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• W2065177675 abstract "Dura mater healing is crucial to prevent cerebrospinal fluid (CSF) leaks after neurosurgical procedures. Biological mechanisms leading to dural closure are only partially understood and have been studied in animals exclusively. We studied an in vitro model of dural closure which uses human cells.We used human dura intended for disposal after surgery. Explant primary cultures were performed. Cells were characterized through common staining and immunohistochemistry. A cell growth curve was elaborated and the effect of dexamethasone on cell count was assessed. Spongostan®, oxidized regenerated cellulose and autologous plastic materials were also evaluated for their effect on cellular growth.All specimens showed growth in fusiform cells, which project pseudopods and fuse into spindles. Cells showed desmin and vimentin positivity, and were negative for all the other stains, behaving phenotypically like fibroblasts. No collagen base was necessary for cell growth. Dexamethasone decreased cell count in the primary culture as well as in the explant, and reduced the cell proliferation marker Ki-67. Spongostan® was successfully used as a graft, and fibroblast cultures were additionally developed with muscle, pericranium, galea, and fascia. Oxidized cellulose induced cell death by lowering the pH of the solution.According to the findings, unlike mini-pigs and rabbits, in humans, dural fibroblast sensitivity to collagen seems to be lower. Dexamethasone inhibits fibroblast invasion, which is the biological base of wound dehiscence in cranial surgery. Although Spongostan is useful, Surgicel® can lower the media pH, thereby inhibiting cellular growth." @default.
• W2065177675 created "2016-06-24" @default.
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• W2065177675 date "2013-04-01" @default.
• W2065177675 modified "2023-10-02" @default.
• W2065177675 title "A new model for dura mater healing: human dural fibroblast culture" @default.
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• W2065177675 doi "https://doi.org/10.1179/1743132812y.0000000136" @default.
• W2065177675 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23336298" @default.
• W2065177675 hasPublicationYear "2013" @default.
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