Results: 5

1.
Fig. 2

Fig. 2. From: Quantitative Salivary Proteomic Differences in Oral Chronic Graft-versus-Host Disease.

Study Workflow. The diagram overviews the procedures used for the identification and quantification of differentially expressed salivary proteins for No oral cGVHD and Oral cGVHD subjects

Carol W Bassim, et al. J Clin Immunol. ;32(6):1390-1399.
2.
Fig. 4

Fig. 4. From: Quantitative Salivary Proteomic Differences in Oral Chronic Graft-versus-Host Disease.

Canonical Pathways identified by Ingenuity Pathway Analyses (IPA). Significant pathways (n=12) were mapped via identified down-regulated proteins. Values on each the y-axis indicate the number of involved proteins in each pathway

Carol W Bassim, et al. J Clin Immunol. ;32(6):1390-1399.
3.
Fig. 5

Fig. 5. From: Quantitative Salivary Proteomic Differences in Oral Chronic Graft-versus-Host Disease.

Label-Free Quantification of Selected Differentially Expressed Proteins between No oral cGVHD and Oral cGVHD groups. Shown are the extracted ion chromatograms showing “peptide elution plotted against intenity” for (a) lactotransferrin, and (b) lactoperoxidase by oral cGVHD classification to illustrate downregulation of each protein in the Oral cGVHD group

Carol W Bassim, et al. J Clin Immunol. ;32(6):1390-1399.
4.
Fig. 3

Fig. 3. From: Quantitative Salivary Proteomic Differences in Oral Chronic Graft-versus-Host Disease.

Distribution of differentially expressed proteins. Differentially expressed proteins (n=180) were categorized using an arbitrary fold ratio change cut-off of ≤0.5 or ≥2 into proteins that did not change in abundance (n=78), proteins that were identified only in the No oral cGVHD group (n=12), and proteins that were down-regulated in the Oral cGVHD samples (n=90). The number of proteins in each pathway is given above each bar

Carol W Bassim, et al. J Clin Immunol. ;32(6):1390-1399.
5.
Fig. 1

Fig. 1. From: Quantitative Salivary Proteomic Differences in Oral Chronic Graft-versus-Host Disease.

Clinical and histological presentation of no oral cGVHD (ad) versus oral cGVHD (eh). Clinical presentation of oral cGVHD includes atrophy, erythema, hyperkeratosis, lichenoid reactions, ulcerations, and edema, here seen on the lower lip (e), maxillary anterior gingiva (f), and buccal mucosa (g) of a patient with oral cGVHD, as compared with the normal intraoral mucosa of a patient with no oral cGVHD (ac). H&E staining of the oral mucosa from the above-matched patients demonstrates characteristic GVHD-like changes in the buccal mucosa compared with No oral cGVHD tissue (d), including prevalent lymphocytic infiltrate and apoptotic bodies (h). Buccal biopsy sections are shown in similar orientation at 10x magnification

Carol W Bassim, et al. J Clin Immunol. ;32(6):1390-1399.

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