Patient Characteristics.

<p>OSA = obstructive sleep apnea, M = male, F = female, Afr Amer = African American, BMI = body mass index, DM = diabetes mellitus, HTN = hypertension, SBP = systolic blood pressure, DBP = diastolic blood pressure, AHI-4% = apnea-hypopnea index of respiratory events per hour with at least 4% oxygen desaturation, RDI = respiratory disturbance index, O2 sat % = percentage oxygen saturation recorded, Stage N1% = percentage of total sleep in non-REM sleep stage I, Stage N2% = percentage of total sleep in non-REM sleep stage II, Stage N3% = percentage of total sleep in non-REM sleep stage III, REM% = percentage of total sleep in rapid eye movement (REM) sleep. Table shows mean (+/- standard deviation) or N = number of patients falling into category.</p

Individual NGAL-to-Creatinine Ratios (NGAL/Cr; ng/mg) versus Apnea-Hypopnea Indices (AHI-4%; events/hour) among All Subjects (Untreated Sleep Apnea and Control).

<p>Individual NGAL-to-Creatinine Ratios (NGAL/Cr; ng/mg) versus Apnea-Hypopnea Indices (AHI-4%; events/hour) among All Subjects (Untreated Sleep Apnea and Control).</p

Individual Urinary NGAL-to-Creatinine Ratios (ng/mg) between Control versus Untreated Sleep Apneic (OSA) Groups.

<p>Horizontal lines within each group of data points indicate the group median.</p

Sleep Apnea Severity between Control Subjects and Affected Patients.

<p>A depicts the individual apnea-hypopnea indices (average number of respiratory events with at least 4% oxygen desaturation per hour; AHI-4%) between control versus sleep apneic groups. B depicts the lowest percent oxygen saturation recorded by overnight pulse oximetry between groups. Horizontal lines within each group of data points indicate the group mean.</p

Urinary NGAL-to-Creatinine Ratios (NGAL/Cr; ng/mg) among 11 Sleep Apneic Patients (OSA) before (Pre-Tx) and after (Post-Tx) Successful Treatment with Continuous Positive Airway Pressure.

<p>Urinary NGAL-to-Creatinine Ratios (NGAL/Cr; ng/mg) among 11 Sleep Apneic Patients (OSA) before (Pre-Tx) and after (Post-Tx) Successful Treatment with Continuous Positive Airway Pressure.</p

Tail-vein injection of AdsFlt-1 significantly increased maternal plasma sFlt-1 levels compared to control and AdEV groups.

<p>All maternal mouse sFlt-1 plasma levels (ng/ml ± SEM) were 0±1.23 at GD0.5 of pregnancy, but at term, both control and AdEV sFlt-1 levels were increased to levels observed in normal pregnancy. Mice injected with AdsFlt-1 measured with significant increases in plasma sFlt-1 levels, and this was not difference when exposed to CO. Similar letters represent data that is not statistically different.</p

Comparison of maternal plasma sFlt-1 concentration and percentage of fetal loss for mice injected with high to low AdsFlt-1 concentrations.

<p>Comparison of maternal plasma sFlt-1 concentration and percentage of fetal loss for mice injected with high to low AdsFlt-1 concentrations.</p

Comparison of maternal blood carbon monoxide levels between groups of mice.

<p>Similar letters denote no difference between groups, using a p-value of 0.05.</p><p>Comparison of maternal blood carbon monoxide levels between groups of mice.</p

Maternal sFlt-1 –induced hypertension (HTN) in late stage pregnancy is completely normalized when mice are exposed to CO.

<p>No difference in BP throughout pregnancy was noted in control ± CO or AdEV ± CO groups throughout pregnancy. The injection of AdsFlt-1 led to HTN at the end of pregnancy (P<0.05), which was completed attenuated in mice exposed to CO and not different from control or AdEV groups (P>0.05).</p

Functional characterization of sEpoR.

<p><b>3a.</b> Western blot showing increasedphospho-Stat-5 in the presence of increasing erythropoietin (25 to 5000 mU/ml) in BaF3/EpoR cell lysates. <b>3b</b>. Representative western blot showing total phospho-Stat-5 and Stat-5 in the presence of erythropoietin 5000 mU/ml and varying concentrations of recombinant sEpoR-Fc (50 -5000 ng/ml). Phospho-Stat-5 decreases with increasing recombinant sEpoR. <b>3c</b>. Quantification of sEpoR-Fc inhibition of phospho-Stat 5 (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0009246#pone-0009246-g003" target="_blank">Figure 3b</a>). Ratios of phospho/total Stat-5 (mean ± SD, n = 3) represented as a percentage of control (Epo alone). *represents p<0.05. <b>3d</b>. Serum from patients with high sEpoR blocks erythropoietin mediated Stat-5 phosphorylation. Shown is the ratio of phospho-Stat-5 to Stat-5 as measured by densitometry. Serum starved BaF3/EpoR cells were exposed to vehicle (negative control), erythropoietin at 50 mU/ml (positive control) and erythropoietin plus 10% serum with Low sEpoR (≤62.5 pg/ml) or serum with high sEpoR (≥4000 pg/ml) for 10 minutes. Cells were lysed in RIPA buffer and 10 ug protein/lane was run on a 4-12% denaturing gel. Gels were transferred and blotted with anti-Stat-5 and anti-phospho-Stat 5. <b>3e</b>. Quantification of western data (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0009246#pone-0009246-g003" target="_blank">Figure 3d</a>). Ratios of phospho/total Stat-5 (mean ± SD, n = 5 individual patient samples each for low sEpoR and high sEpoR) represented as a percentage of control (Epo alone). *represents p<0.05.</p