Hubei University of Science & Technology

The development of cost-effective, high-efficiency oxygen evolution reaction (OER) catalysts through precise compositional and structural design via guest doping engineering represents a significant research challenge. While cobalt silicate (CoSi) has emerged as a promising OER catalyst, its practical application has been limited by relatively high overpotential (η). In this study, we presented a strategic Fe-doping approach to engineer the electronic structure of CoSi, significantly enhancing its OER performance. Through hydrothermal synthesis, we successfully incorporated Fe atoms into the CoSi framework, creating hollow spherical iron-doped cobalt silicate (CoSi-Fe) catalysts. Comprehensive characterization revealed that the geometric and synergistic effects of Fe-doping facilitate: (1) increased exposure of active sites, (2) enhanced activity of Co/Fe dual sites, and (3) improved structural stability of Co species. Density functional theory (DFT) calculations further demonstrated that Fe incorporation optimizes reaction kinetics and improves electrical conductivity, collectively boosting OER activity. The optimized CoSi-Fe-3 catalyst (Co/Fe = 15:5) exhibits exceptional performance, achieving an overpotential of only 289 mV at 10 mA cm^-2 (a 118 mV reduction compared to pristine CoSi of 407 mV) and superior to most reported metal silicate catalysts. We systematically analyzed the structure-activity relationship underlying this performance enhancement. This work establishes an effective doping strategy for developing high-performance silicate-based electrocatalysts, providing valuable insights for advancing renewable energy conversion technologies.

Emerging findings indicate that angiotensin II (Ang II) and its receptors, namely type 1 (AT1R) and type 2 (AT2R), are expressed in dorsal root ganglion (DRG) and involved in the nociception of sensory neurons. However, the mechanisms remain unknown. The purpose of this investigation is to determine the role of Ang II in the regulation of ion channels in nociceptive DRG neurons. Herein, we found that the application of Ang II for 10 min enhanced the electrophysiological activity of acid-sensing ion channels (ASICs) in rat DRG neurons. Ang II increased acid-evoked ASIC currents in a concentration-dependent manner. Ang II increased the maximum response of ASICs to acidic stimuli without changing their sensitivity. Ang II enhanced ASIC currents through AT1R but not AT2R. The enhancing effect of Ang II on ASIC currents was prevented by either the PKC inhibitor GF109203x, or the ERK inhibitor U0126, but not by the p38 inhibitor SB202190 or the JNK inhibitor SP600125. Moreover, Ang II increased the action potentials triggered by acidic stimuli. Finally, intraplantar injection of Ang II dose-dependently exacerbated acid-induced nociceptive behavior in rats through local AT1R. These results indicated that Ang II enhanced the functional activity of ASICs through a mechanism that depended on AT1R, the intracellular PKC, and the ERK signaling pathway. Our findings provided evidence that Ang II is a promising target for developing new treatments for pain, at least for pain associated with tissue acidification.

Lung cancer remains a significant health challenge, with fibroblast growth factor receptor (FGFR) signaling emerging as a critical player in its pathogenesis. This review examines FGFR's roles in endothelial function, angiogenesis, immune modulation, epithelial-to-mesenchymal transition (EMT), and transdifferentiation in lung cancer. Moreover, FGFR signaling is implicated in resistance to receptor tyrosine kinase (RTK) tyrosine kinase inhibitors (TKIs), particularly those targeting EGFR, ALK, and MET, immune checkpoint inhibitors, and chemotherapies in lung cancer. Furthermore, therapeutic approaches targeting FGFR include multitarget TKIs and selective FGFR inhibitors, which have shown promise in individuals with FGFR alterations. The side effects of FGFR inhibitors in clinical settings and associated management strategies have also been outlined. Additionally, challenges in personalizing FGFR therapies include variable FGFR alterations, diagnostic hurdles, biomarker selection and validation, and trial design intricacies. This comprehensive overview underscores the necessity for innovative approaches to optimize FGFR-targeted therapies in lung cancer treatment.