A water strider-inspired intestinal stent actuator for controllable adhesion and unidirectional biofluid picking.

Soft-bodied aquatic organisms exhibit extraordinary navigation and mobility in liquid environments which inspiring the development of biomimetic actuators with complex movements. Stimulus-responsive soft materials including hydrogels and shape-memory polymers are replacing traditional rigid parts that leading to dynamic and responsive soft actuators. In this study, we took inspiration from water strider to develop a biomimetic actuator for targeted stimulation and pH sensing in the gastrointestinal tract. We designed a soft and water-based Janus adhesive hydrogel patch that attaches to specific parts of the intestine and responds to pH changes through external stimulation. The hydrogel patch that forms the belly of the water strider driver incorporates an inverse opal microstructure that enables pH responsive behavior. The hydrogel patch on the water strider's leg uses a sandwich structure of Cu particles to convert light into heat and bend under infrared light to mimic the water strider's leg simulating the efficient and steady movement of the water strider's leg which transporting the biological fluid in one direction. This miniature bionic actuator demonstrates controlled adhesion and unidirectional biofluid delivery capabilities, proving its potential for targeted stimulus response and pH sensing in the gastrointestinal tract, thus opening up new possibilities for medical applications in the growing field of soft actuators.

Microbial interactions facilitating efficient methane driven denitrification via in-situ utilization of short chain fatty acids.

High nitrate pollution in agriculture and industry poses a challenge to emerging methane oxidation coupled denitrification. In this study, an efficient nitrate removal efficiency of 100 % was achieved at an influent loading rate of 400 mg-N/L·d, accompanied by the production of short chain fatty acids (SCFAs) with a maximum value of 80.9 mg/L. Batch tests confirmed that methane was initially converted to acetate, which then served as a carbon source for denitrification. Microbial community characterization revealed the dominance of heterotrophic denitrifiers, including Simplicispira (22.8 %), Stappia (4.9 %), and the high­nitrogen-tolerant heterotrophic denitrifier Diaphorobacter (19.0 %), at the nitrate removal rate of 400 mg-N/L·d. Notably, the low abundance of methanotrophs ranging from 0.24 % to 3.75 % across all operational stages does not fully align with the abundance of pmoA genes, suggesting the presence of other functional microorganisms capable of methane oxidation and SCFAs production. These findings could facilitate highly efficient denitrification driven by methane and contributed to the development of denitrification using methane as an electron donor.

The oncogenic miR-27a/BTG2 axis promotes obesity-associated hepatocellular carcinoma by mediating mitochondrial dysfunction.

Obesity is closely related to the initiation and development of hepatocellular carcinoma (HCC). The regulatory mechanism of obesity-associated HCC remains unclear. HepG2 cells treated with palmitic acid (PA) and diethylnitrosamine (DEN)-induced HCC mice fed a high-fat diet (HFD) were established. The expression of miR-27a and B-cell translocation gene 2 (BTG2) mRNA and protein were detected via qPCR and western blotting. Prediction software and luciferase assays were employed to verify the miR-27a/BTG2 axis. The biological effects of HepG2 cells were evaluated with ORO staining, MTT assays, Transwell assays, Mito-Timer, and Mito-SOX staining. Significantly upregulated miR-27a and downregulated BTG2 mRNA and protein were observed in HepG2 cells and liver tissues of HCC mice. Overexpressing miR-27a (mi-miR-27a) markedly promoted cellular lipid accumulation, proliferation, and invasion, accompanied by aggravated mitochondrial dysfunction (increased fading and ROS products of mitochondria) in HepG2 cells. Additionally, these effects were further reinforced in HepG2 cells treated with mi-miR-27a and PA. BTG2 was identified as a direct target and was negatively regulated by miR-27a. Similarly, BTG2 knockdown (sh-BTG2) had effects identical to those of mi-miR-27a on HepG2 cells. Additionally, PA evidently enhanced these effects of sh-BTG2 in HepG2 cells. Moreover, BTG2 overexpression effectively reversed the effects of miR-27a, including lipotropic and oncogenic effects, and simultaneously promoted mitochondrial imbalance in HepG2 cells. Thus, obesity-associated miR-27a acts as an oncogene to promote lipid accumulation, proliferation, and invasion by negatively regulating BTG2-mediated mitochondrial dysfunction in HCC.

Bile acids elevated by high-fat feeding induce endoplasmic reticulum stress in intestinal stem cells and contribute to mucosal barrier damage.

Long-term high-fat feeding (HF) induces intestinal mucosal barrier damage. However, the mechanism for this remains unclear. HF can elevate the intestinal and circulating bile acid (BA) levels, especially deoxycholic acid (DCA). We hypothesize that BAs elevated by HF regulate intestinal stem cell (ISC) function, which may contribute to mucosal barrier injury in the ileum of mice. In this study, we showed that 2 weeks of HF resulted in a shortening of intestinal villi and a decrease in the tight junction (TJ) protein occludin in the ileum of mice, accompanied by an increase in circulating BA levels. Importantly, 2 weeks of HF also reduced ileal ISCs and goblet cells and decreased the proliferation function of ISCs and their ability to differentiate into goblet cells. Endoplasmic reticulum (ER) stress was found to be involved in the process of ISC damage. All these alterations were reversed by cofeeding with the bile acid binder cholestyramine. In addition, the in vitro studies also confirmed a cytotoxic effect of DCA at a high concentration on ISCs and goblet cells. In conclusion, these data suggested that high levels of BAs induced by HF could impair ISC function by triggering ER stress, resulting in the disruption of the intestinal mucosal barrier.