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Diffstat (limited to 'general/datasets/Jax_d2_mono1vpbmc_ret_rna_seq_0619/summary.rtf')
-rw-r--r-- | general/datasets/Jax_d2_mono1vpbmc_ret_rna_seq_0619/summary.rtf | 3 |
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diff --git a/general/datasets/Jax_d2_mono1vpbmc_ret_rna_seq_0619/summary.rtf b/general/datasets/Jax_d2_mono1vpbmc_ret_rna_seq_0619/summary.rtf new file mode 100644 index 0000000..b5e090d --- /dev/null +++ b/general/datasets/Jax_d2_mono1vpbmc_ret_rna_seq_0619/summary.rtf @@ -0,0 +1,3 @@ +<p>Glaucoma is characterized by the progressive dysfunction and loss of retinal ganglion cells. Recent work in animal models suggests that a critical neuroinflammatory event damages retinal ganglion cell axons in the optic nerve head during ocular hypertensive injury. We previously demonstrated that monocyte-like cells enter the optic nerve head in an ocular hypertensive mouse model of glaucoma (DBA/2 J), but their roles, if any, in mediating axon damage remain unclear.</p>
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+<p><a href="https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-018-0303-3" target="_blank">https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-018-0303-3</a></p>
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