role of soluble intercellular adhesion molecule-1 [SICAM-1] in bronchial asthma

SICAM-l is present in the serum of healthy individuals and its level may be elevated during inflammatory diseases or malignancy. Recent studies have suggested that lCAM-l may be involved in the pathogenesis of bronchial asthma. Hence, this work was carried out to determine weither bronchial asthma is associated with increased serum levels of slCAM-l and to assess the effects of therapy on their levels.Serum levels of slCAM-l was measured in a well known asthmatic patients and in healthy control subjects.Mean value +/- SD of sICAM-l levels in sera of asthmatics [294.2 +/- 94.7 nglml] was significantly higher [P <0.01] than that for healthy subjects [220.6:1 +/- 57.7nglml]. Serum slCAM-1 levels among atopic asthmatics showed a non significant difference [P > 0.05] than those with non atopics [316.2 +/- 12.3 and 274.8 +/- 57.8 respectively]. A significant reduction [P < 0.01] in the serum levels of sICAM-l were observed during remission than during attack among asthmatic parients treated by steroids [199.1 +/- 44.8 ng/ml and 259.4 +/- 40.16 ng/ml respectively], while those not received steroid in their management proved a non- significant reduction [P > 0.05] in serum levels of sICAM-I in remission than during attack [257.3 +/- 49.5 ng/ml and 284 +/- 72.5 ng/ml respectively]

effect of glucose levels in diabetic mothers infant birth weight

This study is done on 20 well known pregnant diabetic women. Both fasting and postprandial blood glucose were measured in each case during the third trimester. There was 6 macrocosmic infants [30%] and 14 infants with average weight for gestational age. Both fasting and postprandial glucose level in maternal blood of the mothers giving birth to macrocosmic infants were found to be significantly higher than in those giving birth to infants weighing less than th 90th percentile [120.7 + 8.3 versus 109.6 + 10.5, t = 3.26 P<0.01 and 134.7 +/- 8.3 versus 116 + 12.2, t = 398 P <0.001 respectively]. It has been concluded that maternal hypoglycemia early in pregnancy stimulates B cell activity with an over response to maternal hypoglycemia late in pregnancy resulting in hyperinsulinemia which enhances lipogenesis that produces fetal macrosomia