Hypothalamic-pituitary-adrenal axis dysfunction during sleep in nocturnal asthma.
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Asthma↗
Biomedical subjects
Misoo C Ellison
Publications and source records attributed to Misoo C Ellison.
Immunomodulatory effects of melatonin in asthma.
Patients with nocturnal asthma demonstrate circadian variations in airway inflammation. We hypothesized that melatonin, a circadian rhythm regulator, modulates circadian inflammatory variations in asthma. The effect of melatonin stimulation on peripheral blood mononuclear cell cytokine production was evaluated at 4:00 P.M. and 4:00 A.M. in normal control subjects, patients with nocturnal asthma, and patients with non-nocturnal asthma. Melatonin was proinflammatory, causing significantly increased production of interleukin-1, interleukin-6, and tumor necrosis factor-alpha at 4:00 P.M. and 4:00 A.M. in all subject groups (range, 12.8 +/- 3.3 to 131.72 +/- 16.4%, p < or = 0.0003). The observed increases in cytokine production did not change between 4:00 P.M. and 4:00 A.M. in control subjects or in patients with nocturnal asthma (p > 0.05, both cases). At 4:00 P.M., the cytokine response to melatonin of patients with nocturnal asthma was greater than that of control subjects or patients with non-nocturnal asthma and did not change significantly at 4:00 A.M. At 4:00 P.M., the cytokine response of patients with non-nocturnal asthma was less than that of patients with nocturnal asthma and rose significantly at 4:00 A.M. (p = 0.0001, all comparisons). Melatonin is proinflammatory in both patients with asthma and healthy subjects. Patients with nocturnal asthma demonstrate the largest daytime cytokine response and cannot be further stimulated at 4:00 A.M., suggesting chronic overstimulation in vivo. These results suggest differential immunomodulatory effects of melatonin based on asthma clinical phenotype and may indicate an adverse effect of exogenous melatonin in asthma.
Adjuvants, Immunologic↗
Longitudinal motion of the atrioventricular annuli in children: reference values, growth related changes, and effects of right ventricular volume and pressure overload.
The goals of this study were to characterize normal patterns of longitudinal motion of atrioventricular annuli in the young, establish reference values and assess growth-related changes (n = 40). Sensitivity to changes in right ventricular volume and pressure load was assessed in patients with atrial septal defect (ASD) (n = 25) and with primary pulmonary hypertension (PPH) (n = 20). M-mode of the annuli were obtained from apical views. In healthy subjects, longitudinal %displacement decreased with growth, lateral tricuspid annulus had highest %displacement, velocity of annular descent did not change with growth, tricuspid lateral annulus had the highest velocity of descent, only ascent velocity of the lateral tricuspid annulus decreased with growth, velocities of ascent for the lateral annuli were similar and higher than the septum, and heart rate had no effect on parameters tested. In patients with ASD, the findings were an exaggerated normal pattern. In patients with PPH, %displacement and ascent velocities were blunted. Our results demonstrate the utility of this technique to assess annular dynamics in pediatric patients.
Adolescent↗
In vivo treatment with granulocyte colony-stimulating factor does not delay apoptosis in human neutrophils by increasing the expression of the vacuolar proton ATPase.
BACKGROUND: Neutrophils die by apoptosis, and in vivo administration of granulocyte colony-stimulating factor (G-CSF) delays this apoptotic cell death. G-CSF administered in vitro correlates delayed apoptosis with upregulation of the vacuolar proton ATPase (v-ATPase). Because this enzyme requires assembly of membrane and cytosolic domains to function, we hypothesized that in vivo G-CSF would increase synthesis and assembly of v-ATPase components to delay apoptosis. METHODS: Volunteers received G-CSF for 5 days, and each had a paired control. Neutrophils were isolated from subjects before the first and after the fifth injection. Proteins from cytosol or plasma membrane or from whole cell lysates were resolved by SDS-polyacrylamide gel electrophoresis and immunoblotted with antibody to the 33kDa v-ATPase E subunit. Densitometry quantified immunoreactivity. RESULTS: No significant increase on the E subunit occurred between treated and control groups. CONCLUSION: In vivo G-CSF does not increase the amount of v-ATPase in neutrophils. Although G-CSF in vivo delays apoptosis, the mechanism(s) by which this occurs is not known.
Adult↗