Sentence examples for mice we showed from inspiring English sources

Using FVB mice we showed, that daily single injections of quinine (10 mg/kg, i.p).

Using green fluorescent protein (GFP) as a reporter of Sox2 transcriptional expression (SOX2 GFP knock-in mice), we showed that SOX2-expressing cells in invasive SCC are greatly enriched in tumour-propagating cells, which further increase upon serial transplantations.

Here, using a modeling approach in humanized mice, we showed that human lymphoid development stemmed from distinct populations of CD127− and CD127+ early lymphoid progenitors (ELPs).

Using global microRNA expression profiling in hippocampus of humanized BDNF Val66Met knock-in mice we showed that this variant results in dysregulation of at least one microRNA, which in turn affects downstream target genes.

Using human blood, serum, and urine spiked with WNV and mouse blood and brain tissues from Karshi virus-infected mice, we showed that these clinical matrices did not inhibit the detection of these viruses.

Using a range of different experimental approaches (and not just analyses of MyD88-deficient mice), we showed that, contrary to the prevailing view, a T-helper response is not sufficient for the generation of optimal T-dependent antibody responses, and that Toll-like-receptor (TLR) signalling in B cells is also required1.

By crossing ENTPD1-null mice with db mice, we show that ENTPD1 deletion has prominent effects on metabolic syndrome traits.

By engineering TGF-β and BMP-reporter mice, we show that TGF-β2 signaling antagonizes BMP signaling in HFSCs but not through competition for limiting Smad4-coactivator.

Functional outcome was assessed with the horizontal ladder test.Using NSC isolated from CCR2+/+ and CCR2-/ mice, we show that receptor deficiency significantly impaired transendothelial diapedesis specifically in response to CCL2.

Using natural killer T (NKT) cell-deficient mice, we show here that allergen-induced airway hyperreactivity (AHR), a cardinal feature of asthma, does not develop in the absence of V alpha 14i NKT cells.

Using genetically engineered mice, we show that precocious Norrin production leads to premature retinal vascular invasion and delayed Norrin production leads to characteristic defects in intraretinal vascular architecture.