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To determine if the bba64 mutant isolate was deposited into the mouse dermis as the infected nymphs feed, we contained infected nymphal ticks within capsules attached to mice, allowed the infected nymphs fed to repletion, and cultured the skin at the bite site.
This statistical equivalency of mice allowed the use of a pseudo-randomization convenience allocation to assign mice to identified cages.
Fertility of single MuRF1 or MuRF2 KO mice allowed the generation of dKO strains by breeding them together.
The cause of the death of the mutated animals was hypothyroidism, and the administration of thyroxine to Pax8-/ mice allowed the animals to survive.
Sequencing of the complete TRB loci in human and mice allowed the repertoire of TRB genes in these species to be fully characterised and also permitted analysis of the organisation, regulation and evolution of this immunologically important locus [ 9, 10].
Adeno-associated viral vector-enforced re-expression of the CB1 receptor in the dorsolateral striatum of R6/2 mice allowed the re-expression of BDNF and the concerted rescue of the neuropathological deficits in these animals.
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Three scientists shared an award for developing a way to eliminate or "knock out" specific genes in mice, allowing the creation of animal models to study many human ailments.
The availability of genetically engineered mice allows the unraveling of the role of specific proteins in mechanisms of ischemic brain injury.
To address these limitations, we examined complete isolated myofibres from mutant mice, allowing the ready scrutiny of all myonuclei and satellite cells (the resident stem cells of adult muscle [17]).
The presence of macrophages in the Rag2−/− γc−/− mice allows the paracrine loop with tumor cells to take place and thus enhances invasiveness in response to EGF.
The lower toxicity of DMXAA in these knockout mice allows the use of higher drug doses, which restored both apoptosis induction and tumour blood flow inhibition responses.
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