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Brain, liver and gastrocnemius muscle were analyzed for BH4, NADPH and arginine, GTP cyclohydrolase-I (GTP-CH) and NOS activities, and NOS protein isoforms.
Diets and fish muscle were analyzed to determine the proximate composition according to standard methods (AOAC 1995).
Extracted DNA samples from blood or muscle were analyzed by Southern blot for mtDNA deletions [16], [17].
Raw signal intensities (before normalization to muscle) were analyzed at this location to verify that control and tinnitus groups experienced similar brain systemic manganese exposure: Between groups, raw signal intensities were similar at the anterior pituitary and adjacent muscle alike (one-way ANOVAs, P>0.05).
The spectra of palmitoyl-ceramide (311 317 m/z for sphingosine; 370 376 m/z for acyl-group) and docosanoyl-ceramide (311 317 m/z for sphigosine; 454 460 m/z for acyl-group) in liver and stearoyl-ceramide (311 317 m/z for sphigosine; 398 404 m/z for acyl-group) in muscle were analyzed.
Several tissues such as spleen, skeletal muscle, esophagus, ileum, colon, and heart muscle were analyzed.
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The level of hypoxia in the GC muscle was analyzed 2 h after intraperitoneal injection of 60 mg/kg pimonidazole into mice at 7 days post ischemia induction.
As a measure of microvascular permeability, leakage of FITC dextran to the postischemic cremaster muscle was analyzed (Fig. 3A).
NF-κB activation in skeletal muscle was analyzed by EMSA as previously described [88] with some modifications.
The mice were euthanized with carbon dioxide, muscles were dissected and weighed, and contraction of the extensor digitorum longus (EDL) muscle was analyzed ex vivo.
In a second set of experiments, leukocyte recruitment to the cremaster muscle was analyzed either 240 min after intraarterial (0.2, 2.0, or 20.0 µg) or 240 min after intrascrotal injection of plasmin (0.02, 0.2, or 2.0 µg in 0.2 ml PBS, Molecular Innovations, Novi, MI, USA).
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