Nitric oxide and endothelin-1,2 in actinic keratosis and basal cell carcinoma: changes in nitric oxide/endothelin ratio

Background Nitric oxide (NO) is an inorganic free radical gas which has cytostatic/cytotoxic actions in tumoral tissues, including gynecologic, breast, and colon cancer. Nitric oxide is also a multifunctional signaling molecule active in many cells of the body, including endothelial cells, macrophages, monocytes, hepatocytes, mast cells, osteoblasts, and astrocytes. Endothelin-1 (ET-1) is a 21-amino acid peptide that stimulates the proliferation of vascular smooth muscle cells, fibroblasts, and keratinocytes, and plays a role in the expression of proto-oncogenes (c-myc, c-fos), which precedes cell proliferation. Similar to NO, ET is secreted by different cell types, including macrophages, monocytes, hepatocytes, endothelial cells, vascular smooth muscle cells, and various tumor cells. Elevated ET-1 levels are observed in pulmonary, hepatocellular, and prostate cancers. Actinic keratosis (AK) and basal cell carcinoma (BCC) are common skin tumors with accentuated hyperkeratinization, hyperpigmentation, and keratinocyte proliferation

Relationship between corrected Timi frame count and collateral flow in patients with recent myocardial infarction

TIMI frame count (TFC) is a quantitative index of coronary now. Catheter based revascularization normalizes resistance to flow and in this condition collateral flow can be considered as an important factor in determining antegrade coronary flow. The aim of this study was to investigate the relationship between corrected TFC (CTFC) which was determined after mechanical recanalization of the infarct related artery (IRA) and collateral flow determined by intracoronary pressure measurement in patients with recent acute myocardial infarction (AMI) who underwent late stent implantation to the IRA

The effects of slow-release verapamil on blood pressure and cardiovascular system in essential hypertension

The study consisted of 26 patients (15 female, 11 male; mean age 43 ± 10 years) with mild to moderate essential hypertension (EH). They were followed for a 2-week washout period and then for another 2-week single-blind placebo phase. Four patients receiving placebo dropped out of the study. Patients qualified for active medication if their sitting diastolic blood pressures (BPs), the median of three readings, were between 95 and 115 mm Hg at the end of the placebo period. Slow-release verapamil 240 mg was given once or twice daily as the sole antihypertensive agent and was continued for 6 weeks. Two patients (9%) were excluded from the trial due to early side effects. A target diastolic BP of <90 mm Hg was obtained in the remaining 20 patients. At the end of the study, the mean value of sitting BP was reduced from an initial 170/103 (125) mm Hg to 130/81 (98) mm Hg (p < 0.001) and the mean standing BP was decreased from 167/103 (125) mm Hg to 130/81 (98) mm Hg (p < 0.001). The drug had no significant effects on the laboratory data, left ventricular performance as assessed by echocardiography and systolic time intervals, and the electrocardiogram parameters with the exception of PR prolongation (p < 0.05). Adverse effects were noted in only three patients (14%). We conclude that slow-release verapamil is an effective, safe, and well-tolerated drug in treating EH. © 1989 Raven Press, Ltd., New York

Relationship between collateral blood flow and microvascular perfusion after reperfused acute myocardial infarction

During acute Occlusion of an epicardial vessel collaterals preserve the microvascular perfusion and limit the extent of myocardial damage. Pressure-derived collateral flow index (CFIp) assessed by intracoronary pressure measurement allow us to quantify collateral vessel development. The angiographic myocardial blush (MB) scores, based on the contrast dye density and washout in the infarcted myocardium, provide important information about microvascular perfusion after acute myocardial infarction (AMI). In this stud), we assessed the microvascular perfusion with MB and studied the relation between CFIp in patients with AMI who treated with thrombolytic therapy and TIMI grade III] now restored in the infarct related artery (IRA)