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Additional strong evidence came from the platelet endothelial cell adhesion molecule (Pecam1 -deficient mice that failed to form endothelial cells and disPecam1 -deficientimiceficathat [46].
As expected, BALF from BLM-injected tnf−/− mice, that failed to develop any inflammatory response and subsequent fibrosis, was almost devoid of any inflammatory cells (Fig. 1 and 3B,C).
The few EAD model mice that failed treatment to normalized BG levels following exogenous insulin (pellets) and anti-CD8 antibody injections (Figure 4C, 6, and data not shown), presumably because they had lost too many β-cells prior to treatment, also maintained increased β-cell proliferation.
The leptin gene was isolated by Friedman's group, through positional cloning from ob/ob mice that failed to produce leptin and displayed extreme obesity and hyperphagia.
All mice that met these three necessary and sufficient conditions had an ablation, while all mice that failed to meet even one condition had no ablation.
There was an overall tendency of reduced locomotion, including climbing, and increased immobility in TG as compared to WT, noticeable across strains and genders, except for male FVB/N mice that failed to show significant changes in locomotion (Fig 1).
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In contrast, UF008/SAP mice that fail to entrain also do not show masking to a 1 hr light pulse administered about 30 minutes after activity onset.
Further dissection of the benefit of these 2 mechanisms in survival will require further studies including the use of knockout mice such as MyD88 mice (toll-like receptor knockout mice that fail to elicit a cytokine storm)[42].
This is in contrast to hippocampal lesioned mice that fail to learn these tasks.
This is not unlike the Tbx22 null mice that fail to thrive except that the tongue defect is considerably milder.
This is consistent with the maintenance of "normal" β-cell mass in POKO mice that fail to expand.
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