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Regional distribution of PRRT2, SLC2A1, PNKD, KCN1A, SNAP25 and CACNA1A mRNA expression in the normal human brain was determined using microarray analysis of human post-mortem brain tissue from the UK Human Brain Expression Consortium (Trabzuni et al., 2011).
In a recent study of fragile X mental retardation 1 (Fmr1) knockout mice, the metabolic profile of the fragile X brain was determined using proton high-resolution magic angle spinning nuclear magnetic resonance spectroscopy.
The infarct area and edema volume in seven coronal sections of each brain was determined using the scanned image with a CCD camera (Samsung, Korea) and quantified with Biovis, Expert vision, (India).
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WldS protein levels in the brain were determined using quantitative fluorescent western blotting.
The frequencies of IFN-γ-producing CD3+CD4+ and CD3+CD8+ T cells among the CD3+ lymphocytes in various tissues (i.e., ileum, spleen, blood, lung and brain) were determined using intracellular staining and flow cytometry.
Expressions of the four isoforms β2L, β2S, β2S1 and β2S2 in DLPFC of postmortem CON, SCZ and BPD brains were determined using quantitative real-time PCR, and normalized by the geometric mean of the three reference genes glyceraldehyde-3-phosphate dehydrogenase (GAPDH), ubiquitin C (UBC) and hydroxymethyl-bilane synthase as described [11].
The anatomical positioning of brain sections was determined using the mouse brain atlas [76].
[11C]AF150(S) specific binding in M1ACh-R-rich brain areas was determined using SRTM with the cerebellum as reference tissue.
Therefore, the ability of Aβ40 derivatives to bind to preformed Aβ fibrils and to amyloid plaques in the APP, PS1 mouse brain sections was determined using surface plasmon resonance (SPR) and emulsion autoradiography techniques, respectively.
Brain infarction was determined using 2,3,5-triphenyl-tetrazolium chloride (TTC) staining as previously described.
Protein concentration of total brain homogenate was determined using a BCA assay.
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