Non-dipping pattern of nocturnal blood pressure in obstructive sleep apnea syndrome: possible role of oxidative stress and endothelin-1 precursor

There is growing evidence suggesting that obstructive sleep apnea OSA is linked to the occurrence of cardiovascular disorders. Lack of normal nocturnal dipping of blood pressure has also been considered a risk factor for the occurrence of cardiovascular disorders. Non-dipping has been described in patients with OSA and is attributed to autonomic dysfunction. However, the search for a causal link between OSA and cardiovascular disease is still underway. To evaluate the occurrence of non-dipping pattern of nocturnal blood pressure, and the possible role of oxidative stress and ET-1 precursor in patients with OSA. Thirty eight patients with OSA and fourteen normal control subjects were enrolled in this study and were subjected to history taking, clinical examination, early morning blood samplings for the measurement of serum malondialdehyde [MDA] and endothelin 1 precursor [ET-1 precursor]. All patients with OSA were subjected to full polysomnographic study and monitoring of nocturnal blood pressure changes. Nocturnal blood pressure measurement of all patients revealed that thirty six patients [94.7%] were non-dippers, 15 patients [39.5%] suffered from ischemic heart disease. Serum endothelin-1 precursor and serum malondialdehyde levels were significantly higher in patients with OSA than in the control group. The systolic blood pressure measured before sleep was also significantly higher in patients than in the control group. The Epworth sleepiness scale and the clinical apnea score were significantly higher in patients than in the control group. The high incidence of non-dipping pattern of nocturnal blood pressure in both normotensive and hypertensive patients with OSA may be considered a warning sign for the occurrence of cardiovascular complications in these patients. Both increased oxidative stress and ET-1 precursor may be among the causative factors responsible for the high prevalence of the non-dipping pattern through increasing sympathetic nervous system activity

Detection of cyclooxygenase-2 [COX-2] expression in non-small cell lung carcinoma. An immunohistochemical and computerized image analysis study

Lung cancer is the leading cause of cancer death all over the world. Evidence is accumulating to suggest that cyclooxygenase-2 [COX-2] is involved the pathogenesis and progression of some types of lung cancer. COX-2 is one of the novel targets under evaluation for non-small cell lung carcinoma [NSCLC] therapy and chemoprevention. The aim of the present study was to detect COX-2 expression in non-small cell lung carcinoma [NSCLC] and to determine its correlation with various clinic pathological parameters. The expression of COX-2 was assessed in 30 patients with NSCLC using immunohistochemistry, followed by quantitative assessment of the immunostaining using computerized image analysis. The present work was conducted on 30 patients with NSCLC: squamous cell carcinoma [15 patients], adenocarcinoma [10 patients], and undifferentiated large cell carcinoma [5 patients]. Overall, 70% of studied NSCLC expressed COX-2. 60% of squamous cell carcinoma [SCC], 80% of adenocarcinoma [ADC] and 80% of undifferentiated large cell carcinoma [ULCC] showed positive immunostaining for COX-2. No significant correlation was found between tumor histological type and each of frequency and degree of COX-2 expression [p=0.569 and p=0.094 respectively]. Though the expression of COX-2 increased with tumor grade, the relation between COX2 expression [both the frequency and degree of expression] and tumor grade was not significant [p=0.778 and p=0.247 respectively for SCC, and p=0.641 and p=0.067 respectively for ADC]. A statistically significant difference was found between node positive and node negative cases as regards the degree of COX2 expression [p=0.05]. No significant relationship was found between COX-2 expression and age and sex of patients, smoking and tumor stage. COX-2 is frequently overexpressed in NSCLC especially in adenocarcinoma and undifferentiated large cell carcinoma. Expression was higher in node-positive tumors and tended to increase with tumor grade, suggesting that COX-2 might play a role in the pathogenesis and/or progression of these tumors. COX-2 appears to be a potentially promising target for therapy and chemoprevention of NSCLC