de Sitter symmetry of Neveu-Schwarz spinors

We study the relations between Dirac fields living on the 2-dimensional Lorentzian cylinder and the ones living on the double-covering of the 2-dimensional de Sitter manifold, here identified as a certain coset space of the group $SL(2,R)$. We show that there is an extended notion of de Sitter covariance only for Dirac fields having the Neveu-Schwarz anti-periodicity and construct the relevant cocycle. Finally, we show that the de Sitter symmetry is naturally inherited by the Neveu-Schwarz massless Dirac field on the cylinder.Comment: 24 page

Thermodynamics of a class of non-asymptotically flat black holes in Einstein-Maxwell-Dilaton theory

We analyse in detail the thermodynamics in the canonical and grand canonical ensembles of a class of non-asymptotically flat black holes of the Einstein-(anti) Maxwell-(anti) Dilaton theory in 4D with spherical symmetry. We present the first law of thermodynamics, the thermodynamic analysis of the system through the geometrothermodynamics methods, Weinhold, Ruppeiner, Liu-Lu-Luo-Shao and the most common, that made by the specific heat. The geometric methods show a curvature scalar identically zero, which is incompatible with the results of the analysis made by the non null specific heat, which shows that the system is thermodynamically interacting, does not possess extreme case nor phase transition. We also analyse the local and global stability of the thermodynamic system, and obtain a local and global stability for the normal case for 0<\gamma<1 and for other values of \gamma, an unstable system. The solution where \gamma=0 separates the class of locally and globally stable solutions from the unstable ones.Comment: 18 pages, version accepted for publication in General Relativity and Gravitatio

Thoracic load carriage-induced respiratory muscle fatigue.

We investigated the effect of carrying a 25 kg backpack upon exercise-induced respiratory muscle fatigue, pulmonary function and physiological and perceptual responses to exercise.N/

Multilocation Corn Stover Harvest Effects on Crop Yields and Nutrient Removal

Corn (Zea mays L.) stover was identified as an important feedstock for cellulosic bioenergy production because of the extensive area upon which the crop is already grown. This report summarizes 239 site-years of field research examining effects of zero, moderate, and high stover removal rates at 36 sites in seven different states. Grain and stover yields from all sites as well as N, P, and K removal from 28 sites are summarized for nine longitude and six latitude bands, two tillage practices (conventional vs no tillage), two stover-harvest methods (machine vs calculated), and two crop rotations {continuous corn (maize) vs corn/soybean [Glycine max (L.) Merr.]}. Mean grain yields ranged from 5.0 to 12.0 Mg ha−1 (80 to 192 bu ac−1). Harvesting an average of 3.9 or 7.2 Mg ha−1(1.7 or 3.2 tons ac−1) of the corn stover resulted in a slight increase in grain yield at 57 and 51 % of the sites, respectively. Average no-till grain yields were significantly lower than with conventional tillage when stover was not harvested, but not when it was collected. Plant samples collected between physiological maturity and combine harvest showed that compared to not harvesting stover, N, P, and K removal was increased by 24, 2.7, and 31 kg ha−1, respectively, with moderate (3.9 Mg ha−1) harvest and by 47, 5.5, and 62 kg ha−1, respectively, with high (7.2 Mg ha−1) removal. This data will be useful for verifying simulation models and available corn stover feedstock projections, but is too variable for planning site-specific stover harvest

PPARα downregulates airway inflammation induced by lipopolysaccharide in the mouse

BACKGROUND: Inflammation is a hallmark of acute lung injury and chronic airway diseases. In chronic airway diseases, it is associated with profound tissue remodeling. Peroxisome proliferator-activated receptor-α (PPARα) is a ligand-activated transcription factor, that belongs to the nuclear receptor family. Agonists for PPARα have been recently shown to reduce lipopolysaccharide (LPS)- and cytokine-induced secretion of matrix metalloproteinase-9 (MMP-9) in human monocytes and rat mesangial cells, suggesting that PPARα may play a beneficial role in inflammation and tissue remodeling. METHODS: We have investigated the role of PPARα in a mouse model of LPS-induced airway inflammation characterized by neutrophil and macrophage infiltration, by production of the chemoattractants, tumor necrosis factor-α (TNF-α), keratinocyte derived-chemokine (KC), macrophage inflammatory protein-2 (MIP-2) and monocyte chemoattractant protein-1 (MCP-1), and by increased MMP-2 and MMP-9 activity in bronchoalveolar lavage fluid (BALF). The role of PPARα in this model was studied using both PPARα-deficient mice and mice treated with the PPARα activator, fenofibrate. RESULTS: Upon intranasal exposure to LPS, PPARα(-/- )mice exhibited greater neutrophil and macrophage number in BALF, as well as increased levels of TNF-α, KC, MIP-2 and MCP-1, when compared to PPARα(+/+ )mice. PPARα(-/- )mice also displayed enhanced MMP-9 activity. Conversely, fenofibrate (0.15 to 15 mg/day) dose-dependently reduced the increase in neutrophil and macrophage number induced by LPS in wild-type mice. In animals treated with 15 mg/day fenofibrate, this effect was associated with a reduction in TNF-α, KC, MIP-2 and MCP-1 levels, as well as in MMP-2 and MMP-9 activity. PPARα(-/- )mice treated with 15 mg/day fenofibrate failed to exhibit decreased airway inflammatory cell infiltrate, demonstrating that PPARα mediates the anti-inflammatory effect of fenofibrate. CONCLUSION: Using both genetic and pharmacological approaches, our data clearly show that PPARα downregulates cell infiltration, chemoattractant production and enhanced MMP activity triggered by LPS in mouse lung. This suggests that PPARα activation may have a beneficial effect in acute or chronic inflammatory airway disorders involving neutrophils and macrophages

The pathophysiological function of peroxisome proliferator-activated receptor-γ in lung-related diseases

Research into respiratory diseases has reached a critical stage and the introduction of novel therapies is essential in combating these debilitating conditions. With the discovery of the peroxisome proliferator-activated receptor and its involvement in inflammatory responses of cardiovascular disease and diabetes, attention has turned to lung diseases and whether knowledge of this receptor can be applied to therapy of the human airways. In this article, we explore the prospect of peroxisome proliferator-activated receptor-γ as a marker and treatment focal point of lung diseases such as asthma, chronic obstructive pulmonary disorder, lung cancer and cystic fibrosis. It is anticipated that peroxisome proliferator-activated receptor-γ ligands will provide not only useful mechanistic pathway information but also a possible new wave of therapies for sufferers of chronic respiratory diseases

Hydroxychloroquine Effectiveness in Reducing Symptoms of Hand Osteoarthritis: A Randomized Trial

Background: Synovitis is believed to play a role in producing symptoms in persons with hand osteoarthritis, but data on slow-acting anti-inflammatory treatments are sparse. Objective: To determine the effectiveness of hydroxychloroquine versus placebo as an analgesic treatment of hand osteoarthritis. Design: Randomized, double-blind, placebo-controlled clinical trial with 12-month follow-up. (ISRCTN registry number: ISRCTN91859104). Setting: 13 primary and secondary care centers in England. Participants: Of 316 patients screened, 248 participants (82% women; mean age, 62.7 years) with symptomatic (pain ≥4 on a 0- to 10-point visual analogue scale) and radiographic hand osteoarthritis were randomly assigned and 210 (84.7%) completed the 6-month primary end point. Intervention: Hydroxychloroquine (200 to 400 mg) or placebo (1:1) for 12 months with ongoing usual care. Measurements: The primary end point was average hand pain during the previous 2 weeks (on a 0- to 10-point numerical rating scale [NRS]) at 6 months. Secondary end points included self-reported pain and function, grip strength, quality of life, radiographic structural change, and adverse events. Baseline ultrasonography was done. Results: At 6 months, mean hand pain was 5.49 points in the placebo group and 5.66 points in the hydroxychloroquine group, with a treatment difference of −0.16 point (95% CI, −0.73 to 0.40 point) (P = 0.57). Results were robust to adjustments for adherence, missing data, and use of rescue medication. No significant treatment differences existed at 3, 6, or 12 months for any secondary outcomes. The percentage of participants with at least 1 joint with synovitis was 94% (134 of 143) on grayscale ultrasonography and 59% on power Doppler. Baseline structural damage or synovitis did not affect treatment response. Fifteen serious adverse events were reported (7 in the hydroxychloroquine group [3 defined as possibly related] and 8 in the placebo group). Limitation: Hydroxychloroquine dosage restrictions may have reduced efficacy. Conclusion: Hydroxychloroquine was no more effective than placebo for pain relief in patients with moderate to severe hand pain and radiographic osteoarthritis

Doom and Boom on a Resilient Reef: Climate Change, Algal Overgrowth and Coral Recovery

Background: Coral reefs around the world are experiencing large-scale degradation, largely due to global climate change, overfishing, diseases and eutrophication. Climate change models suggest increasing frequency and severity of warming-induced coral bleaching events, with consequent increases in coral mortality and algal overgrowth. Critically, the recovery of damaged reefs will depend on the reversibility of seaweed blooms, generally considered to depend on grazing of the seaweed, and replenishment of corals by larvae that successfully recruit to damaged reefs. These processes usually take years to decades to bring a reef back to coral dominance

Global Transcriptome and Deletome Profiles of Yeast Exposed to Transition Metals

A variety of pathologies are associated with exposure to supraphysiological concentrations of essential metals and to non-essential metals and metalloids. The molecular mechanisms linking metal exposure to human pathologies have not been clearly defined. To address these gaps in our understanding of the molecular biology of transition metals, the genomic effects of exposure to Group IB (copper, silver), IIB (zinc, cadmium, mercury), VIA (chromium), and VB (arsenic) elements on the yeast Saccharomyces cerevisiae were examined. Two comprehensive sets of metal-responsive genomic profiles were generated following exposure to equi-toxic concentrations of metal: one that provides information on the transcriptional changes associated with metal exposure (transcriptome), and a second that provides information on the relationship between the expression of ∼4,700 non-essential genes and sensitivity to metal exposure (deletome). Approximately 22% of the genome was affected by exposure to at least one metal. Principal component and cluster analyses suggest that the chemical properties of the metal are major determinants in defining the expression profile. Furthermore, cells may have developed common or convergent regulatory mechanisms to accommodate metal exposure. The transcriptome and deletome had 22 genes in common, however, comparison between Gene Ontology biological processes for the two gene sets revealed that metal stress adaptation and detoxification categories were commonly enriched. Analysis of the transcriptome and deletome identified several evolutionarily conserved, signal transduction pathways that may be involved in regulating the responses to metal exposure. In this study, we identified genes and cognate signaling pathways that respond to exposure to essential and non-essential metals. In addition, genes that are essential for survival in the presence of these metals were identified. This information will contribute to our understanding of the molecular mechanism by which organisms respond to metal stress, and could lead to an understanding of the connection between environmental stress and signal transduction pathways