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Na0.67Ni0.33Mn0.67O2 (NNMO) is one of the most promising cathodes for Sodium‐ion batteries. However, due to undesired P2−O2 phase transition at high voltage during Na+ extraction, its cyclic stability and coulomb efficiency are greatly adversely affected. Herein, electrochemically active Fe3+ ions substituted Na0.67Ni0.23Fe0.1Mn0.67O2 samples were prepared by both sol‐gel method (NNFMO‐SG) and solid phase method (NNFMO‐SP). It has been found that Fe substitution can suppress P2−O2 phase transition with a stable P2 phase during charging and discharging. Additionally, it also suppresses Na+/vacancy ordering, expands the slab‐spacing of the structure and improves the reversibility of the redox of anions. Owing to the combined advantages, NNFMO‐SG material exhibits the enhanced rate capability (70.1 mAh/g at 1000 mA/g) and excellent cycling stability (75.3 % capacity retention after 100 cycles at 200 mA/g). [ABSTRACT FROM AUTHOR]

Human fibroblast growth factor 19 (FGF19, or FGF15 in rodents) plays a central role in controlling bile acid (BA) synthesis through a negative feedback mechanism. This process involves a postprandial crosstalk between the BA‐activated ileal farnesoid X receptor and the hepatic Klotho beta (KLB) coreceptor complexed with fibrobalst growth factor receptor 4 (FGFR4) kinase. Additionally, FGF19 regulates glucose, lipid, and energy metabolism by coordinating responses from functional KLB and FGFR1‐3 receptor complexes on the periphery. Pharmacologically, native FGF19 or its analogs decrease elevated BA levels, fat content, and collateral tissue damage. This makes them effective in treating both cholestatic diseases such as primary biliary or sclerosing cholangitis (PBC or PSC) and metabolic abnormalities such as nonalcoholic steatohepatitis (NASH). However, chronic administration of FGF19 drives oncogenesis in mice by activating the FGFR4‐dependent mitogenic or hepatic regenerative pathway, which could be a concern in humans. Agents that block FGF19 or FGFR4 signaling have shown great potency in preventing FGF19‐responsive hepatocellular carcinoma (HCC) development in animal models. Recent phase 1/2 clinical trials have demonstrated promising results for several FGF19‐based agents in selectively treating patients with PBC, PSC, NASH, or HCC. This review aims to provide an update on the clinical development of both analogs and antagonists targeting the FGF19–FGFR4 signaling pathway for patients with cholestatic, metabolic, and cancer diseases. We will also analyze potential safety and mechanistic concerns that should guide future research and advanced trials. [ABSTRACT FROM AUTHOR]

Research has been conducted on the stromal cell-derived fibroblast growth factors (FGF). The structure of the FGF-7 solved by the molecular replacement with the structure of the FGF-1 and FGF-7 dual function chimera is described and the comparison of the FGF-7 structure with that of FGF-1 and FGF-2 has been carried out and is reported.

Results point out that heme biosynthesis enzymes are regulated by mPer1 and mPer2 encoded proteins, which individually and complemetnarily exhibit influence on the manifestation of circadian rhythms in mice.