Cross-sections of
mouse ventricles show the visible change in size when old hearts are immersed in young blood.
Not exact matches
He and graduate student Yun Yung developed a way to inject one of these lipids, lysophosphatidic acid (LPA), into the
ventricles of a fetal
mouse brain.
When spleen CD4 + T - cells were transferred from heart - attack donor
mice to naïve recipient
mice, they induced long - term left
ventricle dysfunction, fibrosis and enlargement, hallmarks of heart failure.
Treating the
mice with antibodies against CD4 + T - cells four weeks after experimental heart attacks — to deplete that subset of T - cells — prevented the progressive abnormal enlargement of the left
ventricle that leads to heart failure, as compared with untreated
mice.
Our study suggests otherwise, though, as we found that a certain type of B cell is quite abundant in the
ventricles, meninges, and choroid plexus in the brains of young
mice.
This is a heart of a CRISPR gene edited
mice with HLHS (bottom) have a much smaller left
ventricle (LV) compared to a normal
mouse heart (top).
For experimental metastasis assay, nude
mice (7 — 8 weeks) were injected with 50,000 luciferase - labeled CSCs in PBS into left cardiac
ventricle in a total volume of 100 μL.
At
mouse embryonic day (E) 13.5 (Fig. 4b), PRDM16 protein was expressed throughout the left
ventricle but was most prominent in the endocardial and epicardial layers.
SVZ denotes the subventricular zone; LV denotes the lateral
ventricles of the
mouse brain.