Background. Circulating long noncoding RNAs (lncRNAs) have been demonstrated to serve as diagnostic biomarkers for various cancers. We aimed to elucidate the diagnostic efficacy of eight serum lncRNAs HULC, MALAT1, Linc00152, PTENP1, PTTG3P, SPRY4-IT1, UBE2CP3, and UCA1 and their combinations for the diagnosis of hepatocellular carcinoma (HCC). Methods. A total of 129 patients with HCC, 49 patients with liver cirrhosis, 27 patients with chronic hepatitis B, and 93 healthy controls were enrolled in this study. The levels of serum lncRNAs were assessed by quantitative real-time polymerase chain reaction. The correlations between serum lncRNAs and clinicopathological characteristics were further analyzed. The receiver operating characteristic (ROC) curve and area under curve (AUC) were utilized to estimate the diagnostic capacity of serum lncRNAs and their combination with AFP for HCC. A logistic regression model was performed to establish a multiple-lncRNA panel. Results. The levels of serum HULC, MALAT1, Linc00152, PTTG3P, SPRY4-IT1, UBE2CP3, and UCA1 were significantly higher in HCC patients than in patients with benign liver diseases and healthy controls, whereas serum PTENP1 was significantly decreased in HCC patients compared with healthy participants. Positive correlations between serum Linc00152 and GGT, serum PTTG3P and GGT, and serum SPRY4-IT1 and ALT were noted in HCC patients. ROC analysis revealed that all these lncRNAs had a significantly predictive value for HCC except for PTENP1. The best performance of single lncRNA was obtained by Linc00152 with an AUC of 0.877. When combined with AFP, the combination of Linc00152 and AFP gained the highest accuracy, yielding an AUC of 0.906. Through logistic regression analysis, the panel consisting of serum linc00152, UCA1, and AFP provided the greatest predictive ability, obtaining an AUC of 0.912 with 82.9% sensitivity and 88.2% specificity. Conclusion. The panel of serum Linc00152, UCA1, and AFP demonstrates a novel and noninvasive biomarker with relatively high sensitivity and specificity for HCC diagnosis.

No abstract

Switchable selective hydrogenation among the groups in multifunctional compounds is challenging because selective hydrogenation is of great interest in the synthesis of fine chemicals and pharmaceuticals as a result of the importance of key intermediates. Herein, we report a new approach to highly selectively (>99%) reducing CX (X = O, N) over the thermodynamically more favorable nitro groups locating the substrate in a metal−organic capsule containing NADH active sites. Within the capsule, the NADH active sites reduce the double bonds via a typical 2e − hydride transfer hydrogenation, and the formed excited-state NAD + mimics oxidize the reductant via two consecutive 1e − processes to regenerate the NADH active sites under illumination. Outside the capsule, nitro groups are highly selectively reduced through a typical 1e − hydrogenation. By combining photoinduced 1e − transfer regeneration outside the cage, both 1e − and 2e − hydrogenation can be switched controllably by varying the concentrations of the substrates and the redox potential of electron donors. This promising alternative approach, which could proceed under mild reaction conditions and use easy-to-handle hydrogen donors with enhanced high selectivity toward different groups, is based on the localization and differentiation of the 2e − and 1e − hydrogenation pathways inside and outside the capsules, provides a deep comprehension of photocatalytic microscopic reaction processes, and will allow the design and optimization of catalysts. We demonstrate the advantage of this method over typical hydrogenation that involves specific activation via well-modified catalytic sites and present results on the high, well-controlled, and switchable selectivity for the hydrogenation of a variety of substituted and bifunctional aldehydes, ketones, and imines.

Tumor progression requires the communication between tumor cells and tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs) are major components of stromal cells. CAFs contribute to metastasis process through direct or indirect interaction with tumor cells; however, the underlying mechanism is largely unknown. Here, we reported that autophagy was upregulated in lung cancer-associated CAFs compared to normal fibroblasts (NFs), and autophagy was responsible for the promoting effect of CAFs on non-small cell lung cancer (NSCLC) cell migration and invasion. Inhibition of CAFs autophagy attenuated their regulation on epithelial–mesenchymal transition (EMT) and metastasis-related genes of NSCLC cells. High mobility group box 1 (HMGB1) secreted by CAFs mediated CAFs’ effect on lung cancer cell invasion, demonstrated by using recombinant HMGB1, HMGB1 neutralizing antibody, and HMGB1 inhibitor glycyrrhizin (GA). Importantly, the autophagy blockade of CAFs revealed that HMGB1 release was dependent on autophagy. We also found HMGB1 was responsible, at least in part, for autophagy activation of CAFs, suggesting CAFs remain active through an autocrine HMGB1 loop. Further study demonstrated that HMGB1 facilitated lung cancer cell invasion by activating the NFκB pathway. In a mouse xenograft model, the autophagy specific inhibitor chloroquine abolished the stimulating effect of CAFs on tumor growth. These results elucidated an oncogenic function for secretory autophagy in lung cancer-associated CAFs that promotes metastasis potential, and suggested HMGB1 as a novel therapeutic target.

This study show that SP may have a protective effect on DOX-induced cardiotoxicity.

Traditional silicone elastomers are thermoset polymers with crosslink sites linked through covalent bonds. The benefits of silicone elastomers would be improved by the ability to reuse the materials. Here we...

No abstract

Reductive silylation cleaves S–S crosslinks in used automotive rubbers, allowing recovery of polymeric oils in up to 93% yield. The oils can undergo oxidative crosslinking to give new elastomers, closing the loop for sulfur-cured rubbers.