Skin wounds on stretchable parts of the body including the elbows, knees, wrists, and nape usually undergo delayed and poor healing due to the interference of their frequent motion. Ordinary dressings that are not flexible enough face difficulty to promote wound healing due to the mismatching between the mechanics of the dressing materials and the wounds. In this study, an injectable, biocompatible, self‐healable, and conductive material poly(3,4‐ethylenedioxythiophene): poly(styrenesulfonate)/guar slime (PPGS) is developed for healing wounds with various kinds of movements. As a proof‐of‐principle assay, the healing effect of PPGS is explored on a skin wound model on the nape of rats that often experiences frequent movements. PPGS, which can be prepared within 1 min, successfully accelerates the healing of the wounds. The results suggest that PPGS has great potential in the fields of tissue engineering and biomedicine.
Usher syndrome (USH) is the most common inherited deaf-blindness with the majority of USH causative genes also involved in nonsyndromic recessive deafness (DFNB). The mechanism underlying this disease variation of USH genes is unclear. Here, we addressed this issue by investigating the DFNB31 gene, whose mutations cause USH2D or DFNB31 depending on their position. We found that the mouse DFNB31 ortholog (Dfnb31) expressed different mRNA variants and whirlin protein isoforms in the cochlea and retina, where these isoforms played different roles spatially and temporally. Full-length (FL-) whirlin in photoreceptors and hair cell stereociliary bases is important for the USH type 2 protein complex, while FL- and C-terminal (C-) whirlins in hair cell stereociliary tips participate in stereociliary elongation. Mutations in the whirlin N-terminal region disrupted FL-whirlin isoform in the inner ear and retina but not C-whirlin in the inner ear, and led to retinal degeneration as well as moderate to severe hearing loss. By contrast, a mutation in the whirlin C-terminal region eliminated all normal whirlin isoforms but generated a truncated N-terminal whirlin protein fragment, which was partially functional in the retina and thus prevented retinal degeneration. Mice with this mutation had profound hearing loss. In summary, disruption of distinct whirlin isoforms by Dfnb31 mutations leads to a variety of phenotype configurations and may explain the mechanism underlying the different disease manifestations of human DFNB31 mutations. Our findings have a potential to improve diagnosis and treatment of USH disease and quality of life in USH patients.
Ginsenosides, a kind of triterpenoid saponins derived from isopentenyl pyrophosphate (IPP), represent the main pharmacologically active constituents of ginseng. In plants, two pathways contribute to IPP biosynthesis, namely, the mevalonate pathway in cytosol and the non-mevalonate pathway in plastids. This motivates biologists to clarify the roles of the two pathways in biosynthesis of IPP-derived compounds. Here, we demonstrated that both pathways are involved in ginsenoside biosynthesis, based on the analysis of the effects from suppressing either or both of the pathways on ginsenoside accumulation in Panax ginseng hairy roots with mevinolin and fosmidomycin as specific inhibitors for the mevalonate and the non-mevalonate pathways, respectively. Furthermore, the sterol biosynthesis inhibitor miconazole could enhance ginsenoside levels in the hairy roots. These results shed some light on the way toward better understanding of ginsenoside biosynthesis.
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