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Quantitative receptor autoradiography revealed that post-pubertal NVH lesioned animals display increased levels of [3H]pirenzepine/M1-like and [3H]AFDX-384/M2-like receptor binding sites in the striatum, nucleus accumbens, and in subareas of the dorsal hippocampus.
Similar to humans, these animals display increased pancreatic inflammation and associated beta cell death [9], [25].
However, Per2Brdm1 animals display increased bone formation and Cry2−/− mice decreased bone resorption.
In a rat model, male animals display increased daytime activity at an earlier stage of phenotype than female rats [36].
Mouse embryo fibroblasts (MEF) from Hsp70.1/Hsp70.3-deficient animals display increased levels of chromosome end-to-end fusions and reduced viability in response to ionizing radiation (IR).
Interestingly, PARP1 KO animals display increased resistance to streptozotocin induced cell death of pancreatic beta cells [32], ischaemic brain injury [33], and ocular deprivation induced cell death in the lateral geniculate nucleus [34].
Similar(52)
p44+/+ transgenic animals displayed increased latency in entering the goal box (Fig. 1B), increased distance traveled (Fig. 1C), and increased number of errors (Fig. 1D).
SCC animals displayed increased escape/avoidance behavior postinjury, indicating at-level mechanical hypersensitivity.
(D) Fir1 RNAi) animals displayed increased notum+ cells at the wound sites 18 h following head amputation (P < 0.05, two-tailed t test).
(E) Fir1 RNAi) animals displayed increased fst+ cells at the wound sites 18 h following head amputation (P < 0.001, two-tailed t test).
In support of this, mice with heart specific YAP depletion were defective in heart regeneration[67], while LATS1/2 or SAV conditional knock-out animals displayed increased regenerative capacities[79].
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