A semi-Markov model with memory for price changes

We study the high frequency price dynamics of traded stocks by a model of returns using a semi-Markov approach. More precisely we assume that the intraday returns are described by a discrete time homogeneous semi-Markov which depends also on a memory index. The index is introduced to take into account periods of high and low volatility in the market. First of all we derive the equations governing the process and then theoretical results have been compared with empirical findings from real data. In particular we analyzed high frequency data from the Italian stock market from first of January 2007 until end of December 2010

First and second order semi-Markov chains for wind speed modeling

The increasing interest in renewable energy, particularly in wind, has given rise to the necessity of accurate models for the generation of good synthetic wind speed data. Markov chains are often used with this purpose but better models are needed to reproduce the statistical properties of wind speed data. We downloaded a database, freely available from the web, in which are included wind speed data taken from L.S.I. -Lastem station (Italy) and sampled every 10 minutes. With the aim of reproducing the statistical properties of this data we propose the use of three semi-Markov models. We generate synthetic time series for wind speed by means of Monte Carlo simulations. The time lagged autocorrelation is then used to compare statistical properties of the proposed models with those of real data and also with a synthetic time series generated though a simple Markov chain.Comment: accepted for publication on Physica

Weighted-indexed semi-Markov models for modeling financial returns

In this paper we propose a new stochastic model based on a generalization of semi-Markov chains to study the high frequency price dynamics of traded stocks. We assume that the financial returns are described by a weighted indexed semi-Markov chain model. We show, through Monte Carlo simulations, that the model is able to reproduce important stylized facts of financial time series as the first passage time distributions and the persistence of volatility. The model is applied to data from Italian and German stock market from first of January 2007 until end of December 2010.Comment: arXiv admin note: substantial text overlap with arXiv:1109.425

Performance estimation of photovoltaic energy production

This article deals with the production of energy through photovoltaic (PV) panels. The efficiency and quantity of energy produced by a PV panel depend on both deterministic factors, mainly related to the technical characteristics of the panels, and stochastic factors, essentially the amount of incident solar radiation and some climatic variables that modify the efficiency of solar panels such as temperature and wind speed. The main objective of this work is to estimate the energy production of a PV system with fixed technical characteristics through the modeling of the stochastic factors listed above. Besides, we estimate the economic profitability of the plant, net of taxation or subsidiary payment policies, considered taking into account the hourly spot price curve of electricity and its correlation with solar radiation, via vector autoregressive models. Our investigation ends with a Monte Carlo simulation of the models introduced. We also propose the pricing of some quanto options that allow hedging both the price risk and the volumetric risk

High blood levels of IL-6 nicely correlate with animal survival in trained C26 bearing mice

Exercise is a beneficial adjunct therapy to maintain or enhance quality of life in cancer patients. Recently, few studies demonstrated a correlation between high concentrations of IL-6 and a poor survival. This depends on the equilibrium between the concentrations of IL-6 and sIL-6R. Exercise induces a beneficial increase in circulating IL-6 (1). Fresh fragments of solid C26 tumor were inoculated in healthy 3 months-old mice (n=230, M=115 and F=115). The experimental procedure were 12 weeks long. During the first 6 weeks, mice were randomly assigned to one of the experimental conditions: sedentary (SED) or progressive training (TRP). After the first 6 weeks, all mice were inoculated with a fresh fragment of tumor. All trained adult mice after the tumor inoculation were randomly assigned to a different training program: low intensity training (TRL), moderate intensity training (TRM) and high intensity training (TRH). Mice run 5 days per week on a Rota-Rod following one of the specific training program (TRP ,TRL, TRM and TRH) (2). After tumor inoculation the mice were daily weighted and tumor size monitored until death. Moreover, 8 mice for each group were sacrificed when cachexia occurred (>9% body weight loss), and blood samples were stored for CBA Enhanced flex set flow-cytometric assays (IL-6 and TNF-alpha). The TRM and TRH training protocol performed by trained adult male mice extend the median survival compared to the sedentary adult mice and trained female mice. Interesting the beneficial effect of exercise seemed to be mediated extending the survival days. Significant high blood levels of IL-6 were recorded among the male trained mice (TRM and TRH) groups in comparison with sedentary adult mice and trained female mice (TRM and TRH). The results suggest that endurance exercise as adjuvant therapy is gender and physical training level specific. This effect seems to be mediated by IL-6 blood levels

QoT-Driven Optical Control and Data Plane in Multi-Vendor Disaggregated Networks

A novel disaggregated network architecture with independent PCE and optical control based on GNPy is proposed and experimentally validated over a network including two independent OLSs for total 1400 km, ROADM whiteboxes and pluggable transceivers

Interleukin-1 family members in the retina of streptozotocin-injected rats

Diabetic retinopathy (DR) is one of the most common complications of diabetes. It has been demonstrated that pro-inflammatory cytokines are increased in diabetic retina, including interleukin-1β (IL-1β) (Joussen et al., 2001), suggesting that this cytokine might play an important role in the pathogenesis of DR (Kowluru and Odenbach, 2004). The principal components of the IL-1 family are two secreted factors, IL-1α and IL-1β, two transmembrane receptors (IL-1RI and IL-1RII), and a natural antagonist receptor of IL-1 function (IL-1Ra). To date the molecular mechanisms mediated by IL-1 family members in DR have not been fully characterized. In the present study, to explore the role of IL-1, we analyzed the expression and distribution of IL-1α and IL-1β and relative receptors in a model in vivo of DR. Diabetes was induced in adult rats by intraperitoneal injection of streptozotocin (60 mg/kg). Protein expression and distribution of IL-1 members and relative receptors were analyzed in retinas of nondiabetic and diabetic rats three weeks after induction of diabetes by Western blot and confocal microscopy analyses. Hyperglycemia induced a significant increased in IL-1β protein expression levels and distribution as compared to nondiabetic animals. Specifically, IL-1β retinal immunoreactivity was found not only in the rod and cone layer (RCL), but also in the outer plexiform layer (OPL), inner plexiform (IPL) and in the ganglion cell layer (GCL) of diabetic rats. IL-1α transcription levels were unchanged in the retinas of both animal groups. Consistent with expression studies, IL-1α localization did not differ between diabetic and nondiabetic rats. IL-1RI, IL-1RII and IL-1Ra expression was significantly increased in the retina of diabetic rats when compared to controls. Accordingly, IL-1RI positiveness was thoroughly increased in all retinal layers of diabetic rats, while no evident changes were apparent for IL-1RII, which was localized in the RCL layer and in outer nuclear layer (ONL) of both diabetic and nondiabetic rats. These finding point to IL-1 family members as key elements in the pro-inflammatory cascade after hyperglycemia-induced retinal damage, and therefore support the implementation of novel therapeutic strategies aimed at reducing IL-1 production for the treatment of DR

The Melanocortin MC5R as a New Target for Treatment of High Glucose-Induced Hypertrophy of the Cardiac H9c2 Cells

The study explored the anti-hypertrophic effect of the melanocortin MC5R stimulation in H9c2 cardiac myocytes exposed to high glucose. This has been done by using α-MSH and selective MC5R agonists and assessing the expression of GLUT4 and GLUT1 transporters, miR-133 and urotensin receptor levels as a marker of cardiac hypertrophy. The study shows for the first time an up-regulation of MC5R expression levels in H9c2 cardiomyocytes exposed to high glucose medium (33 mM D-glucose) for 48 h, compared to cells grown in normal glucose medium (5.5 mM D-glucose). Moreover, H9c2 cells exposed to high glucose showed a significant reduction in cell viability (-40%), a significant increase in total protein per cell number (+109%), and an increase of the urotensin receptor expression levels as an evidence of cells hypertrophy. The pharmacological stimulation of MC5R with α-MSH (90 pM)of the high glucose exposed H9c2 cells increased the cell survival (+50,8%) and reduced the total protein per cell number (-28,2%) with respect to high glucose alone, confirming a reduction of the hypertrophic state as per cell area measurement. Similarly, PG-901 (selective agonist, 10-10 M) significantly increased cell viability (+61,0 %) and reduced total protein per cell number (-40,2%), compared to cells exposed to high glucose alone. Interestingly, the MC5R agonist reduced the GLUT1/GLUT4 glucose transporters ratio on the cell membranes exhibited by the hypertrophic H9c2 cells and increased the intracellular PI3K activity, mediated by a decrease of the levels of the miRNA miR-133a. The beneficial effects of MC5R agonism on the cardiac hypertrophy caused by high glucose was also observed also by echocardiographic evaluations of rats made diabetics with streptozotocin (65 mg/kg i.p.). Therefore, the melanocortin MC5R could be a new target for the treatment of high glucose-induced hypertrophy of the cardiac H9c2 cells

Dopamine D3 receptor knockout mice exhibit increased hippocampal cAMP response element binding protein (CREB) following acquisition of passive avoidance memory

The dopamine D3 (D3R) receptor seems to be implicated in synaptic plasticity and memory-related processes as identified by several pharmacological and behavioral approaches (Laszy et al., 2005; Swant 2008). In a previous study we have shown that D3Rs mediate an inhibitory effect on learning, since D3R knockout (D3-/-) mice display enhanced cognitive performance in the single trial step-through passive avoidance task (PA) as compared to WTs (Micale et al., 2010; D’Amico et al., 2013). Formation of new memories is known to require de novo synthesis of proteins related to synaptic function, possibly through the activation of a number of signaling pathways including the mitogen-activated protein kinases (MAPKs), protein kinase B (namely Akt) and the activation of nuclear transcription factors such as the cAMP response element binding protein (CREB). However, no clear indications have yet been provided regarding the specific involvement of D3Rs in the activation of these signaling cascades after acquisition of PA. Therefore, in the present study we assessed whether activity/phosphorylation levels of several MAPKs, Akt and CREB were differentially affected by PA in both wild-type (WT) and D3-/- mice. Animals were divided into four groups: naive, unconditioned stimulus trained (USTA), conditioned stimulus trained (CSTA) and conditioned (CA) animals. Phosphorylation of MAPKs, including extracellular signal-regulated kinase 1/2 (ERK 1/2), c-Jun-N-terminal kinase (JNK) and p38, as well as of Akt and CREB were assessed by immunoblotting and immunohistochemical analyses. Results showed that acquisition of PA induced a significant increase in hippocampal pCREB levels both in WT and D3-/- mice. However, the extent of PA-driven increase in pCREB levels was significantly higher in mice lacking D3Rs. Similarly, hippocampal pERK 1/2 were further augmented in D3-/- mice subjected to PA as compared to trained WTs. JNK and p38 phosphorylation was not affected neither by PA nor by genetic background. Finally, a significantly increased Akt activation was observed only when comparing naïve WT and D3-/- mice, but not in response to PA acquisition. This result suggests that the Akt signaling cascade is influenced by the absence of the receptor, but only under basal conditions. In conclusion, the data here presented supports the notion that D3Rs might modulate CREB phosphorylation after acquisition of PA, probably via activation of the ERK signaling pathway

Endurance training induces apoptosis in the tumor mass in the C26-bearing mouse model

Cachexia, sarcopenia and anorexia are characterised by muscle wasting. This condition is a weakening, shrinking, and loss of muscle caused by a disease or lack of use. The loss of muscle causes a decrease in strength and inability to move compromising the quality of life. Recently we demonstrated that the skeletal muscle of endurance trained Balb/c mice release IL-6 and Hsp60 (inside exosomes) in the blood stream. We studied the expression of Hsp60 in the muscles of trained and untrained C26-bearing mice, to understand if Hsp60 was over-expression may improve muscle performance and reduce cachexia. Four different interleukins have been also studied in cachectic mice, to understand which was their effect on Hsp60 expression both in the tumor mass and the trained muscle. In the present study we demonstrated that: 1) IL-6 is released by the trained muscle; 2) IL-6 is release also by the tumor mass, 3) in animals inoculated with the C26 tumor and trained after inoculation, IL-6 is synthesized mainly by the skeletal muscle and the tumor mass undergo apoptosis