Results Participants were allocated to vitamin D 3 vs. placebo in equal numbers; 82% were vitamin D insufficient at baseline. Vitamin D 3 supplementation did not influence time to first severe exacerbation (aHR 1.02, 95% CI 0.69-1.53, P = 0.91) or time to first URI (aHR 0.87, 95% CI 0.64-1.16, P = 0.34). The influence of vitamin D 3 on co-primary outcomes was not modified by baseline vitamin D status or genotype. Of 16 pre-specified secondary outcomes, only one showed a difference between arms: vitamin D supplementation induced a modest improvement in respiratory quality of life as evidenced by a reduction in mean total score for the St George's Respiratory Questionnaire at 2 months (-3.9 points, p = 0.005), 6 months (-3.7 points, p = 0.038) and 12 months (-3.3 points, p = 0.060). Conclusions Vitamin D 3 supplementation did not influence time to exacerbation or URI in a population of adults with ICS-treated asthma with a high prevalence of baseline vitamin D insufficiency. Introduction Severe Asthma, characterised by persistent symptoms despite maximal medical therapy, represents 5% of asthma cases. Bronchial Thermoplasty (BT) is a novel therapy, NICE approved for Severe Asthma patients uncontrolled despite step 4/5 of British Guideline on Asthma Management. BT delivers radiofrequency thermal energy to airways distal to the main-stem bronchi, permanently reducing airway smooth muscle mass. It is unknown whether treatment of smooth muscle hypertrophy impacts persistently upon systemic signs of allergic inflammation. Peripheral blood eosinophils (PBEs) are a marker of allergic inflammation in asthma. We asked: does BT modify signs of allergic inflammation as measured by PBEs and if so, does this effect persist over time? Method A retrospective review of 15 consecutive Severe Asthma cases treated with BT was performed. Serial PBEs measured before and up to 1 year after BT were compared. Blood eosino-phil levels taken peri-procedure were excluded from analysis due to standard protocol concomitant steroid therapy. For time to first detectable high PBE all available post-BT PBE levels were assessed. Results 13 patients had PBE data before and after BT, with an average of 9 and 12 serial PBE levels pre and post-BT respectively. Mean PBE 1 year pre-BT was 0.33 Â 10 9 /L falling to a mean of 0.16 Â 10 9 /L 1 year post-BT (p < 0.05) (see Figure). 9 of 13 patients had a fall in mean PBE, in 2 of 13 levels rouse and 1 of 13 mean PBEs were unchanged post-BT. In 6 patients who converted from normal to high PBE post-BT, average time to first high PBE (>0.4 Â 10 9 /L) was 7 months (range 1-13 months). In 5 patients (38%) PBE remained within normal range persistently post BT. Conclusion Severe Asthma patients undergoing BT had a significant reduction in average peripheral blood eosinophil levels from baseline. In over 1/3 of cases this effect was persistent 1 year post procedure. These findings support the concept that BT not only reduces asthma-associated smooth muscle hypertrophy but impacts upon systemic markers of allergic i...

The VA NSQIP methods and risk models in general and vascular surgery were fully applicable to PS hospitals. Thirty-day postoperative morbidity in PS hospitals was reduced with the implementation of the NSQIP.

(1) Cryopreserved platelet transfusions are superior to liquid-preserved platelets in reducing blood loss and the need for blood product transfusions after cardiopulmonary bypass. (2) The reduction in blood loss in the patients receiving cryopreserved platelet transfusions after cardiopulmonary bypass probably reflects improved in vivo hemostatic function of cryopreserved platelets. (3) Some in vitro measures of platelet quality (aggregation, pH, hypotonic stress) may not reflect in vivo quality of platelet transfusions after cardiopulmonary bypass, whereas other in vitro measures (platelet procoagulant activity and thromboxane) do.

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This new method extends the current preservation limit and avoids time-dependent ischemic injury, thereby allowing for distant procurement of donor organs.

The 24-h post-transfusion survival values of autologous RBC, measured by the 51 disodium chromate/99m technetium double isotope procedure, were not significantly different, whether the roller pump or the centrifugal pump was used in the extracorporeal circuit using membrane oxygenators during cardiopulmonary surgical procedures.

Isolated, isovolumic rat hearts, perfused by Krebs-Henseleit buffer at constant coronary flow rate, were used to explore the hypothesis that endogenous cardiac glutathione provides protection against myocardial dysfunction associated with short periods of ischemia. Experimental animals were depleted of cardiac glutathione to 35% of control levels by intraperitoneal injections of diethylmaleate (DEM). Left ventricular pressure, coronary perfusion pressure, and glutathione levels were measured in control and experimental hearts after 60 minutes of oxygenated perfusion and after 20 minutes of global, no-flow ischemia and 30 minutes of reperfusion. With each protocol, both control and glutathione-depleted hearts received either standard buffer or one supplemented with 2 mM glutathione. Recovery of systolic function after ischemia-reperfusion was impaired in DEM-treated hearts compared with controls. In addition, the rise in perfusion pressure and chamber stiffness was also greater in DEM-treated hearts compared with controls. Recovery in glutathione-depleted hearts was improved when the reperfusate was supplemented with glutathione. In addition, the supplemented reperfusate prevented the decrease in compliance and the increase in coronary perfusion pressure in the glutathione-depleted hearts. Ischemia-reperfusion alone were not associated with a significant alteration in myocardial glutathione levels. Prewashout myocardial levels of glutathione were elevated after reperfusion with glutathione-supplemented bulfer but fell to baseline levels after a short washout period. These studies demonstrate that endogenous glutathione is important in protection of myocardium from injury after ischemia-reperfusion, presumably by modifying levels of active oxygen intermediates. The smaller changes in left ventricular pressure and coronary resistance after administration of GSH probably reflects an extracellular mechanism because benefit is seen soon after reperfusion. (Circulation 1989;80:1449-1457 D uring oxidative metabolism, cells produce potentially toxic oxygen radicals for which both specific and nonspecific scavenging mechanisms are present. Recently, it has been suggested that hypoxia or ischemia, followed by reoxygenation or reperfusion, increases production of oxygen radical species.1-5Administration of exogenous quenchers of free radicals, such as superoxide dismutase (SOD), catalase or both, improve cardiac function and limit infarct size when administered after experimental global ischemia.6,7From the Cardiology Section,