction, is not available in literature. This paper is dedicated to determining a quantitative COF equation in terms of the contact pressure, hoop strain, and sliding velocity. METHODS: The COFs of three commonly-used materials of the CR (i.e., PDMS, white and transparent ABS plastic), are measured under 144 different friction cases (6 contact pressures×4 hoop strains×6 sliding velocities). By analyzing the measurements, the influence law of the three factors on the COFs of the three materials is revealed, and based on which, a general COF equation involving eight fitted constants is determined. RESULTS: The determination coefficients of the COF equation for the three materials are up to 0.9822, 0.9286, and 0.9696, respectively. The COF equation is used to predict the traction force and locomotion resistance of a crawler CR, and the predicting results fit well with the measured ones. CONCLUSION: The COF equation can provide a correct COF for friction force prediction. SIGNIFICANCE: It is promising to enable a better force and locomotion control for the CR in the colon.

Circular RNA circ-AGFG1 contributes to esophageal squamous cell carcinoma progression and glutamine catabolism by targeting microRNA-497-5p/solute carrier family 1 member 5 axis.

Circular RNAs (circRNAs) have been shown to play important regulatory roles in human malignancies. However, the role of circRNA ArfGAP with FG repeats 1 (circ-AGFG1) in esophageal squamous cell carcinoma (ESCC) progression and its associated mechanism are still largely undefined. Cell proliferation was analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and 5-ethynyl-2'-deoxyuridine assay. Cell apoptosis was assessed by flow cytometry analysis. Transwell assay and wound healing assay were used to analyze cell invasion and migration abilities. The uptake of glutamine and the production of α-ketoglutarate and glutamate were analyzed using Glutamine Determination Kit, α-ketoglutarate Assay Kit and Glutamate Determination Kit. A xenograft tumor model was used to analyze the biological role of circ-AGFG1 in vivo . The interaction between microRNA-497-5p (miR-497-5p) and circ-AGFG1 or solute carrier family 1 member 5 (SLC1A5) was verified by dual-luciferase reporter assay. Circ-AGFG1 expression was upregulated in ESCC tissues and cell lines. Circ-AGFG1 silencing suppressed the proliferation, migration, invasion and glutaminolysis and triggered the apoptosis of ESCC cells. Circ-AGFG1 knockdown significantly slowed down tumor growth in vivo . Circ-AGFG1 acted as a sponge for miR-497-5p, and miR-497-5p interacted with the 3' untranslated region (3'UTR) of SLC1A5. miR-497-5p silencing largely abolished circ-AGFG1 silencing-induced effects in ESCC cells. miR-497-5p overexpression-mediated influences in ESCC cells were largely reversed by the addition of SLC1A5 expressing plasmid. Circ-AGFG1 could upregulate SLC1A5 expression by sponging miR-497-5p. In summary, circ-AGFG1 acted as an oncogene to elevate the malignant potential and promote the glutamine catabolism of ESCC cells by targeting the miR-497-5p/SLC1A5 axis.

PDGF-BB promotes vascular smooth muscle cell migration by enhancing Pim-1 expression via inhibiting miR-214.

BACKGROUND: Several studies have indicated that the platelet-derived growth factor/platelet-derived growth factor receptor (PDGF/PDGFR) pathway is involved in the process of atherosclerosis. However, its underlying mechanism remains to be further elucidated. Serine/threonine-protein kinase pim-1 (Pim-1), a member of serine/threonine-specific kinases, is a pro-oncogene published to be related to cell proliferation, apoptosis, and metastasis of cancer cells. Whether Pim-1 is involved in PDGF/PDGFR pathway-mediated coronary atherosclerotic heart disease remains to be elucidated. METHODS: We established a cell model of PDGF-BB-stimulated smooth muscle cells using A7r5 cells. Transwell assay was used to detect the potential of cell migration and invasion. The targeted regulation of Pim-1 by miR-214 was confirmed by luciferase assay. Rescue experiments were performed to determine the role of the PDGF-BB/miR-214/Pim-1 axis on the cell migration of smooth muscle cells by including PDGF-BB treatment, and the overexpression of miR-214 and Pim-1. Quantitative polymerase chain reaction (qPCR) was used to examine the gene expression and western blot was performed to detect the protein expression. RESULTS: Our data indicated that PDGF-BB could effectively enhance smooth muscle cell migration. We also showed Pim-1 was a target of miR-214 in A7r5 cells. The expression of Pim-1 was shown to be upregulated by PDGF-BB via suppression of the expression of miR-214. Moreover, overexpression miR-214 inhibited PDGF-BB-stimulated Pim-1 expression and smooth muscle cell migration via modulating epithelial-mesenchymal transition (EMT), but no change on cell cycle. However, overexpression of Pim-1 reversed miR-214-blocked cell migration by promoting the activation of the STAT3, AKT, and ERK signaling pathways. CONCLUSIONS: Our data suggested that the PDGF/miR-214/Pim-1 axis could be a potential target for coronary atherosclerotic heart disease.

miRNA-425-5p enhances lung cancer growth via the PTEN/PI3K/AKT signaling axis.

BACKGROUND: miRNAs regulate a multitude of cellular processes and their aberrant regulation is linked to human cancer. However, the role of miR-425-5p in lung cancer (LCa) is still largely unclear. Here, we explored the role of miR-425-5p during LCa tumorigenesis. METHODS: Cell proliferation was evaluated by cell counting Kit-8 and colony formation assay. Western blot and real-time PCR were accordingly used to detect the relevant proteins, miRNA and gene expression. Luciferase reporter assays were used to illustrate the interaction between miR-425-5p and PTEN. RESULTS: We demonstrate that miR-425-5p is overexpressed in LCa tissue and enhances the proliferative and colony formation capacity of the LCa cell lines A549 and NCI-H1299. Through predictive binding assays, PTEN was identified as a direct gene target and its exogenous expression inhibited the pro-cancer effects of miR-425-5p. Through its ability to down-regulate PTEN, miR-425-5p activated the PI3K/AKT axis. CONCLUSION: We conclude that miR-425-5p promotes LCa tumorigenesis through PTEN/PI3K/AKT signaling.