| 1. |
- Du, Xueli, et al.
(författare)
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Study of rare-earth oxide sintering aid systems for AlN ceramics
- 2007
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Ingår i: Materials Science & Engineering. - : Elsevier BV. - 0921-5093 .- 1873-4936. ; 460-461, s. 471-474
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Tidskriftsartikel (refereegranskat)abstract
- In the present work, effects of Y2O3 and Dy2O3 sintering aid systems on density and thermal conductivity of AlN ceramics sintered at low temperature were investigated. The AlN powder synthesized by self-propagating high-temperature synthesis (SHS) was mixed individually with six different sintering aids, which were Y2O3, Dy2O3, CaF2–Y2O3, CaF2–Dy2O3, CaF2–Li2CO3–Y2O3 and CaF2–Li2CO3–Dy2O3, and then fabricated by employing press forming technique. The specimens were sintered at 1650 °C in nitrogen atmosphere at atmospheric pressure for 4 h. X-ray diffraction (XRD) was used to identify the secondary phases. The microstructure of the specimen was observed by scanning electron microscopy (SEM). The thermal diffusivity at room temperature was measured by a laser flash technique. Density of sintered specimen was measured by Archimedes displacement method. The result reveals that the density and thermal conductivity of AlN ceramics sintered with one component sintering aids were lower than those of sintered with multiple components sintering aids. The thermal conductivity of AlN ceramics sintered with CaF2–Li2CO3–Y2O3 and CaF2–Dy2O3 were 141 W m−1 K−1 and 142 W m−1 K−1, which were higher than that of any others.
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| 2. |
- Wang, Xiaolei, et al.
(författare)
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Induction of Fibroblast Senescence During Mouse Corneal Wound Healing
- 2019
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Ingår i: Investigative Ophthalmology and Visual Science. - : ASSOC RESEARCH VISION OPHTHALMOLOGY INC. - 0146-0404 .- 1552-5783. ; 60:10, s. 3669-3679
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE. To investigate the presence and role of fibroblast senescence in the dynamic process of corneal wound healing involving stromal cell apoptosis, proliferation, and differentiation.METHODS. An in vivo corneal wound healing model was performed using epithelial debridement in C57BL/6 mice. The corneas were stained using TUNEL, Ki67, and alpha-smooth muscle actin (alpha-SMA) as markers of apoptosis, proliferation, and myofibroblastic differentiation, respectively. Cellular senescence was confirmed by senescence-associated beta-galactosidase (SA-beta-gal) staining and P16(Ink4a) expression. Mitogenic response and gene expression were compared among normal fibroblasts, H2O2-induced senescent fibroblasts, and TGF-beta-induced myofibroblasts in vitro. The senescence was further detected in mouse models of corneal scarring, alkali burn, and penetrating keratoplasty (PKP).RESULTS. The apoptosis and proliferation of corneal stromal cells were found to peak at 4 and 24 hours after epithelial debridement. Positive staining of SA-beta-gal was observed clearly in the anterior stromal cells at 3 to 5 days. The senescent cells displayed P16(Ink4a) thorn vimentin+ alpha-SMA+, representing the major origin of activated corneal resident fibroblasts. Compared with normal fibroblasts and TGF-beta-induced myofibroblasts, H2O2-induced senescent fibroblasts showed a nonfibrogenic phenotype, including a reduced response to growth factor basic fibroblast growth factor (bFGF) or platelet-derived growth factor-BB (PDGF-BB), increased matrix metalloproteinase (MMP) 1/3/13 expression, and decreased fibronectin and collagen I expression. Moreover, cellular senescence was commonly found in the mouse corneal scarring, alkali burn, and PKP models.CONCLUSIONS. Corneal epithelial debridement induced the senescence of corneal fibroblasts after apoptosis and proliferation. The senescent cells displayed a nonfibrogenic phenotype and may be involved in the self-limitation of corneal fibrosis.
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| 3. |
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| 4. |
- Yang, Lingling, et al.
(författare)
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Substance P promotes diabetic corneal epithelial wound healing through molecular mechanisms mediated via the neurokinin-1 receptor.
- 2014
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Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 63:12, s. 4262-4274
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Tidskriftsartikel (refereegranskat)abstract
- Substance P (SP) is a neuropeptide, predominantly released from sensory nerve fibers, with a potentially protective role in diabetic corneal epithelial wound healing. However, the molecular mechanism remains unclear. We investigated the protective mechanism of SP against hyperglycemia-induced corneal epithelial wound healing defects, using type 1 diabetic mice and high glucose-treated corneal epithelial cells. Hyperglycemia induced delayed corneal epithelial wound healing, accompanied with attenuated corneal sensation, mitochondrial dysfunction, and impairments of Akt-, EGFR-, and Sirt1-activation, as well as decreased reactive oxygen species (ROS) scavenging capacity. However, SP application promoted the epithelial wound healing, the recovery of corneal sensation, the improvement of mitochondrial function, and the reactivation of Akt, EGFR and Sirt1, as well as increased ROS scavenging capacity, in both diabetic mouse corneal epithelium and high glucose-treated corneal epithelial cells. The promotion of SP on diabetic corneal epithelial healing was completely abolished by a NK-1 receptor antagonist. Moreover, the subconjunctival injection of NK-1 receptor antagonist also caused diabetic corneal pathological changes in normal mice. In conclusion, the results suggest that SP-NK-1 receptor signaling plays a critical role in the maintenance of corneal epithelium homeostasis, and that SP signaling through the NK-1 recssssseptor contributes to the promotion of diabetic corneal epithelial wound healing by rescued activation of Akt, EGFR, and Sirt1, improvement of mitochondrial function, and increased ROS scavenging capacity.
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| 5. |
- Yang, Lingling, et al.
(författare)
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Trichostatin A Inhibits Transforming Growth Factor-beta-Induced Reactive Oxygen Species Accumulation and Myofibroblast Differentiation via Enhanced NF-E2-Related Factor 2-Antioxidant Response Element Signaling
- 2013
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Ingår i: Molecular Pharmacology. - : American Society for Pharmacology & Experimental Therapeutics (ASPET). - 0026-895X .- 1521-0111. ; 83:3, s. 671-680
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Tidskriftsartikel (refereegranskat)abstract
- Trichostatin A (TSA) has been shown to prevent fibrosis in vitro and in vivo. The present study aimed at investigating the role of reactive oxygen species (ROS) scavenging by TSA on transforming growth factor-beta (TGF-beta)-induced myofibroblast differentiation of corneal fibroblasts in vitro. Human immortalized corneal fibroblasts were treated with TGF-beta in the presence of TSA, the NAD(P) H oxidase inhibitor diphenyleneiodonium (DPI), the antioxidant N-acetyl-cysteine (NAC), the NF-E2-related factor 2-antioxidant response element (Nrf2-ARE) activator sulforaphane, or small interfering RNA. Myofibroblast differentiation was assessed by alpha-smooth muscle actin (alpha-SMA) expression, F-actin bundle formation, and collagen gel contraction. ROS, H2O2, intracellular glutathione (GSH) level, cellular total antioxidant capacity, and the activation of Nrf2-ARE signaling were determined with various assays. Treatment with TSA and the Nrf2-ARE activator resulted in increased inhibition of the TGF-beta-induced myofibroblast differentiation as compared with treatment with DPI or NAC. Furthermore, TSA also decreased cellular ROS and H2O2 accumulation induced by TGF-beta, whereas it elevated intracellular GSH level and cellular total antioxidant capacity. In addition, TSA induced Nrf2 nuclear translocation and up-regulated the expression of Nrf2-ARE downstream antioxidant genes, whereas Nrf2 knockdown by RNA interference blocked the inhibition of TSA on myofibroblast differentiation. In conclusion, this study provides the first evidence implicating that TSA inhibits TGF-beta-induced ROS accumulation and myofibroblast differentiation via enhanced Nrf2-ARE signaling.
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| 6. |
- Zhang, Wei, et al.
(författare)
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Sustained Release of TPCA-1 from Silk Fibroin Hydrogels Preserves Keratocyte Phenotype and Promotes Corneal Regeneration by Inhibiting Interleukin-1β Signaling
- 2020
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Ingår i: Advanced Healthcare Materials. - : Wiley-VCH Verlagsgesellschaft. - 2192-2640 .- 2192-2659. ; 9:17
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Tidskriftsartikel (refereegranskat)abstract
- Corneal injury due to ocular trauma or infection is one of the most challenging vision impairing pathologies that exists. Many studies focus on the pro-inflammatory and pro-angiogenic effects of interleukin-1 beta(IL-1 beta) on corneal wound healing. However, the effect of IL-1 beta on keratocyte phenotype and corneal repair, as well as the underlying mechanisms, is not clear. This study reports, for the first time, that IL-1 beta induces phenotype changes of keratocytes in vitro, by significantly down-regulating the gene and protein expression levels of keratocyte markers (Keratocan, Lumican, Aldh3a1 and CD34). Furthermore, it is found that the NF-kappa B pathway is involved in the IL-1 beta-induced changes of keratocyte phenotype, and that the selective IKK beta inhibitor TPCA-1, which inhibits NF-kappa B, can preserve keratocyte phenotype under IL-1 beta simulated pathological conditions in vitro. By using a murine model of corneal injury, it is shown that sustained release of TPCA-1 from degradable silk fibroin hydrogels accelerates corneal wound healing, improves corneal transparency, enhances the expression of keratocyte markers, and supports the regeneration of well-organized epithelium and stroma. These findings provide insights not only into the pathophysiological mechanisms of corneal wound healing, but also into the potential development of new treatments for patients with corneal injuries.
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