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Neuropathic pain may arise from a direct damage of somatosensory nerves or nerves innervating visceral organs or from a disease affecting the somatosensory nervous system which implies an indirect injury resulting from various causes, including metabolic stress, autoimmune, degenerative, or chronic inflammatory conditions, and idiopathic origins [ 4].
These results suggested that (a) MBs may actually have a negative effect on cognition, independently of other concurrent vascular lesions, and (b) there seems to be an anatomical correlation between the distribution of MBs and the cognitive domains affected, suggesting a direct damage of MBs over the tissue as the pathogenic mechanism.
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The good antioxidant and metal ion chelating properties of monoHER (Haenen et al, 1993; Van Acker et al, 1993) play a role in the protection of endothelial cells against the direct damage of doxorubicin.
ROS likely plays a central role in impairing mitochondrial energy metabolism, through mitochondrial uncoupling, but also through direct damage of mitochondrial components.
Besides direct damage of mitochondria, the reduced supply with NAD+(H) as substrate, which is consumed by an increased poly(ADP-ribose polymerase (PADP-ribose polymerase rePARP under conditions of sepsis wactivitysted [86].
The mechanism(s) that initiates complement activation is not clearly known, although loss of CD59 (protectin) from cells compromised by ischemia/reperfusion may contribute to direct damage of the coronary vascular bed by the terminal complement complex.
Direct damage of the endothelium produced by interaction of ETX with vascular endothelial cells increases the vessel wall permeability [28].
Oxidative stress has several effects on vascular cells, including direct damage of cell membranes [4], and impaired nitric oxide-dependent endothelial-dependent vasomotion [5].
To fulfill distention of the LV, we introduced AR through direct damage of the aortic valve.
However, there is accumulating evidence that direct damage of these vulnerable neurons by misfolded protein species might not be the main reason for their selective degeneration.
Besides direct damage of mitochondria, the reduced supply with NAD+(H) as substrate, which is consumed by an increased poly(ADP-ribose polymerase (PADP-ribose polymerase rePARP under conditions of sepsis wactivitysted [ 86].
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