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Lack of Mg leads to depression because of neuron damage occurring as a result of not meeting the Mg requirement of neurons [ 57].
Given that change of neurite morphology is often the preceding feature of neuron damage (Takeuchi et al. 2005), we next examined the effect of HTRA2 Pro143Ala variant on neurite arborization in rat primary dopaminergic neurons.
At the early stage of SCI, reactive astrocytes start to synthesize abundant GFAP and release various cytokines like NGF (nerve growth factor), bFGF (basic fibroblast growth factor), and IL (interleukin), which is in favor of recovery of neuron damage [ 37].
Consistent with signs of neuron damage, elevated levels of BiP and CHOP were observed in Purkinje cells of the rostral lobules in Sil1−/−; Hyou1+/− mice by 6 weeks after birth (Fig. 5 and Supplementary Material, Fig. S3).
Lactate provides a satisfactory alternative to glucose as the primary energy in brain tissue during recovery from hypoxia [ 24, 25], and lactate infusion can improve the recovery of neuron damage following brain injury [ 20].
These findings suggest that the over-expression of COX-2 may play an important role in the occurrence of neuron damage and neurodegeneration, and the inhibitors of COX-2 may prevent the acute and chronic brain damages induced by aluminium gluconate.
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It can induce an acute stress reaction in glial cells of mouse brains, leading to neuron damage and dysfunction [11].
No clinically relevant electroencephalographic changes occurred, and markers of neuronal damage (neuron specific enolase, S100-β) were found to be slightly reduced following LPS challenge.
Similarly, a much lower level of hippocampal neuron damage was observed in the mice treated with Huperzine A. ELISA results also showed that Aβ25-35 Aβ25-35 administration dramatically decreased ChAT peptide level.
By reducing the magnitude of the initial increase in Ca2+ within CSF during the acute phase of SCI, the degree of excitotoxic secondary neuron damage would be limited.
Taken together, this study identified a novel anti-neurofilament aAb in NPSLE, and established a hitherto undescribed mechanism of aAb-mediated neuron damage that could have relevance to the pathophysiology of NPSLE.
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