Application of degradable organic electronics based on biomaterials, such as polylactic‐co‐glycolic acid and polylactide (PLA), is severely limited by their low thermal stability. Here, a highly thermally stable organic transistor is demonstrated by applying a three‐arm stereocomplex PLA (tascPLA) as dielectric and substrate materials. The resulting flexible transistors are stable up to 200 °C, while devices based on traditional PLA are damaged at 100 °C. Furthermore, charge‐ trapping effect induced by polar groups of the dielectric is also utilized to significantly enhance the temperature sensitivity of the electronic devices. Skin‐like temperature sensor array is successfully demonstrated based on such transistors, which also exhibited good biocompatibility in cytotoxicity measurement. By presenting combined advantages of transparency, flexibility, thermal stability, temperature sensitivity, degradability, and biocompatibility, these organic transistors thus possess a broad applicability such as environment friendly electronics, implantable medical devices, and artificial skin.

Flexible organic phototransistors are fabricated using polylactide (PLA), a polar bio­material, as the dielectric material. The charge trapping effect induced by the polar groups of the PLA layer leads to a photosensitivity close to ≈104. The excellent performance of this new device design is further demonstrated by incorporating the photo­transistors into a sensor array to successfully image a star pattern.

CH3NH3PbI3 perovskite-based optoelectronics have attracted intense research interests recently because of their easy fabrication process and high power conversion efficiency. Herein, we report a novel photodetector based on unique CH3NH3PbI3 perovskite films with island-structured morphology. The light-induced electronic properties of the photodetectors were investigated and compared to those devices based on conventional compact CH3NH3PbI3 films. The island-structured CH3NH3PbI3 photodetectors exhibited a rapid response speed (<50 ms), good stability at a temperature of up to 100 °C, a large photocurrent to dark current ratio (Ilight/Idark > 1 × 10(4) under an incident light of ∼6.59 mW/cm(2), and Ilight/Idark > 1 × 10(2) under low incident light ∼0.018 mW/cm(2)), and excellent reproducibility. Especially, the performance of the island-structured devices markedly exceed that of the conventional compact CH3NH3PbI3 thin-film devices. These excellent performances render the island-structured device to be potentially applicable for a wide range of optoelectronics.

Intestinal barrier dysfunction occurs in critical illnesses and involves the inflammatory and hypoxic injury of intestinal epithelial cells. Researchers are still defining the underlying mechanisms and evaluating therapeutic strategies for restoring intestinal barrier function. The anti-inflammatory drug, emodin, has been shown to exert a protective effect on intestinal barrier function; however, its mechanisms of action remain unknown. In this study, we investigated the protective effects of emodin on intestinal barrier function and the underlying mechanisms in intestinal epithelial cells challenged with lipopolysaccharide (LPS) and hypoxia/reoxygenation (HR). To induce barrier dysfunction, Caco-2 monolayers were subjected to HR with or without LPS treatment. Transepithelial electrical resistance and paracellular permeability were measured to evaluate barrier function. The expression of the tight junction (TJ) proteins, zonula occludens (ZO)-1, occludin, and claudin-1, as well as that of hypoxia-inducible factor (HIF)-1α, phospho-IκB-α, phospho-nuclear factor (NF)-κB p65 and cyclooxygenase (COX)-2 was determined by western blot analysis. The results revealed that emodin markedly attenuated the decrease in transepithelial electrical resistance and the increase in paracellular permeability in the Caco-2 monolayers treated with LPS and subjected to HR. Emodin also markedly alleviated the damage caused by LPS and HR (manifested by a decrease in the expression of the TJ protein, ZO-1), and inhibited the expression of HIF-1α, IκB-α, NF-κB and COX-2 in a dose-dependent manner. In conclusion, our data suggest that emodin attenuates LPS-and HR-induced intestinal epithelial barrier dysfunction by inhibiting the HIF-1α and NF-κB signaling pathways and preventing the damage caused to the TJ barrier (shown by the decrease in the expression of ZO-1).

Radio- and chemo-resistance represent major obstacles in the therapy of non-small-cell lung cancer (NSCLC) and the underlying molecular mechanisms are not known. In the present study, during induction of radio- or chemo-resistance in NSCLC cells, dynamic analyses revealed that decreased expression of let-7 induced by irradiation or cisplatin resulted in increased expression of its target gene LIN28, and increased expression of LIN28 then contributed to further decreased expression of let-7 by inhibiting its maturation and biogenesis. Moreover, we showed that down-regulation of let-7 and up-regulation of LIN28 expression promoted resistance to irradiation or cisplatin by regulating the single-cell proliferative capability of NSCLC cells. Consequently, in NSCLC cells, let-7 and LIN28 can form a double-negative feedback loop through mutual inhibition, and disturbance of the let-7/LIN28 double-negative feedback loop induced by irradiation or chemotherapeutic drugs can result in radio- and chemo-resistance. In addition, low expression of let-7 and high expression of LIN28 in NSCLC patients was associated significantly with resistance to radiotherapy or chemotherapy. Therefore, our study demonstrated that disturbance of the let-7/LIN28 double-negative feedback loop is involved in the regulation of radio- and chemo-resistance, and that let-7 and LIN28 could be employed as predictive biomarkers of response to radiotherapy or chemotherapy in NSCLC patients.