Ink‐based processes, which enable scalable fabrication of flexible devices based on nanomaterials, are one of the practical approaches for the production of wearable electronics. However, carbon nanotubes (CNTs), which possess great potential for flexible electronics, are facing challenges for use in inks due to their low dispersity in most solvents and suspicious cytotoxicity. Here, a stable and biocompatible CNT ink, which is stabilized by sustainable silk sericin and free from any artificial chemicals, is reported. The ink shows stability up to months, which can be attributed to the formation of sericin–CNT (SSCNT) hybrid through non‐covalent interactions. It is demonstrated that the SSCNT ink can be used for fabricating versatile circuits on textile, paper, and plastic films through various techniques. As proofs of concept, electrocardiogram electrodes, breath sensors, and electrochemical sensors for monitoring human health and activity are fabricated, demonstrating the great potential of the SSCNT ink for smart wearables.

Mesenchymal stem cells (MSCs) have been proved to exert considerable therapeutic effects on ischemia‐reperfusion (I/R)‐induced injury, but the underlying mechanism remains unknown. In this study, we aimed to explore the potential molecular mechanism underlying the therapeutic effect of MSCs‐derived exosome reinforced with miR‐20a in reversing liver I/R injury. Quantitative real‐time polymerase chain reaction, Western blot, and IHC were carried out to compare the differential expressions of miR‐20a, Beclin‐I, FAS, Caspase‐3, mTOR and P62 in IR rats and normal rats. TUNEL was performed to assess IR‐induced apoptosis in IR rats, and luciferase assay was used to confirm the inhibitory effect of miR‐20a on Beclin‐I and FAS expression. Among the 12 candidate microRNAs (miRNAs), miR‐486, miR‐25, miR‐24, miR‐20a,miR‐466 and miR‐433‐3p were significantly downregulated in I/R. In particular, miR‐20a, a miRNA highly expressed in umbilical cord‐derived mesenchymal stem cells, was proved to bind to the 3ʹ UTR of Beclin‐I and FAS to exert an inhibitory effect on their expressions. Since Beclin‐I and FAS were aberrantly upregulated in IR, exosomes separated from UC‐MSCs showed therapeutic efficacy in reversing I/R induced apoptosis. In addition, exosomes reinforced with miR‐20a and separated from UC‐MSCs almost fully alleviated I/R injury. Furthermore, our results showed that miR‐20a could alleviate the abnormal expression of genes related to apoptosis and autophagy, such as active Caspase‐3, mTOR, P62, and LC3II. This study presented detailed evidence to clarify the mechanism underlying the therapeutic efficacy of UC‐MSCs in the treatment of I/R injury.

Esophageal microbiota plays important roles in esophageal cancer. Esophagectomy, as the most important therapeutic way, contributes to changes of esophageal microbiome. However, there are few studies examining the esophageal microbiome and the metabolic changes before and after esophagectomy. The present study characterized the esophageal microbiome of 17 patients with esophageal squamous cell carcinoma (ESCC), 11 patients with esophagogastric junction (EGJ) cancer, 15 patients at 9-12 months after radical esophagectomy and 16 healthy controls (HC). 16S ribosomal RNA gene sequencing was used to evaluate the microbiome and predict the metabolic pathways. Our results showed that the microbial diversity was significantly lower in ESCC, EGJ and post-ESCC groups than that in the HC group. The abundance of Fusobacteria was higher (7.01 vs. 1.12%, P = 0.039) and the abundance of Actinobacteria (1.61 vs. 4.04%) was lower in the ESCC group than that in the HC group. We found significant differences in the abundance of Bacteroidetes (20.45 vs. 9.86%, P = 0.026), Fusobacteria (7.01 vs. 1.66%, P = 0.030) between ESCC and post-ESCC groups. The results of microbial composition analysis and PICRUSt demonstrated significant differences between ESCC and HC groups. The β diversity and PICRUSt suggested that the microbial composition and metabolic pathways were similar to HC group after esophagectomy. The monitoring of the esophagus microbiota may be an essential method to predict the recurrence of tumor.

Lung cancer remains the leading cause of cancer-related death all over the world. In spite of the great advances made in surgery and chemotherapy, the prognosis of lung cancer patients is poor. A substantial fraction of long noncoding RNAs (lncRNAs) can regulate various cancers. A recent study has reported that lncRNA HOXB-AS3 plays a critical role in cancers. However, its biological function remains unclear in lung cancer progression. In the current research, we found HOXB-AS3 was obviously elevated in NSCLC tissues and cells. Functional assays showed that inhibition of HOXB-AS3 was able to repress A549 and H1975 cell proliferation, cell colony formation ability and meanwhile, triggered cell apoptosis. Furthermore, the lung cancer cell cycle was mostly blocked in the G1 phase whereas the cell ratio in the S phase was reduced. Also, A549 and H1975 cell migration and invasion capacity were significantly repressed by the loss of HOXB-AS3. The PI3K/AKT pathway has been implicated in the carcinogenesis of multiple cancers. Here, we displayed that inhibition of HOXB-AS3 suppressed lung cancer cell progression via inactivating the PI3K/AKT pathway. Subsequently, in vivo experiments were utilized in our study and it was demonstrated that HOXB-AS3 contributed to lung cancer tumor growth via modulating the PI3K/ AKT pathway. Overall, we implied that HOXB-AS3 might provide a new perspective for lung cancer treatment via targeting PI3K/AKT.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.