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In the adult rodent brain, LIF is localised to neurons within the olfactory sensory layer [ 24, 25] and is upregulated in injury or tissue damage enhancing neural progenitor cell turnover [ 26].
Calorie restriction (CR) is an effective and reproducible intervention for increasing life span, reducing oxidative damage, enhancing stress resistance and delaying/preventing aging and age-associated diseases such as cancer in various species, including mammals (mice, rats, and non- human primates) [ 5- 8].
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This review will focus on potential mechanisms by which zinc deficiency impairs host protective mechanisms designed to protect against DNA damage, enhances susceptibility to DNA-damaging agents and ultimately increases risk for cancer.
A decade ago, stem or progenitor cells held the promise of tissue regeneration in human myocardium, with the expectation that these therapies could rescue ischemic myocyte damage, enhance vascular density and rebuild injured myocardium.
The damage enhanced Anand model developed in this study will enable the tracking of crack fronts during finite element simulations of fatigue crack initiation and propagation in complex solder joint geometries.
In this study, we utilize the maximum entropy fracture model (MEFM) to predict and validate cyclic hysteresis in Sn3.8Ag0.7Cu and Sn3.0Ag0.5 solder alloys through a damage enhanced Anand viscoplasticity model.
Why does DNA damage enhance this interaction?
In contrast, in Nbs1-deficient cerebella endogenous DNA damage enhanced p53-mediated cell death and proliferation arrest.
It was a "vicious cycle" in which initial ROS-induced mitochondria damage enhanced ROS production that, in turn, led to further mitochondrial damage and eventually massive hepatocytes death.
A chronic inflammatory process in the lung could also lead directly to DNA damage, enhance the effects of other carcinogenic exposures, and stimulate cell proliferation and growth (Ohshima and Bartsch 1994).
Importantly, DNA damage enhanced miR-16 and miR-26a expression in U2-OS KDp53 cells at a lower rate compared with U2-OS scr cells with wild-type p53 (2.2 and 4 fold for miR-16 and miR-26a, respectively).
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