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Specifically, overstimulated mice demonstrate increased risk taking/decreased anxiety, poorer short-term memory, and impaired learning.
Concomitantly with the tight skin phenotype at two weeks of age, Tsk2/+ mice demonstrate increased levels of total transforming growth factor beta 1 (TGF-β1) and excessive accumulation of dermal elastic fibers.
In addition, myc overexpressing mice demonstrate increased incidence of tumours (Pelengaris et al, 1999).
In addition, these mice demonstrate increased small intestinal permeability before the onset of colitis.
SHIP1−/− mice demonstrate increased osteoclastogenesis and bone resorption during inflammatory conditions such as arthritis.
Indeed, caspase 12 knock-out mice demonstrate increased resistance to endoplasmic reticulum stress-induced apoptosis, yet remain vulnerable to other apoptotic mechanisms (Nakagawa and Yuan, 2000).
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Following sulfur mustard exposure, primary skin fibroblasts from PARP-deficient mice demonstrated increased internucleosomal DNA cleavage, caspase-3 processing and activity, and annexin V positivity, compared to those derived from PARP+/+ animals.
βOGT-KO mice demonstrated increased ER stress and distended ER architecture, and these changes ultimately caused the loss of β cell mass due to ER-stress-induced apoptosis and decreased proliferation.
S. pneumoniae infected mice demonstrated increased collagen deposition at the pleural and subpleural space when compared to saline-treated mice at 14 days.
S. pneumoniae infected mice demonstrated increased collagen deposition at the pleural surface and in the subpleural region compared to saline-treated mice.
Observations limited to early-stage infection in Irgm1 mice demonstrated increased susceptibility and virtually no inflammatory cell recruitment to heavily-parasitized parenchymal foci but an intact response to chemotherapy.
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