188 research outputs found

    Melatonin Synthesis and Function: Evolutionary History in Animals and Plants

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    Melatonin is an ancient molecule that can be traced back to the origin of life. Melatonin's initial function was likely that as a free radical scavenger. Melatonin presumably evolved in bacteria; it has been measured in both α-proteobacteria and in photosynthetic cyanobacteria. In early evolution, bacteria were phagocytosed by primitive eukaryotes for their nutrient value. According to the endosymbiotic theory, the ingested bacteria eventually developed a symbiotic association with their host eukaryotes. The ingested α-proteobacteria evolved into mitochondria while cyanobacteria became chloroplasts and both organelles retained their ability to produce melatonin. Since these organelles have persisted to the present day, all species that ever existed or currently exist may have or may continue to synthesize melatonin in their mitochondria (animals and plants) and chloroplasts (plants) where it functions as an antioxidant. Melatonin's other functions, including its multiple receptors, developed later in evolution. In present day animals, via receptor-mediated means, melatonin functions in the regulation of sleep, modulation of circadian rhythms, enhancement of immunity, as a multifunctional oncostatic agent, etc., while retaining its ability to reduce oxidative stress by processes that are, in part, receptor-independent. In plants, melatonin continues to function in reducing oxidative stress as well as in promoting seed germination and growth, improving stress resistance, stimulating the immune system and modulating circadian rhythms; a single melatonin receptor has been identified in land plants where it controls stomatal closure on leaves. The melatonin synthetic pathway varies somewhat between plants and animals. The amino acid, tryptophan, is the necessary precursor of melatonin in all taxa. In animals, tryptophan is initially hydroxylated to 5-hydroxytryptophan which is then decarboxylated with the formation of serotonin. Serotonin is either acetylated to N-acetylserotonin or it is methylated to form 5-methoxytryptamine; these products are either methylated or acetylated, respectively, to produce melatonin. In plants, tryptophan is first decarboxylated to tryptamine which is then hydroxylated to form serotonin

    Unprecedented Arctic sea ice thickness loss and multiyear-ice volume export through Fram Strait during 2010-2011

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    The satellite-observed sea ice thickness records from 2003 to 2020 identify an extreme sea ice thickness loss during 2010–2011. Ice thickness budget analysis demonstrates that the thickness loss was associated with an extraordinarily large multiyear ice volume export through the Fram Strait during the season of sea ice advance. High cloudiness led to positive anomalies of net longwave radiation, and positive net surface energy flux anomalies supported enhanced sea ice melt from June to August. Due to the multiyear ice loss, the Arctic sea ice became more sensitive to subsequent atmospheric anomalies. The reduced surface albedo triggering a positive ice-albedo amplifying feedback and contributed to the accelerating loss of ice thickness. These tightly coupled events highlight that the increasingly younger and thinner Arctic sea ice is becoming more vulnerable to external forcing and created the precondition for the rapid reduction in sea ice extent in 2012

    Synthesis and characterisation of novel nopyl-derived phosphonium ionic liquids

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    A series of novel nopyl-derived chiral phosphonium ionic liquids have been successfully synthesised and characterised. Analysis of each novel ionic liquid was conducted in order to confirm structure, purity and thermal stability

    Measurement of the diffractive structure function in deep inelastic scattering at HERA

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    This paper presents an analysis of the inclusive properties of diffractive deep inelastic scattering events produced in epep interactions at HERA. The events are characterised by a rapidity gap between the outgoing proton system and the remaining hadronic system. Inclusive distributions are presented and compared with Monte Carlo models for diffractive processes. The data are consistent with models where the pomeron structure function has a hard and a soft contribution. The diffractive structure function is measured as a function of \xpom, the momentum fraction lost by the proton, of β\beta, the momentum fraction of the struck quark with respect to \xpom, and of Q2Q^2. The \xpom dependence is consistent with the form \xpoma where a = 1.30 ± 0.08 (stat) − 0.14+ 0.08 (sys)a~=~1.30~\pm~0.08~(stat)~^{+~0.08}_{-~0.14}~(sys) in all bins of β\beta and Q2Q^2. In the measured Q2Q^2 range, the diffractive structure function approximately scales with Q2Q^2 at fixed β\beta. In an Ingelman-Schlein type model, where commonly used pomeron flux factor normalisations are assumed, it is found that the quarks within the pomeron do not saturate the momentum sum rule.Comment: 36 pages, latex, 11 figures appended as uuencoded fil

    Negative Regulation of Schistosoma japonicum Egg-Induced Liver Fibrosis by Natural Killer Cells

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    The role of natural killer (NK) cells in infection-induced liver fibrosis remains obscure. In this study, we elucidated the effect of NK cells on Schistosoma japonicum (S. japonicum) egg-induced liver fibrosis. Liver fibrosis was induced by infecting C57BL/6 mice with 18–20 cercariae of S. japonicum. Anti-ASGM1 antibody was used to deplete NK cells. Toll-like receptor 3 ligand, polyinosinic-polycytidylic acid (poly I∶C) was used to enhance the activation of NK cells. Results showed that NK cells were accumulated and activated after S. japonicum infection, as evidenced by the elevation of CD69 expression and IFN-γ production. Depletion of NK cells markedly enhanced S. japonicum egg-induced liver fibrosis. Administration of poly I∶C further activated NK cells to produce IFN-γ and attenuated S. japonicum egg-induced liver fibrosis. The observed protective effect of poly I∶C on liver fibrosis was diminished through depletion of NK cells. Disruption of IFN-γ gene enhanced liver fibrosis and partially abolished the suppression of liver fibrosis by poly I∶C. Moreover, expression of retinoic acid early inducible 1 (RAE 1), the NKG2D ligand, was detectable at high levels on activated hepatic stellate cells derived from S. japonicum-infected mice, which made them more susceptible to hepatic NK cell killing. In conclusion, our findings suggest that the activated NK cells in the liver after S. japonicum infection negatively regulate egg-induced liver fibrosis via producing IFN-γ, and killing activated stellate cells
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