Aprendizaje cooperativo. Un recurso indispensable en la formación universitaria

El Libro “Aprendizaje cooperativo Un recurso indispensable en la formación universitaria”, se enmarca dentro del Proyecto de Innovación docente Finestra Oberta UV_ SFPIE GER 15-314671, bajo la dirección de la Profesora María Elena Cobas Cobiella, del Departamento de Derecho Civil, de la Facultad de Derecho de la Universidad de Valencia. Este libro contiene 19 artículos inéditos de un grupo importante de profesores y especialistas en la temática nacionales e internacionales, así como con la intervención como colaboradores de estudiantes de Grado en Derecho, de la doble titulación Derecho- ADE de la Universidad de Valencia, y de Universidades internacionales. También han intervenido en el mismo estudiantes del Master de Mediación y Arbitraje y solución de conflictos en Derecho Privado 2015/2016 y del Proyecto Unisocietat L’Eliana Curso 2015 – 2016. Constituye una obra que eleva la práctica del aula a la teoría. Altamente recomendable para aquellos que incursionen en el camino de la docencia.The Book "Cooperative learning: an indispensable resource in university education" is part of the Project for teaching innovation "Finestra Oberta,UV_ SFPIE GER 15-314671", under the direction of Professor Maria Elena Cobas Cobiella, from Civil Law department of the Faculty of Law of the University of Valencia. This book contains 19 new articles of a large group of professors and specialists in national and international topics, as well as with the intervention as collaborators of Law degree students from the double degree Law-Business Administration from the University of Valencia, and also from international universities. They have also intervened in the book some students from the Master of Mediation, Arbitration and resolution of conflicts in Private Law 2015/2016 and from the Unisocietat L'Eliana project 2015/2016. It is a work that elevates the classroom practice towards the theory. Highly recommended for those who want to progress in the way of teaching.Los siguientes estudiantes han colaborado en la Parte Especial del Libro, con los resúmenes de sus trabajos de mapas conceptuales y los prezi:Ylenia Martínez, María Gómez Escrivá,Julieta Campora Espí, Blanca Giner Zarranz, Mario Zúñiga Martínez, Alicia Martínez Ruiz, Sandra Gimeno Bascuñana, Héctor Martínez Soler, Amparo García Navarro,Joan De la Haba Herrera,Alberto José Fourrat Calatayud, Juan Ortega Talamantes, Vicente Vila Subiela, Cristina Blázquez Sánchez, Sara Monsalve Alemany, Paula Navarro Román, Carlos Reyes Hernández,Jesús Sanz Carnero,José Guillermo Gil, Aroa Gimeno, José Manuel Aznar, Teresa Pérez, Antonio Fernández, Cristina Martin, Rodrigo Climent, José Ángel Molina Sánchez, Daniel Cabanes Ferrando, David Escobar Haro, Diego Martínez Amor, Mari Carmen Arnau Gil, Raquel Jiménez Gago, Daniel March Quevedo, Laura Alapont Vidal, Gema Canós Ferrandis, Mónica Costa Isabel, Jesús Sanmartín Viturro, Eduardo José Tobio García, Pau Viñuelas LLoria, María del Mar Figueroa Hernández, Minerva Llagunes Picazo, Lucía Olmos, José Olmedo, Brynn De Houwer, Enrique Pla Marcos, Héctor Tabernero Más, Laura Payá González, Blanca Martínez Pons,Alejandro Grima Margarit, Belén Català, Mariam Pérez, David Sánchez, Jorge Seguí ,Sara Tamarit,Fernando Aparisi Escriba, Analía Carballo Quispe,José Luis Moreno Miguel,Candy Priscilla Rojas Campoverde, Ademar Lledó Monfort, Irene Belles Rubio, Clara Calomarde Esteban, Marta Marín de la Dueña, Sergio Pinel Castillo,Maria Simo Martin, Daniel Rocher Camps, Sandra Nicolás Mascarell, Teresa Bartret García, Maria Amparo Monasort Pérez,Joan Vicente Torres Moreno, Belén Cuñat Salavert, Carmen Rodríguez Bertos, Aníbal Sánchez Gómez, Sofía Morant Muñoz, Pedro Ballester Martínez,Akbar Khawar, David Ortíz Soler, Jonathan Pérez Gutiérrez.Jorge Amat Andrés, M.ª Antonia García Juncos, Jenny Maritza González Vergara,Juan José Tocón Torres,Pau Zurita Varela, Manuel Calvo Pereiro, Carolina Luis Tamarit,Beatriz Muñoz Moncholí,Marta Conejero Sarrió, Guillermo Juarez Ginestar, Carolina Más Trullás,Ramón Fernández Pares, Carlos Hervás García,Carolina Tamarit García, Jose Belloch Ortí,Danilo Terán Taborga,Manuel Castillo Martínez, Isabel Martínez Salas, Carlos Javier Castello Domenech, Silvia Juste Frechina, Cristina Barrado Franco, Noemi De Miguel Domingo, Elena Masegosa Laurí, Maryana Seniv, Paula Sanz Perez, Liney Paola Peiró Soriano, José Manuel Zahonero Ferrer,Paula Pons Guillem,Andrea Oviedo Millán,Arnaud Wustefeld, Alba Ruiz-Santa Quiteria Lara,Lydia García Céspedes,Antonio Gomar López,Eva Piqueras García, Claudia Salvador Pérez, Joel David Alvarez Remy, Sheila Jorge Muñoz,Virginia Mendoza Leal,David Benavides Arenas, Mario Perera Sánchez, Vladimir Sarmiento Paizán,Javier Mustelier Armiñán,Diamela Salina Ocaña, Edel Morales Salazar,Fortunato Dong Oñaña,María del Carmen Carvajal Balagué,María del Carmen Daries Coll, Catalina Olmo Brazales,Mª Teresa Sánchez, Julia Serra Figuerola,Mª Nieves Valdearcos Quintín,Carmen Moraga Martín,María José Moragues, Salvador Lluch,Maribel Moreno,José Luis Coello,José Cebriá,Matilde Argente,Consuelo Martínez,Rosi Hernández,Susi García,Graciela Garibotti,Susana Bianchi,Judith Steffan,Susan Humphreys,Jesús Castellano,Ana Preus,Mª José Figueroa,Mª Teresa Carbonell,Lola Lombrera,Luisa Martínez Gordillo,Roberto Soler,Pilar Bezares Martínez, Ramón González Ferrer,Raquel González Sainz,Sacra Martínez Alarcón, Emetério Mirálles Ribot, Ramón Pubill Rocaort,Conchin Ruiz Leal, Isabel Sucarrat Bermejo,Pepa San Román Moñino,InmaTarín Arfella, Maise Tarín Arfella, Pedro Montalban,Carmen Kroebel, Lydia González, Carlos Gómez, Amparo Cuellar,Pilar Navarro,Luisa Vallejo, Encarna Monzó,Carmen Conca,Pilar Alegría, Sonia Almonacil, Inma Fernández, María José García Marcelo,Clara Olivert Pavia, Ana Herrero Martínez, Rosana Crespo Martínez, Carmen Vidal Casañ,José Ramón Villagrasa Tort,Juan Carlos López Cubero,Paco Velayos Sánchez,María de la O Pérez,Carles Montagut Alvarez, José Leopoldo Rodríguez Pla, Amanda Bernat Tinoco,Marta García Montañana, Ioana Roxana Moraru, Jenifer Perujo Plumed,María Ribera Cebolla,Amparo Esteve Cervera, Iris Pla Sempere,Juan Rafael Aranda Perozo,Jesús Collado Mas, Cristina Grimalt Molina,Isabel Rojo Lora, María Teresa Peirats Casanova,Rosana Marin Rausell, Ricardo Mejía Hidalgo,Pablo Pastor Aguilera,Daniel Trujillo Villalba,Yolanda Fuster Llidó, Lucas Lamarca Pedemonte, Gabriel Rosa Felipe

Micromechanical Properties of Injection-Molded Starch–Wood Particle Composites

The micromechanical properties of injection molded starch–wood particle composites were investigated as a function of particle content and humidity conditions. The composite materials were characterized by scanning electron microscopy and X-ray diffraction methods. The microhardness of the composites was shown to increase notably with the concentration of the wood particles. In addition,creep behavior under the indenter and temperature dependence were evaluated in terms of the independent contribution of the starch matrix and the wood microparticles to the hardness value. The influence of drying time on the density and weight uptake of the injection-molded composites was highlighted. The results revealed the role of the mechanism of water evaporation, showing that the dependence of water uptake and temperature was greater for the starch–wood composites than for the pure starch sample. Experiments performed during the drying process at 70°C indicated that the wood in the starch composites did not prevent water loss from the samples.Peer reviewe

Canagliflozin and Cardiovascular and Renal Outcomes in Type 2 Diabetes Mellitus and Chronic Kidney Disease in Primary and Secondary Cardiovascular Prevention Groups

Background: Canagliflozin reduces the risk of kidney failure in patients with type 2 diabetes mellitus and chronic kidney disease, but effects on specific cardiovascular outcomes are uncertain, as are effects in people without previous cardiovascular disease (primary prevention). Methods: In CREDENCE (Canagliflozin and Renal Events in Diabetes With Established Nephropathy Clinical Evaluation), 4401 participants with type 2 diabetes mellitus and chronic kidney disease were randomly assigned to canagliflozin or placebo on a background of optimized standard of care. Results: Primary prevention participants (n=2181, 49.6%) were younger (61 versus 65 years), were more often female (37% versus 31%), and had shorter duration of diabetes mellitus (15 years versus 16 years) compared with secondary prevention participants (n=2220, 50.4%). Canagliflozin reduced the risk of major cardiovascular events overall (hazard ratio [HR], 0.80 [95% CI, 0.67-0.95]; P=0.01), with consistent reductions in both the primary (HR, 0.68 [95% CI, 0.49-0.94]) and secondary (HR, 0.85 [95% CI, 0.69-1.06]) prevention groups (P for interaction=0.25). Effects were also similar for the components of the composite including cardiovascular death (HR, 0.78 [95% CI, 0.61-1.00]), nonfatal myocardial infarction (HR, 0.81 [95% CI, 0.59-1.10]), and nonfatal stroke (HR, 0.80 [95% CI, 0.56-1.15]). The risk of the primary composite renal outcome and the composite of cardiovascular death or hospitalization for heart failure were also consistently reduced in both the primary and secondary prevention groups (P for interaction >0.5 for each outcome). Conclusions: Canagliflozin significantly reduced major cardiovascular events and kidney failure in patients with type 2 diabetes mellitus and chronic kidney disease, including in participants who did not have previous cardiovascular disease

Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy

BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to 300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m 2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years

Atrasentan and renal events in patients with type 2 diabetes and chronic kidney disease (SONAR): a double-blind, randomised, placebo-controlled trial

Background: Short-term treatment for people with type 2 diabetes using a low dose of the selective endothelin A receptor antagonist atrasentan reduces albuminuria without causing significant sodium retention. We report the long-term effects of treatment with atrasentan on major renal outcomes. Methods: We did this double-blind, randomised, placebo-controlled trial at 689 sites in 41 countries. We enrolled adults aged 18–85 years with type 2 diabetes, estimated glomerular filtration rate (eGFR)25–75 mL/min per 1·73 m 2 of body surface area, and a urine albumin-to-creatinine ratio (UACR)of 300–5000 mg/g who had received maximum labelled or tolerated renin–angiotensin system inhibition for at least 4 weeks. Participants were given atrasentan 0·75 mg orally daily during an enrichment period before random group assignment. Those with a UACR decrease of at least 30% with no substantial fluid retention during the enrichment period (responders)were included in the double-blind treatment period. Responders were randomly assigned to receive either atrasentan 0·75 mg orally daily or placebo. All patients and investigators were masked to treatment assignment. The primary endpoint was a composite of doubling of serum creatinine (sustained for ≥30 days)or end-stage kidney disease (eGFR <15 mL/min per 1·73 m 2 sustained for ≥90 days, chronic dialysis for ≥90 days, kidney transplantation, or death from kidney failure)in the intention-to-treat population of all responders. Safety was assessed in all patients who received at least one dose of their assigned study treatment. The study is registered with ClinicalTrials.gov, number NCT01858532. Findings: Between May 17, 2013, and July 13, 2017, 11 087 patients were screened; 5117 entered the enrichment period, and 4711 completed the enrichment period. Of these, 2648 patients were responders and were randomly assigned to the atrasentan group (n=1325)or placebo group (n=1323). Median follow-up was 2·2 years (IQR 1·4–2·9). 79 (6·0%)of 1325 patients in the atrasentan group and 105 (7·9%)of 1323 in the placebo group had a primary composite renal endpoint event (hazard ratio [HR]0·65 [95% CI 0·49–0·88]; p=0·0047). Fluid retention and anaemia adverse events, which have been previously attributed to endothelin receptor antagonists, were more frequent in the atrasentan group than in the placebo group. Hospital admission for heart failure occurred in 47 (3·5%)of 1325 patients in the atrasentan group and 34 (2·6%)of 1323 patients in the placebo group (HR 1·33 [95% CI 0·85–2·07]; p=0·208). 58 (4·4%)patients in the atrasentan group and 52 (3·9%)in the placebo group died (HR 1·09 [95% CI 0·75–1·59]; p=0·65). Interpretation: Atrasentan reduced the risk of renal events in patients with diabetes and chronic kidney disease who were selected to optimise efficacy and safety. These data support a potential role for selective endothelin receptor antagonists in protecting renal function in patients with type 2 diabetes at high risk of developing end-stage kidney disease. Funding: AbbVie

Effect of SGLT2 inhibitors on stroke and atrial fibrillation in diabetic kidney disease: Results from the CREDENCE trial and meta-analysis

BACKGROUND AND PURPOSE: Chronic kidney disease with reduced estimated glomerular filtration rate or elevated albuminuria increases risk for ischemic and hemorrhagic stroke. This study assessed the effects of sodium glucose cotransporter 2 inhibitors (SGLT2i) on stroke and atrial fibrillation/flutter (AF/AFL) from CREDENCE (Canagliflozin and Renal Events in Diabetes With Established Nephropathy Clinical Evaluation) and a meta-Analysis of large cardiovascular outcome trials (CVOTs) of SGLT2i in type 2 diabetes mellitus. METHODS: CREDENCE randomized 4401 participants with type 2 diabetes mellitus and chronic kidney disease to canagliflozin or placebo. Post hoc, we estimated effects on fatal or nonfatal stroke, stroke subtypes, and intermediate markers of stroke risk including AF/AFL. Stroke and AF/AFL data from 3 other completed large CVOTs and CREDENCE were pooled using random-effects meta-Analysis. RESULTS: In CREDENCE, 142 participants experienced a stroke during follow-up (10.9/1000 patient-years with canagliflozin, 14.2/1000 patient-years with placebo; hazard ratio [HR], 0.77 [95% CI, 0.55-1.08]). Effects by stroke subtypes were: ischemic (HR, 0.88 [95% CI, 0.61-1.28]; n=111), hemorrhagic (HR, 0.50 [95% CI, 0.19-1.32]; n=18), and undetermined (HR, 0.54 [95% CI, 0.20-1.46]; n=17). There was no clear effect on AF/AFL (HR, 0.76 [95% CI, 0.53-1.10]; n=115). The overall effects in the 4 CVOTs combined were: Total stroke (HRpooled, 0.96 [95% CI, 0.82-1.12]), ischemic stroke (HRpooled, 1.01 [95% CI, 0.89-1.14]), hemorrhagic stroke (HRpooled, 0.50 [95% CI, 0.30-0.83]), undetermined stroke (HRpooled, 0.86 [95% CI, 0.49-1.51]), and AF/AFL (HRpooled, 0.81 [95% CI, 0.71-0.93]). There was evidence that SGLT2i effects on total stroke varied by baseline estimated glomerular filtration rate (P=0.01), with protection in the lowest estimated glomerular filtration rate (45 mL/min/1.73 m2]) subgroup (HRpooled, 0.50 [95% CI, 0.31-0.79]). CONCLUSIONS: Although we found no clear effect of SGLT2i on total stroke in CREDENCE or across trials combined, there was some evidence of benefit in preventing hemorrhagic stroke and AF/AFL, as well as total stroke for those with lowest estimated glomerular filtration rate. Future research should focus on confirming these data and exploring potential mechanisms

Canagliflozin and renal outcomes in type 2 diabetes and nephropathy

BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to &lt;90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], &gt;300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of &lt;15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P&lt;0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P&lt;0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years

BOLD magnetic resonance imaging in nephrology

Michael E Hall,1,2 Jennifer H Jordan,3 Luis A Juncos,1,2 W Gregory Hundley,3 John E Hall2 1Department of Medicine, University of Mississippi Medical Center, Jackson, MS, USA; 2Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA; 3Department of Internal Medicine, Section on Cardiovascular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA Abstract: Magnetic resonance (MR) imaging, a non-invasive modality that provides anatomic and physiologic information, is increasingly used for diagnosis of pathophysiologic conditions and for understanding renal physiology in humans. Although functional MR imaging methods were pioneered to investigate the brain, they also offer powerful techniques for investigation of other organ systems such as the kidneys. However, imaging the kidneys provides unique challenges due to potential complications from contrast agents. Therefore, development of non-contrast techniques to study kidney anatomy and physiology is important. Blood oxygen level-dependent (BOLD) MR is a non-contrast imaging technique that provides functional information related to renal tissue oxygenation in various pathophysiologic conditions. Here we discuss technical considerations, clinical uses and future directions for use of BOLD MR as well as complementary MR techniques to better understand renal pathophysiology. Our intent is to summarize kidney BOLD MR applications for the clinician rather than focusing on the complex physical challenges that functional MR imaging encompasses; however, we briefly discuss some of those issues. Keywords: functional MRI, kidney, oxygenation, chronic kidney disease&nbsp

Obesity, hypertension, and chronic kidney disease

Michael E Hall,1,2 Jussara M do Carmo,2 Alexandre A da Silva,2 Luis A Juncos,1,2 Zhen Wang,2 John E Hall2 1Department of Medicine, 2Department of Physiology and Biophysics, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, MS, USA Abstract: Obesity is a major risk factor for essential hypertension, diabetes, and other comorbid conditions that contribute to development of chronic kidney disease. Obesity raises blood pressure by increasing renal tubular sodium reabsorption, impairing pressure natriuresis, and causing volume expansion via activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and by physical compression of the kidneys, especially when there is increased visceral adiposity. Other factors such as inflammation, oxidative stress, and lipotoxicity may also contribute to obesity-mediated hypertension and renal dysfunction. Initially, obesity causes renal vasodilation and glomerular hyperfiltration, which act as compensatory mechanisms to maintain sodium balance despite increased tubular reabsorption. However, these compensations, along with increased arterial pressure and metabolic abnormalities, may ultimately lead to glomerular injury and initiate a slowly developing vicious cycle that exacerbates hypertension and worsens renal injury. Body weight reduction, via caloric restriction and increased physical activity, is an important first step for management of obesity, hypertension, and chronic kidney disease. However, this strategy may not be effective in producing long-term weight loss or in preventing cardiorenal and metabolic consequences in many obese patients. The majority of obese patients require medical therapy for obesity-associated hypertension, metabolic disorders, and renal disease, and morbidly obese patients may require surgical interventions to produce sustained weight loss. Keywords: visceral adiposity, type II diabetes, sodium reabsorption, glomerular filtration rate, sympathetic nervous system, renin-angiotensin-aldosterone syste