The present study aimed to evaluate the relationship between OSA and adenotonsillar size in children of different weight status. A total of 451 patients aged 2–13 years with suspected OSA were retrospectively enrolled in the study. Correlations between the apnea-hypopnea index (AHI) and adenotonsillar size in different weight status were investigated. The adenoidal/nasopharyngeal (A/N) ratio of underweight children was significantly higher than that of normal-weight children (
P
= 0.027). Both adenoid and tonsil size were positively correlated with logAHI in children of normal weight (r = 0.210,
P
= 0.001; and r = 0.212,
P
= 0.001) but uncorrelated in the other groups. Gender (OR = 1.49, 95% CI: 1.01–2.20,
P
= 0.043), obese (OR = 1.93, 95% CI: 1.10–3.40,
P
= 0.012), A/N ratio (OR = 1.55, 95% CI: 1.28–1.88,
P
< 0.001) and tonsil size (OR = 1.36, 95% CI: 1.18–1.57,
P
< 0.001) were all associated with the severity of OSA. Adenotonsillar hypertrophy contributed to OSA in normal-weight children. In children of abnormal weight, instead of treatment for adenotonsillar hypertrophy, appropriate treatments for other factors are required.
Abnormal angiogenesis is critical for portal hypertension in cirrhosis. Except for etiological treatment, no efficient medication or regime has been explored to treat the early stage of cirrhosis when angiogenesis is initiated or overwhelming. In this study, we explored an anti-angiogenesis effort through non-cytotoxic drugs octreotide and celecoxib to treat early stage of cirrhotic portal hypertension in an animal model. Peritoneal injection of thioacetamide (TAA) was employed to induce liver cirrhosis in rats. A combination treatment of celecoxib and octreotide was found to relieve liver fibrosis, portal venous pressure, micro-hepatic arterioportal fistulas, intrahepatic and splanchnic angiogenesis. Celecoxib and octreotide exerted their anti-angiogenesis effect via an axis of cyclooxygenase-2/prostaglandin E2/EP-2/somatostatin receptor-2, which consequently down-regulated phosphorylation of extracellular signal-regulated kinase (p-ERK)–hypoxia-inducible factor-1α (HIF-1α)–vascular endothelial growth factor (VEGF) integrated signaling pathways. In conclusions, combination of celecoxib and octreotide synergistically ameliorated liver fibrosis and portal hypertension of the cirrhotic rats induced by TAA via the inhibition of intrahepatic and extrahepatic angiogenesis. The potential mechanisms behind the regimen may due to the inactivation of p-ERK–HIF-1α–VEGF signaling pathway.Electronic supplementary materialThe online version of this article (doi:10.1007/s10456-016-9522-9) contains supplementary material, which is available to authorized users.
Inflammatory transport through the gut-liver axis may facilitate liver cirrhosis. Cyclooxygenase-2 (COX-2) has been considered as one of the important molecules that regulates intestinal epithelial barrier function. This study was aimed to test the hypothesis that inhibition of COX-2 by celecoxib might alleviate liver cirrhosis via reduction of intestinal inflammatory transport in thiacetamide (TAA) rat model. COX-2/prostaglandin E2 (PGE2)/EP-2/p-ERK integrated signal pathways regulated the expressions of intestinal zonula occludens-1 (ZO-1) and E-cadherin, which maintain the function of intestinal epithelial barrier. Celecoxib not only decreased the intestinal permeability to a 4-kDa FITC-dextran but also significantly increased expressions of ZO-1 and E-cadherin. When celecoxib greatly decreased intestinal levels of LPS, TNF-α, and IL-6, it significantly enhanced T cell subsets reduced by TAA. As a result, liver fibrosis induced by TAA was significantly alleviated in the celecoxib group. These data indicated that celecoxib improved the integrity of intestinal epithelial barrier, blocked inflammatory transport through the dysfunctional gut-liver axis, and ameliorated the progress of liver cirrhosis.
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