What impact do thin debris layer have on ablation for debris covered glaciers? A combined fieldmodeling study on Zmuttgletscher

Debris covered glaciers are commonly found in alpine environments. As a result of a protective debris layer, debris covered glaciers respond differently to changes in climate. Current numerical ablation models simulating debris covered glaciers, however, do not account for enhanced melt for thin debris layers as is proven by empirical data. Debris layers thinner than a specific critical debris thickness as well as partially covered surfaces are often found to have increased melt rates compared to clean ice. As current numerical models attribute insulation to debris layers of any thickness, it is of great importance to include enhanced melt for thin layers to analyse how surface mass balance is affected when enhanced melt is incorporated. In a first part, this study focuses on reproducing the Østrem curve with data collected during a field campaign on Zmuttgletscher. Partially covered surfaces were found to enhance melt by up to 20 % the clean ice melt rate, whereas insulating of thicker debris layers reduced surface melt by as much as 61 %, depicting an accurate Østrem curve. Melt rates were shown to be reduced on fully covered surfaces of any thickness, with melt rates decreasing as debris thickness increased. In a second part, simulations of glaciers with and without enhanced melt for thin debris layers were compared and analysed. Step change experiments as well as sinus simulations revealed that, for a glacier building up with a simplified bed geometry, inclusion of enhanced melt for thin debris layers has no significant impact on surface mass balance. Differences increase with a higher selected enhancement factor but do not affect surface mass balance significantly. With an enhancement 1.6 times the clean ice melt rate for debris layers ranging from <0 to 0.03 m thickness, differences stay insignificantly minimal and do not necessitate the need to implement enhanced melt in numeric melt models

Hormonal control of inflammatory responses

Almost any stage of inflammatory and immunological responses is affected by hormone actions. This provides the basis for the suggestion that hormones act as modulators of the host reaction against trauma and infection. Specific hormone receptors are detected in the reactive structures in inflamed areas and binding of hormone molecules to such receptors results in the generation of signals that influence cell functions relevant for the development of inflammatory responses. Diversity of hormonal functions accounts for recognized pro- and anti-inflammatory effects exerted by these substances. Most hormone systems are capable of influencing inflammatory events. Insulin and glucocorticoids, however, exert direct regulatory effects at concentrations usually found in plasma. Insulin is endowed with facilitatory actions on vascular reactivity to inflammatory mediators and inflammatory cell functions. Increased concentrations of circulating glucocorticoids at the early stages of inflammation results in downregulation of inflammatory responses. Oestrogens markedly reduce the response to injury in a variety of experimental models. Glucagon and thyroid hormones exert indirect anti-inflammatory effects mediated by the activity of the adrenal cortex. Accordingly, inflammation is not only merely a local response, but a hormone-controlled process

Role of the protein annexin A1 on the efficacy of anti-TNF treatment in a murine model of acute colitis

TNF-α is involved in the mechanisms that initiate inflammatory bowel diseases (IBDs). Anti-TNF-α drugs, such as infliximab (IFX), cause non-responsiveness and side effects, indicating the need to investigate alternative therapies for these diseases. The anti-inflammatory protein, annexin A1 (AnxA1), has been associated with the protection of the gastrointestinal mucosa. To further address the role of endogenous AnxA1 on the TNF-α blockade efficacy in a murine model, we assessed colitis induced by Dextran Sulfate Sodium (DSS) in wild-type (WT) and AnxA1−/− Balb/c mice treated with IFX. We consistently observed endogenous AnxA1 prevented clinical and physiological manifestations of experimental colitis treated with IFX, additionally the manifestation of the disease was observed earlier in AnxA1−/− mice. Rectal bleeding, diarrhea, histological score, epithelial damages and collagen degradation caused by DSS were prevented following IFX treatment only in WT mice. IL-6 increased during colitis in WT and AnxA1−/− mice, decreasing under IFX treatment in WT. The influx of neutrophils and TNF-α secretion were largely elevated in AnxA1−/− mice when compared to WT mice. In the group WT/DSS + IFX, phagocytes were more susceptible to apoptosis following treatment with IFX. Endogenous expression of AnxA1 increased after DSS and decreased with IFX treatment, demonstrating an attenuated inflammatory response. The data indicate that AnxA1 contributes to the establishment of intestinal homeostasis after blocking of TNF-α was used as a treatment of IBD, constituting a key molecule in the mechanism of action and a potential biomarker of therapeutic efficacy.Fil: De Paula Silva, Marina. Universidade de Sao Paulo; BrasilFil: Barrios, Bibiana Elisabet. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Maccio Maretto, Lisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Sena, Angela. Universidade de Sao Paulo; BrasilFil: Poliselli Farsky, Sandra Helena. Universidade de Sao Paulo; BrasilFil: Correa, Silvia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Oliani, Sonia María. Universidade de Sao Paulo; Brasi

Rapid magma generation or shared magmatic reservoir? Petrology and geochronology of the Rat Creek and Nelson Mountain Tuffs, CO, USA

This study was supported by the ETH Research Grant ETH-34 15-2 (JS).Large-volume silicic volcanism poses global hazards in the form of proximal pyroclastic density currents, distal ash fall and short-term climate perturbations, which altogether warrant the study of how silicic magma bodies evolve and assemble. The southern rocky mountain volcanic field (SRMVF) is home to some of the largest super-eruptions in the geological record, and has been studied to help address the debate over how quickly eruptible magma batches can be assembled–whether in decades to centuries, or more slowly over 100’s of kyr. The present study focuses on the San Luis caldera complex within the SRMVF, and discusses the paradigms of rapid magma generation vs. rapid magma assembly. The caldera complex consists of three overlapping calderas that overlie the sources of three large-volume mid-Cenozoic ignimbrites: first, the Rat Creek Tuff (RCT; zoned dacite-rhyolite, 150 km3), followed by the Cebolla Creek Tuff (mafic dacite, 250 km3) and finally, the Nelson Mountain Tuff (NMT; zoned dacite-rhyolite, 500 km3), which are all indistinguishable in age by 40Ar/39Ar dating. We argue for a shared magmatic history for the three units on the basis of (1) similar mineral trace element compositions in the first and last eruptions (plagioclase, sanidine, biotite, pyroxene, amphibole, titanite, and zircon), (2) overlapping zircon U-Pb ages in all three units, and (3) similar thermal rejuvenation signatures visible in biotite (low-Mn, high-Ba) and zircon (low-Hf, low-U) geochemistry within the RCT and NMT. It is postulated that the NMT was sourced from a pre-existing magma reservoir to the northeast, which is corroborated by the formation of the nearby Cochetopa Caldera during the eruption of the NMT. The inferred lateral magma transport has two important implications: (1) it demonstrates long-distance transport of highly viscosity magmas at volumes (100’s of km3) not previously recorded, and (2) the sourcing of magma from a nearby pre-existing magma reservoir greatly reduces the rate of magma generation necessary to explain the close coincidence of three overlapping, large-volume magma systems. Additionally, the concept of magmatic “flux” (km3 kyr−1) is discussed in this context, and it is argued that an area-normalized flux (km3 kyr–1 km−2) provides a more useful number for measuring magma production rates: it is expected that magmatic volumes will scale with footprint of the thermal anomaly, and not taking this into account may lead to errant volumetric flux (km3 kyr−1) estimates. Meanwhile, area-normalized flux estimates in a given area are similar between units, consistent with evolution in a relatively constant thermal regime. Such estimates also demonstrate similar fluxes for ∼cogenetic volcanic and plutonic units.Publisher PDFPeer reviewe

Pharmacological characterisation of arthritis induced by Bothrops jararaca venom in rabbits: a positive cross talk between bradykinin, nitric oxide and prostaglandin E2.

BACKGROUND: Our previous results showed that nitric oxide (NO) and bradykinin (BK) mediate the arthritis induced by Bothrops jararaca venom (BjV) in rabbits. In this study, we investigated the contribution of each receptor of BK as well as the inter-relationship between NO and eicosanoids in BjV-induced arthritis. METHODS: The arthritis was induced in rabbits with 16 microg of BjV injected intra-articularly. Prostaglandin E2 (PGE2), thromboxane B2 (TxB2), leukotriene B4 (LTB4) (radioimmunoassay) and nitrite/nitrate concentrations (NO2/NO3) (Griess reaction) were evaluated in the synovial fluid 4 h later. The animals were prior treated with NO synthase inhibitor (L-NAME; 20 mg/kg/day for 14 days), the B2 antagonist of BK (HOE-140) and the B1 antagonist of BK (des-Arg9[Leu8]-bradykinin), both at a dose of 0.3mg/kg, 30 min prior to the venom injection. RESULTS: Data show that L-NAME and HOE-140 treatment were equally able to reduce PGE2 and NO2/NO3 levels without interfering with TxB2 and LTB4 production. On the contrary, the B1 antagonist of BK inhibited TxB2 and LTB4 production, and did not alter PGE2 and NO metabolites levels in the inflamed joint. DISCUSSIONS: The results presented clarify the contribution of the kinin system, mainly through the B2 receptor, to the local inflammatory response induced by BjV, as well as its positive interaction with PGE2 and NO production

Synthesis and preliminary biological evaluation of a compound library of triazolylcyclitols

AbstractA small library of compounds was prepared by a combination of toluene dioxygenase (TDO)-catalyzed enzymatic dihydroxylation and copper(I)-catalyzed Hüisgen cycloaddition. Some compounds were obtained by coupling an alkyne and a conduritol derivative, while more complex structures were obtained by a double Hüisgen reaction of a dialkyne and two molecules of the cyclitol. The compounds were fully characterized and subjected to preliminary biological screening

Bothrops asper snake venom and its metalloproteinase BaP-1 activate the complement system. Role in leucocyte recruitment.

The venom of the snake Bothrops asper, the most important poisonous snake in Central America, evokes an inflammatory response, the mechanisms of which are not well characterized. The objectives of this study were to investigate whether B. asper venom and its purified toxins--phospholipases and metalloproteinase--activate the complement system and the contribution of the effect on leucocyte recruitment. In vitro chemotaxis assays were performed using Boyden's chamber model to investigate the ability of serum incubated with venom and its purified toxins to induce neutrophil migration. The complement consumption by the venom was evaluated using an in vitro haemolytic assay. The importance of complement activation by the venom on neutrophil migration was investigated in vivo by injecting the venom into the peritoneal cavity of C5-deficient mice. Data obtained demonstrated that serum incubated with crude venom and its purified metalloproteinase BaP-1 are able to induce rat neutrophil chemotaxis, probably mediated by agent(s) derived from the complement system. This hypothesis was corroborated by the capacity of the venom to activate this system in vitro. The involvement of C5a in neutrophil chemotaxis induced by venom-activated serum was demonstrated by abolishing migration when neutrophils were pre-incubated with antirat C5a receptor antibody. The relevance of the complement system in in vivo leucocyte mobilization was further demonstrated by the drastic decrease of this response in C5-deficient mice. Pre-incubation of serum with the soluble human recombinant complement receptor type 1 (sCR 1) did not prevent the response induced by the venom, but abolished the migration evoked by metalloproteinase-activated serum. These data show the role of the complement system in bothropic envenomation and the participation of metalloproteinase in the effect. Also, they suggest that the venom may contain other component(s) which can cause direct activation of C5a