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These observations, together with the fact that spine head size and geometry are associated with AMPA receptor content and maturation status (Matsuzaki et al., 2001), suggest that MET signaling may control many aspects of glutamatergic synapse development, including the timing of excitatory synapse maturation (Qiu et al., 2014)

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They found that the down-regulation of ACSL4 significantly inhibits lipid peroxidation and neurological damage in SAH

While inflammation, stemming from both early innate and subsequent adaptive immune responses, is a critical element in the vicious cycle of DED [1,2,3,4], existing anti-inflammatory treatments exhibit variable efficacy and carry risks such as glaucoma and cataract from corticosteroids, and ocular burning from cyclosporine A (CsA) [5]

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