Anatomy and Neuroscience - Research Publications

Permanent URI for this collection

http://hdl.handle.net/11343/181

Filters

2013 2
2
Reset filters

Settings
Statistics
Citations
End date: 2013 × Author: Turnley, Ann × Author: Kilpatrick, Trevor ×

Search Results

Now showing 1 - 2 of 2
  • Item
    Thumbnail Image
    Nanodiamonds with silicon vacancy defects for nontoxic photostable fluorescent labeling of neural precursor cells
    Merson, TD ; Castelletto, S ; Aharonovich, I ; Turbic, A ; Kilpatrick, TJ ; Turnley, AM (OPTICAL SOC AMER, 2013-10-15)
    Nanodiamonds (NDs) containing silicon vacancy (SiV) defects were evaluated as a potential biomarker for the labeling and fluorescent imaging of neural precursor cells (NPCs). SiV-containing NDs were synthesized using chemical vapor deposition and silicon ion implantation. Spectrally, SiV-containing NDs exhibited extremely stable fluorescence and narrow bandwidth emission with an excellent signal to noise ratio exceeding that of NDs containing nitrogen-vacancy centers. NPCs labeled with NDs exhibited normal cell viability and proliferative properties consistent with biocompatibility. We conclude that SiV-containing NDs are a promising biomedical research tool for cellular labeling and optical imaging in stem cell research.
  • Item
    Thumbnail Image
    EphA4 Receptor Tyrosine Kinase Is a Modulator of Onset and Disease Severity of Experimental Autoimmune Encephalomyelitis (EAE)
    Munro, KM ; Dixon, KJ ; Gresle, MM ; Jonas, A ; Kemper, D ; Doherty, W ; Fabri, LJ ; Owczarek, CM ; Pearse, M ; Boyd, AW ; Kilpatrick, TJ ; Butzkueven, H ; Turnley, AM ; Fujinami, RS (PUBLIC LIBRARY SCIENCE, 2013-02-04)
    The EphA4 receptor tyrosine kinase is a major regulator of axonal growth and astrocyte reactivity and is a possible inflammatory mediator. Given that multiple sclerosis (MS) is primarily an inflammatory demyelinating disease and in mouse models of MS, such as experimental autoimmune encephalomyelitis (EAE), axonal degeneration and reactive gliosis are prominent clinical features, we hypothesised that endogenous EphA4 could play a role in modulating EAE. EAE was induced in EphA4 knockout and wildtype mice using MOG peptide immunisation and clinical severity and histological features of the disease were then compared in lumbar spinal cord sections. EphA4 knockout mice exhibited a markedly less severe clinical course than wildtype mice, with a lower maximum disease grade and a slightly later onset of clinical symptoms. Numbers of infiltrating T cells and macrophages, the number and size of the lesions, and the extent of astrocytic gliosis were similar in both genotypes; however, EphA4 knockout mice appeared to have decreased axonal pathology. Blocking of EphA4 in wildtype mice by administration of soluble EphA4 (EphA4-Fc) as a decoy receptor following induction of EAE produced a delay in onset of clinical symptoms; however, most mice had clinical symptoms of similar severity by 22 days, indicating that EphA4 blocking treatment slowed early EAE disease evolution. Again there were no apparent differences in histopathology. To determine whether the role of EphA4 in modulating EAE was CNS mediated or due to an altered immune response, MOG primed T cells from wildtype and EphA4 knockout mice were passively transferred into naive recipient mice and both were shown to induce disease of equivalent severity. These results are consistent with a non-inflammatory, CNS specific, deleterious effect of EphA4 during neuroinflammation that results in axonal pathology.