Effect of nasal anti-inflammatory treatment in chronic obstructive pulmonary disease

Sinonasal inflammation and symptoms are often underdiagnosed in chronic obstructive pulmonary disease (COPD) patients. So far, it is not known to what extent anti-inflammatory nasal treatment may reduce sinonasal symptoms in COPD patients. This study was designed to examine the effects of nasal anti-inflammatory treatment on sinonasal symptoms and cough in COPD patients. Thirty-three COPD patients on stable bronchial therapy (salmeterol/fluticasone propionate 50/500 mg b.i.d. for >6 weeks) were randomized to receive fluticasone furoate (FF) or placebo nasal spray at 110 μg once daily for 12 weeks. Sinonasal symptoms and cough were monitored at baseline, at 6 and12 weeks of treatment, and at 4 weeks after cessation of the treatment using a visual analog scale. Levels of cytokines were measured in nasal secretions. In contrast to the placebo group (n = 13), FF patients (n = 14) reported less nasal blockage (10.62 ± 4.21 mm versus 36.57 ± 8.01 mm; p = 0.0026), postnasal drip (1.46 ± 0.29 score versus 2.83 ± 0.38 score; p = 0.03), and nasal discharge (0.23 ± 0.12 score versus 1.77 ± 0.43 score; p = 0.01) after 6 weeks of treatment compared with baseline, which was still present at 12 weeks. FF patients reported less cough compared with baseline (25.54 ± 4.46 mm versus 36.79 ± 5.75 mm; p = 0.04), which was not the case in the placebo group (49.58 ± 10.44 mm versus 42.00 ± 8.05 mm; p = 0.38). Nine of 14 patients in the FF group (64%) reported slight to total relief of nasal symptoms, and this subgroup had a significant decrease in IL-8 levels in nasal secretions after 6 weeks of treatment (850.7 ± 207.2 pg/mL versus 1608 ± 696.5 pg/mL; p = 0.03) compared with baseline. Nasal FF treatment in COPD patients significantly reduced sinonasal symptoms, in parallel with reduced IL-8 in nasal secretion levels and coug

Deletion of the hypoxia-response element in the vascular endothelial growth factor promoter causes motor neuron degeneration

Hypoxia stimulates angiogenesis through the binding of hypoxia-inducible factors to the hypoxia-response element in the vascular endothelial growth factor (Vegf) promotor. Here, we report that deletion of the hypoxia-response element in the Vegf promotor reduced hypoxic Vegf expression in the spinal cord and caused adult-onset progressive motor neuron degeneration, reminiscent of amyotrophic lateral sclerosis. The neurodegeneration seemed to be due to reduced neural vascular perfusion. In addition, Vegf165 promoted survival of motor neurons during hypoxia through binding to Vegf receptor 2 and neuropilin 1. Acute ischemia is known to cause nonselective neuronal death. Our results indicate that chronic vascular insufficiency and, possibly, insufficient Vegf-dependent neuroprotection lead to the select degeneration of motor neurons.status: publishe

Deletion of the hypoxia-response element in the vascular endothelial growth factor promoter causes motor neuron degeneration

Hypoxia stimulates angiogenesis through the binding of hypoxia-inducible factors to the hypoxia-response element in the vascular endothelial growth factor (Vegf) promotor. Here, we report that deletion of the hypoxia-response element in the Vegf promotor reduced hypoxic Vegf expression in the spinal cord and caused adult-onset progressive motor neuron degeneration, reminiscent of amyotrophic lateral sclerosis, The neurodegeneration seemed to be due to reduced neural vascular perfusion. In addition. Vegf(165) promoted survival of motor neurons during hypoxia through binding to Vegf receptor 2 and neuropilin 1. Acute ischemia is known to cause nonselective neuronal death. Our results indicate that chronic vascular insufficiency and, possibly, insufficient Vegf-dependent neuroprotection lead to the select degeneration of motor neurons

Deletion of the hypoxia-response element in the vascular endothelial growth factor promoter causes motor neuron degeneration

Hypoxia stimulates angiogenesis through the binding of hypoxia-inducible factors to the hypoxia-response element in the vascular endothelial growth factor (Vegf) promotor. Here, we report that deletion of the hypoxia-response element in the Vegf promotor reduced hypoxic Vegf expression in the spinal cord and caused adult-onset progressive motor neuron degeneration, reminiscent of amyotrophic lateral sclerosis, The neurodegeneration seemed to be due to reduced neural vascular perfusion. In addition. Vegf(165) promoted survival of motor neurons during hypoxia through binding to Vegf receptor 2 and neuropilin 1. Acute ischemia is known to cause nonselective neuronal death. Our results indicate that chronic vascular insufficiency and, possibly, insufficient Vegf-dependent neuroprotection lead to the select degeneration of motor neurons

Integrated care pathways for airway diseases (AIRWAYS-ICPs)

The objective of Integrated Care Pathways for Airway Diseases (AIRWAYS-ICPs) is to launch a collaboration to develop multi-sectoral care pathways for chronic respiratory diseases in European countries and regions. AIRWAYS-ICPs has strategic relevance to the European Union Health Strategy and will add value to existing public health knowledge by: 1) proposing a common framework of care pathways for chronic respiratory diseases, which will facilitate comparability and trans-national initiatives; 2) informing cost-effective policy development, strengthening in particular those on smoking and environmental exposure; 3) aiding risk stratification in chronic disease patients, using a common strategy; 4) having a significant impact on the health of citizens in the short term (reduction of morbidity, improvement of education in children and of work in adults) and in the long-term (healthy ageing); 5) proposing a common simulation tool to assist physicians; and 6) ultimately reducing the healthcare burden (emergency visits, avoidable hospitalisations, disability and costs) while improving quality of life. In the longer term, the incidence of disease may be reduced by innovative prevention strategies. AIRWAYSICPs was initiated by Area 5 of the Action Plan B3 of the European Innovation Partnership on Active and Healthy Ageing. All stakeholders are involved (health and social care, patients, and policy makers)