To recognize the user’s motion intention, brain-machine interfaces (BMI) usually decode movements from cortical activity to control exoskeletons and neuroprostheses for daily activities. The aim of this paper is to investigate whether self-induced variations of the electroencephalogram (EEG) can be useful as control signals for an upper-limb exoskeleton developed by us. A BMI based on event-related desynchronization/synchronization (ERD/ERS) is proposed. In the decoder-training phase, we investigate the offline classification performance of left versus right hand and left hand versus both feet by using motor execution (ME) or motor imagery (MI). The results indicate that the accuracies of ME sessions are higher than those of MI sessions, and left hand versus both feet paradigm achieves a better classification performance, which would be used in the online-control phase. In the online-control phase, the trained decoder is tested in two scenarios (wearing or without wearing the exoskeleton). The MI and ME sessions wearing the exoskeleton achieve mean classification accuracy of 84.29% ± 2.11% and 87.37% ± 3.06%, respectively. The present study demonstrates that the proposed BMI is effective to control the upper-limb exoskeleton, and provides a practical method by non-invasive EEG signal associated with human natural behavior for clinical applications.
It is challenging to construct high-performing excimer-based luminescent analytic tools at low molecular concentrations.Wereport that enzyme-instructed self-assembly (EISA) enables the monomer-excimer transition of acoumarin dye (Cou)a tl ow molecular concentrations,a nd the resulting higher ordered luminescent supramolecular assemblies (i.e., nanofibers) efficiently record the spatiotemporal details of alkaline phosphatase (ALP) activity in vitro and in vivo. Cou was conjugated to short self-assembly peptides with ah ydrophilic ALP-responsive group.B yA LP triggering,E ISA actuated an anoparticles-nanofibers transition at low peptide concentrations followed by monomer-excimer transition of Cou.Analysis of structure-property relationships revealed that the self-assembly motif was ap rerequisite for peptides to induce the monomer-excimer transition of Cou.L uminescent supramolecular nanofibers of pYD (LSN-pYD)i lluminated the intercellular bridge of cancer cells and distinguished cancer cells (tissues) from normal cells (tissues) efficiently and rapidly,p romising potential use for the early diagnosis of cancer.This work extends the functions of EISA and provides anew application of supramolecular chemistry.
The selective formation of nanomaterials in cancer cells and tumors holds great promise for cancer diagnostics and therapy. Until now, most strategies rely on a single trigger to control the formation of nanomaterials in situ. The combination of two or more triggers may provide for more sophisticated means of manipulation. In this study, we rationally designed a molecule (Comp. 1) capable of responding to two enzymes, alkaline phosphatase (ALP), and reductase. Since the A549 lung cancer cell line showed elevated levels of extracellular ALP and intracellular reductase, we demonstrated that Comp. 1 responded in a stepwise fashion to those two enzymes and displayed a tandem molecular self-assembly behavior. The selective formation of nanofibers in the mitochondria of the lung cancer cells led to the disruption of the mitochondrial membrane, resulting in an increased level of reactive oxygen species (ROS) and the release of cytochrome C (Cyt C). ROS can react with proteins, resulting in endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). This severe ER stress led to disruption of the ER, formation of vacuoles, and ultimately, apoptosis of the A549 cells. Therefore, Comp. 1 could selectively inhibit lung cancer cells in vitro and A549 xenograft tumors in vivo. Our study provides a novel strategy for the selective formation of nanomaterials in lung cancer cells, which is powerful and promising for the diagnosis and treatment of lung cancer.
A strategy for the selectively pericellular hydrogelation via a mechanism that involves alkaline phosphatase expressed outside the cells and CCK2R expressed in the cell membrane.
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