9,518 research outputs found
Asset Prices and Assymetries in the Fed's Interest Rate Rule : a Financial Approach
No full textFinancial Newspapers have for long suggested that the Fed tends to provide additional Liquidity when the Stock Market thumbs. We provide a theoretical Explanation for this Behaviour that builds on the Methodology developed by Romaniuk (2008) for a central Banker with two main Goals, Output and Price stability. In this Paper, the Policymaker behaves as a Portfolio Manager who aims at stabilizing Output, Goods Prices, as well as Asset Prices. An optimal, Time-varying Interest Rate Rule is obtained as the Merton's (1971) continuous Time Solution to the Portfolio Manager's Problem. In a second Step, we infer the optimal Interest Rate Rule of a central Bank that can react differently to positive and negative Variations in the Stock Market.Optimal Interest Rate Rule; Portfolio Choice; Fed; Asset Prices; Options Theory
Study of the origin of platelets coagulation protein S by human megakaryocyte cultures and characterization of platelets protein S in patients with inherited protein S deficiency
No full textProtein S (PS) is a vitamin K dependent plasma glycoprotein with multiple functions in coagulation, inflammation and apoptosis. The molecular weight of PS is approximately 70 kDa and its concentration in plasma is about 25 mg/L. In human plasma 40% of PS circulates as free form and the remaining 60% is complexes with complement C4b-binding protein, a component of the complement system. PS circulating in plasma is mainly derived from liver synthesis but, in addition, endothelial cells, testicular Leydig cells and a megakaryocytic cell line (MEG 01) can synthesize PS. Platelet contain PS, but whether this is derived from megakaryocytic synthesis or from uptake of plasma PS by megakaryocyte (Mk) is not known. Free PS acts as a cofactor for activated protein C (APC) in the inactivation of procoagulant factors Va and VIIIa. However, PS also has APC-independent anticoagulant functions, probably through direct inhibition of both the prothrombinase and the tenase complexes. It is hypothesized that intra-platelets PS, release upon platelets stimulation, plays a crucial role in regulating thrombin generation and therefore controlling procoagulant activity. PS deficiency is inherited as an autosomal dominant disordered and is classified in three types: I) reduced plasma levels of total and free PS antigen (PSAg); II) normal concentration of total and free PSAg but with low PS activity; III) low free PSAg; and
normal total PSAg. Inherited PS deficiency is generally associated with increased risk of deep venous thrombosis, pulmonary embolism and some cases of arterial thrombosis. The risk of venous thrombosis in PS deficiency increased if 2 associated with other genetic or acquired conditions these includes factor V (FV) Leiden, HR2 aplotype of FV and prothrombin mutation. Several
factors influence the concentration of plasma PS, pregnancy, oral contraceptive and oral anticoagulant therapy decreased the levels of PS. To clarify the origin of intra-platelets PS, we development an in vitro model of human megakaryocyte cell culture. Hematopoietic stem cells were isolated by the histopaque system from whole blood of healthy and PS deficiency subjects. Mononuclear cells have been grown in a serum free medium in presence of thrombopoietin (TPO) and interleuchin-3 (IL-3) to stimulate the differentiation into megakaryocytes lineage. The morphology of differentiated mononuclear cells was similar to MKs, and their positive stain with anti-CD41 antibody allowed us to conclude that these cells were indeed Mk. Mk was labeled with ??-tubulin and ?-tubulin antibodies and we observed the cytoplasmatic extensions called proplatelets and the release of platelets. In addition, through immunofluorescence techniques,
we detected FV in their cytoplasm whereas protein C was not present as expected. As for PS, it was present in the cytoplasm of MKs obtained from healthy and PS deficiency individuals. Our study demonstrated the PS biosynthesis by megakaryocyte. To study the mechanisms that regulate the
concentration of plasma and platelets PS we analyzed plasma and platelets PS from normal and PS deficiency subjects. PS contained in platelets have the same immunoblotting pattern respect to plasma PS. Plasma and platelet PS immunoblotting pattern demonstrated different molecular weight of PS in some deficient PS individuals as compared to normal control, suggesting different mutations in PS gene. We analyzed the presence of mutation and the presence of PS Heerlen allele. We investigated platelets PS antigen levels in type I and type III PS deficient patients. In type I subjects total and plasma free PS antigen levels were (PSAg) 62±7% and 37±12% 3 respectively. In carries of type III defect total and free PSAg levels were 85±13% and 41±13% respectively. Platelets PSAg in type I and type III were 66 ±32% and 80±37%.In a subgroup of healthy individuals total, free and platelet PSAg levels were 119±17%, 110±17% and 101±30%, respectively. The results indicate that type I and III subject’s total and plasma free PSAg levels were lower than normal individuals. Intra-platelets PSAg levels in type I and type III were lower than of healthy individuals. Our analysis demonstrates a strict correlation between total and free plasma PS and Plts PS. The reduction of platelet PS mirrors the reduced levels of free and total PSAg present in carries of the defect even though PS levels in Plts appears unexpectedly higher than the free PS counterpart. Moreover, we study the interaction of anticoagulant drugs on PSAg levels on 35 patient treatments with warfarin. The levels of total and free plasma PS decreased during treatment with oral anticoagulant, since PS is a vitamin K-dependent protein. Our study demonstrated significant decreased levels of platelet PS respectively plasma free and total PS. We valuated the effect of
anticoagulant drugs (warfarin) and of vitamin K on Mk cells. The Mk were treatment with 1?g/ml of warfarin or 1?g/ml of vitamin K and analyze synthesis of PS. We observed decreased PS synthesis on MKs with warfarin than control MKs; on the contrary, MKs cultured under vitamin K treatment increase PS synthesis.La proteina S (PS) è una glicoproteina plasmatica, vitamina K-dipendente, con molteplici funzioni nell’ambito della coagulazione, infiammazione e apoptosi. Il suo peso molecolare è di 70 kDa e la sua concentrazione plasmatica di circa 25 mg/L. Nel plasma umano il 40% della PS circola in
forma libera, mentre il restante 60% è legato alla C4b-binding-protein, una proteina del sistema del complemento. La PS circolante nel plasma viene sintetizzata principalmente nel fegato ma anche le cellule endoteliali, le cellule di Leydig e una linea cellulare di megacariociti sono in grado di
sintetizzarla. Le piastrine contengono PS, anche se la sua origine non è ancora stata chiarita. Si ipotizza che derivi dalla sintesi dei megacariociti o che siano gli stessi megacariociti ad assumerla dal pool plasmatico mediante un meccanismo di endocitosi. La PS libera agisce da cofattore per la proteina C attivata (APC) nell’inattivazione dei fattori procoagulanti Va (FVa ) e VIIIa (FVIIIa). La
PS esercita anche un’azione anticoagulante APC-indipendente, probabilmente inibendo direttamente i complessi tenase e protrombinase. Si suppone che la PS rilasciata dalle piastrine in seguito alla loro attivazione regoli la generazione di trombina, controllando perciò l’attività
procoagulante. I difetti di PS sono a trasmissione autosomica dominante e vengono classificati in tre tipi: – difetto di tipo I, caratterizzato da ridotti livelli plasmatici di PS totale e libera; – difetto di tipo II, caratterizzato da livelli fisiologici di PS totale e libera associati ad una ridotta attività; 6 – difetto di tipo III, presenta una PS libera ridotta ed una PS totale nella norma. I difetti di PS sono generalmente associati ad un aumentato rischio di trombosi venosa profonda, embolismo polmonare ed, in qualche caso, a trombosi arteriosa. Nei deficit di PS il rischio di trombosi venosa aumenta se associato ad altre condizioni di carattere genetico o acquisito quali il FV Leiden, l’aplotipo HR2 del FV e mutazioni a carico del gene che codifica per la protrombina. Molteplici fattori, tra cui la gravidanza, la terapia anticoncezionale e anticoagulante orale, riducono la concentrazione plasmatica della PS. Al fine di chiarire l’origine della PS piastrinica, abbiamo messo a punto un
modello in vitro di colture di megacariociti umani. Le cellule staminali ematopoietiche sono state isolate con histopaque da sangue intero di soggetti sani e con difetto di PS. Le cellule mononucleate sono state coltivate in un terreno privo di siero ed in presenza di trombopoietina (TPO) e interleuchina 3 (IL3) per stimolarne la differenziazione in una linea magacariocitaria. Le cellule mononucleate differenziate presentavano una morfologia simile a quella dei megacariociti e risultavano positive all’anticorpo anti-CD41; questi elementi ci hanno permesso di confermare
che si trattasse effettivamente di megacariociti. Inoltre, la marcatura dei megacariociti con anticorpi anti ??-tubulina e ?-tubulina ha evidenziato sia la presenza di estensioni citoplasmatiche denominate “proplatelets” sia il rilascio di piastrine da parte dei megacariociti. In aggiunta, mediante
tecniche di immunofluorescenza, abbiamo rilevato la presenza del FV a livello citoplasmatico, mentre la PC era assente. La PS era presente nel citoplasma dei megacariociti isolati da individui sani e con difetto di PS. La nostra ricerca ha così dimostrato la sintesi di PS da parte dei megacariociti. 7 Per studiare il meccanismo che regola i livelli di PS presenti nel plasma e all’interno delle piastrine, abbiamo determinato la concentrazione di PS plasmatica e piastrinica in soggetti sani e portatori di difetto di PS. La PS piastrinica mostrava lo stesso pattern elettroforetico di quella isolata dal plasma. L’analisi immunologica ha inoltre evidenziato, per alcuni soggetti
portatori del difetto, una PS plasmatica con differente peso molecolare rispetto ai controlli sani; questo ci ha suggerito la presenza di mutazioni nel gene della PS. Abbiamo quindi testato la presenza di eventuali mutazioni e dell’allele Heerlen. In soggetti portatori di difetto di PS di tipo I i livelli di PS totale plasmatici, e libera erano: 62±7% e 37±12% . In soggetti portatori di difetto di PS di tipo III i livelli di PS totale e libera nel plasma erano di 85±13% e 41±13%. I livelli di PS nelle piastrine nei soggetti portatori di difetto di PS di tipo I e di tipo III erano di 66 ±32% e 80±37%. In un gruppo di persone sane i livelli di PS totale, libera e piastrinica erano di 119±17%, 110±17% e 101±30%, rispettivamente. Dall’analisi dei livelli plasmatici e piastrinici di PS in soggetti portatori del difetto di tipo I e III è emerso che a) nei pazienti con difetto i livelli di PS
totale e libera erano più bassi rispetto ai soggetti sani; b) i pazienti con difetto presentavano livelli di PS piastrinica ridotti rispetto agli individui sani utilizzati come controllo. La nostra analisi ha dimostrato una stretta correlazione tra la PS plasmatica (libera e totale) e quella piastrinica. La diminuzione della concentrazione di PS piastrinica, osservata negli individui portatori del difetto, riflette l’abbassamento del livello di PS plasmatica, sebbene la quota di PS all’interno delle piastrine risulti maggiore rispetto a quella della PS presente nel plasma in forma libera. In seguito abbiamo studiato l’effetto di sostanze anticoagulanti sui livelli plasmatici e piastrinici di PS in pazienti 8 sani in trattamento con warfarina. E’ noto che la warfarina abbassa i livelli plasmatici di PS in quanto quest’ultima è una proteina vitamina Kdipendente. Anche i livelli di PS plasmatica, (totale e libera), e piastrinica dei medesimi soggetti in terapia con warfarina risultano ridotti rispetto alla norma ma l’abbassamento della concentrazione di PS appare molto più marcata all’interno delle piastrine piuttosto che nel plasma. Infine abbiamo valutato l’effetto della warfarina e della vitamina K sulla sintesi di PS da parte dei megacariociti. Mediante tecniche di immunofluorescenza abbiamo osservato una ridotta sintesi della PS nei megacariociti trattati con warfarina rispetto alle cellule di controllo; al contrario, i megacariociti coltivati in un terreno supplementato con vitamina K mostravano un incremento della sintesi di PS
Simulation of Heart Rate Variability Model in a Network
No full textWe consider a 1-D model for the simulation of the blood flow in the cardiovascular system. As inflow condition we
consider a model for the aortic valve. The opening and closing of the valve is dynamically determined by the pressure difference
between the left ventricular and aortic pressures. At the outflow we impose a peripheral resistance model. To approximate the
solution we use a numerical scheme based on the discontinuous Galerkin method. We also considering a variation in heart rate and
terminal reflection coefficient due to monitoring of the pressure in the network
Calcium Signaling in Interstitial Cells: Focus on Telocytes
No full textIn this review, we describe the current knowledge on calcium signaling pathways in interstitial cells with a special focus on interstitial cells of Cajal (ICCs), interstitial Cajal-like cells (ICLCs), and telocytes. In detail, we present the generation of Ca(2+) oscillations, the inositol triphosphate (IP3)/Ca(2+) signaling pathway and modulation exerted by cytokines and vasoactive agents on calcium signaling in interstitial cells. We discuss the physiology and alterations of calcium signaling in interstitial cells, and in particular in telocytes. We describe the physiological contribution of calcium signaling in interstitial cells to the pacemaking activity (e.g., intestinal, urinary, uterine or vascular pacemaking activity) and to the reproductive function. We also present the pathological contribution of calcium signaling in interstitial cells to the aortic valve calcification or intestinal inflammation. Moreover, we summarize the current knowledge of the role played by calcium signaling in telocytes in the uterine, cardiac and urinary physiology, and also in various pathologies, including immune response, uterine and cardiac pathologies
An asset pricing model with loss aversion and its stylized facts
No full textA well-defined agent-based model able to match the widely observed properties of financial assets is valuable for testing the implications of various empirically observed heuristics associated with investors behaviour. In this paper, we extend one of the most successful models in capturing the observed behaviour of traders, and present a new behavioural asset pricing model with heterogeneous agents. Specifically, we introduce a new behavioural bias in the model, loss aversion, and show that it causes a major difference in the agents interactions. As we demonstrate, the resulting dynamics achieve one of the major objectives of the field, replicating a rich set of the stylized facts of financial data. In particular, for the first time our model enables us to match the following empirically observed properties: conditional heavy tails of returns, gains/loss asymmetry, volume power-law and long memory and volume-volatility relations
Avoiding regret in an agent-based asset pricing model
No full textWe use an agent-based asset pricing model to test the implications of the disposition effect (avoiding regret) on investors’ interactions and price settings. We show that it has a direct impact on the returns series produced by the model, altering important stylized facts such as its heavy tails and volatility clustering. Moreover, we show that the horizon over which investors compute their wealth has no effect on the dynamics produced by the model
On the next generations of infrastructure-as-a-services
No full textFollowing the wide adoption by industry of the cloud computing technologies, we can talk about a second generation of cloud services and products that are currently under design phase. However, it is not yet clear how the third generation of cloud products and services of the next decade will look like, especially at the delivery level of Infrastructure-as-a-Service. In order to answer at least partially to such a challenging question, we initiated a literature overview and two surveys involving the members of a cluster of European research and innovation actions. The results are interpreted in this paper and a set of topics of interest for the third generation are identified
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