Structural and Optical Properties of Tin Doped Zinc Oxide Fibres Prepared By Electrospinning Technique

The study synthesized ZnO fibers using electrospinning technique. It also characterized and determined the effects of Sn2+ dopant on the optical properties of the fibers synthesized. This was with a view to exploring the potential of improving the performance ZnO semiconductor material in industrial applications. Polyvinyl Alcohol (PVA) solution was prepared and mixed with ZnO source. Zinc acetate was used as the ZnO source while Tin Acetate was used as Sn2+ dopant source. Viscous electrospinning solutions of PVA/Zinc Acetate and three different compositions of Tin Acetate were prepared. The compositions of dopants used were 5, 7 and 9-wt. %. Samples of the depositions from the electrospinning process were annealed at 600o C at a rate of 4o C per minute for 6 hours. Scanning electron microscopy (SEM) was employed to reveal the morphology of the depositions. The structural analysis of the fibers was carried out using x-ray diffractometry (XRD) while the optical properties of the fibers were investigated using ultra violet visible spectrophotometry. The SEM results showed the depositions to be web of fibers. The XRD confirmed the crystallization of undoped and doped ZnO fibers from the acetates. The crystal sizes of the fibers were in the range of 5.566 to 7.202 nm. Furthermore, wide bandgap energy values ranging from 3.26 to 3.46 eV were obtained from the results of the optical properties of the fibers. The results showed that the average crystal sizes of Sn2+ doped ZnO fibers were larger than those of the undoped fibers. However, it was observed that the average crystal size decreases with increase in Sn2+ content. The results also showed that the bandgap energy values of the fibers increase with dopant concentration. The study established the viability of fabricating doped and undoped ZnO structure in form of fibers in order to enhance its performance in industrial applications. Also, the results showed that the optical properties of the fibers improved with increase in Sn2+ dopant concentration. Keywords: ZnO fibers; Electrospinning technique; Structural analysis; Optical properties;  Sn2+ Dopant; Band gap energy value; Crystal siz

Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials

Summary Background The vascular and gastrointestinal eff ects of non-steroidal anti-infl ammatory drugs (NSAIDs), including selective COX-2 inhibitors (coxibs) and traditional non-steroidal anti-infl ammatory drugs (tNSAIDs), are not well characterised, particularly in patients at increased risk of vascular disease. We aimed to provide such information through meta-analyses of randomised trials. Methods We undertook meta-analyses of 280 trials of NSAIDs versus placebo (124 513 participants, 68 342 personyears) and 474 trials of one NSAID versus another NSAID (229 296 participants, 165 456 person-years). The main outcomes were major vascular events (non-fatal myocardial in farction, non-fatal stroke, or vascular death); major coronary events (non-fatal myocardial infarction or coronary death); stroke; mortality; heart failure; and upper gastrointestinal complications (perforation, ob struction, or bleed). Findings Major vascular events were increased by about a third by a coxib (rate ratio [RR] 1·37, 95% CI 1·14-1·66; p=0·0009) or diclofenac (1·41, 1·12-1·78; p=0·0036), chiefl y due to an increase in major coronary events (coxibs 1·76, 1·31-2·37; p=0·0001; diclofenac 1·70, 1·19-2·41; p=0·0032). Ibuprofen also signifi cantly increased major coronary events (2·22, 1·10-4·48; p=0·0253), but not major vascular events (1·44, 0·89-2·33). Compared with placebo, of 1000 patients allocated to a coxib or diclofenac for a year, three more had major vascular events, one of which was fatal. Naproxen did not signifi cantly increase major vascular events (0·93, 0·69-1·27). Vascular death was increased signifi cantly by coxibs (1·58, 99% CI 1·00-2·49; p=0·0103) and diclofenac (1·65, 0·95-2·85, p=0·0187), nonsignifi cantly by ibuprofen (1·90, 0·56-6·41; p=0·17), but not by naproxen (1·08, 0·48-2·47, p=0·80). The proportional eff ects on major vascular events were independent of baseline characteristics, including vascular risk. Heart failure risk was roughly doubled by all NSAIDs. All NSAID regimens increased upper gastrointestinal complications (coxibs 1·81, 1·17-2·81, p=0·0070; diclofenac 1·89, 1·16-3·09, p=0·0106; ibuprofen 3·97, 2·22-7·10, p<0·0001; and naproxen 4·22, 2·71-6·56, p<0·0001). Interpretation The vascular risks of high-dose diclofenac, and possibly ibuprofen, are comparable to coxibs, whereas high-dose naproxen is associated with less vascular risk than other NSAIDs. Although NSAIDs increase vascular and gastrointestinal risks, the size of these risks can be predicted, which could help guide clinical decision making. Funding UK Medical Research Council and British Heart Foundation. Introduction Non-steroidal anti-infl ammatory drugs (NSAIDs) are among the most widely used drugs in the world. They are chiefl y used to treat pain, but their long-term use is limited by serious gastrointestinal side-eff ects. NSAIDs inhibit the two recognised forms of prostaglandin G/H synthase (also referred to as cyclo-oxygenase [COX]), namely COX-1 and COX-2. 1 Since the analgesic and antiinfl ammatory eff ects of NSAIDs are mediated by inhibition of COX-2, and their gastrointestinal side eff ects mostly by inhibition of COX-1, NSAIDs which selectively inhibit COX-2 might reduce the risk of gastrointestinal toxicity compared with other NSAIDs. Several such COX-2 selective drugs (collectively known as coxibs) were developed in the 1990s, and early trials comparing coxibs versus traditional NSAIDs (tNSAIDS) seemed to confi rm that coxibs at doses with similar analgesic effi cacy had less gastrointestinal toxicity. 2,3 Unfortunately, however, subsequent placebo-controlled trials also showed unequivocally that coxibs were associated with an increased risk of atherothrombotic vascular events. 4,5 Soon after these placebo-controlled trials were reported, a meta-analysis of randomised trials comparing a coxib versus placebo or a coxib versus tNSAID indicated that some tNSAIDs might also have adverse eff ects on atherothrombotic events, but that these hazards might depend on the degree and duration of suppression of platelet COX-1