http://hdl.handle.net/2440/10017 Search the Channel search http://digital.library.adelaide.edu.au/dspace/simple-search http://hdl.handle.net/2440/52578 Title: Systematic review of endovenous laser therapy versus surgery for the treatment of saphenous varicose veins <br/> <br/>Author: Hoggan, Benjamin Lee; Cameron, Alun; Maddern, Guy John <br/> <br/>Abstract: This systematic review compares the safety and efficacy of endovenous laser therapy (ELT) and surgery involving saphenous ligation and stripping as treatments for varicose veins. Systematic searches of medical bibliographic databases, the Internet and lists of references were conducted in August 2007 and April 2008 to identify relevant primary studies. Inclusion of papers was resolved through application of a predetermined protocol. Information on the safety and effectiveness of ELT and surgery was analyzed. Fifty-nine studies were included, with seven studies directly comparing ELT with surgery. Serious adverse events after ELT or surgery were rare. While occurrence rates of some minor adverse events appeared higher after ELT in collated data, comparative studies commonly favored ELT over surgery. Few differences were apparent between treatments with respect to clinical effectiveness outcomes, although long-term follow-up was lacking. Nonclinical effectiveness outcomes generally favored ELT over surgery in the first 2 months after treatment. ELT appears to be at least as safe as surgery. While ELT offers short-term benefits and appears to be as clinically effective as surgery up to 12 months after treatment, clinical trials with a minimum of 3 years of follow-up are required to establish the enduring effectiveness of ELT. Wed, 29 Oct 2008 22:58:59 GMT http://hdl.handle.net/2440/49017 Title: Tissue nitrosothiol levels in acute ulcerative colitis A step in disease induction? <br/> <br/>Author: Roediger, W. E. W.; Cummins, Adrian Gerard; Cowled, Prudence Anne <br/> <br/>Abstract: Background and aims: Production of luminal nitric oxide (NO) in the colon is significantly increased in ulcerative colitis (UC) due to bacterial metabolism or activated immune cells. The effect on tissues of prolonged elevation of nitric oxide is unknown. Formation of nitrosothiols has been discounted as these occur under acidic conditions which nevertheless may prevail in acute colitis. The aim was to measure nitrosothiol formation in colonocytes in acute colitis as well as to assess nitrosation of CoA in vitro. Materials and methods: Fresh rectal biopsies obtained at colonoscopies of cases with acute colitis, newly diagnosed or after recurrent attacks, were analysed. Exposure to glutaraldehyde/formaldehyde was avoided and samples stored in the dark at −80 °C. After mechanical homogenization nitrosothiols were measured with the Saville-Griess reaction with and without exposure to mercuric chloride. The reaction with sulphanilamide was measured at 540 nm after azo dye coupling. By calibration curves with GSNO and tissue protein measurement (Bradford reaction) results were expressed as nmoles/mg protein. Purified samples of CoA were obtained for UV spectroscopic analysis after exposure to nitrite or sodium sulphide. Results: Nitrosothiols were not measureable in tissues exposed to formaldehyde. Nitrosothiol levels were 129.3 ± 25.6 (n = 6) in acute UC compared with healthy controls of 53.2 ± 13.8 (n = 6) (p &lt; 0.02). Nitrosothiols of CoA were measureable at acidic pH (2.0) and increased by the presence of sodium sulphide (0.5 mM). Nitroso-CoA formation to a lesser degree occurred at higher pH (6.9) but amplification with sulphide was not clearly identified. Conclusions: Elevated tissue nitrosothiols are found in association with acute colitis. As both CoA and glutathione are known to be depleted in UC, results suggest that these agents could be diminished by nitrosothiol formation. <br/> <br/>Description: Copyright © 2008 Published by Elsevier Inc. Mon, 29 Oct 2007 22:58:59 GMT http://hdl.handle.net/2440/49010 Title: Nitric oxide from dysbiotic nitrate respiration of anaerobic bacteria initiates human ulcerative colitis <br/> <br/>Author: Roediger, W. E. W. <br/> <br/>Abstract: Introduction: Factors initiating human ulcerative colitis (UC) are unknown. Dysbiosis of bacteria has been proposed to initiate UC but to date neither the nature of dysbiosis nor mucosal breakdown has been explained. Method: To assess whether a dysbiosis of anaerobic nitrate respiration could explain the microscopic, biochemical and functional changes observed in colonocytes of ulcerative colitis by measuring the effect of NO on human colonocytes and observing colonic NO production. Results: Anaerobic nitrate respiration yields nitrite, nitric oxide (NO) and nitrous oxide. Colonic bacteria produce NO and UC in remission has a higher luminal NO level than control cases. NO with sulphide but not NO alone impairs lipid and protein synthesis of epithelial cells explaining the membrane, tight junctional, ion channel and beta oxidation changes observed in colonocytes of UC. The observations complement therapeutic mechanisms of those probiotics, prebiotics and antibiotics useful in treating UC. Conclusions: The prolonged production of bacterial NO with sulphide can explain the initiation and barrier breakdown which is central to the pathogenesis of UC. Therapies to alter bacterial nitrate respiration and NO production in pouchitis and human UC need to evolve. <br/> <br/>Description: Copyright © 2008 Published by Elsevier Inc. Mon, 29 Oct 2007 22:58:59 GMT http://hdl.handle.net/2440/49009 Title: Platelet nitric oxide resistance: Pathogenesis and clinical implications <br/> <br/>Author: Chirkov, Yuliy; Horowitz, John D. <br/> <br/>Abstract: Platelet hyperaggregability and associated thrombosis have been documented in a number of cardiovascular diseases. Nitric oxide (NO), via activation of soluble guanylate cyclase, plays an important role in platelet physiology, providing a negative control over platelet aggregation. Endogenous NO is not only of the endothelial source, it is also released from activated platelets. Our extensive studies in patients with angina pectoris, chronic heart failure, diabetes and various cardiovascular risk factors have demonstrated that platelets from these subjects exhibit reduced responsiveness to the anti-aggregating efficacy of NO donors. We have termed this phenomenon “platelet NO resistance”. It results largely from a combination of “scavenging” of NO by superoxide anion radical and inactivation of platelet guanylate cyclase. NO resistance has been also documented in vasculature and is usually paralleled by endothelial dysfunction. In view of the physiological interactions between platelets and the endothelium, impaired responsiveness to NO can be viewed as a mediator of the pathological impact of oxidative stress on hemostasis, with resultant thrombosis in both coronary and peripheral arteries, and increased risk of ischemic events. Furthermore, NO resistance accounts for reduced pharmaco-activity of NO donors used in clinical practice, e.g., organic nitrates. Impaired NO responsiveness creates a potential problem, that ischemic patients, who are in greatest need of nitrate therapy, are least likely to respond. NO resistance may also be a prognostic tool; patients with impaired platelet responsiveness to NO have a significantly higher cardiovascular morbidity and mortality, compared to patients with preserved NO responsiveness. NO resistance is a potential target for pharmacological interventions. We have shown that a number of agents (ACE inhibitors, perhexiline, insulin and statins) ameliorate NO resistance and may exert their beneficial clinical effects partially by enhancing platelet and vascular NO responsiveness. Identification of patients with NO resistance might constitute a means for improved therapeutic decision-making. Mon, 29 Oct 2007 22:58:59 GMT