Sentence examples for mice was designed from inspiring English sources

In this study, a combined treatment of Aβ1-42-bone marrow derived dendritic cells (BMDCs) with intraperitoneal injection of splenocytes from young mice was designed as a novel immunotherapy for AD in APPswe/PSEN1de9 transgenic mice models.

To test this hypothesis, a novel cue-potentiated feeding protocol adapted for use in mice was designed and validated, and then the effects of pharmacologic ghrelin receptor (GHSR) antagonism and GHSR transcriptional blockade (as occurs in GHSR-null mice) were assessed.

The running protocol applied to the mice was designed to provide a strong, but non-exhaustive metabolic stimulus, resembling intensive endurance exercise.

The SCID-hu mouse model, in which human lymphoid organs are implanted into severe-combined immunodeficient (SCID) mice, was designed by McCune et al. [1] to provide a small animal model for the study of human hematopoiesis.

The fMRI part of the study in the hTNFtg mice was designed in a way which is possibly similar to the study of RA patients.

The heritable labeling in our TBI studies using Gli1-CreER T2 driver mice was designed to fate label based on Shh pathway activation with tamoxifen on Days 2 and 3 to capture the early response to injury.

The HA0 cleavage loop peptides used for intranasal immunization of mice were designed and synthesized from specific conserved regions of influenza A/H1N1 & A/H3N2 viruses.

To investigate the role of nuclear CaMKII in cardiac function, transgenic mice were designed and generated to target the expression of a CaMKII inhibitory peptide, AIP (KKALRRQEAVDAL), to the nucleus.

To validate the pathophysiological consequences of the interaction between BRAFV600E and MST1 in vivo, animal experiments using thyroid-specific transgenic BRAFV600E mice (Tg-BRAFV600E mice) and MST1 null mice were designed.

Thus, all cells of Z/AP and Z/EG mice are designed to exhibit a binary readout of Cre activity, expressing β-galactosidase by default and activating expression of hPLAP or EGFP respectively upon exposure to Cre.

Human IL-32α Tg mice were designed to overexpress human IL-32α by using CAG promoter.