Biomarkers of pediatric obstructive sleep apnea syndrome and the assessment of quality of life before and after adenotonsillectomy.

The study aims to explore the inflammatory cytokines and oxidative stress in children with obstructive sleep apnea syndrome (OSAS) triggered by adenoids and/or tonsillar hypertrophy and their changes after adenotonsillectomy (AT) and to investigate the associated behavioral disorders in OSAS, before and after AT. Thirty patients with OSAS and 20 healthy children, aged 3 - 13 years were included in the study. According to apnea-hypopnea index (AHI), OSAS children were classified into 3 groups: mild (n = 19), moderate (n = 5), and severe OSAS (n = 6). Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), interleukin (IL)-6, tumor necrosis factor (TNF)-α, malondialdehyde (MDA) and antioxidant enzymes activities were assessed in serum, preoperative and 6 weeks after AT. TNF-α, IL-6 and malondialdehyde levels were also estimated in adenoid and tonsils tissues. A Pediatric Sleep Questionnaire was completed by the parents before and after AT. As a result of the study, we obtained the following results: TNF-α, IL-6 and malondialdehyde evaluated preoperative increased in serum and tissues in OSAS, especially in severe disease compared to mild and moderate forms. Six weeks after AT, AHI diminished significantly in OSAS, as well as the inflammatory markers and malondialdehyde, in parallel with significant improvement of antioxidant enzymes activities. Daytime sleepiness, hyperactivity and attention deficit in OSAS, even in mild disease were present, with significant improvements of obstructive symptoms after AT. We conclude that OSAS caused by adenoids and/or tonsillar hypertrophy led to changes in the blood parameters, with significant improvement after AT. Postoperatively, a significant improvement in sleep quality and behavior in OSAS patients was also observed.

Decorin-mediated inhibition of proliferation and migration of the human trophoblast via different tyrosine kinase receptors.

Decorin (DCN), a decidua-derived TGFbeta-binding proteoglycan, negatively regulates proliferation, migration, and invasiveness of human extravillous trophoblast (EVT) cells in a TGFbeta-independent manner. The present study examined underlying mechanisms, in particular possible roles of epidermal growth factor receptor (EGFR), IGF receptor (IGFR)-I, and vascular endothelial growth factor receptor (VEGFR)-2. EVT cell sprouting from first-trimester chorionic villus explants in the presence or absence of TGFbeta-neutralizing antibody was inhibited with DCN, suggesting its negative regulatory role in situ. Inhibition of migration of the human EVT cell line HTR-8/SVneo in transwells undercoated with fibronectin was stronger when cells were briefly preincubated with DCN at 4 C (known to retard dissociation of receptor-ligand complex) than at 37 C, suggesting possible DCN action by cell membrane binding. Pretreatment of cells with an IGFR-I blocking agent, but not two EGFR blocking agents or a VEGFR blocking agent, significantly abrogated migration inhibitory effects of DCN, suggesting the involvement of IGFR-I but not EGFR or VEGFR in migration inhibition by DCN. On the other hand, pretreatment with either of the EGFR blocking agents, or the VEGFR blocking agent but not the IGFR-I blocking agent, blocked proliferation inhibitory effects of DCN, indicating the roles of EGFR and VEGFR, but not IGFR-I in antiproliferative action of DCN. EVT cells expressed EGFR, IGFR-I, and VEGFR-2. IGFR-I and VEGF-R2 were phosphorylated in the presence of their natural ligands as well as DCN, and these events were blocked by pretreatment with respective receptor blocking agents indicating DCN-mediated activation of these receptors. In conclusion, DCN effects on EVT cells are mediated selectively by multiple tyrosine kinase receptors.