Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019270 (hernia)
 15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to determine circulating levels of adhesion molecules in serum from patients with congenital diaphragmatic hernia (CDH) to investigate the relationship between soluble ICAM-1, ELAM-1, and VCAM-1 liberated by activated vascular endothelium and the development of persistent pulmonary hypertension (PPH) in patients with CDH. We measured serum levels of ICAM-1, ELAM-1, and VCAM-1 in 20 high-risk neonates with CDH at the time of diagnosis (11 with PPH and 9 without PPH) and 7 age-matched controls using ELISA system. We further examined the lungs of 5 patients with CDH complicated by PPH who died during resuscitation and stabilization, and three control lung specimens for the expression of adhesion molecules using immunohistochemistry. The mean serum ICAM-1 levels in CDH patients with PPH (227.0+/-98.9 ng/ml) were increased compared with levels in CDH patients without PPH (140.29+/-37.4 ng/ml; p<0.05) and controls (130.0+/-23.8 ng/ml; p<0.05). Mean serum ELAM-1 levels in CDH patients with PPH (116.5+/-19.2 ng/ml) were significantly increased compared with levels in CDH patients without PPH (79.3+/-27.9 ng/ml; p<0.01) and controls (58.4+/-14.5 ng/ml; p<0.001). Mean serum VCAM-1 levels in CDH patients with PPH (1596.9+/-460.4 ng/ml) were significantly higher compared with levels in CDH patients without PPH (1069.3+/-444.6 ng/ml; p<0.01) and controls (838.0+/-171.2 ng/ml; p<0.001). But serum adhesion molecule levels in CDH patients without PPH were no different from controls statistically. Pulmonary vascular endothelial cells from CDH lung with PPH had strong expression of adhesion molecules compared with controls. Up-regulated expression of adhesion molecules on the endothelium of pulmonary vessels and high circulating levels of adhesion molecules in CDH patients with PPH suggest that adhesion molecules may play a role in the development of PPH in CDH.
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PMID:Increased levels of circulating adhesion molecules in neonates with congenital diaphragmatic hernia complicated by persistent pulmonary hypertension. 1467 14

Surgical stress induces systemic endocrine-metabolic responses that influence the function of endothelial cells (EC) to cause various systemic reactions. Intercellular adhesion molecule (ICAM)-1 is an adhesion molecule that plays an important role in inflammation, and increased expression of ICAM-1 on EC is a reflection of EC activation. In this study, we investigated the ICAM-1 response to surgical stress in neonates undergoing major surgery. Fifteen neonates (mean age at surgery: 3.5 +/- 1.2 days) were divided into two groups according to indications for surgery: Group I: Congenital diaphragmatic hernia without persistent pulmonary hypertension (n = 5); Group II: Gastrointestinal surgery [n = 10: duodenal atresia (n = 3), intestinal atresia (n = 6), and esophageal atresia (n = 1)]. Serum samples were obtained preoperatively, immediately after completion of surgery (time zero), and 24, 48, 72, 96, and 120 h after surgery to measure ICAM-1 levels using an enzyme-linked immunosorbent assay, C-reactive protein (CRP), and white blood cell count (WBC). Postoperative recovery was uneventful in all cases. ICAM-1 levels in both groups increased significantly within 24 h of surgery (Group I: P = 0.0038, Group II: P = 0.0320). In Group I, ICAM-1 peaked 72 h postoperatively while in Group II it continued to rise until 96 h postoperatively. The difference between peak levels reached was not significant. CRP was first detected 24 h postoperatively in both groups and continued to increase until 48 h postoperatively. Again, the difference between peak levels reached was not significant. No significant changes in WBC were observed in either group. We found that ICAM-1 increases in response to surgical stress in neonates, although there was no significant difference in levels. However, surgical stress as represented by serum ICAM-1 would appear to last longer with intestinal surgery than with non-intestinal surgery. Further research is required to establish the usefulness of ICAM-1 as an easily detectable substance associated with endothelial damage that reflects the host's response to major surgical stress.
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PMID:Intercellular adhesion molecule (ICAM-1) response after major neonatal surgery. 1609 95

Pulmonary hypoplasia is the principal cause of morbidity and mortality in infants with congenital diaphragmatic hernia (CDH). Still, relatively little is known about the mechanisms causing lung hypoplasia associated with CDH. The differentiation from alveolar epithelial cells type II (AECs-II) into alveolar epithelial cells type I (AECs-I) is one of the key processes in lung development in late gestation. It is well known that increased lung expansion promotes differentiation into AECs-I phenotype, whereas reduced lung expansion promotes AECs-II phenotype. The recent availability of cell-specific molecule markers for AECs-I and AECs-II has provided an opportunity to study the various characteristics of these two cell types. To test the hypothesis that the differentiation of AECs-II to AECs-I is impaired in the CDH hypoplastic lung, we investigated molecular markers for AECs-I [ICAM-1, T1alpha, aquaporin 5 (AQP5)] and molecular markers for AECs-II [thyroid transcription factor-1 (Ttf-1), surfactant protein (SP)-B and C] in the nitrofen-induced CDH lung. Fetal rat lungs of normal (n = 7) and nitrofen-treated (n = 14) dams were harvested on embryonic day 21. The expression of the ICAM1, T1alpha, AQP5, SP-B, C and Ttf-1 was analyzed in each lung by real-time reverse transcription polymerase chain reaction. Immunohistochemical studies were performed to evaluate the protein expression level of ICAM1 and Ttf1. Expression levels of ICAM-1, T1alpha and AQP5 were significantly reduced (P < 0.05) in the lungs from nitrofen-treated CDH animals compared to normal controls. ICAM-1 and AQP5 immunohistochemistry showed a diffuse pattern of expression in the alveolar cells in normal lungs. By contrast, the ICAM-1 and AQP5 positive cells were markedly reduced in hypoplastic lungs with CDH. On the other hand, the expression levels of Ttf-1, SP-B and C were significantly (P < 0.05) increased in the lungs from nitrofen-treated CDH animals compared to normal controls. The population of Ttf-1 positive cells was slightly increased in the lungs from nitrofen-treated animals in immunohistochemical study. Our results demonstrate that there is significant reduction in the proportion of AECs-I and increase in the proportion of AECs-II in the hypoplastic lung in the nitrofen-induced CDH. This data provides the first evidence to support the hypothesis that AEC differentiation is impaired in CDH hypoplastic lung.
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PMID:Impaired alveolar epithelial cell differentiation in the hypoplastic lung in nitrofen-induced congenital diaphragmatic hernia. 1724 93