Sentence examples for modified murine models from inspiring English sources

Bone marrow transplantation experiments in genetically modified murine models have been a powerful tool to examine whether immune cells contribute to a given pathology in vivo.

Atherosclerotic lesions have also been observed in genetically modified murine models, that is, LDLR−/− and apoE−/− mice after chronic consumption of an oxidized cholesterol diet [ 129].

Genetically modified murine models are powerful tools for studying the pathophysiological mechanisms of human diseases, and are now increasingly used to study the complex interactions between the gut microbiota and host in normal homeostasis and disease.

Mammary tumors from other genetically modified murine models (FVB/N) were generously provided by Drs. Kim and Alexander (University of Wisconsin) (MMTV-neu [ 28], and Drs. Green and Zi-Yao Liu (NIH-NCI) (C3(1)-SV40 Tag tumors [ 29].

We compared levels of transcripts in the ERα-associated "luminal" signature that defines this subtype of tumors in women and transcripts enriched in various mammary epithelial lineages to other well-studied genetically modified murine models of breast cancer.

The availability of different genetically modified murine models with potentially interesting bone phenotypes increased also the demand for noninvasive methods to effectively compare their differences during growth and development.

This model was the very first line of genetically modified murine model for atherosclerosis studies introduced to the research community.

The present experiments demonstrate, for the first time, an atrial arrhythmic and conduction phenotype in a genetically modified murine model deficient in the β3 subunit of the Na+ channel.

Nevertheless, these findings in the present study demonstrating alterations in the transmural repolarization gradient are in agreement with recent findings describing alterations in apico-basal repolarization patterns in a genetically modified murine model of human LQT3 syndrome (Tian et al. 2007).

Previously, alterations in ventricular transmural gradients of repolarization have been associated with arrhythmogenicity at the whole heart level in the setting of hypokalaemia (Killeen et al. 2007a b) and in genetically modified murine hearts modelling human LQT3 (Stokoe et al. 2007, Thomas et al. 2007a) and LQT5 syndromes (Thomas et al. 2007b).

We explored for empirical means of resolving the causal relationship between EADs and abnormal transmural gradients of repolarization reflected in altered ΔAPD90 values in genetically modified murine whole hearts modelling human long QT syndrome type 3 for the first time.