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It is known that Zn release contributes to neural death [18, 19].
In contrast, on Aβ-containing matrices with large pores, massive neural death is observed when the cells are seeded in the same conditions.
Mathematical studies conducted by Cessac have evidenced the existence of three main regimes (neural death, periodic and chaotic regimes) in the activity of such neuron models.
Importantly, knocking down TPP1 led to multiple abnormalities in zebrafish embryogenesis, including neural death, heart malformation, and caudal defect.
Furthermore, knocking down zfTPP1 by morpholino antisense oligos led to developmental defects including neural death, heart malformation and caudal defect.
However, the recovery rate was remarkably low in part of the data-pixel population in the CA3 cell layer region, which likely reflects acute and CA3-selective neural death.
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A traumatic primary injury to the spinal cord (SCI) induces axonal degeneration, neural cell death, and microvasculature destruction.
Notably, critically ill patients reveal increased insulin levels, and insulin has also been reported to accelerate neural cell death in the hippocampus during low glucose levels, suggesting that insulin might have a double-edged effect on neuron death dependent on glucose concentration (25).
The severe injury to axon could induce neural cell death.
These astrocytic responses are unlikely associated with neural cells death or immunoglobulin leakage around cerebral blood vessels.
Thus, it appears that L11 deficiency, although results in neural cell death, does not change the patterning and localization of the neural cells in the brain.
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