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As to caspases, it is worth noting that all four HDACi induced lesser caspase-3 activation in p53− cells, which, however, in case of vorinostat, apicidin and VPA, was not accompanied by lesser cell death.
After several seizures, Fluoro-Jade C labelling revealed a strong neuronal loss in the CA3 region and a lesser cell death in the CA1 region of LGI1−/− mice aged postnatal day 14 (n = 3, Fig. 8P-R), but not in LGI1+/− or wild-type or postnatal day 8 LGI1−/− mice (not shown).
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For example, myocardial-specific overexpression of caspase-1 induces a massive increase in cardiomyocyte death in young mice without any increase in tissue or plasma levels of IL-1 β, IL-18 or other inflammatory mediators; conversely, Casp1 −/− mice show a lesser degree of cell death after induction of myocardial infarction.
In HCT116 wild type and HCT116 p21-/ knock-out cells, we found a strong correlation between disruption of p21CIP/WAF-1 and in vitro sensitivity towards 5-FU and, to a lesser extent, towards IR-induced cell death.
Finally, activated neutrophils from naive mice were also able to induce T cell death, albeit to a lesser extent than tumour-elicited neutrophils, suggesting that, in general, neutrophil activation is counterproductive to T cell function.
Chemotherapy induced apoptotic cell death to a notably lesser extent in the parental and empty vector-transfected DAOY cells when compared with DAOY M2 cells.
Moreover, cell death occurred to a lesser extent in HeLa-CD95-FR or HeLa-CD95-FL cells compared to HeLa-CD95 cells.
This is supported by the observation that its inactive analogue U0124 also protects against H2O2-induced cell death, albeit to a lesser degree.
Acute exposure to nephrotoxic doses of Hg2+ results primarily in necrosis with apoptotic cell death occurring to a lesser extent at very high doses of Hg2+ [ 35].
Remarkably, deletion of genes encoding apoptosis mediators, such as the Omi yeast homologue (NMA111) or, to a lesser extent, the YCA1 caspase prevented Hog1-induced cell death.
We found that LBW242 increased cell death induced by irinotecan and, to a lesser extent, 5-FU in HT29 cells.
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