Publications

Purpose This paper aims to review the effect of using recycled aggregates (RA) on the properties of recycled aggregate concrete (RAC) following the steady rise in global demand for concrete and the large generation of construction and demolition waste. Design/methodology/approach This study reviewed relevant literature of research work carried out by previous researchers, leading to a deeper understanding of the properties of both RA and RAC. The properties of RA and RAC reported in the various studies were then compared to their corresponding natural aggregate (NA) and natural aggregate concrete, as well as the specifications provided in different codes of practice. In addition, the mix design methods appropriate to RAC and the cost implication of using RA were reviewed. Findings Findings show that the contribution of RA to strength appears inferior in comparison to NA. The shortcoming is attributed to the mortar attached to the RA, which raises its water absorption capacity and lowers its density relative to those of NA. However, it has been reported that the use of regulated quantity of RA, new mixing and proportioning methods, the addition of admixtures and strengthening materials such as steel fibres, can improve both mechanical and durability properties of RAC. Cost evaluation also showed that some savings can be realized by using RA instead of NA. Originality/value This research serves as a guide for future works and suggests that the use of RA as aggregate in new concrete is technically possible, depending on the mix design method adopted.

Background Mesenchymal precursor cells (MPC) are cells that exerted cardio-protective, anti-remodeling, and pro-angiogenic actions in pre-clinical models of acute myocardial infarction (AMI). They ...

Objectives We sought to compare long-term outcomes after coronary bypass surgery with and without an internal thoracic artery graft. Methods We analyzed clinical outcomes over a median follow-up of 6.7 years among 3,087 patients who received coronary bypass surgery as participants in one of 8 clinical trials comparing surgical intervention with angioplasty. We used 2 statistical methods (covariate adjustment and propensity score matching) to adjust for the nonrandomized selection of internal thoracic artery grafts. Results Internal thoracic artery grafting was associated with lower mortality, with hazard ratios of 0.77 (confidence interval, 0.62–0.97; P = .02) for covariate adjustment and 0.77 (confidence interval, 0.57–1.05; P = .10) for propensity score matching. The composite end point of death or myocardial infarction was reduced to a similar extent, with hazard ratios of 0.83 (confidence interval, 0.69–1.00; P = .05) for covariate adjustment to 0.78 (confidence interval, 0.61–1.00; P = .05) for propensity score matching. There was a trend toward less angina at 1 year, with odds ratios of 0.81 (confidence interval, 0.61–1.09; P = .16) in the covariate-adjusted model and 0.81 (confidence interval, 0.55–1.19; P = .28) in the propensity score–adjusted model. Conclusions Use of an internal thoracic artery graft during coronary bypass surgery seems to improve long-term clinical outcomes.

The stunned myocardium has recently become the focus of considerable interest because of its potential role in negating the benefits of reperfusion. A critical but still unresolved issue relates to the mechanism responsible for this contractile abnormality. In recent years an increasing number of studies have provided indirect evidence that postischemic myocardial dysfunction may be mediated in part by the generation of reactive oxygen species, such as superoxide radical, hydrogen peroxide and hydroxyl radical. These oxygen-free radicals could arise from various sources, such as hypoxanthine conversion by xanthine oxidase, catecholamine degradation and mitochondrial electron transport. Direct evidence of injury by free radicals has yet to be shown in the human heart, but many studies of other mammals have linked reactive oxygen metabolites with myocardial injury.1–5 During myocardial ischemia, xanthine dehydrogenase (which appears to be located in the endothelial cells)6 is converted to xanthine oxidase, an enzyme that produces superoxide radical, hydrogen peroxide and uric acid from hypoxanthine or xanthine and molecular oxygen.7 At the same time, ischemia is associated with rapid catabolism of adenosine triphosphate.7 This degradation of adenosine triphosphate causes an efflux of breakdown products that are able to pass through the cell membrane, resulting in an accumulation of hypoxanthine, 1 of 2 substrates for xanthine oxidase. The other substrate (molecular oxygen) is provided by reperfusion, which results in a burst of free-radical generation. 8 These free radicals initiate chain reactions causing peroxidative breakdown of polyunsaturated fatty acids in the membrane bilayer.9–12 The interaction among oxygen-free radicals with polyunsaturated fatty acids has been described as lipid peroxidation and can be measured by formation of malondialdehyde. Until recently, the assessment of alterations in myocardial metabolism in humans early after short and repetitive occlusions of a major coronary artery has not been feasible. However, percutaneous transluminal coronary angioplasty provides a unique opportunity to study the time course of these metabolic changes during transient interruption of coronary flow by the balloon-occlusion sequence in patients with 1-vessel disease and without angiographically demonstrable collateral circulation.13–16 In this report we studied the production of hypoxanthine, urate and malondialdehyde during percutaneous transluminal coronary angioplasty.

We assessed predictors of long-term outcomes after coronary artery bypass grafting (CABG) versus those after percutaneous coronary intervention (PCI) with drug-eluting stents (DES) in 3,230 patients with left main or multivessel coronary artery disease (CAD).Data were pooled from the BEST, PRECOMBAT, and SYNTAX trials. Age, chronic kidney disease, chronic obstructive lung disease, left ventricular dysfunction, and peripheral arterial disease (PAD) were common predictors of all-cause mortality. Diabetes mellitus, previous myocardial infarction (MI), and SYNTAX score were independent predictors of all-cause mortality in the PCI group, but not in the CABG group. In the CABG group, age was the only risk factor for MI; left ventricular dysfunction, hypertension, and PAD were risk factors for stroke. On the other hand, in the PCI group, incomplete revascularization and previous MI were risk factors for MI; age and previous stroke for stroke. In addition, chronic kidney disease significantly correlated with a composite outcome of death, MI, or stroke in the CABG group, and incomplete revascularization and previous MI in the PCI group.Simple clinical variables and SYNTAX score differentially predict long-term outcomes after CABG versus those after PCI with DES for left main or multivessel CAD. Those predictors might help to guide the choice of revascularization strategy. © 2017 Wiley Periodicals, Inc.

No abstract is provided for this article.

We studied the neural control of goblet cell secretion in the lower airways of anesthetized guinea pigs using a semiquantitative morphometric technique. The magnitude of discharge of intracellular mucus was determined in histological sections of the trachea and main bronchi stained for mucus glycoproteins. Bilateral electrical stimulation of the cervical vagus nerves induced goblet cell secretion. The magnitude of the effect was dependent on the frequency, voltage, and pulse width of the stimulus, and the duration of stimulation. At 10 Hz, 5 V, and 5 ms for 3 min, there was a 62% decrease in the amount of intracellular mucus below that with sham stimulation. The secretion was blocked either by atropine or by pretreatment with capsaicin but was not significantly inhibited by idazoxan, an alpha-adrenoceptor antagonist. The magnitude of goblet cell discharge in animals pretreated with propranolol was intermediate between that in controls and that with nerve stimulation, although not significant to either. These results demonstrate that goblet cell secretion is under neural control in guinea pig airways and suggest that cholinergic, nonadrenergic-noncholinergic, and possibly adrenergic neural pathways, may contribute to the secretion.