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 Algae , 2012, Abstract: We report an oxidative burst triggered by prostaglandin A2 (PGA2) in the brown algal kelp Laminaria digitata, constituting the first such discovery in an alga and the second finding of an oxidative burst triggered by a prostaglandin in a living organism. The response is more powerful than the oxidative burst triggered by most other chemical elicitors in Laminaria. Also, it is dose-dependent and cannot be inhibited by diphenylene iodonium, suggesting that another source than NAD(P)H oxidase is operational in the production of reactive oxygen species. Despite the very strong oxidative response, rather few effects at other levels of signal transduction pathways could be identified. PGA2 does not increase lipolysis (free fatty acids) in Laminaria, and only one oxylipin (15-hydroxyeicosatetraenoic acid; 15-HETE) was found to be upregulated in Laminaria. In a subsequent set of experiments in the genome model Ectocarpus siliculosus, none of 5 selected candidate genes, all established participants in various stress responses, showed any significant differences in their expression profiles.
 Brazilian Journal of Biology , 2009, DOI: 10.1590/S1519-69842009000500018 Abstract: innate immune responses are useful to determine the health status of fish and to evaluate the effect of immunomodulatory substances in fish farming. leukocytes respiratory burst was measured in pacu (piaractus mesopotamicus) using chemiluminescence assay and nitroblue tetrazolium (nbt) reduction assay. the nitroblue tetrazolium reduction seemed more adequate than chemiluminescence assay for leukocytes oxidative burst determination, since it was difficult to isolate the blood leucocytes for chemiluminescence assay. plasma and serum lysozyme were measured using a turbidimetric assay. the heating of serum and plasma samples (56 oc for 30 minutes) for complement system inactivation darkened the plasma samples and interfered in the results. the lysozyme activity in serum was higher than in plasma, suggesting that serum samples are more appropriate for the analysis. this study established protocols that can be useful tools in the study of immune mechanisms of the tropical fish pacu.
 PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068963 Abstract: Besides secondary injury at the lesional site, Traumatic brain injury (TBI) can cause a systemic inflammatory response, which may cause damage to initially unaffected organs and potentially further exacerbate the original injury. Here we investigated plasma levels of important inflammatory mediators, oxidative activity of circulating leukocytes, particularly focusing on neutrophils, from TBI subjects and control subjects with general trauma from 6 hours to 2 weeks following injury, comparing with values from uninjured subjects. We observed increased plasma level of inflammatory cytokines/molecules TNF-α, IL-6 and CRP, dramatically increased circulating leukocyte counts and elevated expression of TNF-α and iNOS in circulating leukocytes from TBI patients, which suggests a systemic inflammatory response following TBI. Our data further showed increased free radical production in leukocyte homogenates and elevated expression of key oxidative enzymes iNOS, COX-2 and NADPH oxidase (gp91phox) in circulating leukocytes, indicating an intense induction of oxidative burst following TBI, which is significantly greater than that in control subjects with general trauma. Furthermore, flow cytometry assay proved neutrophils as the largest population in circulation after TBI and showed significantly up-regulated oxidative activity and suppressed phagocytosis rate for circulating neutrophils following brain trauma. It suggests that the highly activated neutrophils might play an important role in the secondary damage, even outside the injured brain. Taken together, the potent systemic inflammatory response induced by TBI, especially the intensively increase oxidative activity of circulating leukocytes, mainly neutrophils, may lead to a systemic damage, dysfunction/damage of bystander tissues/organs and even further exacerbate secondary local damage. Controlling these pathophysiological processes may be a promising therapeutic strategy and will protect unaffected organs and the injured brain from the secondary damage.
 Chinese Science Bulletin , 2001, DOI: 10.1007/BF03187193 Abstract: The respiratory burst is an important physiological function of the neutrophils in killing the bacteria invading in human body. We used chemiluminescence method to measure the exogenous arachidonic acid-stimulated respiratory burst, and measured the cytosolic free calcium concentration in neutrophils by the fluorescence method. It was found that, on one hand, the arachidonic acid-stimulated respiratory burst was enhanced by elevating the cytosolic free calcium concentration in neutrophils with a potent endomembrane Ca2+-ATPase inhibitor, Thapsgargin; on the other hand, chelating the intracellular or extracellular calcium by EGTA or BAPTA inhibited the respiratory burst. Results showed that calcium plays an important regulatory role in the signaling pathway involved in the exogenous arachidonic acid-stimulated respiratory burst of neutrophils.
 科学通报(英文版) , 2001, Abstract: The respiratory burst is an important physiological function of the neutrophils in killing the bacteria invading in human body. We used chemiluminescence method to measure the exogenous arachidonic acid-stimulated respiratory burst, and measured the cytosolic free calcium concentration in neutrophils by the fluorescence method. It was found that, on one hand, the arachidonic acid-stimulated respiratory burst was enhanced by elevating the cytosolic free calcium concentration in neutrophils with a potent endomembrane Ca2+-ATPase inhibitor, Thapsgargin; on the other hand, chelating the intracellular or extracellular calcium by EGTA or BAPTA inhibited the respiratory burst. Results showed that calcium plays an important regulatory role in the signaling pathway involved in the exogenous arachidonic acid-stimulated respiratory burst of neutrophils.
 Physics , 1999, DOI: 10.1063/1.1361627 Abstract: The BeppoSAX Gamma Ray Burst Monitor (GRBM) is triggered any time a statistically significant counting excess is simultaneously revealed by at least two of its four independent detectors. Several spurious effects, including highly ionizing particles crossing two detectors, are recorded as onboard triggers. In fact, a large number of false triggers is detected, in the order of 10/day. A software code, based on an heuristic algorithm, was written to discriminate between real and false triggers. We present the results of the analysis on an homogeneous sample of GRBM triggers, thus providing an estimate of the efficiency of the GRB detection system consisting of the GRBM and the software.
 PLOS Pathogens , 2012, DOI: 10.1371/journal.ppat.1002713 Abstract: In order to establish infections within the mammalian host, pathogens must protect themselves against toxic reactive oxygen species produced by phagocytes of the immune system. The fungal pathogen Histoplasma capsulatum infects both neutrophils and macrophages but the mechanisms enabling Histoplasma yeasts to survive in these phagocytes have not been fully elucidated. We show that Histoplasma yeasts produce a superoxide dismutase (Sod3) and direct it to the extracellular environment via N-terminal and C-terminal signals which promote its secretion and association with the yeast cell surface. This localization permits Sod3 to protect yeasts specifically from exogenous superoxide whereas amelioration of endogenous reactive oxygen depends on intracellular dismutases such as Sod1. While infection of resting macrophages by Histoplasma does not stimulate the phagocyte oxidative burst, interaction with polymorphonuclear leukocytes (PMNs) and cytokine-activated macrophages triggers production of reactive oxygen species (ROS). Histoplasma yeasts producing Sod3 survive co-incubation with these phagocytes but yeasts lacking Sod3 are rapidly eliminated through oxidative killing similar to the effect of phagocytes on Candida albicans yeasts. The protection provided by Sod3 against host-derived ROS extends in vivo. Without Sod3, Histoplasma yeasts are attenuated in their ability to establish respiratory infections and are rapidly cleared with the onset of adaptive immunity. The virulence of Sod3-deficient yeasts is restored in murine hosts unable to produce superoxide due to loss of the NADPH-oxidase function. These results demonstrate that phagocyte-produced ROS contributes to the immune response to Histoplasma and that Sod3 facilitates Histoplasma pathogenesis by detoxifying host-derived reactive oxygen thereby enabling Histoplasma survival.
 Physics , 1998, DOI: 10.1016/S1384-1076(99)00013-5 Abstract: A wide range of mechanisms have been proposed to supply the energy for gamma-ray bursts (GRB) at cosmological distances. It is a common misconception that some of these, notably NS-NS mergers, cannot meet the energy requirements suggested by recent observations. We show here that GRB energies, even at the most distant redshifts detected, are compatible with current binary merger or collapse scenarios involving compact objects. This is especially so if, as expected, there is a moderate amount of beaming, since current observations constrain the energy per solid angle much more strongly and directly than the total energy. All plausible progenitors, ranging from NS-NS mergers to various hypernova-like scenarios, eventually lead to the formation of a black hole with a debris torus around it, so that the extractable energy is of the same order, 1E+54 ergs, in all cases. MHD conversion of gravitational into kinetic and radiation energy can significantly increase the probability of observing large photon fluxes, although significant collimation may achieve the same effect with neutrino annihilation in short bursts. The lifetime of the debris torus is dictated by a variety of physical processes, such as viscous accretion and various instabilities; these mechanisms dominate at different stages in the evolution of the torus and provide for a range of gamma-ray burst lifetimes.
 Physics , 2009, Abstract: There is a difference between the solar ionization concentration in the ionosphere in the daytime and at night-time. At night the E-region ion concentration peak is dramatically reduced due to chemical losses and the rapid change in the vertical polarization electric field at the time around sunset, which is due to the accelerating neutral wind dynamo and which produces a corresponding change in the zonal electric field through curl-free requirements. The result is the formation of a layer of high conductivity, at the daytime-night-time interface. This phenomenon in the South Atlantic Anomaly (SAA) area, provokes an increase in the precipitation of charge particles which is well known and is commonly termed "sunset enhancement". In the following we show five gamma ray burst (GRB) triggers observed by spacecraft GRB detectors in temporal coincidence with muon enhancement observed at ground level by the Tupi telescopes with two different orientations at $\sim 21$ UT (local sunset), and located inside the SAA region. Of these GRB triggers analyzed here, one from Swift, and two from Fermi are probably noise triggers, produced by omni-directional particle precipitation, during the sunset enhancements.
 Physics , 2007, DOI: 10.1103/PhysRevD.76.042004 Abstract: We present a robust strategy to \emph{veto} certain classes of instrumental glitches that appear at the output of interferometric gravitational-wave (GW) detectors.This veto method is physical' in the sense that, in order to veto a burst trigger, we make use of our knowledge of the coupling of different detector subsystems to the main detector output. The main idea behind this method is that the noise in an instrumental channel X can be \emph{transferred} to the detector output (channel H) using the \emph{transfer function} from X to H, provided the noise coupling is \emph{linear} and the transfer function is \emph{unique}. If a non-stationarity in channel H is causally related to one in channel X, the two have to be consistent with the transfer function. We formulate two methods for testing the consistency between the burst triggers in channel X and channel H. One method makes use of the \emph{null-stream} constructed from channel H and the \emph{transferred} channel X, and the second involves cross-correlating the two. We demonstrate the efficiency of the veto by injecting' instrumental glitches in the hardware of the GEO 600 detector. The \emph{veto safety} is demonstrated by performing GW-like hardware injections. We also show an example application of this method using 5 days of data from the fifth science run of GEO 600. The method is found to have very high veto efficiency with a very low accidental veto rate.
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