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1.
Alexandria Journal of Pediatrics. 2005; 19 (2): 379-387
in English | IMEMR | ID: emr-69523

ABSTRACT

The objective of this study was to test the neonatal polymorphism of TNF alpha to measure the day one levels of sL-selectin, sE-selectin and sICAM-1 in sera of neonate and placenta growth factor in cord blood, for the prediction of development of bronchopulmonary dysplasia [BPD]. The study design was a cross sectional one. Forty preterm neonates with respiratory distress and 10 normal full term neonates were enrolled. The neonates were divided into 2 subgroups; 15 who developed bronchopulmonary dysplasia and 25 without. Sampling was done and diagnostic evaluation of all parameters was accomplished. The results proved that infants. None of the infants with BPD carried the AA TNF- alpha -238 genotype, compared with 3 infants without BPD, and only 1 infant with BPD carried the GA TNF- alpha -238 genotype, compared with 7 infants without BPD. Higher sE-selectin has a diagnostic ability [sensitivity 73%, specificity 76%] higher PLGF has a sensitivity of 67% and specificity 68%. Combination of both, improved specificity to 80%. If we add to them, cases which have absence of GA TNF- alpha -238 genotype, we have got a very high sensitivity [93%] but with lower specificity. Combined all data supported a specificity 80% with a sensitivity of 86%. What had been found in this study might clarify the role of adhesion molecules, P1GF and TNF polymorphism as biological marker to determine which premature infants with RDS are at risk for development of BPD and to permit early intervention and might provide a new therapeutic target to prevent BPD


Subject(s)
Humans , Male , Female , Infant, Premature , Bronchopulmonary Dysplasia , Radiography, Thoracic , Intercellular Adhesion Molecule-1 , L-Selectin , E-Selectin , Fetal Blood , Placental Hormones , Tumor Necrosis Factors
2.
Ain-Shams Journal of Forensic Medicine and Clinical Toxicology. 2003; 1 (1): 160-172
in English | IMEMR | ID: emr-61301

ABSTRACT

The discovery of specific cannabinoid receptors in the immune system and a family of endogenous ligands of these receptors provides basis for understanding the cellular and molecular mechanisms of cannabis-induced immunotoxicity. The present study was conducted on 90 non smoker males of high school and university students living in Tanta city of comparable age and socio-economic lifestyle. They were divided into, a control group [30 males] and a bhang user group [60 males], that used bhang by eating its sweetly juice after boiling with little water and drying in an oven, "fola". The bhang group was divided equally into 2 subgroups, subgroup I used bhang for 6-24 months [average 19 +/- 1.2] and subgroup 2 used bhang for 24 to 36 months [average 31 +/- 1.7]. The immunotoxic effects of using bhang appears in the form of significant decrease in serum immunoglobulins [IgG and 1gM], C3 and C4 complement protein concentrations [p<0.05]. In addition, our results demonstrated a significant decrease in absolute number of functionally different subsets of peripheral blood mononuclear lymphocytes, T and B lymphocytes and natural killer cells in bhang users as compared to controls [p<0.05]. Moreover, the fatty acid amide hydrolase [EAAH] showed significant decrease in bhang users as compared to controls and in subgroup 2 as compared to sub-group 1 [p < 0.05] indicating that the decrease in FAAH protein level is closely related to the duration of bhang use. Positive correlations were found between FAAH level and the absolute number of mononuclear cells [T, B lymphocytes and NK cells] among bhang user subgroups. The present study is the first study to report on the effect of bhang on complement proteins and immunoglobulins in humans. Our study revealed that bhang-induced immunotoxicty could be attributed to increased activity of cannabinoid receptors due to decrease in FAAH protein


Subject(s)
Humans , Male , Female , Immunotoxins , Students , Flow Cytometry , Killer Cells, Natural , Immunoglobulin M , Immunoglobulin G , Immunoglobulin A , Complement C3 , Complement C4 , T-Lymphocytes , B-Lymphocytes
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