Myelin sheaths are essential in maintaining the integrity of axons. Development of the platform for in vitro myelination would be especially useful for demyelinating disease modeling and drug screening. In this study, a fiber scaffold with a core–shell structure was prepared in one step by the coaxial electrospinning method. A high-molecular-weight polymer poly-L-lactic acid (PLLA) was used as the core, while the shell was a natural polymer material such as hyaluronic acid (HA), sodium alginate (SA), or chitosan (CS). The morphology, differential scanning calorimetry (DSC), Fourier transform infrared spectra (FTIR), contact angle, viability assay, and in vitro myelination by oligodendrocytes were characterized. The results showed that such fibers are bead-free and continuous, with an average size from 294 ± 53 to 390 ± 54 nm. The DSC and FTIR curves indicated no changes in the phase state of coaxial brackets. Hyaluronic acid/PLLA coaxial fibers had the minimum contact angle (53.1° ± 0.24°). Myelin sheaths were wrapped around a coaxial electrospun scaffold modified with water-soluble materials after a 14-day incubation. All results suggest that such a scaffold prepared by coaxial electrospinning potentially provides a novel platform for oligodendrocyte myelination.

Phase measurement profilometry, or PMP, is undergoing rapid development at present. Combined with defocused projection and advanced multiband phase shift (PS) algorithms, such as heterodyne and number theory, PMP with over thousand framerates has shown great potential in 3-D dynamic scene monitoring, e.g., manufacturing process monitoring and industrial digital twins. PMP’s outstanding advantages include a combination of high lateral resolution, axial precision, and speed; however, the widely used dual-band PS algorithms have limited axial precision compared to low-efficiency tri-band algorithms. In this article, we propose “3–2–1” PMP, which optimizes the existing dual-band approach by adding an extra fringe pattern for projection acquisition to achieve similar precision performance as tri-band PMP. Associated stabilization algorithms in dealing with fringe blur, nonlinear camera responses, phase-jump errors, and related impact factors have also been investigated. Comparative simulation and experiments show that the “3–2–1” approach produces higher precision performance, with a 42%–85% root-mean-square error lower than general dual-band PS methods and famous Fourier transform profilometry ( $\mu $ FTP), but using an equivalent projection pattern number of 6 or less.

Constant light (LL) exposure is an established environmental risk factor for metabolic diseases, in which the whitening of brown adipose tissue (BAT) plays a critical role. This study aimed to elucidate the molecular mechanisms through which cordycepin counteracts LL-induced BAT whitening and improves metabolic function. We established an LL-exposed mouse model and employed an integrative approach combining pharmacological, metabolic, molecular, and computational (docking) assays to define cordycepin’s effects and targets. Cordycepin treatment significantly improved cold tolerance and attenuated BAT whitening in LL mice. Mechanistically, cordycepin directly bound to and enhanced the activity of the NAD⁺-dependent deacetylase SIRT1. This activation mitigated LL-induced impairments in mitochondrial biogenesis, dynamics, and autophagy. Furthermore, SIRT1 activation rebalanced fatty acid metabolism by downregulating CD36 and upregulating CPT1, thereby restoring the coupling of fatty acid uptake to oxidation. All beneficial effects of cordycepin were abolished by the selective SIRT1 inhibitor EX-527. In summary, our work provides strong evidence that cordycepin directly interacts with SIRT1 and enhances its deacetylase activity, thereby restoring mitochondrial function and fatty acid oxidative homeostasis in BAT to counteract constant LL-induced metabolic dysfunction. These findings position cordycepin as a promising natural compound targeting the SIRT1 pathway for metabolic disorders.

Background/Objectives: The transcription factor carbohydrate response element-binding protein (ChREBP) is a key glucose-sensing regulator that governs glucose and lipid metabolic homeostasis. However, its specific functions in skeletal muscle remain insufficiently clarified. The present study aimed to investigate the roles of ChREBP in skeletal muscle exercise capacity, energy metabolism, and adaptive remodeling, as well as muscle regeneration. Methods: We generated a skeletal muscle-specific ChREBP knockout mouse model, and assessed their exercise performance, energy metabolism, skeletal muscle fiber composition, and injury repair capacity. Additionally, hypoxia and high-fructose diet models were established to analyze the function of ChREBP in skeletal muscle adaptive remodeling. C2C12 myoblasts and primary muscle satellite cells were used to explore its effects on myogenic differentiation. Results: Genetic deletion of ChREBP induced no detectable alterations in myofiber composition, overall metabolic status, or muscle adaptive remodeling triggered by hypoxia and high-fructose diet. In vitro assays demonstrated that ChREBP overexpression facilitates C2C12 myogenic differentiation. Adeno-associated virus-mediated ChREBP overexpression enhanced histological markers of regeneration, including desmin-positive regenerative area and the cross-sectional area of newly formed myofibers after cardiotoxin-induced injury. Conclusions: Collectively, our experimental data indicate that ChREBP is largely dispensable for maintaining basal skeletal muscle homeostasis and stress-induced adaptive remodeling. Meanwhile, this study identifies a previously unrecognized regulatory role of ChREBP in the processes of skeletal muscle damage repair and post-injury regeneration.