1,721,100 research outputs found

    The Macroeconomic and Financial Landscape in the Aftermath of the 2007 Crisis: New Challenges and Perspectives

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    On 6 June 2011 the Global Governance Programme at the EUI hosted a High-Level Policy Seminar (HLPS) on the topic “The Macroeconomic and the Financial Landscape in the Aftermath of the 2007 Crisis: New Challenges and Perspectives”. The event consisted of a closed-door roundtable between the vice President of the European Central Bank, Vitor Costancio and a number of academics and policymakers. The discussion centered around three themes: Sovereign debt problems, monetary and fiscal policies, and financial stability and macro prudential policies. In the first theme, the participants discussed various options to deal with the economic situation in Greece. These included the creation of a transfer union among Euro member states and the implications of a possible default for the functioning of the European Central Bank and the stability of the European banking system. In the second theme, it was discussed how to sustain and conduct a single monetary policy in heterogeneously growing countries, how to reach debt sustainability in a low growth environment and the desirability of common fiscal policies. The last part of the event focused on the new architecture for financial regulation and financial stability in Europe. The discussion at the HLPS was very lively. Many different views were discussed and many suggestions and recommendations were put forth. This policy paper consists of seven papers ranging from economics to history and law written by some of the academics participating to the debate. The memoranda were reviewed and expanded after the event to reflect the discussion and to include other topics of interest related to the debate. The papers reflect the aim of the HLPS to contribute to an open debate between academics and policymakers on some key challenges that the economies worldwide are facing. The paper by Thomas Cooley (New York University) discusses the challenges for the European Central Bank in the current situation both in terms of long term fiscal adjustments and of potential fragility of the European Banking system. The pair of papers by Giancarlo Corsetti (Cambridge University and EUI) and Massimiliano Marcellino (EUI) focuses on debt sustainability and the implications of the debt crisis for growth. The paper by Harold James (Princeton University) focuses more specifically on the challenges to monetary and fiscal policies in Europe. The joint paper by Joanna Gray and Patrick O'Callaghan (both Newcastle University) discusses the legitimacy and efficacy of the EU and Member State response to the sovereign debt problems in the Eurozone from a legal perspective. The joint paper by Franklin Allen (University of Pennsylvania) and Elena Carletti (EUI) turn the attention to the issue of systemic risk and the need for macroprudential regulation. Finally, Luigi Guiso (EUI) tackles the issue of trust and risk aversion in the aftermath of the financial crisis. Our hope is that this joint policy paper will contribute to shaping the debate further and help policymakers to tackle the challenges emerged in the aftermath of the financial crisis

    Supraspinal connections and termination patterns of the parabrachial complex determined by the biocytin anterograde tract-tracing technique in the rat

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    We have re-evaluated, using the anterograde tracer biocytin, supraspinal efferent projections from the parabrachial complex (PBN) to gain new information about the nature of its connections and nerve terminal patterns. We selectively injected biocytin into the 3 main regions of the nucleus (lateral PBN, medial PBN and Kölliker-Fuse nucleus). We observed distinct groups of ascending and descending fibres of different calibre from the PBN running throughout the brain and reaching many brain areas involved in the regulation of autonomic function. Here we detected labelled bouton-like terminals and fibres with en-passage varicosities. The ascending efferents from the lateral PBN mainly reached the reticular, raphe and thalamic nuclei, the zona incerta (ZI), central nucleus of the amygdala (CeA) and lateral area of the periaqueductal grey (PAG). Thin descending efferents reached the ventral region of the solitary tract nucleus (STN). The ascending efferents from the medial PBN were seen in the raphe nuclei, reticular nuclei, ventral and lateral areas of the PAG, thalamic nuclei, and in the medial and lateral nuclei of the amygdala. Descending efferents were seen in the STN and in some reticular nuclei. The ascending projections from the Kölliker-Fuse targeted the ventral area of PAG, CeA, ZI, lateral hypothalamic area, ventromedial thalamic nucleus and, with only a few terminals, the ipsi and contralateral reticular area. A large number of descending efferents reached STN, caudal and paragigantocellular reticular nuclei. The higher sensitivity of biocytin compared with other types of markers allowed us to determine more effectively the distribution, nature and extent of the supraspinal PBN connections. This suggested that in several nerve circuits the PBN probably plays a more important role than previously thought

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Cyclosporine-A treatment prevents apoptosis in rat lumbar ganglion cells

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    We evaluated the expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 in lumbar ganglion cells of rats by immunohistochemistry under normal conditions and after 7, 14 and 21 days of cyclosporine-A treatment (7 and 15 mg/kg/daily). In normal rats, Bax was weakly expressed in all types of neurons, whereas satellite cells showed moderate immunostaining. Bcl-2 expression was weak in type A neurons and weak or moderate in type B and C neurons and also into satellite cells. In cyclosporine-A-treated rats, we found changes in Bax staining of neurons: type A neurons and type B neurons were weakly stained, whereas type C neurons were moderately stained. Bax expression in satellite cells was moderate after 7 days of treatment and increased strongly after 14 and 21 days of treatment. Bcl-2 expression increased significantly in neurons after 14 and even more after 21 days of treatment with 7 mg/kg cyclosporine-A, mainly in type B and C neurons. With 15 mg/kg cyclosporine-A, Bcl-2 increased moderately in type A and B neurons and strongly in type C neurons only after 7 days. After 14 and 21 days, Bcl-2 expression was moderate in type A neurons whereas it was strong or even very strong in type B and C neurons. Satellite cells showed a moderate increase in Bcl-2 after 7 and 14 days of treatment whereas after 21 days, expression was strong. We conclude that (1) in normal conditions, Bax and Bcl-2 were differently expressed in neurons and satellite cells; (2) cyclosporine-A treatment rapidly enhanced Bax expression in satellite cells only, whereas Bcl-2 expression increased moderately in type A neurons and was strongly expressed in type B and C neurons; (3) cyclosporine-A has a protective role in neurons but not in satellite cells; and (4) the neuroprotective role of cyclosporine-A is dose dependent. Furthermore, the strong expression of Bax in satellite cells can explain the temporary nature of the neurotoxic effect commonly observed after cyclosporine-A administration

    Distribution of heat shock proteins in kidneys of rats after immunosuppressive treatment with cyclosporine A

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    Cyclosporine A (CsA), a fungal undecapeptide, is the most common immunosuppressive drug used in organ transplantation and auto-immune diseases. However, it has severe side effects mainly on renal structures and functions. Therefore, nephrotoxicity is the major limiting side effect. Heat shock proteins (HSPs) are molecular chaperones, that are induced or expressed at high levels in mammalian cells due to a variety of adverse effects. HSPs have beneficial roles in protein processing and protection against cell injury. In the present study, we examined immunohistochemically levels of expression and localization patterns of various HSPs in rat kidneys after administration of a therapeutic CsA dose during 30 days. After CsA treatment, both constitutive HSP 25 and alpha B-crystallin immunoreactivity became stronger in glomeruli, proximal tubules and collecting ducts. Nuclear translocation of these proteins was detected in renal tubules. HSP 47 was detected in the interstitial space between tubules, vascular smooth muscle and medullary rays. Finally, HSP 72 was induced in the cytoplasm of epithelial cells of proximal and distal tubules, and in the cytoplasm of epithelial cells of Henle limbs and collecting ducts. These data demonstrate that CsA clearly induces increased immunoreactivity of HSPs in defined structures of rat kidneys. These findings suggest that these proteins are functionally involved in the defence against renal cellular damage caused by prolonged drug treatment in rat

    Does methylene blue protect the kidney tissues from damage induced by ciclosporin A treatment?

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    Ciclosporin A (CsA) is the first-choice immunosuppressant universally used in allotransplantation and autoimmune diseases. However, it has been demonstrated that this drug produces negative side effects in several organs and in particular in the lymphoid organs and in the kidney. It has been suggested that the CsA causes deleterious effects because it increases the oxygen free radical production. Here we wanted to test whether antioxidants protect the kidney parenchyma from the toxicity induced by CsA. We used methylene blue (MB), because it inhibits the formation of oxygen free radicals. The study was carried out in four groups of Wistar rats. Group I animals were intraperitoneally injected with MB (1 mg/kg/day) for 21 days; group II animals were subcutaneously injected with CsA (15 mg/kg/day) for 21 days; group III animals were treated with CsA combined with MB at the same doses and for the same periods as groups I and II, and group IV animals were injected subcutaneously with olive oil for 21 days as controls. The kidneys and the thymuses were subsequently removed and examined by conventional morphological staining (hematoxylin-eosin and Masson's trichrome) and enzymatic (NADPH-diaphorase, cytochrome, c oxidase, and superoxide anion production) and immunoenzymatic (inducible nitric oxide synthase - iNOS, endothelial nitric oxide synthase - eNOS) techniques. The thymuses were used to check the persistence of CsA-immunsuppressive effects during MB administration. Group I, III, and IV animals showed a normal kidney architecture and low levels of NADPH-diaphorase and of superoxide anion in all structures studied (proximal and distal tubules, glomeruli and the Henle loops). The cytochrome c oxidase showed a strong activity in proximal tubules, a moderate activity in distal tubules, and a weak activity in glomeruli and in the Henle loops. The expression of iNOS was weak in the proximal tubular epithelial cells and negative in the glomeruli, while eNOS was found to be moderately positive in the glomeruli and in the interstitial arteries, but not in the tubules and in the Henle loops. Degenerative changes with tubulointerstitial injury in the cortex of CsA-treated kidneys (group II) and increases of NADPH-diaphorase levels, iNOS activity, and superoxide staining were found in all structures. The expression of eNOS did not change in group I, III and IV animals. MB combined with CsA prevented the degenerative changes caused by CsA, preserving the structural, enzymatic, and immunoenzymatic integrity of the renal parenchyma. The mechanism by which MB exerts its protective action is not yet clear, but it seems to be due to its ability to inhibit xanthine oxidase and to quench nitric oxide production. Moreover, these data have been also supported by the following: (1) the superoxide anion levels were very high after CsA treatment and reduced after CsA-MB treatment, and (2) the iNOS levels increased in CsA-treated rats and showed normal levels after CsA-MB treatment. Moreover we demonstrated that MB administration did no compromise the CsA immunosuppressive effects, since the thymus showed a cytoarchitecture like that observed in CsA-treated rats. Copyrigh

    Ultrastructural study of the alterations in spinal ganglion cells of rats chronically fed on ethanol

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    A study was conducted to find the effects of chronic alcohol (EtOh) administration on the rat dorsal root ganglion (DRG) cells in vivo. Morphoquantitative changes of the cytoplasmic organelles in neurons and satellite cells (SC) of lumbar DRG of animals fed with 20 and 40% of EtOH for 6 months were determined at the electron microscopic level. Stereological methods were used to quantitatively evaluate the changes in the neuronal Golgi fields, in the lysosomal system components called dense bodies (DB), in the mitochondria, and in the cytoplasmic perikaryal projections (PP) characteristic of DRG neurons. Prolonged consumption of 20% EtOh was well tolerated by neurons. There were, however, some structural modifications in the studied organelles, and there was a significant increase in the neuronal surface. In SC the number of mitochondria and DB increased significantly. Treatment with 40% EtOH produced massive organelle alterations in both neurons and SC, including disruption of the PP, markedly reducing the neuronal surface area. The architecture of the SC sheath appeared disorganized. The alterations resembled those of senescence, and indicated that a high dose of EtOH (or its metabolites) had a profound disruptive effect on the organelles and on the membrane systems of the DRG cells. The SC of the DRG units from the animals fed with EtOH were the first to show significant morphological alterations. When the architecture of the SC sheath already showed evident signs of disorganization, the neuronal body was just beginning to show morphological damage. These results suggest that the progressive disorganization of the SC sheath is a probable source of complication in peripheral neuropathy

    Effects of acute caffeine administration on NOS and Bax/Bcl2 expression in the myocardium of rat

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    Caffeine is the most frequently ingested neuroactive drug in the world and it is largely used to delay fatigue and improve physical activity. Caffeine can modulate NO synthesis in cells and may influence muscular function by modifying the cellular cycle life-death. There is little data concerning the relationship between caffeine in the heart, NOS expression and apoptosis and no data regarding the acute effect of high doses of caffeine in the in vivo myocardium. We therefore studied hemodynamic NOS and Bax/Bcl2 expression in the rat myocardium after a single cafffeine administration. Thirty-two male rats were divided into six groups: the first was iv-injected with caffeine (16 mg/kg), the second with caffeine + l-NAME (30 mg/kg), the third with caffeine + l-arg (0.5 g/kg), the fourth with caffeine + l-NAME + l-arg and finally the fifth with saline. Mean arterial blood pressure (MAP) was monitored for 30 min, then the animals were killed. The sixth group was injected with caffeine and killed after 2 h. The hearts were isolated and processed by immunohistochemistry. We found that caffeine increased MAP temporarily while caffeine + l-NAME increased it for a longer period. In the control myocardium, all NOS isoforms were expressed. The Bcl2 were strongly expressed inside the perinuclear cytoplasm whereas Bax was very faintly detectable in the peripheral cytoplasm. In caffeine and caffeine + l-NAME treated animals, NOS expression disappeared. Bax and Bcl2 expression did not vary. The l-arg administration reversed these caffeine and l-NAME effects on NOS expression. Two hours after caffeine, NOS expression increased and Bax and Bcl2 expression did not vary, although Bcl2 was mainly expressed in the peripheral cytoplasm. We conclude that improved caffeine-induced physical performance could also be related to caffeine's ability to interfere with endogenous myocardial NO synthesis. Furthermore, we suggest that myocardial cell plays an effective anti-apoptotic role against acute caffeine administration

    Cytoplasmic changes in satellite cells of spinal ganglia induced by cisplatin treatment in rats

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    The effects of cisplatin (cis-DDP) therapeutic treatment on the cytoplasmic compartment of satellite cells (SC) of rat dorsal root ganglia (DRG) were evaluated. Female Wistar rats were treated once a week with i.p. injection of cis-DDP (2 mg/kg) for 9 weeks. Morpho-quantitative changes of the cytoplasmatic organelles in SC cytoplasm from L4-L6 DRG were determined at the electron microscopic level. The quantitative changes in the lysosomal system components called dense bodies (DB) and in the mithocondria were stereologically evaluated. The data from SC were compared to those from the neurons. The cis-DDP treatment induced a great increase in DB and mithocondria volume of SC. Furthermore, the SC sheath showed an increase of the cytoplasmic lamellar expansions responsible of the physical dissociation of SC sheath from the nerve cell body surface. The comparative analysis from SC and neurons showed that the drug affected primarily the SC, supporting the idea that SC could be the initial target of cis-DDP molecule. The alterations of the anatomical relationships between SC and neurons could modify the cell control on extracellular solutions, altering the functional role barrier attributed to SC. It appears that not only the DRG neurons but also and principally the SC were involved in the peripheral neuropathy mechanisms caused typically from therapeutic cis-DDP administration
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