Factor analysis of COMPASS autonomic symptom scale scores within pSS patients

Scatterplot of rotated (varimax normalized) COMPASS subscale factor loadings for factor 1 (24% of total variance) and factor 2 (15% of total variance), both with appreciable loadings for the secretomotor subscale. Factor 1 had the highest loadings for secretomotor, orthostatic, gastroparesis, constipation and bladder subscales, which is indicative of a substantial clustering of these symptoms within patients who have primary Sjögren's syndrome (pSS). The highest loadings for factor 2 were observed with both the secretomotor and pupillomotor subscales. Scatterplot of the COMPASS factor 1 scores for each pSS patient by results of the contemporaneous 15-minute unstimulated salivary flow test. The horizontal bars represent mean scores for each group. Factor 1 scores were significantly higher in patients with this objective measure of dryness (= 0.025), whereas factor 2 scores were not (= 0.40; data not shown). Scatterplot of the COMPASS factor 1 scores for each pSS patient by the FACIT-F scores. Factor 1 scores were significantly correlated with fatigue scores (= 0.035), whereas factor 2 scores were not (= 0.18; data not shown). COMPASS, Composite Autonomic Symptom Scale; FACIT-F, Functional Assessment of Chronic Illness Therapy-Fatigue.<p><b>Copyright information:</b></p><p>Taken from "Mild autonomic dysfunction in primary Sjögren's syndrome: a controlled study"</p><p>http://arthritis-research.com/content/10/2/R31</p><p>Arthritis Research & Therapy 2008;10(2):R31-R31.</p><p>Published online 7 Mar 2008</p><p>PMCID:PMC2453776.</p><p></p

Factor analysis of abnormal postural change cardiovascular autonomic indices within pSS patients

RR intervals, low frequency RR power (HRV), proportion of successive RR intervals differing by more than 50 ms (pNN50), change in systolic blood pressure on standing (ΔSBP), low frequency systolic blood pressure power (BPV) and the 30/15 ratio were all decreased in patients who have primary Sjögren's syndrome (pSS) relative to control individuals on standing. Three-dimensional scatterplot of rotated (varimax normalized) factor loadings. Factor 1 had the highest loadings for HRV, pNN50 and the 30/15 RR ratio. Factor 2 had the highest loadings for ΔSBP and BPV. Factor 3 had the highest loading for RR intervals during standing. Scatterplot of the HRV factor 1 scores for each pSS patient by the presence of Raynaud's phenomenon. The horizontal bars represent mean scores for each group. Factor 1 scores were significantly lower (more abnormal) in patients without Raynaud's (= 0.025). Scatterplot of the HRV factor 1 scores (y-axis) versus COMPASS factor 1 scores (x-axis) for each pSS patient. There was a negative correlation that did not quite reach statistical significance (= 0.08).<p><b>Copyright information:</b></p><p>Taken from "Mild autonomic dysfunction in primary Sjögren's syndrome: a controlled study"</p><p>http://arthritis-research.com/content/10/2/R31</p><p>Arthritis Research & Therapy 2008;10(2):R31-R31.</p><p>Published online 7 Mar 2008</p><p>PMCID:PMC2453776.</p><p></p

Summary of analysis results for each of the studies performed. Sens = sensitivity.

<p>Spec = specificity; NA = Not applicable.</p

Paired comparison of z-scores.

<p>Z-scores were calculated for paired samples with previously described GC normalized, repeat masked z-scores on the x-axis <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0057381#pone.0057381-Palomaki1" target="_blank">[7]</a> and z-scores from the same libraries sequenced in 12-plex on the y-axis. Samples classified by karyotype analysis as trisomies for A) Chromosome 21, B) Chromosome 13, or C) Chromosome 18 are shown in blue; unaffected samples for each aneuploidy condition are shown in gray. Red horizontal and vertical lines in each plot represent the respective classification cutoff for that chromosome (z = 3 for chromosome 21, z = 3.95 for chromosomes 13 and 18).</p

Paired comparison of z-scores.

<p>Z-scores were calculated for 1269 paired samples with previously described GC normalized, repeat masked z-scores on the x-axis <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0057381#pone.0057381-Palomaki1" target="_blank">[7]</a> and z-scores from the high-throughput assay on the y-axis. Samples classified by karyotype analysis as trisomies for A) Chromsome 21, B) Chromosome 13, or C) Chromosome 18 are shown in blue; unaffected samples for each aneuploidy condition are shown in gray. Red horizontal and vertical lines in each plot represent the respective classification cutoff for that chromosome (z = 3 for chromosome 21, z = 3.95 for chromosomes 13 and 18). Black line in plot represents y = x.</p

Summary of sample types utilized for each of the studies performed.

<p>Summary of sample types utilized for each of the studies performed.</p

Microarray Results and Corresponding Quantitative Real-Time PCR for Differentially Regulated Genes in CD or UC Compared to Normal Controls

<p>Genes were chosen on the basis of their dysregulation in IBD and represent both known genes from functional groups discussed and genes of unknown function. Quantitative real-time PCR was carried out on individual samples from group 2 patients (14–18 normal controls, 19–33 UC, and 17–22 CD samples, depending on the availability of the patient samples at the time the plates were produced), except for IL-8 and TNF-α (not on array), which were tested in group 1 patients (11 normal controls, ten UC, and ten CD patient samples) as a proof-of-principle measure. The extended cohort of group 2 patients includes those with active disease and using anti-inflammatory drugs (but not immunosuppressants or biologicals), whereas group 1 patients had active disease and were medication-free for 6 wk. Results are summarised by a ratio of medians (CD:normal or UC:normal). Complete results, including box-plots and number of samples analysed in each assay, are included in <a href="http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0020199#sg001" target="_blank">Figure S1</a>. All results were significantly differentially regulated except for marked results; single dagger indicates that array result was not significant (<i>p</i> > 0.0015 or fold-change < 1.2); asterisk indicates that real-time PCR result was not significant (<i>p</i> > 0.05). A dashed line represents the fold-change level of 1.2.</p

Immunohistochemical Localization of CEACAM1, CSNK1D, and PRKCB1 in Colonic Mucosa

<div><p>Staining of a representative mucosal tissue samples from five normal controls (N), five Crohn disease (CD), and six ulcerative colitis (UC) patients using antibodies against (A) CEACAM1, (B) CSNK1D, and (C) PRKCB1.</p> <p>(A) CEACAM1 immunoreactivity was found in the apical epithelial lining (1), crypts of inflamed tissue (2, 4). Additional staining was detected in immune cells (3) and blood vessels (5).</p> <p>(B) CSNK1D immunoreactivity showed a strong granular staining pattern in normal (6) and the UC group (8), which was located basolaterally. Weaker staining of the apex of the crypts could be detected in CD (7).</p> <p>(C) For PRKCB1, weak staining could be observed in the apical epithelial layer in the normal (9) and CD (10) mucosa and, interestingly, immunoreactivity was found nearly exclusively in the marginal zone of small lymph follicles (11), whereas the lamina propria was immunonegative. In contrast, strong staining was detected in the apical epithelial layer of UC mucosa (12). Furthermore, lamina propria mononuclear cells underlying the epithelial layer were also positive in the UC mucosa (13).</p></div