EVALUATION OF A FOAM BUFFER TARGET DESIGN FOR SPATIALLY UNIFORM ABLATION OF LASER-IRRADIATED PLASMAS

Experimental observations are presented demonstrating that the use of a gold-coated foam layer on the surface of a laser-driven target substantially reduces its hydrodynamic breakup during the acceleration phase. The data suggest that this results from enhanced thermal smoothing during the early-time imprint stage of the interaction. The target's kinetic energy and the level of parametric instability growth are shown to remain essentially unchanged from that of a conventionally driven target.

Efficacy and mechanism of hypoxic postconditioning in salvage of ex vivo human rectus abdominis muscle from hypoxia/reoxygenation injury

In reconstructive surgery, skeletal muscle may endure protracted ischemia before reperfusion, which can lead to significant ischemia/reperfusion injury. Ischemic postconditioning induced by brief cycles of reperfusion/reocclusion at the end of ischemia has been shown to salvage skeletal muscle from ischemia/reperfusion injury in several animal models. However, ischemic postconditioning has not been confirmed in human skeletal muscle. Using an established in vitro human skeletal muscle hypoxic conditioning model, we tested our hypothesis that hypoxic postconditioning salvages ex vivo human skeletal muscle from hypoxia/reoxygenation injury and the mechanism involves inhibition of opening of the mitochondrial permeability transition pore (mPTP) and preservation of ATP synthesis. Muscle strips (~0.5×0.5×15mm) from human rectus abdominis muscle biopsies were cultured in Krebs-Henseleit-HEPES buffer, bubbled with 95%N(2)/5%CO(2) (hypoxia) or 95%O(2)/5%CO(2) (reoxygenation). Samples were subjected to 3h hypoxia/2h reoxygenation. Hypoxic postconditioning was induced by one or two cycles of 5min reoxygenation/5min hypoxia after 3h hypoxia. Muscle injury, viability and ATP synthesis after 2h of reoxygenation were assessed by measuring lactate dehydrogenase (LDH) release, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) reduction and ATP content, respectively. Hypoxic postconditioning or treatment with the mPTP-opening inhibitors Cyclosporine A (CsA, 5×10(-6)M) or N-Methyl-4-isoleucine Cyclosporine (NIM811, 5×10(-6)M) 10min before reoxygenation decreased LDH release, increased MTT reduction and increased muscle ATP content (n=7 patients; P

Development of an in vitro model for study of the efficacy of ischemic preconditioning in human skeletal muscle against ischemia-reperfusion injury

Ischemia-reperfusion (I/R) injury causes skeletal muscle infarction and ischemic preconditioning (IPC) augments ischemic tolerance in animal models. To date, this has not been demonstrated in human skeletal muscle. This study aimed to develop an in vitro model to investigate the efficacy of simulated IPC in human skeletal muscle. Human skeletal muscle strips were equilibrated in oxygenated Krebs-Henseleit-HEPES buffer (37 degrees C). Aerobic and reperfusion phases were simulated by normoxic incubation and reoxygenation, respectively. Ischemia was simulated by hypoxic incubation. Energy store, cell viability, and cellular injury were assessed using ATP, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT), and lactate dehydrogenase (LDH) assays, respectively. Morphological integrity was assessed using electron microscopy. Studies were designed to test stability of the preparation (n = 5-11) under normoxic incubation over 24 h; the effect of 1, 2, 3, 4, or 6 h hypoxia followed by 2 h of reoxygenation; and the protective effect of hypoxic preconditioning (HPC; 5 min of hypoxia/5 min of reoxygenation) before 3 h of hypoxia/2 h of reoxygenation. Over 24 h of normoxic incubation, muscle strips remained physiologically intact as assessed by MTT, ATP, and LDH assays. After 3 h of hypoxia/2 h of reoxygenation, MTT reduction levels declined to 50.1 +/- 5.5% (P <0.05). MTT reduction levels in HPC (82.3 +/- 10.8%) and normoxic control (81.3 +/- 10.2%) groups were similar and higher (P <0.05) than the 3 h of hypoxia/2 h of reoxygenation group (45.2 +/- 5.8%). Ultrastructural morphology was preserved in normoxic and HPC groups but not in the hypoxia/reoxygenation group. This is the first study to characterize a stable in vitro model of human skeletal muscle and to demonstrate a protective effect of HPC in human skeletal muscle against hypoxia/reoxygenation-induced injury.

Process of debonding in RC beams shear-strengthened with FRP U-strips or side strips

Reinforced concrete (RC) beams may be strengthened for shear using externally bonded fiber reinforced polymer (FRP) composites in the form of side bonding, U-jacketing or complete wrapping. The shear failure of almost all RC beams shear-strengthened with side bonded FRP and the majority of those strengthened with FRP U-jackets, is due to debonding of the FRP. The bond behavior between the externally-bonded FRP reinforcement (referred to as FRP strips for simplicity) and the concrete substrate therefore plays a crucial role in the failure process of these beams. Despite extensive research in the past decade, there is still a lack of understanding of how debonding of FRP strips in such a beam propagates and how the debonding process affects its shear behavior. This paper presents an analytical study on the progressive debonding of FRP strips in such strengthened beams. The complete debonding process is modeled and the contribution of the FRP strips to the shear capacity of the beam is quantified. The validity of the analytical solution is verified by comparing its predictions with numerical results from a finite element analysis. This analytical treatment represents a significant step forward in understanding how interaction between FRP strips, steel stirrups and concrete affects the shear resistance of RC beams shear-strengthened with FRP strips.

The principles and practice of interpreting cardiac rhythm strips: a seven-step model

This open learning zone article examines the cardiac cycle and the interpretation of cardiac rhythm strips. The article begins with a brief revision of related physiology followed by a description of normal sinus rhythm and the main cardiac rhythm abnormalities. The article concludes by providing easy to follow steps for use in the interpretation of cardiac rhythm strips with practice examples presented in the CPD task section.