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The Notch mutant mice rather succumb to MPD by high G-CSF levels since lowering G-CSF concentrations in Notch mutant mice is sufficient to drastically prolong their survival.
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For the study of Ngn2 targets, data from the cortex of Mash1-/; Ngn2-/ double mutant mice was utilized rather than Ngn2-/ single mutants in order to avoid the compensation due to de-repression of Mash1 in the cortex of the later mutants [ 2].
Thus, it appears that an outright knock-out of G6PD is too drastic, whereas in the available mutant mice G6PD deficiency is rather mild.
Dclk -/- mice also exhibited a rather mild cortical phenotype, but Dcx/Dclk double mutant mice displayed severe cortical defects [ 23, 24].
As such, the short lifespan of Tsc1c/− /hGFAP2- Cre+ mutant mice was probably a consequence of the onset of status epilepticus, rather than of cachexia and wasting.
Thus, we believe that the VF depots in these mutants are functionally distinct from the same fat depots in N mice and are beneficial, rather than detrimental, to the overall health of these mutant mice.
The loss of CD103+CD11b+ DCs in SIRPα mutant mice appears to reflect enhanced susceptibility of these cells to die by apoptosis rather than defective generation from DC progenitors.
Most of the mutant mice, such as mice in the control groups, die of some form of neoplasia, rather than of metabolic diseases such as diabetes or atherosclerosis.
In mutant mice lacking V0 neurons, the left and right motor neurons fire at the same time, rather than alternating.
As p21Cip1 is absent in triple mutant mice, p53 signals are likely to favor apoptotic cell death instead of cell-cycle arrest in these mutant mice.
You've got some normal mice and some mutant mice.
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