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These data reveal mouse models with various levels of heterogeneity and illustrate some of the tumor phenotypes that drive relationships between different mouse models.
Furthermore, strain-specific disparities in the proportion of lymphocyte subsets (such as CD4+, CD8+ and TReg cells) influence the phenotype between different mouse models of GvHD.
In addition, our ability to identify protein biomarkers conserved between different mouse models of SMA and human SMA patients suggests that common biomarkers can be utilized in both pre-clinical testing of new treatments in animal models as well as in human clinical trials.
This may be caused by higher hydrophobicity since two charges are lost during conversion [ 71]. pE-Aβ has been detected in a variety of AD mouse models, yet the time of first appearance during pathology varies strongly between different mouse models – ranging from 2 months in the APP/PS1KI model [ 72], to 16 months in the Tg2576 model [ 73], to 15 months in the APP23 model [ 20].
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This agreement between different mice models and AD cases strongly support the involvement of autophagy in the development of AD.
In addition, it is possible that the genetic background of the two mouse models or some other undefined mechanism may affect the tumor latency and spectrum between the different mouse models of Pten heterozygosity [8], [11], [12], [36].
Any discrepancies between the different mouse models may be explained by genetic modifiers.
This variation in phenotype between the different mouse models indicates that either PDK1 has PI-3 kinase/Akt-independent roles, or that the PI3Kα/PI3Kδ pro-B cells still had a low level of Akt activity.
The most reasonable explanations of the observed discrepancy between the two studies lie in the different mouse models used, coupled to a putative role of IL-1 α in atherosclerosis development in the ApoE mouse model.
The discrepancy may come from the different mouse models and delivery systems used between these two studies.
Different mouse models have been developed to study the mechanism underlying human breast cancer development.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com