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Skeletal muscle has a robust endocrine function as a powerful organ and can secrete and release cytokines or polypeptides known as myokines. These myokines have significant regulatory effects on signal transduction in skeletal muscle and the metabolism of peripheral tissues and organs and exert biological effects via autocrine, paracrine, or endocrine forms. Obesity and aging cause myokine secretion dysregulation, and hastening sarcopenic obesity (SO) development. Exercise is currently an excellent intervention and prevention method for SO. Meanwhile, exercise impacts many organs and tissues. These organs and tissues will produce various myokines in response to movement and metabolism throughout the body to govern muscle differentiation, growth, and remodeling. According to accumulating data, exercise can increase the release of myokines from diverse tissues into the blood and postpone the SO onset and progression by influencing protein metabolism, inflammation, mitochondrial quality control, and other mechanisms.

Nuclear RNA export into the cytoplasm is one of the key steps in protein expression to realize biological functions. Despite the broad availability of nucleic acid dyes, tracking and quantifying the highly dynamic process of RNA export in live cells is challenging. When dye-labeled RNA enters the cytoplasm, the dye molecules are released upon degradation of the RNA, allowing them to re-enter the cell nucleus. As a result, the ratio between the dye exported with RNA into the cytoplasm and the portion staying inside the nucleus cannot be determined. To address this common limitation, we report the design of a smart probe that can only check into the nucleus once. When adding to cells, this probe rapidly binds with nuclear RNAs in live cells and reacts with intrinsic H2S. This reaction not only activates the fluorescence for RNA tracking but also changes the structure of probe and consequently its intracellular localization. After disassociating from exported RNAs in cytoplasm, the probe preferentially enters lysosomes rather than cell nucleus, enabling real-time quantitative measurement of nuclear RNA exports. Using this probe, we successfully evaluated the effects of hormones and cancer drugs on nuclear RNA export in live cells. Interestingly, we found that hormones inhibiting RNA exports can partially offset the effect of chemotherapy.

Osteonecrosis of femoral head (ONFH) is a pathological state caused by lack of blood supply in femoral head. This study aimed to explore the function of Lycium barbarum polysaccharide (LBP), an antioxidant agent extracted from L. barbarum, on ONFH.Osteonecrosis rat model was generated using lipopolysaccharide (LPS) and methylprednisolone followed by examination of body weight, blood glucose, morphology, and BMSC osteoblast differentiation. The effect and underlying mechanism of LBP on the proliferation, apoptosis, and osteoblast differentiation of BMSC were determined with or without LPS or hypoxia treatment using CCK-8. Alizarin Red S staining, flow cytometry, and western blot, respectively.LBP could protect against glucocorticoid-induced ONFH in rats, resulting in improved sparse trabecular bone, empty lacunae and bone cell coagulation. Moreover, LBP promoted the proliferation and osteoblast differentiation of bone mesenchymal-derived stem cells (BMSCs) in a dose-dependent manner. Furthermore, LBP enhanced osteoblast differentiation of BMSCs under hypoxia condition. Mechanistically, we found that LBP treatment enhanced Runx2 and ALP expression in BMSCs. LBP restored the expression of Runx2 and ALP under hypoxia, suggesting that LBP might be involved in regulating Runx2/ALP expression and contributed to osteoblast differentiation. Knockdown of Runx2 significantly inhibited BMSCs proliferation, while LBP treatment did not rescue the osteoblast differentiation ability of BMSCs with Runx2 knockdown.Our findings suggested that LBP protects against ONFH via regulating Runx2 expression, which could be utilized to treat patients suffering ONFH.

The collective oscillation of free electrons at the nanoscale surface of gold nanostructures is closely modulated by tuning the size, shape/morphology, phase, composition, hybridization, assembly, and nanopatterning, along with the surroundings of the plasmonic surface located at a dielectric interface with air, liquid, and solid. This review first introduces the physical origin of the intrinsic optical properties of gold nanostructures and further summarizes stimuli-responsive changes in optical properties, metal-field-enhanced optical signals, luminescence spectral shaping, chiroptical response, and photogenerated hot carriers. The current success in the landscape of nanoscience and nanotechnology mainly originates from the abundant optical properties of gold nanostructures in the thermodynamically stable face-centered cubic (fcc) phase. It has been further extended by crystal phase engineering to prepare thermodynamically unfavorable phases (e.g., kinetically stable) and heterophases to modulate their intriguing phase-dependent optical properties. A broad range of promising applications, including but not limited to full-color displays, solar energy harvesting, photochemical reactions, optical sensing, and microscopic/biomedical imaging, have fostered parallel research on the multitude of physical effects occurring in gold nanostructures. This article is protected by copyright. All rights reserved.