Flexible pressure sensors have attracted increasing interest because of their potential applications on wearable sensing devices for human−machine interface connections, but challenges regarding material cost, fabrication robustness, signal transduction, sensitivity improvement, detection range, and operation convenience still need to be overcome. Herein, with a simple, low-cost, and scalable approach, a flexible and wearable pressure-sensing device fabricated by utilizing filter paper as the solid support, poly(3,4-ethylenedioxythiophene) to enhance conductivity, and silver nanoparticles to provide a rougher surface is introduced. Sandwiching and laminating composite material layers with two thermoplastic polypropylene films lead to robust integration of sensing devices, where assembling four layers of composite materials results in the best sensitivity toward applied pressure. This practical pressure-sensing device possessing properties such as high sensitivity of 0.119 kPa −1 , high durability of 2000 operation cycles, and an ultralow energy consumption level of 10 −5 W is a promising candidate for contriving point-of-care wearable electronic devices and applying it to human−machine interface connections.
Programmable surface-patterned functional DNA density is achieved via manipulation of molecular-level defects through chemical lift-off lithography. Artificial SAM defects are well-tunable by a contact-induced reaction, enabling molecular environment guidance and DNA insertion to be spatially and quantitatively addressable. This straightforward molecular density control creates an advanced avenue toward fabricating multiplexed bioactive substrates.
The classical alkanethiol post-passivation can prevent nonspecific binding of nucleotide bases onto supporting substrates and help aptamers transition from a "lying down" to a "standing up" orientation. However, the surface probes display lower binding affinity towards targets than those in bulk solutions due to unsatisfied hybridization spaces on the alkanethiol passivated substrate. To overcome this challenge, an artificial defect-rich matrix possessing an aptamer "self-standing" property created by chemical lift-off lithography (CLL) is demonstrated. This approach provided artificial defects on a hydroxyl-terminated alkanethiol self-assembled monolayer (SAM), which allowed the insertion of thiolated aptamers. The diluted surface molecular environment assisted aptamers not only to "self-stand" on the surface, but also to separate from each other, providing a suitable surface aptamer density and sufficient space for capturing targets. With this approach, the binding affinity of the aptamer towards a target was comparable to solution-type probes, showing higher recognition efficiency than that in conventional methods.
The aim of the present study was to investigate the effect of the nuclear factor‑κB (NF‑κB) inhibitor, pyrrolidine dithiocarbamate (PDTC), on high‑mobility group protein B1 (HMGB1) expression in a rat model of chronic obstructive pulmonary disease (COPD). The COPD model was developed by administering lipopolysaccharides to the airways of rats and smudging (group B). In addition, a model of COPD complicated with hypoxia was established by administering lipopolysaccharides to the airways of rats, smudging and hypoxia (group C). PDTC was administered to the treatment groups by intraperitoneal injection. Reverse transcription polymerase chain reaction (RT‑PCR) and western blot analysis were used to detect the expression of HMGB1 and NF‑κB in lung tissue. RT‑PCR and western blot analysis demonstrated that HMGB1 mRNA and protein expression in groups B and C increased significantly (P<0.05) compared with control group A. In addition, HMGB1 expression in groups B and C gradually increased. HMGB1 mRNA and protein expression in groups B1 and C1 decreased (P<0.05) compared with B and C. NF‑κB protein expression in groups B and C increased significantly (P<0.05) compared with A. NF‑κB protein expression in groups B1 and C1 decreased compared with B and C. Therefore, HMGB1 mRNA and protein expression was identified to be positively correlated with NF‑κB protein expression. The NF‑κB inhibitor, PDTC, was demonstrated to significantly inhibit HMGB1 expression in lung tissues of rats with COPD and this mechanism may be associated with the NF‑κB signal transduction pathway.
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