Demeter high resolution observations of the ionospheric thermal plasma response to magnetospheric energy input during the magnetic storm of November 2004

High resolution Demeter plasma and wave observations were available during one of the geomagnetic storms of November 2004 when the ionospheric footprint of the plasmasphere was pushed below 64 degrees in the midnight sector. We report here onboard observations of thermal/suprathermal plasma and HF electric field variations with a temporal resolution of 0.4 s, which corresponds to a spatial resolution of 3 km. Local perturbations of the plasma parameters at the altitude of 730 km are analysed with respect to the variation of the field-aligned currents, electron and proton precipitation and large-scale electric fields, measured in-situ by Demeter and by remote optical methods from the IMAGE/Polar satellites. <br><br> Flow monitoring in the 21:00 and 24:00 MLT sectors during storm conditions reveals two distinct regions of O<sup>+</sup> outflow, i.e. the region of the field-aligned currents, which often comprises few layers of opposite currents, and the region of velocity reversal toward dusk at sub-auroral latitudes. Average upward O<sup>+</sup> velocities are identical in both local time sectors and vary between 200 and 450 m s<sup>−1</sup>, with an exception of a few cases of higher speed (~1000 m s<sup>−1</sup>) outflow, observed in the midnight sector. Each individual outflow event does not indicate any heating process of the thermal O<sup>+</sup> population. On the contrary, the temperature of the O<sup>+</sup>, outflowing from auroral latitudes, is found to be even colder than that of the ambient ion plasma. The only ion population which is observed to be involved in the heating is the O<sup>+</sup> with energies a few times higher than the thermal energy. Such a population was detected at sub-auroral latitudes in the region of duskward flow reversal. Its temperature raises up to a few eV inside the layer of sheared velocity. <br><br> A deep decrease in the H<sup>+</sup> density at heights and latitudes, where, according to the IRI model, these ions are expected to comprise ~50% of the positive charge, indicates that the thermospheric balance between atomic oxygen and hydrogen was re-established in favour of oxygen. As a consequence, the charge exchange between oxygen and hydrogen does not effectively limit the O<sup>+</sup> production in the regions of the electron precipitation. According to Demeter observations, the O<sup>+</sup> concentration is doubled inside the layers with upward currents (downward electrons). Such a density excess creates the pressure gradient which drives the plasma away from the overdense regions, i.e. first, from the layers of precipitating electrons and then upward along the layers of downward current. <br><br> In addition, the downward currents are identified to be the source regions of hiss emissions, i.e. electron acoustic mode excited via the Landau resonance in the multi-component electron plasma. Such instabilities, which are often observed in the auroral region at 2–5 Earth radii, but rarely at ionospheric altitudes, are believed to be generated by an electron beam which moves through the background plasma with a velocity higher than its thermal velocity

Experimental nitrogen addition alters structure and function of a boreal bog: critical load and thresholds revealed

Bogs and fens cover 6% and 21%, respectively, of the 140,329 km2 Oil Sands Administrative Area in northern Alberta. Development of the oil sands has led to increasing atmospheric N deposition, with values as high as 17 kg N.ha-1yr-1; regional background deposition is N.ha-1yr-1. Bogs, being ombrotrophic, may be especially susceptible to increasing N deposition. To examine responses to N deposition, over five years, we experimentally applied N (as NH4NO3) to a bog near Mariana Lake, Alberta, unaffected by oil sands activities, at rates of 0, 5, 10, 15, 20, and 25 kg N.ha-1yr-1, plus controls (no water or N addition). Increasing N addition: (1) stimulated N2 fixation at deposition .ha-1yr-1, and progressively inhibited N2 fixation as N deposition increased above this level; (2) had no effect on Sphagnum fuscum net primary production (NPP) in years 1, 2, and 4, but inhibited S. fuscum NPP in years 3 and 5; (3) stimulated dominant shrub and Picea mariana NPP; (4) led to increased root biomass and production; (5) changed Sphagnum species relative abundance (decrease in S. fuscum, increase in S. magellanicum, no effect on S. angustifolium); (6) led to increasing abundance of Rhododendron groenlandicum and Andromeda polifolia, and to vascular plants in general; (7) led to increasing shrub leaf N concentrations in Andromeda polifolia, Chamaedaphne calyculata, Vaccinium oxycoccos, V. vitis-idaea, and Picea mariana; (8) stimulated cellulose decomposition, with no effect on S. fuscum peat or mixed vascular plant litter decomposition; (9) had no effect on net N mineralization rates or on porewater NH4+-N, NO3--N, or DON concentrations; and (10) had minimal effects on peat microbial community composition. Increasing experimental N addition led to a switch from new N being taken up primarily by Sphagnum to being taken up primarily by shrubs. As shrub growth and cover increase, Sphagnum abundance and NPP decrease. Because inhibition of N2 fixation by increasing N deposition plays a key role in bog structural and functional responses, we recommend a N deposition critical load of 3 kg N.ha-1yr-1 for northern Alberta bogs

Genetic and Psychological Factors Interact to Predict Physical Impairment Phenotypes Following Exercise-Induced Shoulder Injury

Background: We investigated interactions between genetic and psychological factors in predicting shoulder impairment phenotypes. We hypothesized that pro-inflammatory genes would display stronger relationships compared with pain-related genes when combined with psychological factors for predicting phenotypic changes.Subjects and methods: Altogether, 190 participants completed a 5-day experimental protocol. An experimental shoulder injury model was used to induce physical impairment, and a priori selected genetic (pain-related, pro-inflammatory) and psychological (anxiety, depressive symptoms, pain catastrophizing, fear of pain, kinesiophobia) factors were included as predictors of interest. Impairment phenotypes were injury-induced deficits in range of motion (ROM) and strength. After controlling for age, sex, and race, genetic and psychological predictors were entered separately as main effects and interaction terms in regression models for each phenotype.Results: Strong statistical evidence was provided for interactions between: 1) IL-1β (rs1143634) and fear of pain for predicting loss of shoulder flexion and abduction, 2) IL-1β (rs1143634) and anxiety for predicting loss of flexion, and 3) IL-1β (rs1143634) and depressive symptoms for predicting loss of internal rotation. In addition, the interaction between OPRM1 (rs1799971) and fear of pain as well as COMT (rs4818) and pain catastrophizing provided strong statistical evidence for predicting strength loss.Conclusion: Pro-inflammatory gene variants contributed more to physical impairment with two single nucleotide polymorphisms (SNPs; IL-1β [rs1143634] and TNF/LTA [rs2229094]) interacting with psychological factors to predict six shoulder impairment phenotypes. In comparison, two pain-related gene SNPs (OPRM1 [rs1799971] and COMT [rs4818]) interacted with psychological factors to predict four shoulder impairment phenotypes (abduction: 5-day average loss; strength loss: 5-day average, peak, and relative loss)

A computational model for sex-specific genetic architecture of complex traits in humans: Implications for mapping pain sensitivity

Understanding differences in the genetic architecture of complex traits between the two sexes has significant implications for evolutionary studies and clinical diagnosis. However, our knowledge about sex-specific genetic architecture is limited largely because of a lack of analytical models that can detect and quantify the effects of sex on the complexity of quantitative genetic variation. Here, we derived a statistical model for mapping DNA sequence variants that contribute to sex-specific differences in allele frequencies, linkage disequilibria, and additive and dominance genetic effects due to haplotype diversity. This model allows a genome-wide search for functional haplotypes and the estimation and test of haplotype by sex interactions and sex-specific heritability. The model, validated by simulation studies, was used to detect sex-specific functional haplotypes that encode a pain sensitivity trait in humans. The model could have important implications for mapping complex trait genes and studying the detailed genetic architecture of sex-specific differences

Modeling genetic imprinting effects of DNA sequences with multilocus polymorphism data

Single nucleotide polymorphisms (SNPs) represent the most widespread type of DNA sequence variation in the human genome and they have recently emerged as valuable genetic markers for revealing the genetic architecture of complex traits in terms of nucleotide combination and sequence. Here, we extend an algorithmic model for the haplotype analysis of SNPs to estimate the effects of genetic imprinting expressed at the DNA sequence level. The model provides a general procedure for identifying the number and types of optimal DNA sequence variants that are expressed differently due to their parental origin. The model is used to analyze a genetic data set collected from a pain genetics project. We find that DNA haplotype GAC from three SNPs, OPRKG36T (with two alleles G and T), OPRKA843G (with alleles A and G), and OPRKC846T (with alleles C and T), at the kappa-opioid receptor, triggers a significant effect on pain sensitivity, but with expression significantly depending on the parent from which it is inherited (p = 0.008). With a tremendous advance in SNP identification and automated screening, the model founded on haplotype discovery and statistical inference may provide a useful tool for genetic analysis of any quantitative trait with complex inheritance

Mental Stress Provokes Ischemia in Coronary Artery Disease Subjects Without Exercise- or Adenosine-Induced Ischemia

ObjectivesThe purpose of this study was to investigate the possibility that some patients with coronary artery disease (CAD) but negative exercise or chemical stress test results might have mental stress-induced ischemia. The study population consisted solely of those with negative test results.BackgroundMental stress-induced ischemia has been reported in 20% to 70% of CAD subjects with exercise-induced ischemia. Because mechanisms of exercise and mental stress-induced ischemia may differ, we studied whether mental stress would produce ischemia in a proportion of subjects with CAD who have no inducible ischemia with exercise or pharmacologic tests.MethodsTwenty-one subjects (14 men, 7 women) with a mean age of 67 years and with a documented history of CAD were studied. All subjects had a recent negative nuclear stress test result (exercise or chemical). Subjects completed a speaking task involving role playing a difficult interpersonal situation. A total of 30 mCi 99mTc-sestamibi was injected at one minute into the speech, and imaging was started 40 min later. A resting image obtained within one week was compared with the stress image. Images were analyzed for number and severity of perfusion defects. The summed difference score based on the difference between summed stress and rest scores was calculated. Severity was assessed using a semiquantitative scoring method from zero to four.ResultsSix of 21 (29%) subjects demonstrated reversible ischemia (summed difference score ≥3) with mental stress. No subject had chest pain or electrocardiographic changes during the stressor. Mean systolic and diastolic blood pressure and heart rate all increased between resting and times of peak stress.ConclusionsMental stress may produce ischemia in some subjects with CAD and negative exercise or chemical nuclear stress test results

On wind-driven electrojets at magnetic cusps in the nightside ionosphere of Mars

Mars has a complex magnetic topology where crustal magnetic fields can interact with the solar wind magnetic field to form magnetic cusps. On the nightside, solar wind electron precipitation can produce enhanced ionization at cusps while closed field regions adjacent to cusps can be devoid of significant ionization. Using an electron transport model, we calculate the spatial structure of the nightside ionosphere of Mars using Mars Global Surveyor electron measurements as input. We find that localized regions of enhanced ionospheric density can occur at magnetic cusps adjacent to low density regions. Under this configuration, thermospheric winds can drive ionospheric electrojets. Collisional ions move in the direction of the neutral winds while magnetized electrons move perpendicular to the wind direction. This difference in motion drives currents and can lead to charge accumulation at the edges of regions of enhanced ionization. Polarization fields drive secondary currents which can reinforce the primary currents leading to electrojet formation. We estimate the magnitude of these electrojets and show that their magnetic perturbations can be detectable from both orbiting spacecraft and the surface. The magnitude of the electrojets can vary on diurnal and annual time scales as the strength and direction of the winds vary. These electrojets may lead to localized Joule heating, and closure of these currents may require field-aligned currents which may play a role in high altitude acceleration processes

Gender Differences in Acute and Chronic Pain in the Emergency Department: Results of the 2014 Academic Emergency Medicine Consensus Conference Pain Section

Pain is a leading public health problem in the United States, with an annual economic burden of more than $630 billion, and is one of the most common reasons that individuals seek emergency department (ED) care. There is a paucity of data regarding sex differences in the assessment and treatment of acute and chronic pain conditions in the ED. The Academic Emergency Medicine consensus conference convened in Dallas, Texas, in May 2014 to develop a research agenda to address this issue among others related to sex differences in the ED. Prior to the conference, experts and stakeholders from emergency medicine and the pain research field reviewed the current literature and identified eight candidate priority areas. At the conference, these eight areas were reviewed and all eight were ratified using a nominal group technique to build consensus. These priority areas were: 1) gender differences in the pharmacological and nonpharmacological interventions for pain, including differences in opioid tolerance, side effects, or misuse; 2) gender differences in pain severity perceptions, clinically meaningful differences in acute pain, and pain treatment preferences; 3) gender differences in pain outcomes of ED patients across the life span; 4) gender differences in the relationship between acute pain and acute psychological responses; 5) the influence of physician-patient gender differences and characteristics on the assessment and treatment of pain; 6) gender differences in the influence of acute stress and chronic stress on acute pain responses; 7) gender differences in biological mechanisms and molecular pathways mediating acute pain in ED populations; and 8) gender differences in biological mechanisms and molecular pathways mediating chronic pain development after trauma, stress, or acute illness exposure. These areas represent priority areas for future scientific inquiry, and gaining understanding in these will be essential to improving our understanding of sex and gender differences in the assessment and treatment of pain conditions in emergency care settings

Brain-predicted age difference mediates the association between PROMIS sleep impairment, and self-reported pain measure in persons with knee pain

Knee pain, the most common cause of musculoskeletal pain (MSK), constitutes a severe public health burden. Its neurobiological causes, however, remain poorly understood. Among many possible causes, it has been proposed that sleep problems could lead to an increase in chronic pain symptomatology, which may be driven by central nervous system changes. In fact, we previously found that brain cortical thickness mediated the relationship between sleep qualities and pain severity in older adults with MSK. We also demonstrated a significant difference in a machine-learning-derived brain-aging biomarker between participants with low-and high-impact knee pain. Considering this, we examined whether brain aging was associated with self-reported sleep and pain measures, and whether brain aging mediated the relationship between sleep problems and knee pain. Exploratory Spearman and Pearson partial correlations, controlling for age, sex, race and study site, showed a significant association of brain aging with sleep related impairment and self-reported pain measures. Moreover, mediation analysis showed that brain aging significantly mediated the effect of sleep related impairment on clinical pain and physical symptoms. Our findings extend our prior work demonstrating advanced brain aging among individuals with chronic pain and the mediating role of brain-aging on the association between sleep and pain severity. Future longitudinal studies are needed to further understand whether the brain can be a therapeutic target to reverse the possible effect of sleep problems on chronic pain