Wearable transdermal iontophoresis eliminating the need for external power sources offers advantages for patient-comfort when deploying epidermal diseases treatments. However, current self-powered iontophoresis based on energy harvesters is limited to support efficient therapeutic administration over the long-term operation, owing to the low and inconsistent energy supply. Here we propose a simplified wearable iontophoresis patch with a built-in Mg battery for efficient and controllable transdermal delivery. This system decreases the system complexity and form factors by using viologen-based hydrogels as an integrated drug reservoir and cathode material, eliminating the conventional interface impedance between the electrode and drug reservoir. The redox-active polyelectrolyte hydrogel offers a high energy density of 3.57 mWh cm−2, and an optimal bioelectronic interface with ultra-soft nature and low tissue-interface impedance. The delivery dosage can be readily manipulated by tuning the viologen hydrogel and the iontophoresis stimulation mode. This iontophoresis patch demonstrates an effective treatment of an imiquimod-induced psoriasis mouse. Considering the advantages of being a reliable and efficient energy supply, simplified configuration, and optimal electrical skin-device interface, this battery-powered iontophoresis may provide a new non-invasive treatment for chronic epidermal diseases.
Cardiac fibrosis is a basic process in cardiac remodeling. It is related to almost all types of cardiovascular diseases (CVD) and has become an important global health problem.
THOR is a long noncoding RNA that is highly conserved and highly expressed in a variety of human tumor cells. A large number of studies show that THOR is deeply involved in the occurrence and development of a variety of cancers. However, the role and potential molecular mechanisms of THOR in the initiation and progression of CRC have not been fully elucidated. Here, we demonstrate that THOR is crucial for the occurrence of CRC; it interacts with IGF2BP1 to regulate the downstream Wnt/β-catenin signaling pathway. To clarify the contribution of THOR in the occurrence and development of CRC, we established THOR-deficient APCMin/+ mice and human colorectal cancer cells (SW480) using CRISPR/Cas9 technology. The results showed that the body weight and survival rate of THOR-deficient APCMin/+ mice increased; hyperlipidemia in elderly mice was alleviated, and changes in intestinal structure were attenuated. THOR knockout inhibited the growth, proliferation, and migration of SW480 cells. Downstream regulator genes, including c-MYC, APC, SOX9, Wnt1, CDH1, Axin1, Axin2, LEF 1, were knocked down with THOR knockout. In summary, our results indicate that THOR knockout inhibits the growth and migration of CRC cells and that THOR is a promising prognostic indicator for CRC patients. Moreover, the THOR-IGF2BP1-Wnt/β-catenin axis may be a potential therapeutic target for CRC, providing new insights into the important role of lncRNAs in cancer.
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