40 research outputs found
Interrelationship between serum and sputum inflammatory mediators in chronic obstructive pulmonary disease
Little is known about airway inflammatory markers in chronic obstructive pulmonary disease (COPD). The objective of the present study was to identify and try to correlate pulmonary and peripheral blood inflammatory markers in COPD. In a cross-sectional study on patients with stable COPD, induced sputum and blood samples were collected for the determination of C-reactive protein, eosinophilic cationic protein, serum amyloid A protein, a-1 antitrypsin (a-1AT), and neutrophil elastase. Twenty-two patients were divided into two groups according to post-bronchodilator forced expiratory volume in the first second (%FEV1): group 1 (N = 12, FEV1 <40%) and group 2 (N = 10, FEV1 ³40%). An increase in serum elastase, eosinophilic cationic protein and a-1AT was observed in serum markers in both groups. Cytology revealed the same total number of cells in groups 1 and 2. There was a significantly higher number of neutrophils in group 1 compared to group 2 (P < 0.05). No difference in eosinophils or macrophages was observed between groups. Serum elastase was positively correlated with serum a-1AT (group 1, r = 0.81, P < 0.002 and group 2, r = 0.83, P < 0.17) and negatively correlated with FEV1 (r = -0.85, P < 0.03 and -0.14, P < 0.85, respectively). The results indicate the presence of chronic and persistent pulmonary inflammation in stable patients with COPD. Induced sputum permitted the demonstration of the existence of a subpopulation of cells in which neutrophils predominated. The serum concentration of all inflammatory markers did not correlate with the pulmonary functional impairment
Elevated serum neutrophil elastase is related to prehypertension and airflow limitation in obese women
<p>Abstract</p> <p>Background</p> <p>Neutrophil elastase level/activity is elevated in a variety of diseases such as atherosclerosis, systolic hypertension and obstructive pulmonary disease. It is unknown whether obese individuals with prehypertension also have elevated neutrophil elastase, and if so, whether it has a deleterious effect on pulmonary function. Objectives: To determine neutrophil elastase levels in obese prehypertensive women and investigate correlations with pulmonary function tests.</p> <p>Methods</p> <p>Thirty obese prehypertensive women were compared with 30 obese normotensive subjects and 30 healthy controls. The study groups were matched for age. Measurements: The following were determined: body mass index, waist circumference, blood pressure, lipid profile, high sensitivity C-reactive protein, serum neutrophil elastase, and pulmonary function tests including forced expiratory volume in one second (FEV<sub>1</sub>), forced vital capacity (FVC) and FEV<sub>1</sub>/FVC ratio.</p> <p>Results</p> <p>Serum neutrophil elastase concentration was significantly higher in both prehypertensive (405.8 ± 111.6 ng/ml) and normotensive (336.5 ± 81.5 ng/ml) obese women than in control non-obese women (243.9 ± 23.9 ng/ml); the level was significantly higher in the prehypertensive than the normotensive obese women. FEV1, FVC and FEV1/FVC ratio in both prehypertensive and normotensive obese women were significantly lower than in normal controls, but there was no statistically significant difference between the prehypertensive and normotensive obese women. In prehypertensive obese women, there were significant positive correlations between neutrophil elastase and body mass index, waist circumference, systolic blood pressure, diastolic blood pressure, total cholesterol, triglyceride, low density lipoprotein cholesterol, high sensitivity C-reactive protein and negative correlations with high density lipoprotein cholesterol, FEV1, FVC and FEV1/FVC.</p> <p>Conclusion</p> <p>Neutrophil elastase concentration is elevated in obese prehypertensive women along with an increase in high sensitivity C-reactive protein which may account for dyslipidemia and airflow dysfunction in the present study population.</p
Chemical modification of niobium layered oxide by tetraalkylammonium intercalation
Chemical modification of the layered K4Nb6O17 material was systematically investigated through the reaction of its proton-exchanged form (H2K2Nb6O17) in alkaline solutions containing tetramethylammonium (tma+), tetraethylammonium (tea+) or tetrapropylammonium (tpa+) cations. The intercalated amount reaches 50% (for tma+), 25% (for tea+) and 15% (for tpa+) of the H2K2Nb6O17 negative charge (concerning the exchange at interlayer I) due to the steric hindrance of larger cations. Hexaniobate samples present (020) basal reflections equal to 23.0, 26.3 and 26.5 Å once intercalated respectively with tma+, tea+ and tpa+. When samples are heated above 200-250 ºC, CO2 evolution is observed; Hofmann elimination reaction is also detected for hexaniobate-tpa+ samples. Scanning electron microscopy images show the predominance of plate-like particles; stick-like particles are also observed for samples containing bulky ions. The intercalation reaction is promoted in the order tma+ > tea+ > tpa+, while the formation of a dispersion of colloidal particles is facilitated in the inverse order.A modificação química do material lamelar K4Nb6O17 foi investigada sistematicamente através da reação de sua forma protônica (H2K2Nb6O17) em soluções alcalinas contendo os cátions tetrametilamônio (tma+), tetraetilamônio (tea+) ou tetrapropilamônio (tpa+). A quantidade intercalada corresponde a 50% (para tma+), 25% (para tea+) e 15% (para tpa+) da carga negativa do H2K2Nb6O17 (considerando a troca iônica na região interlamelar I). As amostras de hexaniobato apresentam reflexões basais (020) de 23,0, 26,3 e 26,5 Å quando intercaladas, respectivamente, com tma+, tea+ e tpa+. Aquecendo-se as amostras acima de 200-250 ºC, observa-se a liberação de CO2; a reação de eliminação de Hofmann também é observada para as amostras de hexaniobato-tpa+. As imagens de microscopia eletrônica de varredura mostram a presença predominante de partículas em forma de placas; partículas em forma de bastões também são observadas nas amostras contendo íons volumosos. A reação de intercalação é promovida na ordem tma+ > tea+ > tpa+, enquanto a formação de uma dispersão de partículas coloidais é facilitada na ordem inversa
Dissimilarity Between Prostaglandin E1 And Nitric Oxide Donors As Potentiators Of Plasma Exudation In The Rabbit Skin In Vivo.
The ability of prostaglandin E1 (PGE1) and nitric oxide (NO) donor compounds such as sodium nitroprusside (SNP), glyceryl trinitrate (GTN), and 3-morpholino-sydnonimine (SIN-1) to modulate the histamine- and bradykinin-induced increase in microvascular permeability have been investigated in rabbit skin. The effect of the NO synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) on the plasma exudation induced by histamine and bradykinin was also studied. Local edema formation was evaluated using [125I]human serum albumin. New Zealand white rabbits received an intravenous injection of [125I]human albumin followed immediately by the intradermal injection of edematogenic agents into the shaved dorsolateral skin. PGE1 (0.1 nmol/site) significantly potentiated both histamine- and bradykinin-induced edema. In contrast, SNP (0.4-400 nmol/site), SIN-1 (0.4-400 nmol/site), and GTN (0.4-40 nmol/site) did not affect the edematogenic response induced by either histamine or bradykinin. GTN (0.4-40 nmol/site) also had no effect on the increase in plasma exudation induced by histamine and bradykinin in the presence of PGE1. L-NAME (50-400 nmol/site, but not its enantiomer D-NAME, dose-dependently reduced the edema formation induced by a combination of either histamine or bradykinin with PGE1. This inhibition was significantly reversed by SNP (4-400 nmol/site) and by high doses (2.5 mumol/site) of L-arginine (but not by D-arginine). Our results thus demonstrate that PGE1, but not nitrovasodilators, can actually potentiate histamine- and bradykinin-induced edema in rabbit skin.(ABSTRACT TRUNCATED AT 250 WORDS)52399-40