Serum ICAM-1 in asthmatic children

The recruitment of leukocytes to inflamed tissues depends on the function of adhesive molecules of the leukocytes and of vascular endothelium. Intercellular adhesion molecules-1 [ICAM-1, CD.54] is a number of the immunoglobulin super-family of adhesion proteins. It is expressed by a number of blood cells and by endothclial, fibroblastic, and epithelial cells. The expression of ICAM-1 is upregulated by a number of cytokines that are released at sites of inflammation. It is probable that ICAM-1 participates in the recruitment of eosmophils to asthmatic airways and contributes to the pathogenesis of asthma. Serum ICAM-1 contains most of the structure of the extracellular portion of membrane-bound ICAM-1 could potentially have physiologic function, perhaps as a modifier of lymphocyte function-associated antigen-1 [LFA-1] dependent leukocyte adhesion. The principle objective of this work is to assess serum soluble intercellular adhesion molecules-1 [slCAM-1] level in asthmatic children during acute asthma exacerbation of their symptoms. We will pay attention to the effect of corticosteroid therapy on serum ICAM-1 level when administered for a short period of time during the acute episode. The study included 30 wheezy children with age from [6 months to 12 year] and 10 normal controls with the same age range. All children and controls undergo good history taking and thorough clinical examination, plain chest X-ray and laboratory investigations including; serum IgE, CBC with differential, serum ICAM-1 determination. Bacterial infection is excluded by clinical examination, leukocytic count, and chest X-ray. Our results showed that serum soluble intercellular adhesion molecules-1 [sICAM-1] level is significantly higher during acute asthma exacerbation in comparison to its level in serum of healthy controls. Also the level of serum soluble adhesion molecules-1 [slCAM-1] is reduced significantly 10 days following the acute episode after a short period of oral corticosteroid therapy

Possible role of plasminogen activator inhibitor-1 in bronchial asthma

Asthma represents a chronic inflammatory process of the airways. The plasminogen activator inhibitor-1 gene [PAI-1] has an essential role in promoting fibrosis after inflammation. The tissue-type plasminogen activator [t-PA] and urokinasc type plasminogen activator [u-PA] convert plasminogen to plasmin, which enhance proteolytic degradation of the extracellular matrix [ECM]. Among the inhibitors of plasminogen activators, PAI-1 is the most important in the process of lung fibrosis. The main role in the inhibition of fibrinolysis through the blockade of activators is ascribed to PAI-1. It is synthesized in endothelium, megakaryocytes, smooth muscle cells of vessels, and in the liver, with the help of cytokines, growth factors, cyclic nucleotides. hormones including glycocorticosteriods and bacterial endotoxins. The study is designed to investigate the correlation between plasma PAI-1 and bronchial asthma severity and whether steroid medications could affect its levels. The study included 40 children with bronchial asthma and 20 healthy children as control subjects. Estimation of plasma PAI-1 carried out for them using ELISA technique. There was a significant lowering of PAI-1 in all asthmatic groups in comparison to control group. The moderate asthmatic subgroups showed highly significant difference in comparison to mild asthmatic and to control group. The mild subgroups showed also significant difference to control group but with lesser mean value compared to moderate subgroups. The results suggest that PAI-1 may play an important role in the pathogenesis of bronchial asthma

Progression of disease in extra hepatic biliary atresia is associated with reduced total hepatic blood flow: descriptive results of a prospective pilot study

Hepatic fibrosis and cirrhosis develop progressively in extrahepatic biliary atresia despite timely surgical intervention. We aimed to study total hepatic blood flow [hepatic artery and portal vein flow] as a possible predictive factor of outcome of infants having biliary atresia who had underwent Kasai portoenterostomy. Twenty Infants having biliary atresia underwent colored and pulsed Doppler ultrasound studies. They were done before and 2-3 months after portoenterostomy. Hepatic artery, portal vein and single hepatic vein mean flow, mean diameter, mean velocity, hepatic arterial to portal venous flow ratio and total hepatic flow/kg were calculated and correlated to final outcome. The detected mean total hepatic flow and total hepatic flow/kg preoperatively was 685.5 +/- 296 ml/min and 147.1 +/- 51.4 ml/min/kg and post-operatively in those who became anicteric was 854.4 +/- 107 ml/min and 149.5 +/- 37.2 ml/min/kg, 539.2 +/- 337.7 ml/min and 112.1 +/- 78.6 ml/min/kg in those who developed chronic disease and in those who died was 157.6 +/- 79.6 and 30.9 +/- 16.1 ml/min/kg respectively. Unresolving cholestasis in infants having biliary atresia with poor outcome following portoenterostomy is associated with decreased post-operative total hepatic flow. Preoperative total hepatic flow did not correlate with postoperative total hepatic flow

Plasma antioxidative enzymes in down syndrome

Numerous biochemical abnormalities are present in Down syndrome [DS] patients, and these abnormalities have not yet been completely-clarified, the antioxidant defense system enzymes have shown to be altered due to increased gene on chromosome 21. In this study we investigated the activities of plasma superoxide dismutase [SOD-1] and glutathione peroxidase [GSH-Px] enzymes and the levels of their cofactors zinc[zn] and selenium [Se] in plasma of 20 Down Syndrome patients 14 males and 6 females with age ranging from 3-14 years, comparing the results with age and sex- matched controls [n=15]. Plasma GSH-Px, SOD-1 were significantly decreased in DS patient group [p<0.001]. Also their cofactors Zn and se were significantly; decreased with [p<0.05] and these changes in the plasma enzyme levels and their cofactors were not correlated to age or sex of the patients. We conclude that evaluation of these antioxidative enzymes and their cofactors are of great importance in DS patients