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Results: 4

1.
Figure 2

Figure 2. From: Novel Immune Response to Gluten in Individuals with Schizophrenia.

A) Chromatogram of gluten proteins eluted from the BioGel P-100 size exclusion column, following acetic acid extraction. B) SDS-PAGE profile (Coomassie-stained) of fractions 1–6 of gluten proteins collected from the column.

Diana Samaroo, et al. Schizophr Res. ;118(1-3):248-255.
2.
Figure 4

Figure 4. From: Novel Immune Response to Gluten in Individuals with Schizophrenia.

Characterization of the specificity of serum antibody to the ~33 kDa doublet. Protein bands were individually excised, extracted, and re-analyzed by immunoblotting with the serum of representative individuals with schizophrenia in order to identify the target protein. Lane 1) Protein doublet, containing upper and lower bands; lane 2) upper protein band; lane 3) lower protein band. Patient immune reactivity was found to be directed primarily at the upper band.

Diana Samaroo, et al. Schizophr Res. ;118(1-3):248-255.
3.
Figure 3

Figure 3. From: Novel Immune Response to Gluten in Individuals with Schizophrenia.

Pattern of antibody reactivity to gluten proteins of the Cheyenne cultivar in individuals with schizophrenia and controls. A) SDS-PAGE profile of fractions 1–6 of gluten proteins. B–E) Reactivity of serum antibodies from gliadin-immunized rabbits (B), a representative healthy control (C), representative patients 1–4 with celiac disease (D), and representative patients 1–4 with schizophrenia and elevated anti-gliadin antibody (E) towards transferred gluten proteins from panel A. Detection of bound antibodies was by the ECL system and autoradiography film. Arrows in panels A and E point to the ~33 kDa doublet to which antibody reactivity was found in schizophrenia patients.

Diana Samaroo, et al. Schizophr Res. ;118(1-3):248-255.
4.
Figure 1

Figure 1. From: Novel Immune Response to Gluten in Individuals with Schizophrenia.

Comparison of mean antibody levels in celiac disease and gluten-sensitive schizophrenia patients. A) Antibodies to native gliadin. Individuals with schizophrenia that were positive for anti-gliadin antibodies had lower levels of IgG (P<0.05) and IgA (P<0.005) antibodies to gliadin than celiac disease patients. B) Antibodies to a deamidated (glutamine-glutamate substituted) trimer of a fusion gliadin peptide containing PLQPEQPFP and PEQLPQFEE sequences in the same patients as in panel A. Individuals with schizophrenia who were positive for anti-gliadin antibodies had significantly lower mean IgG and IgA antibody reactivity to deamidated gliadin than celiac disease patients (P<0.001). C) IgA antibodies to recombinant human TG2. Levels were significantly lower in the schizophrenia group than the celiac disease group (P<0.001). Dotted lines indicate established cutoff values for positivity. Error bars represent the standard error of the mean.

Diana Samaroo, et al. Schizophr Res. ;118(1-3):248-255.

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