Primer sequences and conditions for the TNF-α promoter gene.

<p>Mg_: Magnesium concentration.</p><p>Primer sequences and conditions for the TNF-α promoter gene.</p

Cytokine production and disease characteristics.

<p>Cytokine levels (pg/ml) are presented as medians with the interquartile range [IQR]. HC, Healthy control; TNF-α, Tumor necrosis factor alpha; IL, Interleukin; L1, ileal disease; L2, colonic disease; L3, ileocolonic disease; P-, no peri-anal disease; P+, peri-anal disease; IQR, interquartile range.</p><p>Cytokine production and disease characteristics.</p

cytokine production in healthy controls versus patients with quiescent CD.

<p>Cytokine levels (pg/ml) are presented as medians with the interquartile range [IQR]. TNF-α, Tumor necrosis factor alpha; IL, Interleukin; IQR, interquartile range; CD, Crohn's disease.</p><p>cytokine production in healthy controls versus patients with quiescent CD.</p

Relation between cytokine production and disease severity.

<p>Values are presented as medians (pg/ml) with the interquartile range. For the number of bowel resections and treatment exposure patients were dichotomized in a low and high group according to the number of resections or the percentage of years in which they were treated with steroids, thiopurines, biologicals, methotrexate or cyclosporine, corrected for disease duration. Two patients were excluded for the analysis for treatment exposure, because no complete drug history was available. TNF-α, Tumor necrosis factor alpha; IL, Interleukin; L1, ileal disease; L3, ileocolonic disease; P-, no fistulas; P+, fistulating disease.</p

Baseline characteristics of the included patients with CD and HC.

<p>CD, Crohn’s disease; HC, healthy controls; SD, standard deviation; 5-ASA, 5-aminosalicylic acid.</p><p>Baseline characteristics of the included patients with CD and HC.</p

Mouse anti-hAAT antibody formation and its correlation with urine levels of KIM-1 during the recovery phase of renal I/R Injury (IRI).

<p><b>A.</b> Mouse anti-hAAT antibody levels in plasma were measured before surgery (pre-op) and at different time-points after IRI. One-way analysis of variance (ANOVA) followed by <i>Dunnett’s</i> post-test. ***<i>P</i><0.001 (<i>n</i> = 4–8 animals). <b>B.</b> Correlation between protein levels of KIM-1 in urine and mouse anti-hAAT antibodies in serum at day 15 post-op. Spearman´s correlation. *<i>P</i><0.05 (<i>n</i> = 6 animals).</p

hAAT (80 mg/kg/day; i.p.) treatment ameliorates AKI after I/R Injury (IRI).

<p><b>A.</b> Plasma NGAL levels at day 7 pre-op and at different time-points after IRI. <b>B.</b> Urine NGAL levels at day 7 pre-op and at different time-points after IRI. <b>C.</b> Urine KIM-1 levels at day 7 pre-op and at different time-points after IRI. Grey boxes represent the control group treated with hAlb. White boxes represent the group treated with hAAT. Two-way analysis of variance (ANOVA) followed by <i>Bonferroni</i> post-test: *<i>P</i><0.05, ***<i>P</i><0.001. Mann-Whitney U test (two-tailed) to analyze the effect of treatment at each time-point. ^#<i>P</i><0.05, ^##<i>P</i><0.01 (<i>n</i> = 6–8 animals per group).</p

Effect of hAAT (80 mg/kg/day; i.p.) treatment on renal leukocyte influx at different time-points after I/R Injury (IRI).

<p><b>A, B.</b> Immunofluorescence analysis of granulocytes in ischemic kidneys. Kidney sections were stained with a specific anti-Gr-1 antibody. <b>A</b> representative image of ischemic control mouse kidney at day 1 after IRI. <b>B</b> representative image of ischemic mouse kidney treated with hAAT at day 1 after IRI. Scale bar = 50 μm (original magnification <i>x200</i>). <b>D, E.</b> Immunofluorescence analysis of macrophages in ischemic kidneys. Kidney sections were stained with a specific anti-CD68 antibody. <b>D</b> representative image of ischemic kidney of a control mouse at day 1 after IRI. <b>E</b> representative image of ischemic kidney of a mouse treated with hAAT at day 1 after IRI. Scale bar = 20 μm (original magnification <i>x400</i>). Solid arrows indicate intertubular cell infiltration. The open arrow indicates cellular influx in the glomeruli. <b>C.</b> Gr-1⁺ cells were counted in non-overlapping fields and subsequently averaged. <b>F.</b> Macrophage staining was scored semi-quantitatively on a scale from 0 to 5 based on the extent of CD68 immunofluorescence staining. Grey boxes represent the control group treated with hAlb. White boxes represent the group treated with hAAT (dark green = autofluorescence of the tubuli; red = agrin; bright green = immune cells). Mann-Whitney U test (two-tailed) to analyze the effect of treatment at each time-point. ^#<i>P</i><0.05 (<i>n</i> = 6–8 animals per group).</p

hAAT (80 mg/kg/day; i.p.) treatment decreases acute tubular necrosis after I/R Injury (IRI).

<p><b>A-F.</b> PAS-stained frontal sections of mouse kidney: <b>A, D</b> PAS-stained frontal sections of naïve mouse kidney without any histological damage and with the intact brush border in the proximal tubules. <b>B, C</b> representative images of ischemic kidney of control mouse at different time-points after IRI. <b>E, F</b> representative images of ischemic kidney of mouse treated with hAAT at different time-points after IRI. C = cortex; CMJ = cortico-medullary junction; M = medullar region; PT = proximal tubules; G = glomeruli. The solid arrow indicates areas of cast formation. Open arrows indicate debris deposition in the tubular lumen. Scale bar = 100 μm (original magnification <i>x100</i>). <b>G.</b> Kidney histological damage score. The percentage of damaged tubules in 3 different areas of the kidney was estimated using a 5-point scale. Grey boxes represent the control group treated with hAlb. White boxes represent the group treated with hAAT. Two-way analysis of variance (ANOVA) followed by <i>Bonferroni</i> post-test: *<i>P</i><0.05. Mann-Whitney U test (two-tailed) to analyze the effect of treatment at each time-point. ^#<i>P</i><0.05 (<i>n</i> = 6–8 animals per group).</p

<i>Rs2149356</i> genotype and association with risk of gout in NZ and Europe sample sets using ARIC and FHS controls.

<p><i>Rs2149356</i> genotype and association with risk of gout in NZ and Europe sample sets using ARIC and FHS controls.</p