Exact(9)
The multi-faced inhibitory nature of the CNS lesion suggests that therapies used in combination may be more effective.
The marked increase in carbonylation seen in ependymal layers distant from the lesion suggests a mechanism involving the transmission of a cerebral spinal fluid-borne factor to these sites.
Identical genetic mutations between the adenomatous and squamous parts of a single Ad-SCC lesion suggests that the phenotypic transition between ADC and SCC occurs according to the cancer monoclonal theory (Hofmann et al., 1994; Toyooka et al., 2006; Kang et al., 2007; Ichinokawa et al., 2011).
Second, observations of persistent error in human patients after ACC lesion suggests that the ACC also plays a role in attentiveness processing [3], [4], [9], but only sparse evidence exists for a direct role for the ACC in performance adjustment.
A radiolucent lesion suggests that there has been lysis of normal bone.
On the other hand, the disappearance of the NeuN signals around the cystic lesion suggests the loss of neuron cells in the damaged area (Fig. 5b).
Similar(51)
c Narrow-band imaging of the lesion suggested irregularity of intraepithelial papillary capillary loops.
Interestingly, RARγ agonist also weakened deterioration of muscle architecture adjacent to the heterotopic ossification lesion, suggesting that RARγ agonist may oppose skeletal muscle damage.
Left eye fundus revealed an elevated mound in the inferotemporal quadrant corresponding externally to the mass lesion suggesting indentation effect by the mass.
To confirm this potential link, at 48 hours, GPR17+ neurons are no longer present inside the lesion suggesting that they have indeed undergone death.
There is excellent overlap of the eccentricity versus distance curves in foveal V1, outside the area of the lesion, suggesting that the magnification factor remains unchanged in nearby V1 cortex following the lesion.
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