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Due to alternative splicing, the phenotype of this new mouse model resembles that of knockout mice.
A "knock-in" mouse model resembles human TBS more closely, indicating that domain-negative effort is responsible for the pathogenesis of TBS.
This mouse model resembles most major features of the human syndrome, such as neonatal hyperbilirubinemia and early lethality due to bilirubin-induced neurological damage.
Interestingly, the more physiologic Aq mouse model resembles the CII response in RA better than the more artificial but humanized DR4 mouse.
The Nkx3.1 Pten mutant mouse model resembles that of human prostate cancer progression in which spontaneous PIN lesions form and progress to adenocarcinomas and eventually hormone refractory tumors upon androgen deprivation.
To determine how well our novel MMTV-Wnt10b-IRES-LacZ (Wnt10b Lac Z) mouse model resembles human TNBC, we conducted IHC for estrogen receptor-alpha (ERα), progesterone receptor (PR) and HER2 protein expression levels (Fig 2A).
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We aimed to develop an integrated and representative pneumococcal meningitis mouse model resembling the human situation.
These models were then combined with a clinically relevant in vivo I/R mouse model, resembling a common clinical course of events in patients with MI who undergo revascularization therapy.
MS, for a long time, was considered as a Th1-dependent disease, until studies revealed the key role of Th17 cells and IL-17 family cytokines in the development of MS using EAE, a mouse model resembling human MS. Th17 cells and associated cytokines are the major force that drives the related central nervous system inflammation and lesion formation.
Despite the prevalence of ERα+ tumors clinically, very few mouse models resemble this breast cancer subtype.
Using our established cell and knockout/transgenic mouse models resembling human NS harboring the R246Q or C321R mutation respectively, we have shown that both R246Q and C321R mutations cause defective secretion of laminin-521 from podocytes to the GBM [ 49, 50].
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