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Human ovarian adenocarcinoma cells N.1 secrete an autocrine activity that stimulates active cell death under serum-reduced conditions.
Important to keep in mind is the fact that cells undergoing apoptosis (active cell death) maintain considerable levels of metabolic activity respective ATP in order to perform the energy-requiring steps during the apoptotic cascade [ 67– 72].
The rationale for using IL-2 and subsequent anti-IL-2 treatments is that IL-2 generally promotes activation-induced T cell death (AICD) [8], [9], the active cell death, and that subsequent anti-IL-2 treatments neutralize IL-2, a growth factor, and promote passive T cell death via "IL-2 withdrawal".
Moreover, addition of Ca2+ chelators or Ca2+ channel blockers resulted in a significant inhibition of an O3-induced [Ca2+]cyt increase and subsequent cell death suggesting that the uptake of extracellular Ca2+ via the activation of PM Ca2+ channels is required for the induction of active cell death [4], [10].
Apoptosis is an active cell death pathway involved in a variety of pathological conditions, including noise-induced outer hair cell (OHC) death.
PCD as an active cell death process mainly consists of apoptosis, autophagy, necroptosis, and pyroptosis.
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To get the detail action mechanisms of cinnamon in vivo, we tried to investigate whether anti-tumoral effects of cinnamon in vivo melanoma model is also mediated by the similar mechanisms of in vitro system such as active tumor cell death and inhibition of NFκB and AP1 activities.
Apoptosis is an active programmed cell death, consisting of an essential sequence of physiological processes caused in response to specific stimuli [ 20].
Sevoflurane was administered before, during and after cerebral ischemia, and has been found to modulate the balance between pro- and anti-apoptotic key proteins towards a reduction of active programmed cell death by increasing the hippocampal concentration of the anti-apoptotic proteins Bcl-2, and by inhibiting the ischemia-induced upregulation of the pro-apoptotic protein Bax [ 54].
Cell death, induced by anticancer therapeutics in targeted cancer cells can be divided into two types: active or programmed cell death that requires active participation of cellular machinery and passive cell death or necrosis.
As caspases require post-translational activation to become catalytically active and mediate cell death, we investigated whether the loss of TGF β-induced caspase expression due to P/CAF knockdown was followed by a decrease in caspase activity.
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