Prescribed asthma medication comparison between asthma patients with and without kidney stones matched by age gender and BMI.

<p>Prescribed asthma medication comparison between asthma patients with and without kidney stones matched by age gender and BMI.</p

Clinical-demographic data comparison between asthma-stone patients and stone patients without asthma.

<p>Clinical-demographic data comparison between asthma-stone patients and stone patients without asthma.</p

24 hour urine comparison between asthma patients with stone and those with stone only diagnosis (Cr = Creatinine, SD = Standard deviation).

24 hour urine comparison between asthma patients with stone and those with stone only diagnosis (Cr = Creatinine, SD = Standard deviation).</p

The prevalence of asthma at our institution in all children and children with nephrolithiasis.

<p>The prevalence of asthma at our institution in all children and children with nephrolithiasis.</p

The prevalence of nephrolithiasis at our institution in all children and children with asthma.

<p>The prevalence of nephrolithiasis at our institution in all children and children with asthma.</p

Clinical-Demographic data for current pediatric patients stratified by asthma and kidney stone diagnosis.

<p>Clinical-Demographic data for current pediatric patients stratified by asthma and kidney stone diagnosis.</p

C3d deposition in chronic hypoxia-induced PH in mice.

<p>(A–D) Lungs from normoxic and hypoxic C57Bl/6J mice were stained with α-C3d and α-SMA antibody and counterstained with DAPI to detect nuclei(n = 4). (E) Quantification of C3d staining in WT vs. C3−/− mice in normoxia and hypoxia. Bars represent the mean ± SD (n = 4). *<i>P</i><0.05. (F) Representative Western blot for C3d in normoxic vs. hypoxic C57Bl/6J mice. (G) Quantification of Western blots for C3d in normoxic vs. hypoxic mice. Bars represent the mean ± SD (n = 4). *<i>P</i><0.05. (H) C5a was immunoprecipitated from lung or plasma of normoxic and hypoxic C57Bl/6J mice and analyzed by Western blot (rC5a = recombinant mouse C5a).</p

Markers of Inflammation and endothelial dysfunction in WT vs. C3 −/− mice.

<p>(A) IL-6 mRNA was measured by quantitative rtPCR in RNA prepared from normoxic or hypoxic WT and C3−/− lungs. IL-6 levels were normalized to the house keeping gene β2-microglobulin. (B) ICAM-1 was quantified by ELISA in lung homogenates from normoxic or hypoxic WT or C3−/− mice. (C) ET-1 was quantified by ELISA in plasma from normoxic or hypoxic WT or C3−/− mice. Bars represent mean ± SD (n = 4) for A–C. *<i>P</i><0.05.</p

Loss of C3 prevents platelet activation caused by CH.

<p>(A) Bleeding time of WT and C3−/− mice exposed to normoxia or CH (n = 5–7). (B) Scatter plot showing platelet population in platelet rich plasma. All experiments were similarly gated to the area encircled. (C) Flow cytometry histogram demonstrating that the gated cell population is positive for the platelet marker CD41. (D–E) Representative flow cytometry histograms of platelets from (D) hypoxic WT or (E) hypoxic C3−/− mice stained with P-selectin antibody or isotype control. (F) Percent P-selectin positive platelets in PRP isolated from normoxic and hypoxic WT or C3−/− mice (n = 6). Bars represent mean ± SD. *<i>P</i><0.05; n.s. = not significant.</p

Loss of C3 prevents hypoxia-induced TF upregulation.

<p>(A) Representative Western blot analysis of normoxic or hypoxic WT and C3−/− lungs for TF expression. (B) Densitometric anlysis of Western blots from (A). Bars represent the mean ± SD (n = 4 animals per group). *<i>P</i><0.05.</p