Bioavailable estradiol concentrations are elevated and predict mortality in septic patients: a prospective cohort study.

Background: Experimental studies demonstrate beneficial immunological and hemodynamic effects of estradiol in animal models of sepsis. This raises the question whether estradiol contributes to sex differences in the incidence and outcomes of sepsis in humans. Yet, total estradiol levels are elevated in sepsis patients, particularly nonsurvivors.

The ratio of arginine to dimethylarginines is reduced and predicts outcomes in patients with severe sepsis.

Objectives: Arginine deficiency may contribute to microvascular dysfunction, but previous studies suggest that arginine supplementation may be harmful in sepsis. Systemic arginine availability can be estimated by measuring the ratio of arginine to its endogenous inhibitors, asymmetric and symmetric dimethylarginine. We hypothesized that the arginine-to-dimethylarginine ratio is reduced in patients with severe sepsis and associated with severity of illness and outcomes.

Vascular effects of ultrafine particles in persons with type 2 diabetes.

Background: Diabetes confers an increased risk for cardiovascular effects of airborne particles.

Objective: We hypothesized that inhalation of elemental carbon ultrafine particles (UFP) would activate blood platelets and vascular endothelium in people with type 2 diabetes.

Methods: In a randomized, double-blind, crossover trial, 19 subjects with type 2 diabetes inhaled filtered air or 50 µg/m³ elemental carbon UFP (count median diameter, 32 nm) by mouthpiece for 2 hr at rest.

Effect of inhaled carbon ultrafine particles on reactive hyperemia in healthy human subjects.

Background: Ultrafine particles (UFP) may contribute to the cardiovascular effects of exposure to particulate air pollution, partly because of their relatively efficient alveolar deposition and potential to enter the pulmonary vascular space.

Objectives: This study tested the hypothesis that inhalation of elemental carbon UFP alters systemic vascular function.

Methods: Sixteen healthy subjects (mean age, 26.

Smokers have reduced nitric oxide production by conducting airways but normal levels in the alveoli.

Air exhaled by cigarette smokers contains reduced amounts of nitric oxide (NO). Measurement of NO at different expiratory flow rates permits calculation of NO production by the conducting airways (Vaw(NO)) and alveolar concentration of NO (P(ALV)). An independent measurement of diffusing capacity of the alveolar compartment (D(LNO)) multiplied by P(ALV) allows calculation of NO production by the alveoli (V(LNO)).

Inhalation of ultrafine particles alters blood leukocyte expression of adhesion molecules in humans.

Ultrafine particles (UFPs; aerodynamic diameter < 100 nm) may contribute to the respiratory and cardiovascular morbidity and mortality associated with particulate air pollution. We tested the hypothesis that inhalation of carbon UFPs has vascular effects in healthy and asthmatic subjects, detectable as alterations in blood leukocyte expression of adhesion molecules. Healthy subjects inhaled filtered air and freshly generated elemental carbon particles (count median diameter approximately 25nm, geometric standard deviation approximately 1.

Effects of exposure to ultrafine carbon particles in healthy subjects and subjects with asthma.

Increased levels of particulate air pollution are associated with increased respiratory and cardiovascular mortality and morbidity as well as worsening of asthma. Ultrafine particles (UFP; less than 0.1 microm in aerodynamic diameter) may contribute to the health effects of particulate matter (PM) for a number of reasons.

Pulmonary function, diffusing capacity, and inflammation in healthy and asthmatic subjects exposed to ultrafine particles.

Particulate air pollution is associated with asthma exacerbations and increased morbidity and mortality from respiratory causes. Ultrafine particles (particles less than 0.1 microm in diameter) may contribute to these adverse effects because they have a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity when compared with larger particles on a mass basis.

Nitrogen dioxide exposure: effects on airway and blood cells.

This study examined the effects of nitrogen dioxide (NO(2)) exposure on airway inflammation, blood cells, and antiviral respiratory defense. Twenty-one healthy volunteers were exposed on separate occasions to air and 0.6 and 1.