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Ductal hyperplasias are frequently observed in genetically engineered models where specific oncogenes have been deregulated.
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The paper presents a rigorous process for building the domain model, where specific roles, activities and artifacts are identified.
These data indicate that mislocalization in the LMNA E161K is not a general phenomenon and instead supports a model where specific genes are mislocalized.
A reduced rank model is, in essence, a FA model where specific effects are assumed absent, i.e. Ψ = 0.
We believe these materials should find use in manufacturing of cells through providing architectures/environments similar to those occurring in vivo, and also in tissue modeling, where specific placement of different cell types is necessary to recapitulate the cell organization of normal tissue.
In contrast to many other CP mouse models where the specific genetic background had significant impact on either penetrance or severity, for example as described in the Tgfb3 mutant (31), our analysis in CD1, 129Sv and C57Bl6 strains has shown similar phenotypes and with a similar penetrance for each.
The utility and effectiveness of the CIR approach have been demonstrated in a variety of animal models where tumor-specific CIRs drove the adoptive transferred autologous T lymphocytes to accumulate at the tumor site in vivo and prevented tumor growth [13], [14].
Evidence for a role for these amyloid disease proteins in muscle disease also comes from transgenic models, where muscle-specific expression of PrP, Aβ or SOD1 also produced localized accumulation.
Additionally, once the autoimmune process has begun it might become progressively more difficult to alter, as suggested by animal models where antigen-specific therapies used prior to the onset of disease can be far more effective than the same treatments given at the time of disease onset.
A construct for examining the multi-dimensional nature of reward is used, the type-system-criterion (TSC) model, to identify where specific differences in reward preference lie.
This was further confirmed in a mouse osteotomy model where a specific depletion of CD8+ T cells led to an improved bone healing [13].
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