Control cells (wt/wt) and the homozygous cell line from the Finnish patient (W262X/W262X) were treated with 100 μg/ml cycloheximide (CHX) for 3 hours

<p><b>Copyright information:</b></p><p>Taken from "A minor alternative transcript of the fumarylacetoacetate hydrolase gene produces a protein despite being likely subjected to nonsense-mediated mRNA decay"</p><p>BMC Molecular Biology 2005;6():1-1.</p><p>Published online 7 Jan 2005</p><p>PMCID:PMC546004.</p><p></p> Total RNA was extracted and subjected to RT-PCR. RAR serves as a control for RNA quantity in each sample. Control amplifications (showing an increasing number of cycles) for del100, del231 and RAR are displayed on the left to show that, with the conditions used, each PCR reaction is in the exponential phase. (A) [αP]-dATP was incorporated during the PCR reaction and the products loaded on a 6% acrylamide gel. The gel was used to directly expose an X-ray film and the signal was quantified using the NIH Image 1.2 software. FAH was amplified from exons 6 to 14 (the del100 transcript which is detected using these primers is indicated by a star). Del100 and del231 were amplified using the specific primers RT84 and RT85. (B) Quantification of the amount of del100 mRNA in 3 different experiments, normalized to RAR levels. The error bars represent standard deviations. Del100 is stabilized between 4- to 7-fold in homozygous cells (W262X/W262X) and normal cells (wt/wt) following the cycloheximide treatment (yellow bars: - cycloheximide; purple bars: + cycloheximide). (C) del231 is relatively unaffected by translation inhibition

Additional file 3 of Aligning the unalignable: bacteriophage whole genome alignments

Detailed comparison of Alpha and Mauve alignments for the four S. aureus phages phiETA3, phiNM2, phiNM1 and B236. (XLSX 83 kb

Additional file 2 of Assisted transcriptome reconstruction and splicing orthology

Results.tar. Compressed folder containing csv files listing the results. (GZ 3942 kb

Additional file 3 of Assisted transcriptome reconstruction and splicing orthology

TableS1. Data for Figure 3. (PDF 21 kb

Increased naive and transitional but decreased memory blood B cells in active chronic sarcoidosis patients.

<p>(A) Representative flow cytometry dot plots of naive (CD27⁻IgD⁺) and memory (CD27⁺) B cell subsets among CD19⁺ B cells in a healthy control (healthy), active sarcoidosis patient (active) and inactive sarcoidosis patient (inactive). Numbers represent the percentage of the indicated B cell subset among CD19⁺ B cells. (B) Representative flow cytometry dot plots of the transitional (CD24^hiCD38^hi) B cell subset among CD19⁺ B cells in a healthy control, active sarcoidosis patient and inactive sarcoidosis patient. Numbers represent the percentage of the indicated B cell subset among CD19⁺ B cells. (C, D, E) Scatter plots showing the percentages (upper panel) and absolute numbers (lower panel) of naive (C), memory (D) and transitional (E) B cell subsets in the peripheral blood of the three subject groups as indicated. Each dot represents individual subjects, and horizontal bars represent the group means. The patients are described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0043588#pone-0043588-t001" target="_blank">Table 1</a>. Significant differences between the means of the patient groups and healthy controls are indicated: NS, not significant; *p<0.05, **p<0.01.</p

Additional file 1 of Inefficient antiviral response in reconstituted small-airway epithelium from chronic obstructive pulmonary disease patients following human parainfluenza virus type 3 infection

Supplementary Material

Increased blood IL-10-producing B cells in patients with active chronic sarcoidosis.

<p>(A) Representative B cell cytoplasmic IL-10 expression of 15 healthy donors (healthy), 14 active sarcoidosis patients (active) and 11 inactive sarcoidosis patients (inactive). IL-10 production by B cells was induced by 72 hours of CpG stimulation, with PMA, ionomycin and monensin being added during the final 6 hours of culture. The percentages indicate IL-10⁺ B cell frequencies among CD19⁺ B cells. (B, C) IL-10⁺ B cell frequencies (B) and IL-10⁺ B cell absolute numbers (C) as in panel A, with each dot representing individual subjects. Horizontal bars represent group means. Significant differences between the means of patient groups and healthy controls are indicated: *p<0.05; **p<0.01.</p

Demographic, clinical and biological characteristics of 18 healthy donors and 18 active and 15 inactive chronic sarcoidosis patients.

<p>M = male, F = female, values are given as mean ± SEM,</p>**<p>p<0.01 and *p<0.05 compared with active sarcoidosis,</p>†<p>Visceral sarcoidosis lesions that occurred at any time of the patient’s history. Each organ defined was either clinically active at the time of inclusion in the active group or previously involved but not actively involved at the time of inclusion in the inactive group,</p>$<p>Upper respiratory tract sarcoidosis involvement was biopsy proved in 2/9 patients.</p

Increased serum BAFF levels in patients with active chronic sarcoidosis correlates with serum hypergammaglobulinemia.

<p>(A) Increased serum BAFF levels in active sarcoidosis patients. Scatter plots show the serum BAFF concentrations in 18 healthy donors (healthy), 18 active chronic sarcoidosis patients (active) and 15 inactive sarcoidosis patients (inactive). Each dot represents individual subjects, and horizontal bars represent the group means. Significant differences between the means of patient groups and healthy controls are indicated: **p<0.01. (B) BAFF levels correlate with serum hypergammaglobulinemia in sarcoidosis. The graph shows a linear regression analysis of BAFF levels (pg/ml) versus serum immunoglobulin levels (g/l) in sarcoidosis patients. Each dot represents individual subjects. The Pearson’s correlation coefficient is represented by “r”. The significance of the strength of the linear relationship is indicated: **p<0.01.</p

Distribution of the different alleles in the 106 samples tested for the intronic (A), exonic (B) and intergenic (C) markers.

<p>Distribution of the different alleles in the 106 samples tested for the intronic (A), exonic (B) and intergenic (C) markers.</p