Bioelectricity generation, by Shewanella oneidensis (S. oneidensis) MR-1, has become particularly alluring, thanks to its extraordinary prospects for energy production, pollution treatment, and biosynthesis. Attempts to improve its technological output by modification of S. oneidensis MR-1 remains complicated, expensive and inefficient. Herein, we report on the augmentation of S. oneidensis MR-1 with carbon dots (CDs). The CDs-fed cells show accelerated extracellular electron transfer and metabolic rate, with increased intracellular charge, higher adenosine triphosphate level, quicker substrate consumption and more abundant extracellular secretion. Meanwhile, the CDs promote cellular adhesion, electronegativity, and biofilm formation. In bioelectrical systems the CDs-fed cells increase the maximum current value, 7.34 fold, and power output, 6.46 fold. The enhancement efficacy is found to be strongly dependent on the surface charge of the CDs. This work demonstrates a simple, cost-effective and efficient route to improve bioelectricity generation of S. oneidensis MR-1, holding promise in all relevant technologies.

Nanomaterials for killing pathogenic bacteria under light irradiation.

Solar steam generation (SSG) is a promising approach to address the global shortage of freshwater by seawater treatment, but commonly suffers from salt-accumulation related issues, drastically reducing the operational efficiency and lifetime of SSG systems. Herein, we propose a strategy for sustainable SSG from seawater, enabling powerful self-salt-discharge and self-water-pumping by constructing a closed loop between water and salt. As a result, besides an evaporation rate as high as 2.8 kg m⁻² h⁻¹ (under one sun), neither salt accumulation nor evaporation rate decline is observed upon long-term cycling of over one month or constant floating on seawater over eight months. Even upon continuous desalination in a highly concentrated solution (20 wt% NaCl) for over 400 h or under high-intensity irradiation for over 12 h, the high evaporation rate is successfully maintained. This work thus provides an effective solution for salt accumulation, addressing the top challenge for long-term sustainable desalination.

Background: Exosomes have been implicated in tumour progression and metastatic spread. Little is known of the effect of mechanical and innate immune interactions of malignant cell‐derived exosomes on endothelial integrity, which may relate to increased extravasation of circulating tumour cells and, therefore, increased metastatic spread.Methods: Exosomes isolated from non‐malignant immortalized HCV‐29 and isogenic malignant non‐metastatic T24 and malignant metastatic FL3 bladder cells were characterized by nanoparticle tracking analysis and quantitative nanomechanical mapping atomic force microscopy (QNM AFM) to determine size and nanomechanical properties. Effect of HCV‐29, T24 and FL3 exosomes on human umbilical vein endothelial cell (HUVEC) monolayer integrity was determined by transendothelial electrical resistance (TEER) measurements and transport was determined by flow cytometry. Complement activation studies in human serum of malignant and non‐malignant cell‐derived exosomes were performed.Results: FL3, T24 and HCV‐29 cells produced exosomes at similar concentration per cell (6.64, 6.61 and 6.46×10⁴ exosomes per cell for FL3, T24 and HCV‐29 cells, respectively) and of similar size (120.2 nm for FL3, 127.6 nm for T24 and 117.9 nm for HCV‐29, respectively). T24 and FL3 cell‐derived exosomes exhibited a markedly reduced stiffness, 95 MPa and 280 MPa, respectively, compared with 1,527 MPa with non‐malignant HCV‐29 cell‐derived exosomes determined by QNM AFM. FL3 and T24 exosomes induced endothelial disruption as measured by a decrease in TEER in HUVEC monolayers, whereas no effect was observed for HCV‐29 derived exosomes. FL3 and T24 exosomes traffic more readily (11.6 and 21.4% of applied exosomes, respectively) across HUVEC monolayers than HCV‐29 derived exosomes (7.2% of applied exosomes). Malignant cell‐derived exosomes activated complement through calcium‐sensitive pathways in a concentration‐dependent manner.Conclusions: Malignant (metastatic and non‐metastatic) cell line exosomes display a markedly reduced stiffness and adhesion but an increased complement activation compared to non‐malignant cell line exosomes, which may explain the observed increased endothelial monolayer disruption and transendothelial transport of these vesicles.