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Exact(6)
Since age appeared to determine the extent of differences between C57Bl6 ctsk−/− and WT animals, metabolic parameters (Table 1) were measured using 5 8 week old male (defined as young) and 12 20 week old male mice (defined as adult).
Initially, the protocol employs a qualitative criterion of differentiation into submissive vs. non-submissive mice, defined as an absence or presence of attacks towards the partner, respectively.
Mutant mice with targeted Atrx inactivation in the embryonic mouse forebrain were previously described (Atrx Foxg1Cre mice, defined as Atrx-null hereafter) (Bérubé et al., 2005).
For example, successive stages of mTEC maturation have been shown to exist in mice, defined as immature MHCIIloCD80loAire− (mTEClo), mature MHCIIhiCD80hiAirehi (mTEChi), and recently identified terminally differentiated MHCIIloCD80loAireloInvolucrin+ (also residing within the originally defined mTEClo) 22, 37, 38.
As in treated infections, parasite clearance in untreated mice (defined as the rate of decline in parasite numbers between day 6 and day 11 PI, see Methods) significantly correlated with peak infection density (parasite density at day 6 PI; = 5.11, P = 0.036), and there was significant variation between parasite lines (= 6.48, P < 0.005; Fig. 2C; Table S1.4).
More importantly, we identified 63 'rescued' genes in SOD/OXR1 mice; defined as those genes that are significantly altered by >1.3-fold in the SOD/+ spinal cord, but not significantly changed or altered by <1.2-fold in SOD/OXR1 tissue (Fig. 5A and B, and Supplementary Table 3).
Similar(54)
Indeed, alternative splicing isoforms of SMO have been described in human and mouse, defined as "major" (i.e., SMO1 and SMOα for human and mouse proteins, respectively) and "long" isoforms (i.e., SMO5 and SMOμ for human and mouse proteins, respectively) [ 17, 18].
BM cells were sterilely isolated from donor mice (defined hereafter as WT/GFP or CCR2/GFP) by flushing the femurs and tibiae with Dulbecco's modified Eagle's medium (DMEM) (Invitrogen, Carlsbad, CA, USA).
RW mice are defined as those mice fed a regular diet (PMI 5002 Rodent Diet®, Richmond, IN, USA; ~5kal% fat) throughout the study.
As mentioned above, gene therapy was not effective in all treated mice; 4 out of 16 mice, here defined as non-responders (NRs), failed to recover FIX expression and activity and 3 of them maintained FIX inhibitors in the plasma (Table 1).
Early work in the Col6a1 −/− mice defined mitochondrial deficiency and apoptosis as hallmarks of this disease, clearly linking mitochondrial dysfunction to this muscle disease.
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