Nuevas perspectivas para la investigación en Internet: la Web 2.0 y la Empresa 2.0.

Desde su creación en 1989, la World Wide Web (la Web) ha revolucionado Internet, facilitando el acceso a información a muchos usuarios potenciales. Dos décadas más tarde, la Web forma parte de la vida diaria de muchas personas en todo el mundo, originando profundas transformaciones sociales que los investigadores en ciencias sociales batallan por comprender. Además, a lo largo de los últimos cinco años la Web ha sufrido importantes cambios debido al surgimiento y popularización de la llamada Web 2.0. Esto ha provocado una democratización en las herramientas de generación de información permitiendo que millones de personas se involucren en una conversación a escala global. Las tecnologías de la Web 2.0 y sus dinámicas de funcionamiento constituyen un área de gran futuro en la que profundizar en la investigación en ciencias sociales y, particularmente, en la investigación en el campo económico y de empresa. El concepto de Empresa 2.0 se deriva directamente de este nuevo contexto tecnológico. Since its creation in 1989, the World Wide Web (the Web) has revolutionised the Internet, facilitating the access to information to many potential users. Two decades later, the Web has become part of the daily lives of many people all over the world, causing deep social transformations that social scientists struggle to understand. Moreover, for the past five years, the Web has undergone significant changes by the popularisation of the so-called Web 2.0. This has provoked a democratisation of the information creation tools in such a way that millions of people have started to participate in a global conversation. The Web 2.0 technologies and dynamics represent a promising area to deepen into social science research and, particularly, into economics and business research. The concept Enterprise 2.0 derives directly from this new technological context.Web 2.0, Web, Internet, negocios, Empresa 2.0. Web 2.0, Web, Internet, business, Enterprise 2.0.

Nuevas perspectivas para la investigación en Internet: la Web 2.0 y la Empresa 2.0

Desde su creación en 1989, la World Wide Web (la Web) ha revolucionado Internet, facilitando el acceso a información a muchos usuarios potenciales. Dos décadas más tarde, la Web forma parte de la vida diaria de muchas personas en todo el mundo, originando profundas transformaciones sociales que los investigadores en ciencias sociales batallan por comprender. Además, a lo largo de los últimos cinco años la Web ha sufrido importantes cambios debido al surgimiento y popularización de la llamada Web 2.0. Esto ha provocado una democratización en las herramientas de generación de información permitiendo que millones de personas se involucren en una conversación a escala global. Las tecnologías de la Web 2.0 y sus dinámicas de funcionamiento constituyen un área de gran futuro en la que profundizar en la investigación en ciencias sociales y, particularmente, en la investigación en el campo económico y de empresa. El concepto de Empresa 2.0 se deriva directamente de este nuevo contexto tecnológico.Since its creation in 1989, the World Wide Web (the Web) has revolutionised the Internet, facilitating the access to information to many potential users. Two decades later, the Web has become part of the daily lives of many people all over the world, causing deep social transformations that social scientists struggle to understand. Moreover, for the past five years, the Web has undergone significant changes by the popularisation of the so-called Web 2.0. This has provoked a democratisation of the information creation tools in such a way that millions of people have started to participate in a global conversation. The Web 2.0 technologies and dynamics represent a promising area to deepen into social science research and, particularly, into economics and business research. The concept Enterprise 2.0 derives directly from this new technological context

The diclosure of corporate social responsibility information in public administrations: an empirical study in local governments

Las prácticas de divulgación de Responsabilidad Social Corporativa (RSC) son cada vez más utilizadas por las grandes compañías como instrumentos para eliminar las asimetrías de información entre los stakeholders. En el caso de las administraciones públicas, aunque las exigencias de los ciudadanos son cada vez mayores en materia de transparencia y de rendición de cuentas, la difusión de información RSC es un tema todavía poco estudiado. Este trabajo pretende realizar una primera aproximación a la difusión de información RSC en las administraciones locales españolas y su finalidad principal es conocer las debilidades y fortalezas que, en materia de RSC, tienen los sistemas de información de estas entidades, identificando oportunidades de mejora que orienten futuras investigaciones. Para ello, hemos analizado los sitios web de 55 grandes gobiernos locales, obteniendo conclusiones sobre la difusión de información general acerca de RSC así como sobre la publicación de información económica, social y medioambiental. Los resultados revelan que las mayores carencias de publicación de información RSC corresponden a la información medioambiental, mientras que la información social es la más divulgada. Asimismo, el tamaño de la entidad, la competencia política y el signo del partido gobernante, no explican el desarrollo de las prácticas de difusión de información RSC.The disclosure practices of Corporate Social Responsibility (CSR) are increasingly used by large companies in order to eliminate information asymmetries between stakeholders. Instead, the disclosure of CSR information for governments is a topic little studied yet, though the demands of citizens are increasing in transparency and accountability. This paper attempts a first approach to information CSR dissemination in Spanish local governments. Its main purpose is to know the strengths and weaknesses about CSR of information systems of these entities, identifying opportunities for improvement to guide future research. To do this, we analyzed the websites of 55 large local governments, drawing conclusions about the disclosure of CSR general information and about the publication of on economic, social and environmental information. The results reveal that the major shortcomings in CSR disclosure are related to environmental information, while social information is the most published. Also, the size of the entity, political competition and the political sign of the government, do not explain the development of disclosure of RSC information.Esta investigación fue realizada con la financiación de la Comunidad Autónoma de Andalucía, Consejería de Innovación, Ciencia y Empresa (Proyecto de Investigación nº ECO2010-17463 y Proyecto de Investigación nº ECO2010- 20522) así como del Ministerio de Ciencia e Innovación (Proyecto de Innovación ECO 2010-17463, ECON-FEDER)

Enhancing Sustainability Transparency in Local Governments—An Empirical Research in Europe

In the current socioeconomic context, the question of local government sustainability transparency is of great interest to policymakers, managers, citizens and other stakeholders, and yet one to which previous research has devoted little specific attention. At the same time, the Internet has become an instrument of good governance worldwide and government entities in Europe have strived to promote e-government to improve transparency towards citizens. The aim of this study was to identify factors that can help politicians and managers improve practices of sustainability information disclosed by European local governments. To do so, an empirical study was conducted of 91 municipalities in nine countries, comparing three main administrative cultures. Our analysis of the study results highlights various demographic, socioeconomic, financial and legal factors that may be useful to policymakers and managers in promoting the online provision of sustainability information in Anglo-Saxon, Nordic and Southern European countries

Addressing Profiles of Systemic Inflammation Across the Different Clinical Phenotypes of Acutely Decompensated Cirrhosis

ACLF; Acute decompensation; CirrhosisInsuficiencia hepática aguda sobre crónica; Descompensación aguda; CirrosisInsuficiència hepàtica aguda sobre crònica; Descompensació aguda; CirrosiBackground: Patients with acutely decompensated cirrhosis (AD) may or may not develop acute-on-chronic liver failure (ACLF). ACLF is characterized by high-grade systemic inflammation, organ failures (OF) and high short-term mortality. Although patients with AD cirrhosis exhibit distinct clinical phenotypes at baseline, they have low short-term mortality, unless ACLF develops during follow-up. Because little is known about the association of profile of systemic inflammation with clinical phenotypes of patients with AD cirrhosis, we aimed to investigate a battery of markers of systemic inflammation in these patients. Methods: Upon hospital admission baseline plasma levels of 15 markers (cytokines, chemokines, and oxidized albumin) were measured in 40 healthy controls, 39 compensated cirrhosis, 342 AD cirrhosis, and 161 ACLF. According to EASL-CLIF criteria, AD cirrhosis was divided into three distinct clinical phenotypes (AD-1: Creatinine<1.5, no HE, no OF; AD-2: creatinine 1.5-2, and or HE grade I/II, no OF; AD-3: Creatinine<1.5, no HE, non-renal OF). Results: Most markers were slightly abnormal in compensated cirrhosis, but markedly increased in AD. Patients with ACLF exhibited the largest number of abnormal markers, indicating "full-blown" systemic inflammation (all markers). AD-patients exhibited distinct systemic inflammation profiles across three different clinical phenotypes. In each phenotype, activation of systemic inflammation was only partial (30% of the markers). Mortality related to each clinical AD-phenotype was significantly lower than mortality associated with ACLF (p < 0.0001 by gray test). Among AD-patients baseline systemic inflammation (especially IL-8, IL-6, IL-1ra, HNA2 independently associated) was more intense in those who had poor 28-day outcomes (ACLF, death) than those who did not experience these outcomes. Conclusions: Although AD-patients exhibit distinct profiles of systemic inflammation depending on their clinical phenotypes, all these patients have only partial activation of systemic inflammation. However, those with the most extended baseline systemic inflammation had the highest the risk of ACLF development and death

The specialized pro-resolving lipid mediator maresin 1 protects hepatocytes from lipotoxic and hypoxia-induced endoplasmic reticulum stress.

Endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) are hallmarks of nonalcoholic fatty liver disease (NAFLD), which is the hepatic manifestation of the metabolic syndrome associated with obesity. The specialized proresolving lipid mediator maresin 1 (MaR1) preserves tissue homeostasis by exerting cytoprotective actions, dampening inflammation, and expediting its timely resolution. Here, we explored whether MaR1 protects liver cells from lipotoxic and hypoxia-induced ER stress. Mice were rendered obese by high-fat diet feeding, and experiments were performed in primary hepatocytes, Kupffer cells, and precision-cut liver slices (PCLSs). Palmitate-induced lipotoxicity increased ER stress and altered autophagy in hepatocytes, effects that were prevented by MaR1. MaR1 protected hepatocytes against lipotoxicity-induced apoptosis by activating the UPR prosurvival mechanisms and preventing the excessive up-regulation of proapoptotic pathways. Protective MaR1 effects were also seen in hepatocytes challenged with hypoxia and TNF-α-induced cell death. High-throughput microRNA (miRNA) sequencing revealed that MaR1 actions were associated with specific miRNA signatures targeting both protein folding and apoptosis. MaR1 also prevented lipotoxic-triggered ER stress and hypoxia-induced inflammation in PCLSs and enhanced Kupffer cell phagocytic capacity. Together, these findings describe the ability of MaR1 to oppose ER stress in liver cells under conditions frequently encountered in NAFLD.-Rius, B., Duran-Güell, M., Flores-Costa, R., López-Vicario, C., Lopategi, A., Alcaraz-Quiles, J., Casulleras, M., Lozano, J. J., Titos, E., Clària, J. The specialized proresolving lipid mediator maresin 1 protects hepatocytes from lipotoxic and hypoxia-induced endoplasmic reticulum stress

Inhibition of soluble epoxide hydrolase modulates inflammation and autophagy in obese adipose tissue and liver. Role for omega-3 epoxides

Soluble epoxide hydrolase (sEH) is an emerging therapeutic target in a number of diseases that have inflammation as a common underlying cause. sEH limits tissue levels of cytochrome P450 (CYP) epoxides derived from omega-6 and omega-3 polyunsaturated fatty acids (PUFA) by converting these antiinflammatory mediators into their less active diols. Here, we explored the metabolic effects of a sEH inhibitor (t-TUCB) in fat-1 mice with transgenic expression of an omega-3 desaturase capable of enriching tissues with endogenous omega-3 PUFA. These mice exhibited increased CYP1A1, CYP2E1, and CYP2U1 expression and abundant levels of the omega-3-derived epoxides 17,18-epoxyeicosatetraenoic acid (17,18-EEQ) and 19,20-epoxydocosapentaenoic (19,20-EDP) in insulin-sensitive tissues, especially liver, as determined by LC-ESI-MS/MS. In obese fat-1 mice, t-TUCB raised hepatic 17,18-EEQ and 19,20-EDP levels and reinforced the omega-3-dependent reduction observed in tissue inflammation and lipid peroxidation. t-TUCB also produced a more intense antisteatotic action in obese fat-1 mice, as revealed by magnetic resonance spectroscopy. Notably, t-TUCB skewed macrophage polarization toward an antiinflammatory M2 phenotype and expanded the interscapular brown adipose tissue volume. Moreover, t-TUCB restored hepatic levels of Atg12-Atg5 and LC3-II conjugates and reduced p62 expression, indicating up-regulation of hepatic autophagy. t-TUCB consistently reduced endoplasmic reticulum stress demonstrated by the attenuation of IRE-1α and eIF2α phosphorylation. These actions were recapitulated in vitro in palmitate-primed hepatocytes and adipocytes incubated with 19,20-EDP or 17,18-EEQ. Relatively similar but less pronounced actions were observed with the omega-6 epoxide, 14,15-EET, and nonoxidized DHA. Together, these findings identify omega-3 epoxides as important regulators of inflammation and autophagy in insulin-sensitive tissues and postulate sEH as a druggable target in metabolic diseases

Stimulation of soluble guanylate cyclase exerts antiinflammatory actions in the liver through a VASP/NF-κB/NLRP3 inflammasome circuit

Soluble guanylate cyclase (sGC) catalyzes the conversion of guanosine triphosphate into cyclic guanosine-3',5'-monophosphate, a key second messenger in cell signaling and tissue homeostasis. It was recently demonstrated that sGC stimulation is associated with a marked antiinflammatory effect in the liver of mice with experimental nonalcoholic steatohepatitis (NASH). Here, we investigated the mechanisms underlying the antiinflammatory effect of the sGC stimulator praliciguat (PRL) in the liver. Therapeutic administration of PRL exerted antiinflammatory and antifibrotic actions in mice with choline-deficient l-amino acid-defined high-fat diet-induced NASH. The PRL antiinflammatory effect was associated with lower F4/80- and CX3CR1-positive macrophage infiltration into the liver in parallel with lower Ly6CHigh- and higher Ly6CLow-expressing monocytes in peripheral circulation. The PRL antiinflammatory effect was also associated with suppression of hepatic levels of interleukin (IL)-1β, NLPR3 (NACHT, LRR, and PYD domain-containing protein 3), ASC (apoptosis-associated speck-like protein containing a caspase-recruitment domain), and active cleaved-caspase-1, which are components of the NLRP3 inflammasome. In Kupffer cells challenged with the classical inflammasome model of lipopolysaccharide plus adenosine triphosphate, PRL inhibited the priming (expression of Il1b and Nlrp3) and blocked the release of mature IL-1β. Mechanistically, PRL induced the protein kinase G (PKG)-mediated phosphorylation of the VASP (vasodilator-stimulated phosphoprotein) Ser239 residue which, in turn, reduced nuclear factor-κB (NF-κB) activity and Il1b and Nlrp3 gene transcription. PRL also reduced active cleaved-caspase-1 levels independent of pannexin-1 activity. These data indicate that sGC stimulation with PRL exerts antiinflammatory actions in the liver through mechanisms related to a PKG/VASP/NF-κB/NLRP3 inflammasome circuit

Role of bioactive lipid mediators in obese adipose tissue inflammation and endocrine dysfunction.

White adipose tissue is recognized as an active endocrine organ implicated in the maintenance of metabolic homeostasis. However, adipose tissue function, which has a crucial role in the development of obesity-related comorbidities including insulin resistance and non-alcoholic fatty liver disease, is dysregulated in obese individuals. This review explores the physiological functions and molecular actions of bioactive lipids biosynthesized in adipose tissue including sphingolipids and phospholipids, and in particular fatty acids derived from phospholipids of the cell membrane. Special emphasis is given to polyunsaturated fatty acids of the omega-6 and omega-3 families and their conversion to bioactive lipid mediators through the cyclooxygenase and lipoxygenase pathways. The participation of omega-3-derived lipid autacoids in the resolution of adipose tissue inflammation and in the prevention of obesity-associated hepatic complications is also thoroughly discussed

Small fragments of hyaluronan are increased in individuals with obesity and contribute to low-grade inflammation through TLR-mediated activation of innate immune cells.

Background and aim: Extracellular matrix (ECM) components released during excessive fat mass expansion are considered potential endogenous danger/alarm signals contributing to innate immune system activation. The aim of the current study was to specifically measure plasma levels of low molecular weight (LMW) hyaluronan (HA) and to evaluate its role as pro-inflammatory damage-associated molecular pattern (DAMP) on leukocyte response in the context of human obesity. Subjects and methods: Participants were selected according to their body mass index (BMI, kg/m2) as non-obese (BMI 29.9, n = 33). Plasma samples were size-dependent fractionated using ion-exchange chromatography to specifically obtain LMW HA fractions that were subsequently quantified by ELISA. Cell incubation experiments with synthetic HA molecules were performed on freshly Ficoll-isolated neutrophils (PMN) and peripheral blood monocytes (PBMC). Leukocyte and adipose tissue gene expression was assessed by real-time PCR and NF-κB activation by western blot. Plasma cytokine levels were measured by fluorescent bead-based (Luminex) immunoassay. Results: We observed a statistically significant increase in the circulating levels of HA fragments of LMW in individuals with obesity which were consistent with significant up-regulated expression of the LMW HA synthesizing enzyme hyaluronan synthase-1 (HAS-1) in obese adipose tissue. Gene expression assessment of HA receptors revealed up-regulated levels for TLR2 in both obese PMN and PBMC. Synthetic HA molecules of different sizes were tested on leukocytes from healthy donors. LMW HA fragments (15-40 kDa) and not those from intermediate molecular sizes (75-350 kDa) induced a significant up-regulation of the expression of major pro-inflammatory cytokines such as IL-1β, MCP-1 and IL-8 in PBMC. Importantly, LMW HA was able to induce the phosphorylation of IKK α/β complex supporting its pro-inflammatory role through NF-κB activation. Conclusion: Circulating LMW HA molecules are elevated in obesity and may play an important role in triggering low-grade inflammation and the development of metabolic complications