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Evidence from clinical and mouse samples has consistently demonstrated that TR3 is highly expressed and that TSC2 is weakly expressed in patients or mice with left ventricular hypertrophy.
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GAPDH for human samples and rer1 for mouse samples have been additionally tested, in several cases, to confirm the results.
Data from both human and mouse samples have been included.
The reactivities of antibodies to ANG and VE-cadherin in human and mouse samples have been confirmed by the manufacturers.
Thus, each mouse sample had a unique multiplex adaptor tag that allowed simultaneous hybridization to a single MGS array.
Although the mouse is the most widely used laboratory animal [ 10], and heparin is probably the most widely used anticoagulant, the heparin-effect on cytokines in mouse blood samples has not been systematically investigated.
Additional human skeletal muscle and isolated mature adipocytes, also 3T3-L1 and mouse WAT samples have been explained in past studies [9], [44].
Mouse cortex samples had greater 5-hmdC content than ES cell samples, as expected (Szwagierczak et al. 2010).
Another researcher's mouse stem cell samples had "started to mysteriously die" with "no obvious cause".
Cellular studies of mice and patient samples have been complemented by genetic studies (Box 1), which have helped to clarify and confirm many aspects of disease pathophysiology.
Proteomic and genomic approaches in NOD mice and patients samples have allowed the identification of several apoptotic and inflammatory factors as well as acinar cell components as putative biomarkers of Sjögren's syndrome [ 36- 38].
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