Dynamic auroral storms on Saturn as observed by the Hubble Space Telescope.

We present observations of significant dynamics within two UV auroral storms observed on Saturn using the Hubble Space Telescope in April/May 2013. Specifically, we discuss bursts of auroral emission observed at the poleward boundary of a solar wind-induced auroral storm, propagating at ∼330% rigid corotation from near ∼01 h LT toward ∼08 h LT. We suggest that these are indicative of ongoing, bursty reconnection of lobe flux in the magnetotail, providing strong evidence that Saturn's auroral storms are caused by large-scale flux closure. We also discuss the later evolution of a similar storm and show that the emission maps to the trailing region of an energetic neutral atom enhancement. We thus identify the auroral form with the upward field-aligned continuity currents flowing into the associated partial ring current.

Decades-long changes of the interstellar wind through our solar system.

The journey of the Sun through the dynamically active local interstellar medium creates an evolving heliosphere environment. This motion drives a wind of interstellar material through the heliosphere that has been measured with Earth-orbiting and interplanetary spacecraft for 40 years. Recent results obtained by NASA's Interstellar Boundary Explorer mission during 2009-2010 suggest that neutral interstellar atoms flow into the solar system from a different direction than found previously. These prior measurements represent data collected from Ulysses and other spacecraft during 1992-2002 and a variety of older measurements acquired during 1972-1978. Consideration of all data types and their published results and uncertainties, over the three epochs of observations, indicates that the trend for the interstellar flow ecliptic longitude to increase linearly with time is statistically significant.

Water vapour jets inside the plume of gas leaving Enceladus.

A plume of water vapour escapes from fissures crossing the south polar region of the Saturnian moon Enceladus. Tidal deformation of a thin surface crust above an internal ocean could result in tensile and compressive stresses that would affect the width of the fissures; therefore, the quantity of water vapour released at different locations in Enceladus' eccentric orbit is a crucial measurement of tidal control of venting. Here we report observations of an occultation of a star by the plume on 24 October 2007 that revealed four high-density gas jets superimposed on the background plume. The gas jet positions coincide with those of dust jets reported elsewhere inside the plume. The maximum water column density in the plume is about twice the density reported earlier. The density ratio does not agree with predictions-we should have seen less water than was observed in 2005. The ratio of the jets' bulk vertical velocities to their thermal velocities is 1.5 +/- 0.2, which supports the hypothesis that the source of the plume is liquid water, with gas accelerated to supersonic velocity in nozzle-like channels.

Enceladus' water vapor plume.

The Cassini spacecraft flew close to Saturn's small moon Enceladus three times in 2005. Cassini's UltraViolet Imaging Spectrograph observed stellar occultations on two flybys and confirmed the existence, composition, and regionally confined nature of a water vapor plume in the south polar region of Enceladus. This plume provides an adequate amount of water to resupply losses from Saturn's E ring and to be the dominant source of the neutral OH and atomic oxygen that fill the Saturnian system.

Control of Jupiter's radio emission and aurorae by the solar wind.

Radio emissions from Jupiter provided the first evidence that this giant planet has a strong magnetic field and a large magnetosphere. Jupiter also has polar aurorae, which are similar in many respects to Earth's aurorae. The radio emissions are believed to be generated along the high-latitude magnetic field lines by the same electrons that produce the aurorae, and both the radio emission in the hectometric frequency range and the aurorae vary considerably. The origin of the variability, however, has been poorly understood. Here we report simultaneous observations using the Cassini and Galileo spacecraft of hectometric radio emissions and extreme ultraviolet auroral emissions from Jupiter. Our results show that both of these emissions are triggered by interplanetary shocks propagating outward from the Sun. When such a shock arrives at Jupiter, it seems to cause a major compression and reconfiguration of the magnetosphere, which produces strong electric fields and therefore electron acceleration along the auroral field lines, similar to the processes that occur during geomagnetic storms at the Earth.

Ultraviolet emissions from the magnetic footprints of Io, Ganymede and Europa on Jupiter.

Io leaves a magnetic footprint on Jupiter's upper atmosphere that appears as a spot of ultraviolet emission that remains fixed underneath Io as Jupiter rotates. The specific physical mechanisms responsible for generating those emissions are not well understood, but in general the spot seems to arise because of an electromagnetic interaction between Jupiter's magnetic field and the plasma surrounding Io, driving currents of around 1 million amperes down through Jupiter's ionosphere. The other galilean satellites may also leave footprints, and the presence or absence of such footprints should illuminate the underlying physical mechanism by revealing the strengths of the currents linking the satellites to Jupiter. Here we report persistent, faint, far-ultraviolet emission from the jovian footprints of Ganymede and Europa. We also show that Io's magnetic footprint extends well beyond the immediate vicinity of Io's flux-tube interaction with Jupiter, and much farther than predicted theoretically; the emission persists for several hours downstream. We infer from these data that Ganymede and Europa have persistent interactions with Jupiter's magnetic field despite their thin atmospheres.

Quinoid redox cycling as a mechanism for sustained free radical generation by inhaled airborne particulate matter.

The health effects of airborne fine particles are the subject of government regulation and scientific debate. The aerodynamics of airborne particulate matter, the deposition patterns in the human lung, and the available experimental and epidemiological data on health effects lead us to focus on airborne particulate matter with an aerodynamic mean diameter less than 2.5 microm (PM(2.5)) as the fraction of the particles with the largest impact in health. In this article we present a novel hypothesis to explain the continuous production of reactive oxygen species produced by PM(2.5) when it is deposited in the lung. We find PM(2.5) contains abundant persistent free radicals, typically 10(16) to 10(17) unpaired spins/gram, and that these radicals are stable for several months. These radicals are consistent with the stability and electron paramagnetic resonance spectral characteristics of semiquinone radicals. Catalytic redox cycling by semiquinone radicals is well documented in the literature and we had studied in detail its role on the health effects of cigarette smoke particulate matter. We believe that we have for the first time shown that the same, or similar radicals, are not confined to cigarette smoke particulate matter but are also present in PM(2.5). We hypothesize that these semiquinone radicals undergo redox cycling, thereby reducing oxygen and generating reactive oxygen species while consuming tissue-reducing equivalents, such as NAD(P)H and ascorbate. These reactive oxygen species generated by particles cause oxidative stress at sites of deposition and produce deleterious effects observed in the lung.

Role of free radicals in the toxicity of airborne fine particulate matter.

Exposure to airborne fine particles (PM2.5) is implicated in excess of 50 000 yearly deaths in the USA as well as a number of chronic respiratory illnesses. Despite intense interest in the toxicity of PM2.5, the mechanisms by which it causes illnesses are poorly understood. Since the principal source of airborne fine particles is combustion and combustion sources generate free radicals, we suspected that PM2.5 may contain radicals. Using electron paramagnetic resonance (EPR), we examined samples of PM2.5 and found large quantities of radicals with characteristics similar to semiquinone radicals. Semiquinone radicals are known to undergo redox cycling and ultimately produce biologically damaging hydroxyl radicals. Aqueous extracts of PM2.5 samples induced damage to DNA in human cells and supercoiled phage DNA. PM2.5-mediated DNA damage was abolished by superoxide dismutase, catalase, and deferoxamine, implicating superoxide radical, hydrogen peroxide, and the hydroxyl radical in the reactions inducing DNA damage.

A prevalence survey for zoonotic enteric bacteria in a research monkey colony with specific emphasis on the occurrence of enteric Yersinia.

Transmissible pathogenic and opportunistic zoonotic enteric bacteria comprise a recognized occupational health threat to exposed humans from non-human primates (NHPs). In an effort to evaluate the occurrence of selected enteric organisms with zoonotic and biohazard potential in a research colony setting, we performed a prevalence study examining 61 juvenile and young adult rhesus macaques participating in a transplant immunology project. Primary emphasis was directed specifically to detection of pathogenic enteric Yersinia, less well-documented and reported NHP pathogens possessing recognized significant human disease potential. NHPs were surveyed by rectal culture during routine health monitoring on three separate occasions, and samples incubated using appropriate media and specific selective culture methods. Enteric organisms potentially transmissible to humans were subcultured and identified to genus and species. Significant human pathogens of the Salmonella/Shigella, Campylobacter, and enteric Yersinia groups were not isolated throughout the survey, suggesting prevalence of these organisms may generally be quite low.

Reaction of uric acid with peroxynitrite and implications for the mechanism of neuroprotection by uric acid.

Peroxynitrite, a biological oxidant formed from the reaction of nitric oxide with the superoxide radical, is associated with many pathologies, including neurodegenerative diseases, such as multiple sclerosis (MS). Gout (hyperuricemic) and MS are almost mutually exclusive, and uric acid has therapeutic effects in mice with experimental allergic encephalomyelitis, an animal disease that models MS. This evidence suggests that uric acid may scavenge peroxynitrite and/or peroxynitrite-derived reactive species. Therefore, we studied the kinetics of the reactions of peroxynitrite with uric acid from pH 6.9 to 8.0. The data indicate that peroxynitrous acid (HOONO) reacts with the uric acid monoanion with k = 155 M(-1) s(-1) (T = 37 degrees C, pH 7.4) giving a pseudo-first-order rate constant in blood plasma k(U(rate))(/plasma) = 0.05 s(-1) (T = 37 degrees C, pH 7.4; assuming [uric acid](plasma) = 0.3 mM). Among the biological molecules in human plasma whose rates of reaction with peroxynitrite have been reported, CO(2) is one of the fastest with a pseudo-first-order rate constant k(CO(2))(/plasma) = 46 s(-1) (T = 37 degrees C, pH 7.4; assuming [CO(2)](plasma) = 1 mM). Thus peroxynitrite reacts with CO(2) in human blood plasma nearly 920 times faster than with uric acid. Therefore, uric acid does not directly scavenge peroxynitrite because uric acid can not compete for peroxynitrite with CO(2). The therapeutic effects of uric acid may be related to the scavenging of the radicals CO(*-)(3) and NO(*)(2) that are formed from the reaction of peroxynitrite with CO(2). We suggest that trapping secondary radicals that result from the fast reaction of peroxynitrite with CO(2) may represent a new and viable approach for ameliorating the adverse effects associated with peroxynitrite in many diseases.

Beta carotene: from biochemistry to clinical trials.

Three large-scale clinical trials tested the effects of supplemental beta-carotene on the risk for chronic diseases such as cancer. The populations involved were Finnish male heavy smokers (the Alpha Tocopherol Beta Carotene [ATBC] trial), male asbestos workers and male and female heavy smokers (Beta-Carotene and Retinol Efficacy Trial [CARET]), and U.S. male physicians, 11% of whom were current smokers (Physician's Health Study). All three trials concluded that beta-carotene provided no protection against lung cancer; however, quite unexpectedly, two of the trials found a higher risk for lung cancer for those subjects given beta-carotene compared with those that were not. Several authors concluded from these beta-carotene trials that the protective effects of antioxidants against chronic disease are not as great as had been hoped. As reviewed here, however, beta-carotene may or may not be an antioxidant; it certainly differs in many respects from the prototypical antioxidant, vitamin E. In any case, the majority of beta-carotene's effects in vivo are probably not derived from any antioxidant properties that it may possess, but rather from its effect on a number of biochemical systems. Whether taking supplemental antioxidants can reduce the risk for chronic diseases remains to be established, although the case for vitamin E and heart disease appears strong. However, the association between eating a diet sufficient in fruits and vegetables and reduced risk for a number of diseases is consistent. There is no evidence at present that consuming small amounts of supplemental beta-carotene, i.e., amounts in foods or in a multivitamin tablet, is unwise for any population. The role of supplementation, however, particularly at high levels, with compounds that may be anti-oxidants but that are less well understood than vitamin E (e.g., carotenoids, plant polyphenols, and other phytochemicals), is less clear. The surprising results of the ATBC and CARET trials are a red flag, signaling the need for further research; a number of areas for future work are suggested here. Future research should lead to a clearer understanding of the effects of beta-carotene and other phytochemicals, as well as to more refined strategies for intervention, with important clinical and public health implications.

Vitamin E and heart disease: basic science to clinical intervention trials.

A review is presented of studies on the effects of vitamin E on heart disease, studies encompassing basic science, animal studies, epidemiological and observational studies, and four intervention trials. The in vitro, cellular, and animal studies, which are impressive both in quantity and quality, leave no doubt that vitamin E, the most important fat-soluble antioxidant, protects animals against a variety of types of oxidative stress. The hypothesis that links vitamin E to the prevention of cardiovascular disease (CVD) postulates that the oxidation of unsaturated lipids in the low-density lipoprotein (LDL) particle initiates a complex sequence of events that leads to the development of atherosclerotic plaque. This hypothesis is supported by numerous studies in vitro, in animals, and in humans. There is some evidence that the ex vivo oxidizability of a subject's LDL is predictive of future heart events. This background in basic science and observational studies, coupled with the safety of vitamin E, led to the initiation of clinical intervention trials. The three trials that have been reported in detail are, on balance, supportive of the proposal that supplemental vitamin E can reduce the risk for heart disease, and the fourth trial, which has just been reported, showed small, but not statistically significant, benefits. Subgroup analyses of cohorts from the older three trials, as well as evidence from smaller trials, indicate that vitamin E provides protection against a number of medical conditions, including some that are indicative of atherosclerosis (such as intermittent claudication). Vitamin E supplementation also produces an improvement in the immune system and protection against diseases other than cardiovascular disease (such as prostate cancer). Vitamin E at the supplemental levels being used in the current trials, 100 to 800 IU/d, is safe, and there is little likelihood that increased risk will be found for those taking supplements. About one half of American cardiologists take supplemental vitamin E, about the same number as take aspirin. In fact, one study suggests that aspirin plus vitamin E is more effective than aspirin alone. There are a substantial number of trials involving vitamin E that are in progress. However, it is possible, or even likely, that each condition for which vitamin E provides benefit will have a unique dose-effect curve. Furthermore, different antioxidants appear to act synergistically, so supplementation with vitamin E might be more effective if combined with other micronutrients. It will be extremely difficult to do trials that adequately probe the dose-effect curve for vitamin E for each condition that it might affect, or to do studies of all the possible combinations of other micronutrients that might act with vitamin E to improve its effectiveness. Therefore, the scientific community must recognize that there never will be a time when the science is "complete." At some point, the weight of the scientific evidence must be judged adequate; although some may regard it as early to that judgement now, clearly we are very close. In view of the very low risk of reasonable supplementation with vitamin E, and the difficulty in obtaining more than about 30 IU/day from a balanced diet, some supplementation appears prudent now.

Induction of inflammatory mediators in human airway epithelial cells by lipid ozonation products.

We have proposed that exposure of epithelial cell membrane lipids in the lung (mainly phospholipids) to ozone will generate lipid ozonation products (LOP), which could be responsible for the proinflammatory effects of ozone. The ozonation of phosphocholine, the principal membrane phospholipid, produces a limited number of LOP, including hydroxyhydroperoxides and aldehydes. We now report that exposure of cultured human bronchial epithelial cells to the ozonized 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) product, 1-palmitoyl-2-(9-oxononanoyl)-sn-glycero-3-phosphocholine (PC-ALD), a phospholipase A(2) (PLA(2))-stimulatory LOP, resulted in a 113 +/- 11% increase in the amounts of tritiated platelet-activating factor ((3)H-PAF) released apically. (3)H-PAF release was also induced by 1-hydroxy-1-hydroperoxynonane of ozonized POPC (HHP-C9), a phospholipase C (PLC)- stimulatory LOP (134 +/- 40% increase in (3)H-PAF). PC-ALD at 10 microM, but not HHP-C9, induced a 127 +/- 24% increase in prostaglandin E(2) (PGE(2)) release (n = 6, p < 0.05). In contrast, HHP-C9, but not PC-ALD, induced interleukin (IL)-6 release (178 +/- 23% increase, n = 6, p < 0.05) and IL-8 release (101 +/- 23% increase, n = 8, p < 0. 05). These results suggest that LOP-dependent release of proinflammatory mediators may play an important role in the early inflammatory response seen during exposure to ozone.

Antioxidant transport modulates peripheral airway reactivity and inflammation during ozone exposure.

We examined the effects of ozone (O(3)) and endogenous antioxidant transport on canine peripheral airway function, central airway function, epithelial integrity, and inflammation. Dogs were either untreated or pretreated with probenecid (an anion-transport inhibitor) and exposed for 6 h to 0.2 parts/million O(3). Peripheral airway resistance (Rpa) and reactivity (DeltaRpa) were monitored in three sublobar locations before and after exposure to either air or O(3). Pulmonary resistance and transepithelial potential difference in trachea and bronchus were also recorded. Bronchoalveolar lavage fluid (BALF) was collected before, during, and after exposure. O(3) increased Rpa and DeltaRpa only in probenecid-treated dogs and in a location-dependent fashion. Pulmonary resistance and potential difference in bronchus increased after O(3) exposure regardless of treatment. O(3) markedly increased BALF neutrophils only in untreated dogs. With the exception of hexanal, O(3) did not alter any BALF constituent examined. Probenecid reduced BALF ascorbate, BALF protein, and plasma urate. We conclude that 1) a 6-h exposure to 0.2 parts/million O(3) represents a subthreshold stimulus in relation to its effects on peripheral airway function in dogs, 2) antioxidant transport contributes to the maintenance of normal airway tone and reactivity under conditions of oxidant stress, 3) O(3)-induced changes in Rpa and DeltaRpa are dependent on location, and 4) peripheral airway hyperreactivity and inflammation reflect independent responses to O(3) exposure. Finally, although anion transport mitigates the effect of O(3) on peripheral airway function, it contributes to the development of airway inflammation and may represent a possible target for anti-inflammatory prevention or therapy.

Activation and inactivation of cyclo-oxygenase in rat alveolar macrophages by aqueous cigarette tar extracts.

Cyclo-oxygenase (COX) activity and its level of expression, the release of arachidonic acid (AA), and the accumulation of prostaglandins (PGs) were determined in isolated rat pulmonary alveolar macrophages (PAM) exposed to aqueous cigarette tar (ACT) extracts. COX activity increased 3-fold above the initial activity within 2 h of incubation with ACT extracts and gradually decreased below the initial activity after 8 h of incubation. The increased COX activity after 2 h of incubation did not lead to increased accumulation of PGE2. Accumulated levels of PGE2 increased dramatically after 12 h of incubation despite decreased COX activity in cells incubated with ACT extracts. This increased accumulation of PGE2 was greater in cells derived from vitamin E deficient rats compared with control rats. Release of AA from cells was dramatically increased in cells incubated with ACT extracts in parallel to PG accumulation. Thus increased accumulation of PGE2 despite decreased COX activity after 12 h of incubation is likely the result of increased substrate availability. These results suggest that, contrary to earlier reports, cigarette smoke stimulates the formation of PGs in alveolar macrophages. Increased PG production may lead to suppressed immune response and enhanced risk of tumorigenesis in smokers' lungs.

Reaction of peroxynitrite with melatonin: A mechanistic study.

The pH profile of the peroxynitrite/melatonin reaction suggests that both peroxynitrous acid (ONOOH) and its anion (ONOO-) are reactive toward melatonin, but at physiological pH most of the reaction with melatonin involves ONOOH and the activated form of peroxynitrous acid (ONOOH). The formation of hydroxylated products (mainly 6-hydroxymelatonin) suggests that melatonin also reacts with ONOOH. The overall peroxynitrite/melatonin reaction is first-order in melatonin and first-order in peroxynitrite, but the hydroxylation of melatonin is presumed to be zero-order in melatonin. Melatonin is metabolized in the liver, mainly to 6-hydroxymelatonin, so we do not think this metabolite is a useful biomarker for melatonin's antioxidant activity; however, 6-hydroxymelatonin is a better chain-breaking antioxidant than melatonin and may contribute to the beneficial effects of melatonin in vivo. As is now well-known, CO2 modulates the reactions of peroxynitrite. The reaction of peroxynitrite with melatonin in the absence of added bicarbonate produces mainly 6-hydroxymelatonin and 1,2,3,3a,8, 8a-hexahydro-1-acetyl-5-methoxy-8a-hydroxypyrrolo[2,3-b]indole, with some isomeric 1,2,3,3a,8, 8a-hexahydro-1-acetyl-5-methoxy-3a-hydroxypyrrolo[2,3-b]indole. In the presence of added bicarbonate, product yields decrease and 6-hydroxymelatonin is not formed. These facts suggest that melatonin scavenges reactive species (such as CO3*- and *NO2) that are produced from the peroxynitrite/CO2 reaction. The spectrum of the melatoninyl radical cation is observed both in the absence and in the presence of added bicarbonate, suggesting that the melatoninyl radical cation is the initial product and the hydroxypyrrolo[2, 3-b]indole products are derived from it. Unlike tyrosine, where both nitrated and hydroxylated products can be isolated, nitromelatonin is not found in the final products from the melatonin/peroxynitrite reaction in either the absence or presence of added bicarbonate. However, we suggest that 2-hydroxy-3-nitro- and/or 2-hydroxy-3-peroxynitro-2,3-dihydromelatonin are formed as intermediates and subsequently decompose to give 1,2,3,3a,8, 8a-hexahydro-1-acetyl-5-methoxy-8a-hydroxypyrrolo[2,3-b]indole. Since peroxynitrite/CO2 governs the reactions of peroxynitrite in vivo, we suggest that the hydroxypyrrolo[2,3-b]indole products are the main products from the oxidation of melatonin by peroxynitrite-derived species in vivo, and that these products may serve as indexes for melatonin's antioxidant activity.

Ozone exposure increases aldehydes in epithelial lining fluid in human lung.

We hypothesized that exposure of healthy humans to ozone causes both ozonation and peroxidation of lipids in lung epithelial lining fluid. Twelve smokers and 15 nonsmokers (eight lung function "responders" and seven "nonresponders") were exposed once to air and twice to 0. 22 ppm ozone for 4 h with exercise in an environmental chamber, with each exposure separated by at least 3 wk. Bronchoalveolar lavage (BAL) was performed immediately after one ozone exposure and 18 h after the other ozone exposure. BAL fluid was analyzed for the aldehyde products of ozonation and lipid peroxidation, nonanal (C9) and hexanal (C6), as well as total protein, albumin, and immunoglobulin M as markers of changes in epithelial permeability. Ozone exposure resulted in a significant early increase in C9 (p = 0. 0001), with no statistically significant relationship between increases in C9 and lung function changes, airway inflammation, or changes in epithelial permeability. Increases in C6 levels were not statistically significant (p = 0.16). Both C9 and C6 levels returned to baseline by 18 h after exposure. These studies confirm that exposure to ozone with exercise, at concentrations relevant to urban outdoor air, results in ozonation of lipids in the airway epithelial lining fluid of humans.

Direct and simultaneous ultraviolet second-derivative spectrophotometric determination of nitrite and nitrate in preparations of peroxynitrite.

We have determined the initial concentrations of nitrite and nitrate for three different methods of synthesizing peroxynitrite using an ultraviolet second-derivative spectroscopy method (Fig. 3). As expected, the net nitrogen balance in these preparations (Fig. 4) and the yields of nitrite and nitrate (Table II) indicate that, at pH 6.0, peroxynitrite decomposes to give essentially NO3-. Stock solutions of peroxynitrite prepared using method I (ozonation of azide) consistently contain more NO2- and NO3- than method II (isoamyl nitrite with hydrogen peroxide) and method III (hydrogen peroxide with nitrous acid). Method II gives the least amount of NO2- contaminants, and NO3- impurities are the lowest in method III (Table I).