171,025 research outputs found
Introduzione
No full textLa società italiana è pervasa da fenomeni di razzismo, spesso considerati un residuo del passato. Il volume riflette sui tracciati ideologici, sulle derive del linguaggio e della comunicazione, sugli atteggiamenti quotidiani e su un persistente immaginario razzista, che sono alla radice del rinnovarsi del rifiuto di ciò e di chi è vissuto come una minaccia alla propria integrità e all'ordine costituito, identificando nel razzismo una falsa razionalità
Structural contagion and vulnerability to unexpected liquidity shortfalls
No full textThis paper assumes that financial fluctuations are the result of the dynamic interaction
between liquidity and solvency conditions of individual economic units. The framework
is an extention of Sordi and Vercelli (2012) designed as an heterogeneous agent model
which proceeds through discrete time steps within a finite time horizon. The interaction
at the micro-level between economic units monitors the spread of contagion and systemic
risk, producing interesting complex dynamics. The model is analysed by means of numerical
simulations and systemic risk modelling, where local interaction of units is captured
and analysed by the bilateral provision of liquidity among units. The behaviour and evolution
of economic units are studied for different parameter regimes in order to investigate
the relation between units’ expectations, liquidity regimes and contagion. Liquidity policy
implications are briefly discusse
Structural contagion and vulnerability to unexpected liquidity shortfalls
No full textThis paper assumes that financial fluctuations are the result of the dynamic interaction between liquidity and solvency conditions of individual economic units. The framework is an extention of Sordi and Vercelli (2012) designed as an heterogeneous agent model which proceeds through discrete time steps within a finite time horizon. The interaction at the micro-level between economic units monitors the spread of contagion and systemic risk, producing interesting complex dynamics. The model is analysed by means of numerical simulations and systemic risk modelling, where local interaction of units is captured and analysed by the bilateral provision of liquidity among units. The behaviour and evolution of economic units are studied for different parameter regimes in order to investigate the relation between units' expectations, liquidity regimes and contagion. Liquidity policy implications are briefly discussed. © 2012 Elsevier B.V
Time-course of c-Jun N-terminal kinase activation after cerebral ischemia and effect of D-JNKI1 on c-Jun and caspase-3 activation
No full textThe c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in ischemic brain injury. The d-retro-inverso form of c-Jun N-terminal kinase-inhibitor (D-JNKI1), a cell-permeable inhibitor of JNK, powerfully reduces neuronal death induced by permanent and transient ischemia, even when administered 6 h after the ischemic insult, offering a clinically relevant window. We investigated the JNK molecular cascade activation in rat cerebral ischemia and the effects of D-JNKI1 on this cascade. c-Jun activation starts after 3 h after ischemia and peaks at 6 h in the ischemic core and in the penumbra at 1 h and at 6 h respectively. The 6 h c-Jun activation peak correlates well with that of P-JNK. We also examined the activation of the two direct JNK activators, MAP kinase kinase 4 (MKK4) and MAP kinase kinase 7 (MKK7). MKK4 showed the same time course as JNK in both core and penumbra, reaching peak activation at 6 h. MKK7 did not show any significant increase of phosphorylation in either core or penumbra. D-JNKI1 markedly prevented the increase of P-c-Jun in both core and penumbra and powerfully inhibited caspase-3 activation in the core. These results confirm that targeting the JNK cascade using the TAT cell-penetrating peptide offers a promising therapeutic approach for ischemia, raising hopes for human neuroprotection, and elucidates the molecular pathways leading to and following JNK activation
Blood colony-forming cells (CFU-C) and leucocyte colony-stimulating activity (CSA) in patients with neutrophilic leucocytosis.
No full textBlood - CFU-C- leucocyte - CSA- neutrophilic leucocytosi
c-Jun N-terminal kinase signaling pathway in excitotoxic cell death following kainic acid-induced status epilepticus
No full textSystemic injections of kainic acid (KA) cause epileptic seizures with delayed neuronal damage in the limbic system, particularly in the hippocampus. KA excitotoxicity activates complex signal transduction events that trigger apoptotic cell death. The c-Jun N-terminal kinase (JNK) pathway plays an important role in cell death, and the peptide D-JNKI1, a competitive JNK inhibitor, is a potent neuroprotective agent. To analyse the role of JNK and the effects of D-JNKI1 administration on excitotoxic neuronal death, we induced epileptic seizures by intraperitoneal (i.p.) injection of KA in adult male Sprague-Dawley rats; a group of rats received i.p. D-JNKI1 2 h after KA. KA caused massive cell death in the hippocampus: in Nissl-stained sections, stereological counts showed a significant decrease in neuronal density in all CA fields, both at 1 and 5 days after seizures, which was partially prevented by D-JNKI1 treatment. These results were confirmed by counts of degenerating neurons in CA3 in FluoroJade B-stained sections. Seizure activity also induced marked gliosis as observed with glial fibrillary acidic protein (GFAP) immunohistochemistry. We also analysed c-Jun activation as a target of JNK and central transcriptional effector in the adult rat brain following KA injection. Phospho-c-Jun immunoreactivity was absent in the hippocampus of untreated animals, whereas strong nuclear neuronal labeling could be observed, starting from 3 h after KA administration, in microtubule-associated protein-2-positive neurons but not in GFAP-positive astrocytes. D-JNKI1 treatment also reduced the positivity for phospho-c-Jun in the hippocampus, thus confirming the specificity of the peptide in blocking JNK. Therefore, JNK is a promising target for blocking seizure-induced cell death
Globalisation, Inequality and Health
No full textAs we suggested in a previous work (Borghesi and Vercelli, Sustainable globalisation, Ecological Economics, vol.44, n.1, 2003), the process of globalisation affects the sustainability of development mainly through three channels: economic growth, inequality and environmental degradation. This conceptual framework may help us to understand also the causal influence of globalisation on health that represents a fundamental dimension of the quality of life enjoyed by the people and of sustainability. For this purpose, the present paper aims to investigate both the direct and the indirect effects of post-war globalisation, with particular attention to the role played by inequality in the globalisation-health relationship. A few policy implications emerging from the analysis are also discussed, suggesting a policy strategy that can at the same time improve health and make the current globalisation process more compatible with sustainable development.globalisation, inequality, health, sustainable development
Neuroprotection by DJNKI1 following seizure activity.
No full textSystemic injections of kainic acid (KA) cause epileptic seizures with delayed neuronal damage in the limbic system, particularly in the hippocampus. KA excitotoxicity activates complex signal transduction events that trigger apoptotic cell death. The c-Jun N-terminal kinase (JNK) pathway plays an important role in cell death, and the peptide DJNKI1, a competitive JNK inhibitor, represents a potent neuroprotective agent.
To analyze the role of JNK and the effects of DJNKI1 administration on excitotoxic neuronal death we induced epileptic seizures on adult male Sprague-Dawley rats by i.p. injection of KA (15 mg/kg) with or without DJNKI1 i.p. administration, 2h after KA treatment. KA caused massive cell death in the hippocampus, which could be quantified in Cresyl violet stained sections. In fact, stereological counts showed a significant decrease in neuronal density in all CA fields, but not in the dentate gyrus, both at one and five days after seizures, which was partially prevented by DJNKI1 treatment. Evaluation of neuronal degeneration showed that DJNKI1 treatment prevented the appearance of Fluoro-Jade B positive-profiles in all CA fields. Seizure activity also induced marked gliosis as observed with GFAP immunohistochemistry. The peptide reduced the size of damaged area in the entorhinal cortex. We also analyzed c-Jun activation as target of JNK and central trascriptional effector in the adult rat brain following KA injection. Phospho-c-Jun immunoreactivity was absent in the limbic system of untreated animals, but starting from 3h after KA a strong nuclear neuronal labeling was seen in the limbic system. DJNKI1 treatment also reduced positivity for phospho-c-Jun in the hippocampus, thus confirming the specificity of the peptide in blocking JNK.
Therefore, JNK is a promising target for blocking seizure-induced cell death.
Support: EEC Stressprotect project
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