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For the other markers, we stained synovial tissues from at least two different patients per diagnosis.
In order to test whether aPKC inhibition also affected the expression of earlier PrE markers, we stained embryos for NANOG and the early PrE marker GATA6.
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To examine the sites of marker expression, we stained sections of 18 human oral SCCs, one adenoid cystic carcinoma, one lymph node metastasis of an oral SCC and two specimens of normal skin, as well as four samples of normal oral mucosa.
To assess the accuracy of the aforementioned nuclear CM markers, we exemplarily stained nuclei from H2B-mCh+ hearts for PCM-1.
To assess the correlation between the expression of TAM and CSC markers in human OSCCs, we stained the tumor sections from human tissue arrays for OSCC with antibodies for CD68, CD163, SOX2, ALDH1, and CD44 and compared them with normal oral mucosa samples.
DOI: http://dx.doi.org/10.7554/eLife.04437.010 > -wrap-foot> To determine whether Egfr f24 FSC clones retained other markers of epithelial identity we stained for FasIII, which is commonly used to identify follicle cells, and found that it was consistently detectable on the cell membrane.
In order to determine if the observed reduction in Aire levels were the result of a reduction in mature medullary TECs (mTECs) or an alteration in another thymic population, we stained for markers of thymic stromal cells.
To confirm the specificity of the Col1a1- GFP mouse model and distinguish differences between salivary gland epithelium and mesenchyme, we stained for markers specific of salivary gland epithelium, CD44, E-cadherin (E-cad), amylase (AMY-1), aquaporin-5, and LAMP-1.
To determine whether organoids could recapitulate the cortical spatial lamination, we stained for cortical layer markers on day 65.
To investigate whether these DPCs expressed neural crest markers, we performed immunofluorescent staining.
Extracellular markers were stained with fluorochrome-labeled monoclonal antibodies (mAb).
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