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  • American Scientific Publishers  (4)
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  • American Scientific Publishers  (4)
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  • 1
    In: Journal of Nanoelectronics and Optoelectronics, American Scientific Publishers, Vol. 14, No. 12 ( 2019-12-01), p. 1771-1775
    Abstract: In this investigation we have showed the synthesis of TiO 2 -NPs using Rosa hybrida leaf extract and studied using various spectroscopic and microscopic techniques. The as prepared photosensitive TiO 2 -NPs based nanocomposite have been used, to alter the epoxy-based light-sensitive resin, by carrying the goal of achieving express prototyping dental resources, where TiO 2 -NPs acted as reinforcing fillers. We enhanced the hardness of the nanocomposite material using TiO 2 -NPs filler, which plays as a significant parameter in the technique of dental impression. Further, the prepared composites are also studied about the light absorption, mechanical properties and viscosity. It is found the enhanced mechanical properties of the nanocomposites indicating the potential of TiO 2 -NPs for stereolithography and digital light processing that can be useful for preparation of the high dimensional accuracy dental model.
    Type of Medium: Online Resource
    ISSN: 1555-130X
    Language: English
    Publisher: American Scientific Publishers
    Publication Date: 2019
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  • 2
    Online Resource
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    American Scientific Publishers ; 2021
    In:  Journal of Biomedical Nanotechnology Vol. 17, No. 8 ( 2021-08-01), p. 1679-1689
    In: Journal of Biomedical Nanotechnology, American Scientific Publishers, Vol. 17, No. 8 ( 2021-08-01), p. 1679-1689
    Abstract: We established a self-decomposable SiO 2 encapsulated mitochondrial targeting short peptide SS31 drug loading system (SiO 2 @SS31) to determine its nano-sustained release characteristics in eukaryotic cells. We explored the protection of SiO 2 @SS31 on the 661W cells after oxidative injury by H 2 O 2 . After the drug loading, we detected the morphology of SiO 2 @SS31 by transmission electron microscopy (TEM). Moreover, high-pressure liquid chromatography (HPLC) was used to determine the drug capacity and encapsulation efficiency of the nanoparticles. Then, the release curve in vitro was drawn. The 661W cells were cultured in vitro to allow the detection of cytotoxicity by the MTT assay. The SS31loaded nanoscale microspheres labeled with fluorescein isothiocyanate (SiO 2 @FITC-SS31) were prepared, and their sustained release effect was detected with intracellular endocytosis, using confocal microscopy and flow cytometry. Within 15 days, the SiO2@SS31 nanoparticles were completely decomposed and simultaneously released the SS31 peptide in deionized water and normal saline. Nonetheless, the process was faster in simulated body fluid and serum. The MTT assay suggested that SiO 2 @SS31 has sustained protection compared with SS31 in the 661W cells at 48 h. Flow cytometry proved SiO 2 @FITC-SS31 could maintain a high level and last longer after 24 h. The SS31 peptide, which has excellent medical application prospects, can be slowly and continuously released from self-decomposable SiO 2 and targeted to concentrate on mitochondria.
    Type of Medium: Online Resource
    ISSN: 1550-7033
    Language: English
    Publisher: American Scientific Publishers
    Publication Date: 2021
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  • 3
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    Online Resource
    American Scientific Publishers ; 2020
    In:  Journal of Biomedical Nanotechnology Vol. 16, No. 5 ( 2020-05-01), p. 603-615
    In: Journal of Biomedical Nanotechnology, American Scientific Publishers, Vol. 16, No. 5 ( 2020-05-01), p. 603-615
    Abstract: The goal of this study was to examine the impact of the mitochondrial-targeted antioxidant peptide, SS31, and its role in promoting autophagy in cone photoreceptor 661W cells that were subjected to oxidative damage. To do so, we examined the viability of 661W cells in the presence of increasing concentrations of H 2 O 2 with or without SS31 pre-treatment using the MTT assay and by expression of autophagy and apoptosis-associated proteins LC3-II/I, P62, and caspase-3. Autophagy was evaluated by fluorescence microscopy in cells stained with monodansyl cadaverine (MDC). Autophagy was induced with rapamycin (Rap) and inhibited with bafamycin A1 (bafA1) followed by examination of Reactive oxygen species (ROS) levels in target 661W cells by fluorescence microscopy and flow cytometry. Annexin V/PI staining was used to evaluate the rate of apoptosis and mRNA sequencing (mRNA-seq) analysis (Illumina platform) was performed on H 2 O 2 -exposed 661W cells treated with SS31. Among our results, we observed a substantial and concentration-dependent decrease in 661W cell viability in response to H 2 O 2 -exposure; production of ROS, autophagy and apoptosis were induced at 8 h in response to exposure to 100 μ M of H 2 O 2 . Pre-treatment with 100 nM SS31 resulted in significant attenuation of H 2 O 2 -mediated cytotoxicity, together with reduced ROS production and enhanced autophagy observed in response to oxidative stress. Both Rap and bafA1 were used to modulate SS31-mediated autophagy; the impact of Rap was similar to that of SS31. By contrast, administration of bafA1 counteracted autophagy induced by SS31. Furthermore, mRNAseq analysis revealed that SS31 promoted significant alterations in gene expression in 661W cells and suggested that autophagy was induced via the mTORC1-mediated signaling. In conclusion, our results indicate that exposure to H 2 O 2 resulted in reduced 661W cell viability via mechanisms associated with oxidative damage, apoptosis, and autophagy. Notably, we demonstrated that pre-treatment with SS31 protects 661W cells from H 2 O 2 -induced oxidative damage that may result in part from induction of autophagy via mTORC1-mediated signaling pathways.
    Type of Medium: Online Resource
    ISSN: 1550-7033
    Language: English
    Publisher: American Scientific Publishers
    Publication Date: 2020
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  • 4
    Online Resource
    Online Resource
    American Scientific Publishers ; 2021
    In:  Journal of Biomedical Nanotechnology Vol. 17, No. 2 ( 2021-02-28), p. 279-290
    In: Journal of Biomedical Nanotechnology, American Scientific Publishers, Vol. 17, No. 2 ( 2021-02-28), p. 279-290
    Abstract: Retinopathy is an eye disease caused by the death of retinal cells in the macular area and the surrounding choroid. As the retinal rod cell dysfunction and death lead to the loss of night vision, the disease will lead to visual dysfunction and blindness as the disease progresses. Because of the irreversible nature of cell death, gene therapy has become a research hotspot in the field of retinopathy. But the technology is still in animal studies or clinical trials, and more research is needed to prove its feasibility. In this study, oxidative damage cell model was established and divided into a control group, H 2 O 2 group, SS31 +NEC1 group, SS31 +H 2 O 2 group, and SS31 +NEC1 +H 2 O 2 group, for different interventions. The cell survival rate of the H 2 O 2 group was significantly increased compared with those of the SS31 + H 2 O 2 group, SS31 +NEC1 +H 2 O 2 group, and NEC1 +H 2 O 2 group. Nec1 combined treatment significantly reduced reactive oxygen species (ROS) production compared with that in the H 2 O 2 group. The level of MDA in the SS31 group, Nec-1 group and combined treatment of SS31 +NEC1 group decreased significantly compared with the H 2 O 2 group. The proportion of cells with decreased mitochondrial membrane potential in the H 2 O 2 group significantly increased, and the rate of positivity for propidium iodide (PI) of 661W cells in the H 2 O 2 group and the control group significantly increased. Nine hours after H 2 O 2 treatment of 661W cells, the RIP3 expression level began to increase, and peaked at 24 h. The level of RIP3 in the H 2 O 2 group was significantly increased, while this level was downregulated in the SS31 and NEC1 treatment groups. Therefore, this study suggests that SS31 has a partial protective effect on 661W cells by inhibiting necrosis, which has certain guiding significance for the treatment of retinal diseases.
    Type of Medium: Online Resource
    ISSN: 1550-7033
    Language: English
    Publisher: American Scientific Publishers
    Publication Date: 2021
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