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A high mortality rate of ∼85% in mice was documented following intravenous infusion of mouse ADSCs within 24 h due to the observation of pulmonary embolism.
Recently, a causal role for HMGB1 in acute myocardial infarction injury in mice was documented [ 15].
The appearance of the mice was documented using a Kodak MDS-120 digital camera and Polaroid Photo Max software.
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All mice were documented to remain free of helicobacter infection throughout the study.
Since MyD88−/− mice are documented to possess an atypical immune response [60], [61], no conclusions can be reliably drawn from the apparent reduction of peritonitis in MyD88−/− mice versus wild-type mice; it may be that there is a MyD88-dependent component to the full response or it may be due to strain differences.
Protective anti-inflammatory effects of PAR2 activation in mice were documented in rodent models of LPS-induced lung injury [ 59, 60].
The copy number of DRIM loci and the integrity of chromosome 12 material was evaluated in a panel of 6 human breast tumor cell lines commonly used in research, and whose metastatic propensity in athymic mice is documented.
One mouse Cpeb2 protein sequence was documented in the UniProt database (Q812E0).
As in the human cell experiment, a stimulatory role for rhIGF-1 in mouse Treg cell function was documented in vitro by robust proliferation and FoxP3 activation in FACS-purified Treg cells treated with rhIGF-1 (Fig 2A and Supplementary Fig S1B).
The deficiency was documented in mouse ES cells, mouse neural progenitors, and human CD34+ haematopoietic progenitors.
Previously, abnormal accumulation of material at the photoreceptor-RPE interface was documented in Nrl−/– mice, another mouse model of ESCS (Mustafi et al., 2011).
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