RESUMO
Semiconductor quantum dot (QD) arrays can be useful for optical devices such as lasers, solar cells and light-emitting diodes. As the size distribution influences the band-gap, it is worthwhile to investigate QDs prepared using different solvents because each of them could influence the overall morphology differently, depending on the ligand network around individual QDs. Here, we follow the nucleation and growth of gold (Au) on CdSe QD arrays to investigate the influence of surface ligands and thereby realized interparticle distance between QDs on Au growth behaviour. We particularly emphasize on the monolayer stage as the Au decoration on individual QDs is expected at this stage. Therefore, we sputter-deposit Au on each QD array to investigate the morphological evolution in real-time using time-resolved grazing-incidence small-angle X-ray scattering (GISAXS). The growth kinetics - independent of the template - signifies that the observed template-mediated nucleation is limited only to the very first few monolayers. Delicate changes in the Au growth morphology are seen in the immediate steps following the initial replicated decoration of the QD arrays. This is followed by a subsequent clustering and finally a complete Au coverage of the QD arrays.
RESUMO
Background: Chronic obstructive pulmonary disease (COPD) is characterized by irreversible expiratory airflow obstruction, and its chronic course is worsened by recurrent acute exacerbations. Our previous microarray assay identified microRNA (miR)-301a-5p as being associated with progression of acute exacerbation of COPD (AE-COPD); however, the mechanism underlying COPD pathogenesis remains unknown. Methods: Samples of serum and peripheral blood mononuclear cells (PBMCs) were isolated from healthy control subjects and patients with stable COPD (R-COPD) or with an acute exacerbation of COPD (AE-COPD). Human HULEC-5a and human bronchial epithelial (HBE) cells were transfected with methyl-CpG-binding domain protein 2 (MBD2), sh-MBD2, miR-301a-5p mimics or an inhibitor, and then stimulated with cigarette smoke extract (CSE). Conditioned medium co-culture assays were performed by adding the supernatant of medium derived from HULEC-5a cells transfected with miR-301a-5p mimics or inhibitor into wells containing si-c-x-c motif chemokine receptor 4 (CXCR4)-transfected-lung fibroblasts or human leukemic THP-1 cell line macrophages. Transwell assays were performed to analyze cell migration. Results: Our analysis of clinical samples showed that decreased miR-301a-5p levels in patients with AE-COPD were positively correlated with levels of MBD2 expression, but negatively correlated with levels of chemokine ligand C-X-C motif chemokine ligand 12 (CXCL12) expression. MBD2 overexpression significantly promoted miR-301a-5p production, but suppressed CXCL12 production in HULEC-5a and HBE cells. CXCL12 was confirmed to be a direct target of miR-301a-5p. CXCR4 knockdown significantly enhanced the suppressive effect of miR-301a-5p mimics and attenuated the promotional effects of the miR-301a-5p inhibitor on the migration of circulating fibroblasts and macrophages, as well as the expression levels of phospho-mitogen-activated protein kinase (p-MEK) and phospho-protein kinase B (p-AKT). Conclusion: In summary, the MBD2/miR-301a-5p/CXCL12/CXCR4 pathway was shown to affect the migration of lung fibroblasts and monocyte-derived macrophages, which may play an important role during COPD exacerbations.
