Sensitive and specific detection of tumor exosomes is of great significance for early cancer diagnosis. In this paper, we report an aptamer strategy for exosome detection based on aptamer recognition-induced multi-DNA release and cyclic enzymatic amplification. First, we use aptamer-magnetic bead bioconjugates to capture tumor exosomes derived from LNCaP cells, leading to the release of three kinds of messenger DNAs (mDNAs). After magnetic separation, the released mDNAs hybridized with the probe DNAs immobilized on a gold electrode. Electroactive Ru(NH) was used as the signal reporter because of its electrostatic attraction to DNA. Subsequent Exo III cyclic digestion caused the electrochemical signal to "turn off". Because the electrochemical signal reflects the concentration of Ru(NH) and the concentration of Ru(NH) is correlated with the mDNA concentration, which is correlated with the exosome concentration, the tumor exosomes can be detected by examining the decrease in the peak current of Ru(NH). In this paper, the signal was amplified by the numerous mDNAs released from the magnetic bead and the Exo III-assisted mDNA recycling. Under the optimal conditions, a detection limit down to 70 particles/μL was achieved, which is lower than the LODs of most currently available methods. Furthermore, this assay can be used to detect tumor exosomes in complex biological samples, demonstrating potential application in real sample diagnosis.

No abstract

For the organic memory device with vertically arranged electrodes, controlling the film‐packing to achieve highly oriented crystallite arrangement is critical but challenging for obtaining the satisfied performance. Here, the effect of backbone planarity on the crystallite orientation is studied. Two diketopyrrolopyrrole‐based small molecules (NI2PDPP and NI2FDPP) are synthesized with increasing planarity by furan substitution for phenyl rings. Upon thin‐film analysis by atomic force microscopy, X‐ray diffraction, and grazing‐incidence small‐angle X‐ray scattering, the orientations of these crystallites are demonstrated to be well controlled through tailoring molecular planarity. The highly planar NI2FDPP in film prefers out‐of‐plane crystallite orientation with respect to the substrate normal while the nonplanar NI2PDPP displays less ordered packing with a broad orientation distribution relative to the substrate. As a result, NI2FDPP‐based memory device exhibits superior multilevel performance. More importantly, the oriented crystallite arrangement favors uniformity in NI2FDPP thin film, thus, the device displays higher reproducibility of memory effects. This study provides an effective synthetic strategy for designing multilevel memory materials with favorable crystallite orientation.

Synthesis of cyclic peptides with novel Cβ–Ar crosslinks has been achieved by C(sp3)–H activation, and their biological properties have been evaluated for the first time.

Background Sepsis leads to severe acute lung injury/acute respiratory distress syndrome (ALI/ARDS) that is associated with enhanced endoplasmic reticulum (ER) stress. Heme oxygenase-1 (HO-1), an ER-anchored protein, exerts antioxidant and protective functions under ALI. However, the role of HO-1 activation in the development of endoplasmic reticulum (ER) stress during sepsis remains unknown. Methods Cecal ligation and puncture (CLP) model was created to induce septic ALI. Lung tissue ER stress was measured 18 hours after CLP. The effects of HO-1 on ER stress during septic ALI were investigated in vivo using HO-1 agonist hemin and antagonist ZnPP. Results Compared with the sham group, ER stress in septic lung increased significantly 18 hours after CLP, which was significantly reduced by pretreatment with the ER inhibitor 4-phenylbutyrate (4-PBA). The lung injury score and the lung wet to dry (W/D) ratio in lungs were significantly reduced in septic rats after ER stress inhibition. Similarly, lung ER stress-related genes' (PERK, eIF2-α, ATF4, and CHOP) levels were attenuated after ER stress inhibition. Furthermore, HO-1 activation by hemin reduced p-PERK, p-eIF2-α, ATF4, and CHOP protein expression and oxidative stress and lung cell apoptosis. Additionally, HO-1 antagonist could aggregate the ER stress-related ALI. Conclusions ER stress was activated during CLP-induced ALI, which may represent a mechanism by which CLP induces ALI. HO-1 activation could inhibit CLP-induced lung ER stress and attenuate CLP-induced ALI.