Diagnostic flexible versus rigid bronchoscopy for the assessment of tracheomalacia in children.

OBJECTIVE: This project compares the degree of tracheal collapse determined by rigid and flexible bronchoscopy in paediatric patients with tracheomalacia. METHODS: A total of nine patients with tracheomalacia underwent both rigid and flexible video bronchoscopy. All patients were breathing spontaneously. Cross-sectional images of the airway were processed using the ImageJ program and analysed via colour histogram mode technique in order to delineate the luminal area. Paired t-tests (conducted using Stata software version 13.0) quantified differences between rigid and flexible bronchoscopes regarding the ratios of luminal pixels at maximum airway collapse to expansion. Correlation between both techniques in terms of airway collapse to expansion ratios was determined by calculating the Pearson correlation coefficient (R). RESULTS: The difference in ratios of maximum collapse to expansion between rigid and flexible bronchoscopy was not statistically significant (p = 0.4656) and was positively correlated (R = 0.523). CONCLUSION: The ratios suggest that rigid and flexible bronchoscopy are equally efficacious in assessing tracheomalacia severity, and may be used interchangeably in a clinical setting.

Apolipoprotein(a) induces monocyte chemotactic activity in human vascular endothelial cells.

BACKGROUND: Elevated levels of lipoprotein(a) [Lp(a)] are associated with premature atherosclerosis; however, the mechanisms are not known. Recruitment of monocytes to the blood vessel wall is an early event in atherogenesis. METHODS AND RESULTS: This study has found that unoxidized Lp(a) induced human umbilical vein endothelial cells (HUVECs) to secrete monocyte chemotactic activity (MCA), whereas LDL under the same conditions did not. In the absence of HUVECs, Lp(a) had no direct MCA. Endotoxin was shown not to be responsible for the induction of MCA. Actinomycin D and cycloheximide inhibited the HUVEC response to Lp(a), indicating that protein and RNA synthesis were required. The apolipoprotein(a) [apo(a)] portion of Lp(a) was identified as the structural component of Lp(a) responsible for inducing MCA. Lp(a) and apo(a) also stimulated human coronary artery endothelial cells to produce MCA. Granulocyte-monocyte colony-stimulating factor (GM-CSF) antigen was not detected in the Lp(a)-conditioned medium, nor was monocyte chemoattractant protein-1 mRNA induced in HUVECs by Lp(a). CONCLUSIONS: These findings suggest that Lp(a) may be involved in the recruitment of monocytes to the vessel wall and provide a novel mechanism for the participation of Lp(a) in the atherogenic process.

Apolipoprotein(a) is a human vascular endothelial cell agonist: studies on the induction in endothelial cells of monocyte chemotactic factor activity.

Elevated levels of lipoprotein(a), Lp(a), are associated with premature atherosclerosis; however, the mechanisms of its atherogenicity are not known. Recruitment of monocytes to the blood vessel wall is an early event in atherogenesis. Since Lp(a) is associated with macrophages in the plaque, we have examined the effect of Lp(a) on inducing monocyte chemotactic activity (MCA) in vascular endothelial cells. We report that Lp(a) and apo(a) induced human umbilical vein (HUVEC) and coronary artery endothelial cells to secrete monocyte chemotactic activity as early as 30 min of incubation. In the absence of cells, Lp(a) had no direct monocyte chemotactic activity. Actinomycin D and cycloheximide inhibited the HUVEC response, indicating that protein and RNA synthesis were required. Endotoxin was shown not to be responsible for the induction of monocyte chemotactic activity. Granulocyte monocyte-colony stimulating factor antigen was not detected in the Lp(a)-conditioned medium, nor was monocyte chemoattractant protein-1 mRNA induced by Lp(a). These results suggest that Lp(a) may be involved in the recruitment of monocytes to the vessel wall, thus providing a novel mechanism for the participation of Lp(a) in the atherogenic process.

Angiopeptin, a somatostatin-14 analogue, decreases adhesiveness of rat leukocytes to unstimulated and IL-1 beta-activated rat heart endothelial cells.

We have previously demonstrated that somatostatin-14 and its octapeptide analogue, angiopeptin, decrease the ability of rat heart endothelial cells to bind leukocytes [Leszczynski, et al., Reg. Pept. 43 (1993) 131-140]. Here, we examined whether exposure of leukocytes to angiopeptin modifies their adhesiveness to the unstimulated and to IL-1 beta-activated endothelium. Monolayers of unstimulated endothelial cells bind 274 +/- 12 leukocytes/mm2. Exposure of leukocytes for 1, 4 and 24 hours to angiopeptin (1 microM) reduced significantly (p < 0.05) adhesion of leukocytes from 274 +/- 12 to 188 +/- 10, 185 +/- 8 and 172 +/- 3 cells/mm2, respectively. Stimulation of endothelial cells with Il-1 beta (100 U/ml) for 24 hours increased endothelial adhesiveness from 274 +/- 12 to 381 +/- 17 adhering leukocytes/mm2. Exposure of leukocytes for 1, 4 and 24 hours to angiopeptin (1 microM) reduced significantly (p < 0.05) binding of leukocytes to IL-1 beta-activated endothelium from 381 +/- 17 to 237 +/- 8, 254 +/- 11 and 248 +/- 13 cells/mm2, respectively. Angiopeptin had no effect on the expression of lymphocyte function-associated molecule-1 (LFA-1; CD11a/CD18) by leukocytes, as assessed by flow cytometry. This suggests that angiopeptin modulates adhesive properties of leukocytes by (1) altering the expression of other than LFA-1 adhesion molecule(s) and/or (2) modulating the affinity of adhesion molecule(s) expressed by leukocytes. In conclusion, our results demonstrate that angiopeptin reduces leukocyte adhesiveness to unstimulated and to IL-1 beta-activated endothelium. It suggests that angiopeptin may suppress immune response via modulation of the leukocyte-endothelial interaction.