Argumentive Writing as a Collaborative Activity

Although converging evidence indicates that argumentive thinking and writing are best promoted by collaboration with others, it is still unclear which instructional approaches exert most benefits. The present study builds on the success of using a dialogic approach to develop argumentation skills in middle school students. The key component of the approach used here is the creation of an adversarial classroom setting in which students engage deeply in dialogic argumentation, which is viewed here as a process involving two or more individuals who hold opposing views. In dialogic argumentation, the focus of students’ attention will tend to center on the discursive goals of strengthening their own positions and weakening the position of the opponents. These goals of discourse ensure that students not only exercise supporting their claims with reasons and evidence but also practice making and responding to critiques, which is said to promote students’ mastery of the argument-counterargument-rebuttal structure. While the literature describes compelling advantages of dialogic approaches, it also reports valid concerns. A main concern is that during dialogic argumentation arguers have diverging goals of advancing their own positions, which may prevent the integration of opposing arguments. In an attempt to explore whether this disadvantage can be minimized, the present study examines whether the addition of a collaborative writing activity, as a form of peer argumentation that draws students’ attention towards a converging goal, to the dialogic curriculum provides students a further degree of support in developing their argumentive writing skills. It is hypothesized that collaborative writing would serve as a bridge between dialogic and individual argumentation by changing the focus of students’ attention from the adversarial to the collaborative dimensions of argumentation. To examine this hypothesis, two classes of sixth grade students participated in a month-long intervention that promoted deep engagement in dialogic argumentation on a series of challenging topics. Groups differed only with respect to participation in collaborative writing. Analysis of individual essays on the final intervention topic indicates that students who participated in collaborative writing showed gains relative to students who didn’t in coordinating evidence with claims, specifically in drawing on evidence to make claims that are inconsistent as well as consistent with their favored positions. On a transfer topic, students in the collaborative writing condition continued to surpass students in the individual writing condition; however, the gains were restricted to drawing on evidence to make claims that are consistent with the students’ favored positions. The results support the claim that the combination of adversarial and collaborative forms of peer argumentation in classroom instruction is a promising path for developing middle school students’ argumentive writing skills. Theoretical and practical implications are discussed

Oleic acid inhibits lung Na/K-ATPase in mice and induces injury with lipid body formation in leukocytes and eicosanoid production

Submitted by sandra infurna ([email protected]) on 2016-01-26T11:43:07Z No. of bitstreams: 1 cassiano_albuquerque_etal_IOC_2013.pdf: 2143360 bytes, checksum: 8f5e5674d7c469c0ea089e8c27de22ed (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-01-26T12:03:05Z (GMT) No. of bitstreams: 1 cassiano_albuquerque_etal_IOC_2013.pdf: 2143360 bytes, checksum: 8f5e5674d7c469c0ea089e8c27de22ed (MD5)Made available in DSpace on 2016-01-26T12:03:05Z (GMT). No. of bitstreams: 1 cassiano_albuquerque_etal_IOC_2013.pdf: 2143360 bytes, checksum: 8f5e5674d7c469c0ea089e8c27de22ed (MD5) Previous issue date: 2013Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense.Instituto de Biologia. Departamento de Biologia Celular e Molecular. Niterói, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Departamento de Química Analítica. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Departamento de Química Analítica. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Universidade do Estado do Rio de Janeiro. Faculdade de Ciências Mèdicas. Departamento de Medicina Interna. Rio de Janeiro, RJ, Brasil.Background: Acute respiratory distress syndrome (ARDS) can emerge from certain pathologies, such as sepsis, fat embolism and leptospirosis, in which the levels of unesterified fatty acids are increased in the patient’s plasma. ARDS is characterized by edema formation, and edema resolution occurs mainly due to the pneumocyte Na/K-ATPase activity. As previously described, increased oleic acid (OA) plasma concentrations induce lung injury by interfering with sodium transport. The first aim of this study was to develop a radioactivity-free assay to detect Na,K-ATPase activity ex vivo using a model of OA-induced lung injury in mice. We also investigated the relationship between Na/K-ATPase inhibition and OA-induced lung injury using ouabain-induced lung injury as a comparison, because of the well-described effect of ouabain as a Na/K-ATPase inhibitor. Methods: We developed a Na/K-ATPase assay based on the capture of non-radioactive Rb+ ions by mice lung tissue in the absence or presence of ouabain, a specific Na/K-ATPase inhibitor. Rb+ incorporation into the lung was measured by inductively coupled plasma-optical emission spectrometry (ICP-OES) after lung tissue mineralization. Na/K-ATPase activity was considered as the difference between Rb+ incorporation in the absence and in the presence of ouabain. Bronchoalveolar lavage fluid was collected for lung injury assessment. For this assessment, cell counting, lipid body enumeration and lipid mediator concentrations were measured. Histological analyses were used to determinate lung pathology. Whole body plethysmographic analysis was performed to assay lung function. Results: The lung Na/K-ATPase activity of mice was completely inhibited by an OA dose of 10 μmol, an effect also obtained with 10-3 μmol of ouabain, as demonstrated by the decreased Rb+ incorporation in the lungs. The same OA dose induced lung edema and inflammation with cell influx, lipid body formation, and leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) production. Ouabain also induced lung inflammation, as detected by histological examinations. As far as we know, this is the first time that ouabain-induced lung injury was shown. Both OA and ouabain induced functional lung pathology in mice simultaneously with inhibition of the lung Na/K-ATPase activity. Conclusions: We developed a new non-radioactive assay to quantified Na/K-ATPase in vivo. OA and ouabain inhibited in vivo Na/K-ATPase activity in the lungs and induced lung injury. Our data reinforce the idea that Na/K-ATPase inhibitors may worsen lung injury in specific pathological conditions

Omega-9 Oleic Acid, the Main Compound of Olive Oil, Mitigates Inflammation during Experimental Sepsis

The Mediterranean diet, rich in olive oil, is beneficial, reducing the risk of cardiovascular diseases and cancer. Olive oil is mostly composed of the monounsaturated fatty acid omega-9. We showed omega-9 protects septic mice modulating lipid metabolism. Sepsis is initiated by the host response to infection with organ damage, increased plasma free fatty acids, high levels of cortisol, massive cytokine production, leukocyte activation, and endothelial dysfunction. We aimed to analyze the effect of omega-9 supplementation on corticosteroid unbalance, inflammation, bacterial elimination, and peroxisome proliferator-activated receptor (PPAR) gamma expression, an omega-9 receptor and inflammatory modulator. We treated mice for 14 days with omega-9 and induced sepsis by cecal ligation and puncture (CLP). We measured systemic corticosterone levels, cytokine production, leukocyte and bacterial counts in the peritoneum, and the expression of PPAR gamma in both liver and adipose tissues during experimental sepsis. We further studied omega-9 effects on leukocyte rolling in mouse cremaster muscle-inflamed postcapillary venules and in the cerebral microcirculation of septic mice. Here, we demonstrate that omega-9 treatment is associated with increased levels of the anti-inflammatory cytokine IL-10 and decreased levels of the proinflammatory cytokines TNF-alpha and IL-1 beta in peritoneal lavage fluid of mice with sepsis. Omega-9 treatment also decreased systemic corticosterone levels. Neutrophil migration from circulation to the peritoneal cavity and leukocyte rolling on the endothelium were decreased by omega-9 treatment. Omega-9 also decreased bacterial load in the peritoneal lavage and restored liver and adipose tissue PPAR gamma expression in septic animals. Our data suggest a beneficial anti-inflammatory role of omega-9 in sepsis, mitigating leukocyte rolling and leukocyte influx, balancing cytokine production, and controlling bacterial growth possibly through a PPAR gamma expression-dependent mechanism. The significant reduction of inflammation detected after omega-9 enteral injection can further contribute to the already known beneficial properties facilitated by unsaturated fatty acid-enriched diets

Omega-9 Oleic Acid Induces Fatty Acid Oxidation and Decreases Organ Dysfunction and Mortality in Experimental Sepsis

Submitted by sandra infurna ([email protected]) on 2016-06-19T21:56:40Z No. of bitstreams: 1 flora_oliveira_etal_IOC_2016.PDF: 1127513 bytes, checksum: 2b33c8a8ebdd6279e2e149aaedca5a3a (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-06-19T22:20:25Z (GMT) No. of bitstreams: 1 flora_oliveira_etal_IOC_2016.PDF: 1127513 bytes, checksum: 2b33c8a8ebdd6279e2e149aaedca5a3a (MD5)Made available in DSpace on 2016-06-19T22:20:25Z (GMT). No. of bitstreams: 1 flora_oliveira_etal_IOC_2016.PDF: 1127513 bytes, checksum: 2b33c8a8ebdd6279e2e149aaedca5a3a (MD5) Previous issue date: 2016Made available in DSpace on 2016-07-08T12:22:05Z (GMT). No. of bitstreams: 3 flora_oliveira_etal_IOC_2016.PDF.txt: 55221 bytes, checksum: 6263327453588b424db910e20fddf55b (MD5) flora_oliveira_etal_IOC_2016.PDF: 1127513 bytes, checksum: 2b33c8a8ebdd6279e2e149aaedca5a3a (MD5) license.txt: 2991 bytes, checksum: 5a560609d32a3863062d77ff32785d58 (MD5) Previous issue date: 2016Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense. Faculdade de Ciências Médicas. Instituto de Biologia. Departamento de Biologia Celular e Molecular. Niterói, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Universidade do Estado do Rio de Janeiro. Faculdade de Ciências Médicas. Departamento de Medicina Interna. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil / Universidade Estácio de Sá. Programa de Produtividade Científica. Rio de Janeiro, RJ, Brasil .Sepsis is characterized by inflammatory and metabolic alterations, which lead to massive cytokine production, oxidative stress and organ dysfunction. In severe systemic inflammatory response syndrome, plasma non-esterified fatty acids (NEFA) are increased. Several NEFA are deleterious to cells, activate Toll-like receptors and inhibit Na+/K+-ATPase, causing lung injury. A Mediterranean diet rich in olive oil is beneficial. Themain component of olive oil is omega-9 oleic acid (OA), a monounsaturated fatty acid (MUFA).We analyzed the effect of OA supplementation on sepsis. OA ameliorated clinical symptoms, increased the survival rate, prevented liver and kidney injury and decreased NEFA plasma levels inmice subjected to cecal ligation and puncture (CLP). OA did not alter food intake and weight gain but diminished reactive oxygen species (ROS) production and NEFA plasma levels. Carnitine palmitoyltransferase IA (CPT1A) mRNA levels were increased, while uncoupling protein 2 (UCP2) liver expression was enhanced in mice treated with OA. OA also inhibited the decrease in 5' AMPactivated protein kinase (AMPK) expression and increased the enzyme expression in the liver of OA-treated mice compared to septic animals.We showed that OA pretreatment decreased NEFA concentration and increased CPT1A and UCP2 and AMPK levels, decreasing ROS production.We suggest that OA has a beneficial role in sepsis by decreasing metabolic dysfunction, supporting the benefits of diets high inmonounsaturated fatty acids (MUFA)

Simvastatin Posttreatment Controls Inflammation and Improves Bacterial Clearance in Experimental Sepsis

Sepsis is characterized by a life-threatening organ dysfunction caused by an unbalanced host response to microbe infection that can lead to death. Besides being currently the leading cause of death in intensive care units worldwide, sepsis can also induce long-term consequences among survivors, such as cognitive impairment. Statins (lipid-lowering drugs widely used to treat dyslipidemia) have been shown to possess pleiotropic anti-inflammatory and antimicrobial effects. These drugs act inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, an enzyme that catalyzes the conversion of HMG-CoA to mevalonate, the limiting step in cholesterol biosynthesis. In this work, we evaluated the therapeutic effects of simvastatin in an animal model of sepsis. In previous study from our group, statin pretreatment avoided cognitive damage and neuroinflammation in sepsis survivors. Herein, we focused on acute inflammation where sepsis was induced by cecal ligation and puncture (CLP), and the animals were treated with simvastatin (2 mg/kg) 6 h after surgery. We measured plasma biochemical markers of organ dysfunction, cell migration, cell activation, bacterial elimination, production of nitric oxide 24 h after CLP, survival rate for 7 days, and cognitive impairment 15 days after CLP. One single administration of simvastatin 6 h after CLP was able to prevent both liver and kidney dysfunction. In addition, this drug decreased cell accumulation in the peritoneum as well as the levels of TNF-α, MIF, IL-6, and IL-1β. Simvastatin diminished the number of bacterial colony forming units (CFU) and increased the production of nitric oxide production in the peritoneum. Simvastatin treatment increased survival for the first 24 h, but it did not alter survival rate at the end of 7 days. Our results showed that posttreatment with simvastatin hampered organ dysfunction, increased local production of nitric oxide, improved bacterial clearance, and modulated inflammation in a relevant model of sepsis

Na/K-ATPase assay in the intact mice lung subjected to perfusion

Made available in DSpace on 2015-05-27T13:39:50Z (GMT). No. of bitstreams: 2 license.txt: 1914 bytes, checksum: 7d48279ffeed55da8dfe2f8e81f3b81f (MD5) adriana_silvaetal_IOC_2014.pdf: 350633 bytes, checksum: 5135d467f38c8b0fb3cbe9daca32f22b (MD5) Previous issue date: 2014Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense. Instituto de Biologia. Departamento de Biologia Celular e Molecular. Niterói, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Tecnologia em Imunobiológicos. Bio-Manguinhos. Departamento de Reativos para Diagnóstico. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto de Tecnologia em Imunobiológicos. Bio-Manguinhos. Departamento de Reativos para Diagnóstico. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Departamento de Química Analítica. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Imunofarmacologia. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Departamento de Química Analítica. Rio de Janeiro, RJ, Brasil.Among the characteristics of acute respiratory distress syndrome (ARDS) is edema formation and its resolution depends on pneumocyte Na/K-ATPase activity. Increased concentration of oleic acid (OA) in plasma induces lung injury by targeting Na/K-ATPase and, thus, interfering in sodium transport. FINDINGS: Presently, we adapted a radioactivity-free assay to detect Na/K-ATPase activity in perfused lung mice, comparing the inhibitory effect of ouabain and OA. We managed to perfuse only the lung, avoiding the systemic loss of rubidium. Rb+ incorporation into lung was measured by inductively coupled plasma optical emission spectrometry (ICP OES) technique, after lung tissue digestion. Na/K-ATPase activity was the difference between Rb+ incorporation with or without ouabain. Lung Na/K-ATPase was completely inhibited by perfusion with ouabain. However, OA caused a partial inhibition. CONCLUSIONS: In the present work the amount of incorporated Rb+ was greater than seen in our previous report, showing that the present technique is trustworthy. This new proposed assay may allow researchers to study the importance of Na/K-ATPase activity in lung pathophysiology

Oleic acid administration improves survival and ameliorates clinical score in septic mice.

<p>Animals were treated with oleic acid for 14 days. On the 15^th day, mice were subjected to CLP, and (A) 6 and (B) 24 hours after surgery, the clinical score was evaluated as described in the Materials and Methods. (C) The survival rate was assessed for 7 days after CLP. Control groups received saline. Each group consisted of 15 to 23 animals (clinical score at 6 hours: sham = 15 animals, sham + OA = 18 animals and CLP and CLP + OA = 23 animal; at 24 hours: sham and sham + OA = 18 animals, CLP = 18 animals, CLP + OA = 22 animals) in 3 independent experiments. For survival rates, 10 animals from each group were analyzed. This is a representative curve from 3 independent experiments. p < 0.05 * CLP vs sham, # CLP vs CLP plus oleic acid; log-rank test for mortality and one-way ANOVA followed by Newman-Keuls test for the clinical score.</p

Oleic acid increases the transcription of the CPT1A gene in septic mice.

<p>Swiss mice were treated for 14 days with oleic acid. On the 15^th day, mice were subjected to CLP. The liver was removed 24 hours after CLP. CPT1A mRNA was detected by RT-PCR. A representative gel of (A) CPT1A and of the (B) control GAPDH gene transcription. The loading control was GAPDH. (C)The bands were analyzed by densitometry and are represented as the CPT1A/GAPDH ratio. Values represent mean and SEM from 5–6 animals per group.</p