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Presented as an electronic poster in the 17th European Cataract and Refractive Surgery Society winter meeting (Warsow 2013)., The purpose of this study is to measure the impact of tamsulosin intake on five postoperative cataract surgery complications (toxic anterior segment syndrome, rebound uveitis, retinal detachment, macular edema, and postoperative endophthalmitis). This retrospective cohort study was conducted at University Hospital of Henares. The study included 660-eyes of 660 patients submitted to cataract surgery at the ophthalmology unit of Hospital del Henares (Madrid) between 2 March 2009 and 28 February 2010. Extracapsular cataract extraction, combined glaucoma and cataract surgery phacovitrectomy, posterior capsule rupture and zonular damage were considered exclusion criteria. Clinical charts were reviewed during July 2012. Patients were divided in two groups (exposed and non-exposed to tamsulosin). Cumulative incidence of toxic anterior segment syndrome, rebound uveitis, retinal detachment, macular edema and postoperative endophthalmitis were compared in both groups. Rebound uveitis (relative risk [RR] 3.39; confidence interval [CI] 1.63–7.08) and macular edema (RR 4.15; CI 1.06–16.22) were more common in the tamsulosin-exposed group. Retinal detachment had a similar incidence in both groups. We observed no cases of endophthalmitis or toxic anterior segment syndrome in either of the two groups. Tamsulosin exposure in this cohort was associated with a higher risk of rebound uveitis and macular edema but the other three studied postoperative complications had a similar incidence in both groups., Depto. de Optometría y Visión, Fac. de Óptica y Optometría, TRUE, pub

Presented as an electronic poster in the 17th European Cataract and Refractive Surgery Society winter meeting (Warsow 2013)., The purpose of this study is to measure the impact of tamsulosin intake on five postoperative cataract surgery complications (toxic anterior segment syndrome, rebound uveitis, retinal detachment, macular edema, and postoperative endophthalmitis). This retrospective cohort study was conducted at University Hospital of Henares. The study included 660-eyes of 660 patients submitted to cataract surgery at the ophthalmology unit of Hospital del Henares (Madrid) between 2 March 2009 and 28 February 2010. Extracapsular cataract extraction, combined glaucoma and cataract surgery phacovitrectomy, posterior capsule rupture and zonular damage were considered exclusion criteria. Clinical charts were reviewed during July 2012. Patients were divided in two groups (exposed and non-exposed to tamsulosin). Cumulative incidence of toxic anterior segment syndrome, rebound uveitis, retinal detachment, macular edema and postoperative endophthalmitis were compared in both groups. Rebound uveitis (relative risk [RR] 3.39; confidence interval [CI] 1.63–7.08) and macular edema (RR 4.15; CI 1.06–16.22) were more common in the tamsulosin-exposed group. Retinal detachment had a similar incidence in both groups. We observed no cases of endophthalmitis or toxic anterior segment syndrome in either of the two groups. Tamsulosin exposure in this cohort was associated with a higher risk of rebound uveitis and macular edema but the other three studied postoperative complications had a similar incidence in both groups., Depto. de Optometría y Visión, Fac. de Óptica y Optometría, TRUE, pub

Excess post-exercise oxygen consumption (EPOC), once known as 'oxygen debt,' has been well documented in a wide variety of organisms. There are many factors implicated as responsible for EPOC. These include elevated lactate and hormone levels, depressed glycogen concentrations, increased body temperature (in endotherms), increased ventilation and heart rate, decreased phosphagen levels, and depressed oxygen concentrations in hemoglobin and myoglobin. Both the intensity and duration of exercise have been found to influence the length and magnitude of EPOC. Most of the previous research done on EPOC has focused on long duration, sustainable locomotion. For many animals, exercise of short duration is more ecologically relevant, yet little is known about EPOC under these conditions. There were three purposes for this study. First, I have focused on determining the influence of exercise duration on EPOC for short, (<= 60 seconds) maximal burst locomotion in the desert iguana, Dipsosaurus dorsalis. I have found that the length and magnitude of EPOC is positively affected by sprint duration. Secondly, I investigated the relationship between the adrenal hormones, epinephrine and norepinephrine, and EPOC. These hormones are known to elevate recovery metabolism and previous research has revealed that these hormones are increased in D. dorsalis following five minutes of treadmill exercise. I have found that administration of the alpha-blocker, phentolamine, and the beta-blocker, propranolol, prior to treadmill exercise significantly reduces EPOC duration and magnitude below saline injected control values. A third purpose of this research was to establish the energetic cost of non-sustainable transport, C(ns), for these animals.

Introduction Significant developments have been made in the treatment and prevention of cancer. Despite these developments, a third of the population of the UK will get cancer in their lifetime and a quarter of the population are likely to die from it, making it a leading cause of death in the UK[1, 2]. There is an increase in the numbers of cancers being largely driven by the ageing and expanding population.[2, 3]Conventional anti-cancer and anti-metastatic approaches such as chemotherapy and radiotherapy are effective because these approaches mostly inhibit cell division in proliferating cancer cells or make the tissue environment hostile to cancer cell growth and migration. However, the non-selectiveness of these approaches often causes serious side effects leading to the damage of healthy tissue. Significant gains have been made through the development of targeted therapies and early detection with the benefit of personalising medicine for a specific target thereby minimising harm. However, there is a problem of drug resistance in about 50% of patients with these forms of treatment. Progress in developing these treatments for disease remain slow, with traditional approaches inadequate and rational new therapies needed to tackle cancer. As a result, an alternative strategy for drug development such as using previously approved drugs for new medical indications is beginning to be explored.[4] This strategy will potentially remove substantial risks, costs and time from the pathway of drug development.[4] Recent evidence has shown the potential anti-neoplastic effects of some cheaper and safer medications. Among the best examples of this is the near 50% reduction in cancer specific mortality from colorectal cancer recently shown in those starting Aspirin after diagnosis[5], which has already led to a randomised controlled trial.[6] In vitro and in vivo studies suggest a role for beta blockers and alpha blockers in inhibiting the proliferation and migration of cancer