A Discolorable Flexible Synaptic Transistor for Wearable Health Monitoring.

Multifunctional intelligent wearable electronics, providing integrated physiological signal analysis, storage, and display for real-time and on-site health status diagnosis, have great potential to revolutionize health monitoring technologies. Advanced wearable systems combine isolated digital processor, memory, and display modules for function integration; however, they suffer from compatibility and reliability issues. Here, we introduce a flexible multifunctional electrolyte-gated transistor (EGT) that integrates synaptic learning, memory, and autonomous discoloration functionalities for intelligent wearable application. This device exhibits synergistic light absorption coefficient changes during voltage-gated ion doping that modulate the electrical conductance changes for synaptic function implementation. By adaptively changing color, the EGT can differentiate voltage pulse inputs with different frequency, amplitude, and duration parameters, exhibiting excellent reversibility and reliability. We developed a smart wearable monitoring system that incorporates EGT devices and sensors for respiratory and electrocardiogram signal analysis, providing health warnings through real-time and on-site discoloration. This study represents a significant step toward smart wearable technologies for health management, offering health evaluation through intelligent displays.

miR-26a-5p mediates TLR signaling pathway by targeting CTGF in LPS-induced alveolar macrophage.

To explore the regulation mechanism of miR-26a-5p and connective tissue growth factor (CTGF) in lipopolysaccharide (LPS)-induced alveolar macrophages, which is a severe pneumonia cell model. MH-S cells were grouped into Normal group, Model group, negative control (NC) group, miR-26a-5p mimic group, oe-CTGF group, miR-26a-5p mimic + oe-CTGF group. The expression level of miR-26a-5p, CTGF and Toll-like receptor (TLR) signaling related molecules (TLR2, TLR4 and nuclear factor-κB p65) were detected by qRT-PCR and WB, respectively. The cell viability and apoptosis rate were detected by methyl thiazolyl tetrazolium (MTT) and flow cytometry, respectively. Compared with the Normal group, the expression level of miR-26a-5p was significantly decreased, while CTGF protein level was significantly increased in the Model group. Compared with the Model group, MH-S cells with miR-26a-5p overexpression showed enhanced cell viability, decreased apoptosis rate, declined expression level of TLR signaling related molecules and reduced level of tumor necrosis factor-α (TNF-α), interleukin (IL) 6 (IL-6) and IL-1ß, while those with CTGF overexpression had an opposite phenotype. In conclusion, miR-26a-5p can inhibit the expression of CTGF and mediate TLR signaling pathway to inhibit the cell apoptosis and reduce the expression of proinflammatory cytokines in alveolar macrophages which is a cell model of severe pneumonia.