In this work, ZnO hollow nanofibers with diameters of 120-150 nm were successfully fabricated by electrospinning the precursor solution consisting of polyacrylonitrile (PAN), polyvinylpyrrolidone (PVP), and zinc acetate composite through a facile single capillary, followed by thermal decomposition for removal of the above polymers from the precursor fibers. The as-prepared nanofibers were characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), X-ray diffraction (XRD), resonant Raman spectra, thermal gravimetric and differential thermal analysis (TG-DTA), and Fourier transform infrared spectroscopy (FT-IR) spectra, respectively. The results indicated that, during the electrospinning process, there occurred phase separation between the electrospun composite materials, while the obtained precursor nanofibers of PAN, PVP, and zinc acetate composite might possess a core-shell structure (PAN as the core and PVP/zinc acetate composite as the shell). Furthermore, the composite nanofibers with core/shell structure could play a structural directing template role for preparing ZnO hollow nanofibers during the calcination process. The ZnO hollow nanofibers exhibited excellent sensing properties against ethanol due to their special one-dimensional nanostructural properties.

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Summary Sarcopenia, the loss of skeletal muscle mass and function with advancing age, is a significant cause of disability and loss of independence in the elderly, and, thus, represents a formidable challenge for the aging population. Nevertheless, the molecular mechanism(s) underlying sarcopenia-associated muscle dysfunction remain poorly understood. In this study, we employed an integrated approach combining top-down targeted proteomics with mechanical measurements to dissect the molecular mechanism(s) in age-related muscle dysfunction. Top-down targeted proteomic analysis uncovered a progressive age-related decline in the phosphorylation of myosin regulatory light chain (RLC), a critical protein involved in the modulation of muscle contractility, in the skeletal muscle of aging rats. Top-down tandem mass spectrometry analysis identified a previously un-reported bis-phosphorylated proteoform of fast skeletal RLC and localized the sites of decreasing phosphorylation to Ser14/15. Of these sites, Ser14 phosphorylation represents a previously unidentified site of phosphorylation in RLC from fast-twitch skeletal muscle. Subsequent mechanical analysis of single fast-twitch fibers isolated from the muscles of rats of different ages revealed that the observed decline in RLC phosphorylation can account for age-related decreases in the contractile properties of sarcopenic fast-twitch muscles. These results strongly support a role for decreasing RLC phosphorylation in sarcopenia-associated muscle dysfunction, and suggest therapeutic modulation of RLC phosphorylation may represent a new avenue for the treatment of sarcopenia.

Increased aerobic glycolysis is a hallmark of cancer metabolism. How cancer cells coordinate glucose metabolism with extracellular glucose levels remains largely unknown. Here, we report that coactivator-associated arginine methyltransferase 1 (CARM1 or PRMT4) signals glucose availability to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and suppresses glycolysis in liver cancer cells. CARM1 methylates GAPDH at arginine 234 (R234), inhibiting its catalytic activity. Glucose starvation leads to CARM1 upregulation, further inducing R234 hypermethylation and GAPDH inhibition. The re-expression of wild-type GAPDH, but not of its methylation-mimetic mutant, sustains glycolytic levels. CARM1 inhibition increases glycolytic flux and glycolysis. R234 methylation delays tumor cell proliferation in vitro and in vivo. Compared with normal tissues, R234 is hypomethylated in malignant clinical hepatocellular carcinoma samples. Notably, R234 methylation positively correlates with CARM1 expression in these liver cancer samples. Our findings thus reveal that CARM1-mediated GAPDH methylation is a key regulatory mechanism of glucose metabolism in liver cancer.

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Sarcopenia, the age-related loss of skeletal muscle mass and strength, is a significant cause of morbidity in the elderly and is a major burden on health care systems. Unfortunately, the underlying molecular mechanisms in sarcopenia remain poorly understood. Herein, we utilized top-down proteomics to elucidate sarcopenia-related changes in the fast- and slow-twitch skeletal muscles of aging rats with a focus on the sarcomeric proteome, which includes both myofilament and Z-disc proteins-the proteins that constitute the contractile apparatuses. Top-down quantitative proteomics identified significant changes in the post-translational modifications (PTMs) of critical myofilament proteins in the fast-twitch skeletal muscles of aging rats, in accordance with the vulnerability of fast-twitch muscles to sarcopenia. Surprisingly, age-related alterations in the phosphorylation of Cypher isoforms, proteins that localize to the Z-discs in striated muscles, were also noted in the fast-twitch skeletal muscle of aging rats. This represents the first report of changes in the phosphorylation of Z-disc proteins in skeletal muscle during aging. In addition, increased glutathionylation of slow skeletal troponin I, a novel modification that may help protect against oxidative damage, was observed in slow-twitch skeletal muscles. Furthermore, we have identified and characterized novel muscle type-specific proteoforms of myofilament proteins and Z-disc proteins, including a novel isoform of the Z-disc protein Enigma. The finding that the phosphorylation of Z-disc proteins is altered in response to aging in the fast-twitch skeletal muscles of aging rats opens new avenues for the investigation of the role of Z-discs in age-related muscle dysfunction.

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Cerebrovascular disease involves various medical disorders that obstruct brain blood vessels or deteriorate cerebral circulation, resulting in ischemic or hemorrhagic stroke. Platinum coils with or without biological modification have become routine embolization devices in the cerebral aneurysm sac to reduce the risk of bleeding. Many intracranial stents, flow diverters and stent retrievers have been invented with uniquely designed structures. To accelerate the translation of these devices into clinical usage, an indepth understanding of the mechanical and material performance of these metal-based devices is critical. However, considering the more distal location and tortuous anatomic characteristics of cerebral arteries, present devices still risk failing to arrive at target lesions. Consequently, more flexible endovascular devices and novel designs are under urgent demand to overcome the deficiencies of existing devices. Herein, we discuss the pros and cons of the current structural designs when these devices are applied to the treatment of diseases ranging broadly from hemorrhages to ischemic strokes, in order to encourage further development of such kind of devices and investigation of their use in the clinic. Moreover, novel biodegradable materials and drug elution techniques, and the design, safety and efficacy of personalized devices for further clinical applications in cerebral vasculature are discussed.