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Background 3,4-Methylenedioxymethamphetamine (MDMA) produces a neuroinflammatory reaction in rat brain characterized by an increase in interleukin-1 beta (IL-1β) and microglial activation. The CB2 receptor agonist JWH-015 reduces both these changes and partially protects against MDMA-induced neurotoxicity. We have examined MDMA-induced changes in IL-1 receptor antagonist (IL-1ra) levels and IL-1 receptor type I (IL-1RI) expression and the effects of JWH-015. The cellular location of IL-1β and IL-1RI was also examined. MDMA-treated animals were given the soluble form of IL-1RI (sIL-1RI) and neurotoxic effects examined. Methods Dark Agouti rats received MDMA (12.5 mg/kg, i.p.) and levels of IL-1ra and expression of IL-1RI measured 1 h, 3 h or 6 h later. JWH-015 (2.4 mg/kg, i.p.) was injected 48 h, 24 h and 0.5 h before MDMA and IL-1ra and IL-1RI measured. For localization studies, animals were sacrificed 1 h or 3 h following MDMA and stained for IL-1β or IL-1RI in combination with neuronal and microglial markers. sIL-1RI (3 μg/animal; i.c.v.) was administered 5 min before MDMA and 3 h later. 5-HT transporter density was determined 7 days after MDMA injection. Results MDMA produced an increase in IL-ra levels and a decrease in IL-1RI expression in hypothalamus which was prevented by CB2 receptor activation. IL-1RI expression was localized on neuronal cell bodies while IL-1β expression was observed in microglial cells following MDMA. sIL-1RI potentiated MDMA-induced neurotoxicity. MDMA also increased IgG immunostaining indicating that blood brain-barrier permeability was compromised. Conclusions In summary, MDMA produces changes in IL-1 signal modulators which are modified by CB2 receptor activation. These results indicate that IL-1β may play a partial role in MDMA-induced neurotoxicity.

Background Preconditioning is a phenomenon by which tolerance develops to injury by previous exposure to a stressor of mild severity. Previous studies have shown that single or repeated low dose MDMA can attenuate 5-HT transporter loss produced by a subsequent neurotoxic dose of the drug. We have explored the mechanism of delayed preconditioning by low dose MDMA. Methods Male Dark Agouti rats were given low dose MDMA (3 mg/kg, i.p.) 96 h before receiving neurotoxic MDMA (12.5 mg/kg, i.p.). IL-1β and IL1ra levels and 5-HT transporter density in frontal cortex were quantified at 1 h, 3 h or 7 days. IL-1β, IL-1ra and IL-1RI were determined between 3 h and 96 h after low dose MDMA. sIL-1RI combined with low dose MDMA or IL-1β were given 96 h before neurotoxic MDMA and toxicity assessed 7 days later. Results Pretreatment with low dose MDMA attenuated both the 5-HT transporter loss and elevated IL-1β levels induced by neurotoxic MDMA while producing an increase in IL-1ra levels. Low dose MDMA produced an increase in IL-1β at 3 h and in IL-1ra at 96 h. sIL-1RI expression was also increased after low dose MDMA. Coadministration of sIL-1RI (3 μg, i.c.v.) prevented the protection against neurotoxic MDMA provided by low dose MDMA. Furthermore, IL-1β (2.5 pg, intracortical) given 96 h before neurotoxic MDMA protected against the 5-HT neurotoxicity produced by the drug, thus mimicking preconditioning. Conclusions These results suggest that IL-1β plays an important role in the development of delayed preconditioning by low dose MDMA.

The behavior of composite beads of Zea mays rachis and sodium alginate (AL) for Pb (II) adsorption was studied. The Zea mays rachis–sodium alginate was prepared and characterized. The IR spectra showed interactions of the functional groups and the metal ions after adsorption. The kinetic data were fitted to the pseudo-first- and pseudo-second-order models, the maximum adsorption capacity was 60 mg/g for Pb (II), and the isotherm data were best adjusted to the Freundlich model, indicating that the adsorbent is heterogeneous. The thermodynamic study shows that the process is physisorption. The service time of columns increases as the height of columns increases, and this behavior was attributed to the active sites available in the columns. The initial concentration of Pb (II) had a significant effect on the breakthrough curves. As the concentration increases, the saturation time decreases. The material was regenerated four times (adsorption–desorption cycles), without a significant change in the removal efficiencies.

In this study, we prepared Al2O3-TiO2 (AT) mixed oxides to synthesize NiW catalysts for sulfur removal reactions. The AT support samples were prepared with various surfactants. Additionally, gallium atoms (2.4 wt%) were introduced as an additive to coat the outer surface layers of AT support that lacked Al3+ or Ti2+ cations. Characterization results showed substantial differences in textural properties, chemical composition, and surface acidity. The x-ray Photoelectron Spectroscopy (XPS) and High-Resolution Transmission Electron Microscopy (HR-TEM) results demonstrated that the NiW/AT-L-Ga sample has a better combination of dispersion, sulfidation, and promotion among materials. The sulfided NiW/AT-L-Ga catalyst had the highest catalytic activity. After incorporating Ga, XPS observed that the activity could be associated with an increase in the NiWS active phase; however, including a surfactant in the synthesis of the support allowed an increase in the amount of NiWS phase. The active phase was modeled considering the HR-TEM results for the slab length, revealing the atoms at the border susceptible to promotion.

Preconditioning is a phenomenon by which tolerance develops to injury by previous exposure to a stressor of mild severity. Previous studies have shown that single or repeated low dose MDMA can attenuate 5-HT transporter loss produced by a subsequent neurotoxic dose of the drug. We have explored the mechanism of delayed preconditioning by low dose MDMA. Male Dark Agouti rats were given low dose MDMA (3 mg/kg, i.p.) 96 h before receiving neurotoxic MDMA (12.5 mg/kg, i.p.). IL-1[beta] and IL1ra levels and 5-HT transporter density in frontal cortex were quantified at 1 h, 3 h or 7 days. IL-1[beta], IL-1ra and IL-1RI were determined between 3 h and 96 h after low dose MDMA. sIL-1RI combined with low dose MDMA or IL-1[beta] were given 96 h before neurotoxic MDMA and toxicity assessed 7 days later. Pretreatment with low dose MDMA attenuated both the 5-HT transporter loss and elevated IL-1[beta] levels induced by neurotoxic MDMA while producing an increase in IL-1ra levels. Low dose MDMA produced an increase in IL-1[beta] at 3 h and in IL-1ra at 96 h. sIL-1RI expression was also increased after low dose MDMA. Coadministration of sIL-1RI (3 [mu]g, i.c.v.) prevented the protection against neurotoxic MDMA provided by low dose MDMA. Furthermore, IL-1[beta] (2.5 pg, intracortical) given 96 h before neurotoxic MDMA protected against the 5-HT neurotoxicity produced by the drug, thus mimicking preconditioning. These results suggest that IL-1[beta] plays an important role in the development of delayed preconditioning by low dose MDMA.

If neutrinos are their own antiparticles the otherwise-forbidden nuclear reaction known as neutrinoless double beta decay can occur. The very long lifetime expected for these exceptional events makes its detection a daunting task. In order to conduct an almost background-free experiment, the NEXT collaboration is investigating novel synthetic molecular sensors that may capture the Ba dication produced in the decay of certain Xe isotopes in a high-pressure gas experiment. The use of such molecular detectors immobilized on surfaces must be explored in the ultra-dry environment of a xenon gas chamber. Here, using a combination of highly sensitive surface science techniques in ultra-high vacuum, we demonstrate the possibility of employing the so-called Fluorescent Bicolor Indicator as the molecular component of the sensor. We unravel the ion capture process for these molecular indicators immobilized on a surface and explain the origin of the emission fluorescence shift associated to the ion trapping. One of the possible events signaling a neutrinoless double beta decay is a Xe atom decaying into a Ba ion and two electrons. Aiming at the realisation of a detector for such a process, the authors show that Ba ions can be efficiently trapped (chelated) in vacuum by an organic molecule layer on a surface.

Hickson Compact Groups (HCGs) are dense configurations of 4 to 10 galaxies, whose HI (neutral gas) morphology appears to follow an evolutionary sequence of three phases, with gas initially confined to galaxies, then significant amounts spread throughout the intra-group medium, and finally with almost no gas remaining in the galaxies themselves. The HI deficiency of HCGs is expected to increase as the HI morphological phase progresses along this sequence, potentially making it a useful proxy for evolutionary phase. We test this hypothesis for the first time with a large sample of 38 HCGs with VLA HI observations that are uniformly reduced and analysed with a purpose-built pipeline. However, we find little evidence that HI deficiency can be used as a proxy for the evolutionary phase of a HCG in either of the first two phases, with the distribution of HI deficiency being consistent in both, although it does greatly increase in the third phase. This appears to be the result to three factors: a) there is already a broad range of HI deficiencies in Phase 1 HCGs, possibly due to their differing locations relative to large scale structures; b) the timescale for major interactions and morphological changes is, in general, considerably shorter than the timescale for the destruction or consumption of HI gas; and c) some groups have their HI content rejuvenated by the late addition of a new gas-rich member (for which we added a new sub-phase, 3c, to the established evolutionary sequence). Finally, across all HCGs studied, we identify only a few cases where there is strong evidence for the existence of a previously proposed diffuse HI component in the intra-group medium, which might be detectable with improved observations. This work was completed with considerable attention paid to scientific reproducibility, and all reduction and analysis has been made public via Github and Zenodo. (Abridged)

3,4-Methylenedioxymethamphetamine (MDMA) produces a neuroinflammatory reaction in rat brain characterized by an increase in interleukin-1 beta (IL-1[beta]) and microglial activation. The CB2 receptor agonist JWH-015 reduces both these changes and partially protects against MDMA-induced neurotoxicity. We have examined MDMA-induced changes in IL-1 receptor antagonist (IL-1ra) levels and IL-1 receptor type I (IL-1RI) expression and the effects of JWH-015. The cellular location of IL-1[beta] and IL-1RI was also examined. MDMA-treated animals were given the soluble form of IL-1RI (sIL-1RI) and neurotoxic effects examined. Dark Agouti rats received MDMA (12.5 mg/kg, i.p.) and levels of IL-1ra and expression of IL-1RI measured 1 h, 3 h or 6 h later. JWH-015 (2.4 mg/kg, i.p.) was injected 48 h, 24 h and 0.5 h before MDMA and IL-1ra and IL-1RI measured. For localization studies, animals were sacrificed 1 h or 3 h following MDMA and stained for IL-1[beta] or IL-1RI in combination with neuronal and microglial markers. sIL-1RI (3 [mu]g/animal; i.c.v.) was administered 5 min before MDMA and 3 h later. 5-HT transporter density was determined 7 days after MDMA injection. MDMA produced an increase in IL-ra levels and a decrease in IL-1RI expression in hypothalamus which was prevented by CB2 receptor activation. IL-1RI expression was localized on neuronal cell bodies while IL-1[beta] expression was observed in microglial cells following MDMA. sIL-1RI potentiated MDMA-induced neurotoxicity. MDMA also increased IgG immunostaining indicating that blood brain-barrier permeability was compromised. In summary, MDMA produces changes in IL-1 signal modulators which are modified by CB2 receptor activation. These results indicate that IL-1[beta] may play a partial role in MDMA-induced neurotoxicity.

Proteins are complex biological polymers that are commonly considered the workhorses of cells. They mediate virtually all the cellular functions. Correctly identifying and characterizing Protein-Protein interactions (PPIs) is an important task for thoroughly understanding the molecular mechanisms within cells. Despite great efforts that have been made by life science researchers to identify PPIs through experiments and then document them through publications, there still lacks an effective means for retrieving PPI data from literature: manual curation of documents provides accurate results, but is a slow and tedious task that requires a large amount of effort. In this thesis we present a comprehensive system to automatically extract PPI-related information from biomedical articles by mining both textual and graphical information. Our framework aims to assist life scientist to accurately and efficiently curate relevant PPI information from literature. We first develop a solution for robustly harvesting figure-caption pairs from biomedical literature. Our approach relies on the idea that the PDF specification of the document layout can be used to identify encoded figures and figure boundaries within the PDF and enforce constraints among figure-regions. This allows us to harvest fragmented figures from the PDF, correctly identify subfigures that belong to the same figure, and identify the captions associated with each figure. Our method simultaneously recovers figures and captions and applies additional filtering process to remove irrelevant figures such as logos, to eliminate text passages that were incorrectly identified as captions, and to re-group subfigures to generate a putative figure. We then present a robust solution for automatically segmenting each figure into unimodal panels. Our approach analyzes figure captions to estimate the number of panels and then combines it with geometric constrains obtained from the position of the panel labels for conducting robust panel extraction. We further develop a hybrid image-text based classification scheme to automatically identify experimental evidence (methods) of PPIs in each panel. We store all processed results (the raw documents, their figures and captions, PPI methods, etc.) in a relational database and construct a new content-based image retrieval (CBIR) system called ePPI (Experimental PPIs). Life scientists can use cascaded queries in ePPI to easily and effectively retrieve PPI-related figures within each article as well as capture essential facts (e.g., experimental methods) regarding specific pairs of PPIs.

The NEXT experiment aims at the sensitive search of the neutrinoless double beta decay in \\(^{136}\\)Xe, using high-pressure gas electroluminescent time projection chambers. The NEXT-White detector is the first radiopure demonstrator of this technology, operated in the Laboratorio Subterráneo de Canfranc. Achieving an energy resolution of 1% FWHM at 2.6 MeV and further background rejection by means of the topology of the reconstructed tracks, NEXT-White has been exploited beyond its original goals in order to perform a neutrinoless double beta decay search. The analysis considers the combination of 271.6 days of \\(^{136}\\)Xe-enriched data and 208.9 days of \\(^{136}\\)Xe-depleted data. A detailed background modeling and measurement has been developed, ensuring the time stability of the radiogenic and cosmogenic contributions across both data samples. Limits to the neutrinoless mode are obtained in two alternative analyses: a background-model-dependent approach and a novel direct background-subtraction technique, offering results with small dependence on the background model assumptions. With a fiducial mass of only 3.50\\(\\pm\\)0.01 kg of \\(^{136}\\)Xe-enriched xenon, 90% C.L. lower limits to the neutrinoless double beta decay are found in the T\\(_{1/2}^{0\\nu}>5.5\\times10^{23}-1.3\\times10^{24}\\) yr range, depending on the method. The presented techniques stand as a proof-of-concept for the searches to be implemented with larger NEXT detectors.