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By applying an in vitro chondrogenesis model with genetically modified hBMSC, it was subsequently shown that genetic upregulation of DIO2 expression resulted in a marked reduction of the capacity of chondrocytes to deposit ECM components, concurrent with induction of OA-specific markers of cartilage matrix degeneration (ADAMTS5 and MMP13) and mineralisation (ALPL) (figure 3).
To study the role of CGRP in these disorders, we have characterized the photophobic phenotype of nestin/hRAMP1 mice, a transgenic model with genetically engineered increased sensitivity to CGRP.
Metabolic homeostasis is achieved by complex molecular and cellular networks that differ significantly among individuals and are difficult to model with genetically engineered lines of mice optimized to study single gene function.
In vivo phage panning in a GEM model with genetically identical mice can offer the advantage of isolating peptides that directly accumulate into tumor tissue, binding to either endothelial cells within tumor vasculature [37], epithelial cells through extravasation [38], or extracellular matrix.
In a model with genetically augmented Aβ42 levels in skeletal muscle, there was no inflammation [ 50].
In 2004, an in vivo model with genetically modified skin-humanized mice was proposed.
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In quantitative genetics, Markov chain Monte Carlo (MCMC) methods are indispensable for statistical inference in non-standard models like generalized linear models with genetic random effects or models with genetically structured variance heterogeneity.
Recent studies in mouse models with genetically altered connexin expression have shown that Cx43 is the principal coupling protein in ventricular myocardium, whereas Cx40 fulfills this function in the atria.
This chapter summarizes the design, planning, and execution of 2-year rodent carcinogenicity studies as well as the same features in newer alternative (6-month) studies that use mouse models with genetically engineered predispositions to develop xenobiotic-induced cancers (e.g., the rasH2 mouse and p53+/− mouse).
Models with genetically induced biliary injury and strong autoimmune effects can give valuable information about inflammatory cell migration and recruitment.
In the future, the pneumonectomy mouse model combined with genetically modified mouse lines, lineage tracing approaches, and single-cell transcriptomic analyses will be powerful tools to shed new lights on the regenerative aspects associated with de novo alveologenesis.
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