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Additive effects of genetic risk markers were documented in schizophrenia (Purcell et al., 2009) and in ADHD (Jain et al., 2011).
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As an exogenous protein, GFP marker was documented to be immunogenic [ 12, 14, 15].
If the size of the PCR products from the male or hermaphrodite were distinctively different from that of the females of SunUp and AU9, the marker was documented as Y-specific.
Body temperature, positive microbiological results, white cell count and inflammatory markers (C-reactive protein, procalcitonin) were documented.
The biopsy sites were documented by marker acquisition using a neuronavigation system to illustrate the anatomical region and the gross tumor structure at the site of analysis as well as the distance between the biopsy sites.
Data on electrocardiographic findings, biochemical markers, procedural details and adjunctive therapy were documented.
The RHs were genotyped by PCR amplification, followed by gel electrophoresis, and the results of genotyping for a marker, designated as an RH vector, were documented as described.
Postoperative markers of myocardial injury, inflammation, and renal function were documented.
were documented.
Similar changes in these markers have been documented in a nonhuman primate model of PD (Chen et al. 2008).
Within flatfish, sex-associated markers have been documented in species of the family Pleuronectidae (Hippoglossus hippoglossus, Palaiokostas et al. 2013; Verasper variegatus, Ma et al. 2010) and Cynoglossidae (Cynoglossus semilaevis; Chen et al. 2014), in addition to turbot (Scophthalmidae).
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