3,221 research outputs found

    Brazilian Contemporary Art in the International Art Market

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    With changes in the art world, the Brazilian Contemporary art becomes an interesting subject to be analyzed in its relationship to the art market dynamics. The international art market has been growing since late 90s thanks to globalization. In this sense, the problematization of the research lies in an economical perspective of the art market to understand Brazilian Contemporary art internationalization through art fairs, biennials, art galleries and auction houses. With this analysis, the objective is to present an opinion about the panorama of Brazilian Contemporary art and its international market insertion

    Scavenging activity of Magnéli phases as a function of Ti(4+)/Ti(3+) ratios

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    TiO2 is able to scavenge reactive oxygen and nitrogen species (ROS and RNS) in the absence of light. The scavenging mechanism has been related to the chemistry of defects (oxygen vacancy reduced oxidation states of Ti) but it is still unknown. This study describes the ROS scavenging activity of different titanium oxide phases and relates their scavenging activities with the Ti4+/Ti3+ molar ratio as well as the band gap value. The Ti5O9 phase, with a mixture of both oxidation states, presented a substantially higher percentage of 2,2-diphenyl-1-picrylhydracyl radicals (DPPH) eliminated per m2 of specific surface area in comparison to phases with predominant oxidation states Ti4+ or Ti3+ such as TiO2 and Ti2O3, respectively. The obtained results indicate that the DPPH scavenging mechanism corresponds to a catalytic process on the Ti5O9 surface which is facilitated by the presence of charges that can easily move through the material. The mobility of charges and electrons in the semiconductor surface, related to the presence of oxidation states Ti4+ and Ti3+ and a small band gap, could create an attractive surface for radical species such as DPPH. This puts forward Ti5O9 as a promising candidate coating for implantable biomedical devices, as an electrode, since it can cushion inflammatory processes which could lead to device encapsulation and, consequently, failure.The authors would like to thank the Fundación General CSIC and Obra Social “La Caixa” (Project BIOAMD) for providing financial support to this work. Dr Canillas acknowledges the financial support received from the CSIC for her PhD JAEpre grant and Dr Moreno is grateful to the Fondo Social Europeo and CSIC for her JAEDoc contract

    Clinical and quality-of-life assessment among women with temporomandibular disorder

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    OBJETIVOS: Este estudo teve como objetivo avaliar sintomas de dor, apertamento dos dentes, qualidade do sono e sensibilidade dolorosa nos principais músculos mastigatórios e estabilizadores cervicais e qualidade de vida de mulheres com Disfunção Temporomandibular (DTM). MÉTODOS: Foram avaliadas 45 mulheres, divididas em dois grupos. O grupo I, composto por 27 mulheres (30,1±5,8anos) com diagnóstico de DTM e o grupo II, controle, composto por 18 mulheres saudáveis (23,4±2,3 anos). A intensidade dos sintomas de dor, cefaleia, cervicalgia, de apertamento dos dentes e dificuldade de dormir foram avaliados por escala visual analógica (EVA), o limiar de dor dos músculos masseter, temporal anterior, trapézio superior e esternocleidomastoideo, com dolorímetro e a qualidade de vida, pelo SF-36. Foi realizada análise estatística e o nível de significância foi &#945;=0,05. RESULTADOS: Os resultados mostram que mulheres com DTM têm sintomas mais intensos de cefaleia (p<0,001), cervicalgia (p<0,001), intensidade de apertamento dos dentes (p<0,001) e dificuldade de dormir (p<0,001). Também apresentam limiar de dor mais baixo nos músculos masseter (p<0,001), temporal anterior (p<0,001), trapézio superior (p<0,001), esternocleidomastoideo (p<0,001) e pior qualidade de vida em todos os domínios avaliados (p<0,05), quando comparados com o grupo controle. CONCLUSÕES: Mulheres com DTM têm maior intensidade dos sintomas de dor, apertamento dos dentes, dificuldade de dormir, maior sensibilidade dolorosa em músculos mastigatórios e cervicais e pior qualidade de vida quando comparadas com mulheres sem DTM.OBJECTIVES: The aim of this study was to evaluate pain symptoms, teeth clenching, quality of sleep, sensitivity to pain in the main masticatory and stabilizer muscles, and quality of life among women with temporomandibular disorder (TMD). METHODS: Forty-five women were evaluated and divided into two groups. Group I included 27 women (mean age 30.1±5.8 years) with a diagnosis of TMD and Group II (control) included 18 healthy women (mean age 23.4±2.3 years). The intensity of pain symptoms (headache, neck pain), teeth clenching and trouble sleeping was evaluated using a visual analog scale (VAS). The pain thresholds of the masseter, anterior temporalis, upper trapezius and sternocleidomastoid muscles were evaluated using a dolorimeter. Quality of life was evaluated using SF-36. Statistical analysis was performed and the significance level was &#945;<0.05. RESULTS: The results showed that the women with TMD presented more intense headache (p<0.001), neck pain (p<0.001), teeth clenching (p<0.001) and trouble sleeping (p<0.001). They also presented lower pain threshold in the masseter (p<0.001), anterior temporalis (p<0.001), upper trapezius (p<0.001) and sternocleidomastoid (p<0.001) muscles and lower quality of life in all evaluated domains (p<0.05) when compared with the control group. CONCLUSIONS:Women with TMD had greater intensity of pain symptoms, teeth clenching, trouble sleeping, sensitivity to pain in the masticatory and neck muscles and lower quality of life, compared with women without TMD

    Therapeutic antisense oligonucleotides against cancer: Hurdling to the clinic

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    Under clinical development since the early 90's and with two successfully approved drugs (Fomivirsen and Mipomersen), oligonucleotide-based therapeutics has not yet delivered a clinical drug to the market in the cancer field. Whilst many pre-clinical data has been generated, a lack of understanding still exists on how to efficiently tackle all the different challenges presented for cancer targeting in a clinical setting. Namely, effective drug vectorization, careful choice of target gene or synergistic multi-gene targeting are surely decisive, while caution must be exerted to avoid potential toxic, often misleading off-target-effects. Here a brief overview will be given on the nucleic acid chemistry advances that established oligonucleotide technologies as a promising therapeutic alternative and ongoing cancer related clinical trials. Special attention will be given toward a perspective on the hurdles encountered specifically in the cancer field by this class of therapeutic oligonucleotides and a view on possible avenues for success is presented, with particular focus on the contribution from nanotechnology to the field.The authors would like to acknowledge the FEDER funds through the Programa Operacional Factores de Competitividade - COMPETE and the Portuguese funds through FCT – Fundação para a Ciência e a Tecnologia (PTDC/CTM-NAN/115124/2009, HMSP-ICT/0020/2010 and PEst-C/SAU/LA0002/2013) that supported this work. Pedro M. D. Moreno is supported by a Marie Curie Action of the European Community’s Seventh Framework Program (PIEF-GA2 011300485)

    Impact of carvedilol on the mitochondrial damage induced by hypoxanthine and xantine oxidase: what role in myocardial ischemia and reperfusion?

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    OBJECTIVES: The cardioprotective effects of carvedilol (CV) may be explained in part by interactions with heart mitochondria. The objective of this work was to study the protection afforded by CV against oxidative stress induced in isolated heart mitochondria by hypoxanthine and xanthine oxidase (HX/XO), a well-known source of reactive oxygen species (ROS) in the cardiovascular system. METHODS: Mitochondria were isolated from Wistar rat hearts (n = 8) and incubated with HX/XO in the presence and in the absence of calcium. Several methods were used to assess the protection afforded by CV: evaluation of mitochondrial volume changes (by measuring changes in the optical density of the mitochondrial suspension), calcium uptake and release (with a fluorescent probe, Calcium Green 5-N) and mitochondrial respiration (with a Clark-type oxygen electrode). RESULTS: CV decreased mitochondrial damage associated with ROS production by HX and XO, as verified by the reduction of mitochondrial swelling and increase in mitochondrial calcium uptake. In the presence of HX and XO, CV also ameliorated mitochondrial respiration in the active phosphorylation state and prevented decrease in the respiratory control ratio (p < 0.05) and in mitochondrial phosphorylative efficiency (p < 0.001). CONCLUSIONS: The data indicate that CV partly protected heart mitochondria from oxidative damage induced by HX and XO, which may be useful during myocardial ischemia and reperfusion. It is also suggested that mitochondria may be a priority target for the protective action of some compounds

    Three-dimensional image surface acquisition in vertebrate paleontology: A review of principal techniques

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    Three-dimensional (3D) surface scanning includes techniques of image acquisition and image processing. Among the former, hardware devices (e.g., portable and non-portable scanners, camera) capture images from the target, whereas image processing is conducted via specialized software, in which acquired images are processed to merge them into a single 3D surface model. Image surface scanning comprises a wide variety of devices which incorporate different image acquisition techniques, all of them with potential high standards results. We describe four different scanning devices and techniques commonly used in vertebrate paleontology in order to compare them in terms of pros and cons, considering different variables, such as scanning time, post-processing time, costs and image resolution. The decision on which device to choose will depend on the budget available, the portability as well as the nature of the fossil material being analyzed (e.g., size, weight, accessibility). In the light of this, photogrammetry constitutes the image surface technique which fulfills these requirements, having the best cost-benefit relationship

    Advantages in the use of carvedilol versus propranolol for the protection of cardiac mitochondrial function

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    BACKGROUND: Carvedilol is a neurohormonal antagonist of multiple action which is used in clinical practice for the treatment of congestive heart failure, mild to moderate hypertension and myocardial infarction. Previous results from our group have demonstrated that one of the main targets for the protective effect of carvedilol is the cardiac mitochondrial network. In-this work, we compare the effect of carvedilol with propranolol in different models of mitochondrial dysfunction and in the generation of transmembrane electric potential (EP). We further tested if carvedilol was able to inhibit the mitochondrial permeability transition (MPT) induced by doxorubicin and calcium-dependent cytochrome c release, a phenomenon frequently associated with apoptotic cell death. METHODS: Cardiac mitochondria were isolated by differential centrifugation. Oxygen consumption and mitochondrial EP were determined using an oxygen electrode and a tetraphenylphosphonium-sensitive electrode, respectively. Changes in mitochondrial volume and the release of cytochrome c were measured with spectrophotometric techniques. RESULTS: Propranolol, compared with carvedilol, had only a marginal effect, not only in protection against MPT induction, but also against oxygen consumption linked to the oxidation of external NADH, a process that is considered by several authors as key in the cardiotoxicity of doxorubicin. Regarding EP generation, propranolol had no effect, in contrast to carvedilol, which was confirmed to act as a protonophore. For the first time we also show that carvedilol inhibits the MPT induced by doxorubicin and calcium-dependent cytochrome c release. CONCLUSIONS: With this work, we further support the notion that carvedilol is effective in several models of mitochondrial dysfunction, particularly those involving oxidative stress. The results demonstrate that for some pathological conditions, carvedilol and propranolol have different mechanisms of action at the sub-cellular level, as propranolol seems to lack effectiveness in the protection of cardiac mitochondria

    Histological changes and impairment of liver mitochondrial bioenergetics after long-term treatment with alpha-naphthyl-isothiocyanate (ANIT)

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    This study was designed to evaluate the effects of long-term treatment with alpha-naphthyl-isothiocyanate (ANIT) on liver histology and at the mitochondrial bioenergetic level. Since, ANIT has been used as a cholestatic agent and it has been pointed out that an impairment of mitochondrial function is a cause of hepatocyte dysfunction leading to cholestatic liver injury, serum markers of liver injury were measured and liver sections were analyzed in ANIT-treated rats (i.p. 80 mg/kg/week x 16 weeks). Mitochondrial parameters such as transmembrane potential, respiration, calcium capacity, alterations in permeability transition susceptibility and ATPase activity were monitored. Histologically, the most important features were the marked ductular proliferation, proliferation of mast cells and the presence of iron deposits in ANIT-treated liver. Mitochondria isolated from ANIT-treated rats showed no alterations in state 4 respiration, respiratory control ratio and ADP/O ratio, while state 3 respiration was significantly decreased. No changes were observed on transmembrane potential, but the repolarization rate was decreased in treated rats. Consistently with these data, there was a significant decrease in the ATPase activity of treated mitochondria. Associated with these parameters, mitochondria from treated animals exhibited increased susceptibility to mitochondrial permeability transition pore opening (lower calcium capacity). Since, human cholestatic liver disease progress slowly overtime, these data provide further insight into the role of mitochondrial dysfunction in the process

    Antisense Oligonucleotides Modulating Activation of a Nonsense-Mediated RNA Decay Switch Exon in the ATM Gene

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    ATM (ataxia-telangiectasia, mutated) is an important cancer susceptibility gene that encodes a key apical kin ase in the DNA damage response pathway. ATM mutations in the germ line result in ataxia-telangiectasia (A-T), a rare genetic syndrome associated with hypersensitivity to double-strand DNA breaks and predisposition to lymphoid malignancies. ATM expression is limited by a tightly regulated nonsense-mediated RNA decay (NMD) switch exon (termed NSE) located in intron 28. In this study, we identify antisense oligonucleotides that modulate NSE inclusion in mature transcripts by systematically targeting the entire 3.1-kb-long intron. Their identification was assisted by a segmental deletion analysis of transposed elements, revealing NSE repression upon removal of a distant antisense Alu and NSE activation upon elimination of a long terminal repeat transposon MER51A. Efficient NSE repression was achieved by delivering optimized splice-switching oligonucleotides to embryonic and lymphoblastoid cells using chitosan-based nanoparticles. Together, these results provide a basis for possible sequence-specific radiosensitization of cancer cells, highlight the power of intronic antisense oligonucleotides to modify gene expression, and demonstrate transposon-mediated regulation of NSEs.The authors wish to thank Professor Steven Marsh (UCL and the Anthony Nolan Trust) for a generous gift of the VAVY cell line. This work was funded by Bloodwise (grant 12060 to I.V. and N.C.P.C), Santa Casa da Misericordia de Lisboa—Premio Melo e Castro (grant MC-1068-2015 to A.P.P.), and Fundacão para a Ciência e Tecnologia (grant SFRH/BPD/108738/2015 to P.M.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

    Hydrogel-Assisted Antisense LNA Gapmer Delivery for In Situ Gene Silencing in Spinal Cord Injury

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    After spinal cord injury (SCI), nerve regeneration is severely hampered due to the establishment of a highly inhibitory microenvironment at the injury site, through the contribution of multiple factors. The potential of antisense oligonucleotides (AONs) to modify gene expression at different levels, allowing the regulation of cell survival and cell function, together with the availability of chemically modified nucleic acids with favorable biopharmaceutical properties, make AONs an attractive tool for novel SCI therapy developments. In this work, we explored the potential of locked nucleic acid (LNA)-modified AON gapmers in combination with a fibrin hydrogel bridging material to induce gene silencing in situ at a SCI lesion site. LNA gapmers were effectively developed against two promising gene targets aiming at enhancing axonal regeneration—RhoA and GSK3ß. The fibrin-matrix-assisted AON delivery system mediated potent RNA knockdown in vitro in a dorsal root ganglion explant culture system and in vivo at a SCI lesion site, achieving around 75% downregulation 5 days after hydrogel injection. Our results show that local implantation of a AON-gapmer-loaded hydrogel matrix mediated efficient gene silencing in the lesioned spinal cord and is an innovative platform that can potentially combine gene regulation with regenerative permissive substrates aiming at SCI therapeutics and nerve regeneration.This work was supported by Fundação para a Ciência e a Tecnologia ( FCT , Portugal) in the framework of the Harvard-Portugal Medical School Program ( HMSP-ICT/0020/2010 ); Project NORTE-01-0145-FEDER-000008 , supported by the Norte Portugal Regional Operational Programme (NORTE 2020) , under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF) ; Fundo Europeu de Desenvolvimento Regional funds through COMPETE 2020 - Operational Program for Competitiveness and Internationalization (POCI) , Portugal 2020; by Portuguese funds through FCT/Ministério da Ciência, Tecnologia e Ensino Superior in the framework of the project “Institute for Research and Innovation in Health Sciences” ( POCI-01-0145-FEDER-007274 ); Marie Curie Actions of the European Community’s 7th Framework Program ( PIEF-GA-2011-300485 to P.M.D.M.); Santa Casa da Misericordia de Lisboa – Prémio Neurociências Mello e Castro , and FCT fellowship SFRH/BPD/108738/2015 (to P.M.D.M). Funding for open access charge: Project NORTE-01-0145-FEDER-000012 , financed by Norte Portugal Regional Operational Programme (NORTE 2020) , under the PORTUGAL 2020 Partnership Agreement, through the ERDF . We would like to acknowledge the support from Paula Magalhães and Tânia Meireles from the i3S Cell Culture and Genotyping Core Facility in real-time PCR experiments
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