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To assess whether apoptosis is involved in this liver damage, the activation of the apoptotic machinery was measured using the activated caspase 3 and the extent of TUNEL staining.
In our study, the apoptosis is involved in this liver damage; the activation of the apoptotic machinery was measured with the higher expression of activated caspase 3 and the more extent of TUNEL staining in the prenatal steroid administration group.
This study was designed to investigate oxidative DNA damage, the activation of ATM, a reporter of DNA damage, and redox-sensitive signal transduction through mitogen-activated protein kinases (MAPKs) by the monomer triethylene glycol dimethacrylate (TEGDMA).
The DNA damage response is an intricate cellular system that coordinates the repair of DNA damage, the activation of cell-cycle checkpoints to facilitate repair, and apoptosis in order to eliminate cells with extensive DNA damage [20].
Upon DNA damage, the activation of p53 leads to cell cycle arrest enabling the cells to repair the damaged DNA.
In an attempt to further pinpoint the exact localisation of the radiation-induced damage, the activation of PKC α was assessed.
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A key event in the cellular response to DNA damage is the activation of DNA damage checkpoints that arrest progress in the cell cycle to ensure that DSBs can be repaired.
Severe or sustained stress accompanied by irreversible damage, such as extreme genotoxic damage or the activation of oncogenes, results in the induction of cell death or senescence.
Suggested protective factors of the KD are antioxidant activity, the prevention of mitochondrial damage and the activation of anti-inflammatory mechanisms31, however, the cross-talk among all these aspects remain unelucidated.
First, the rapid signal transduction pathway responds to DNA damage by the activation of p53 and AMPK, which in turn activates TSC2 via phosphorylation [ 176, 177].
Impairment of redox equilibrium causes both oxidative damage and the activation of pathways leading to chronic inflammation.
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