The Trading Performance of Dynamic Hedging Models: Time Varying Covariance and Volatility Transmission Effects

In this paper, we investigate the value of incorporating implied volatility from related option markets in dynamic hedging. We comprehensively model the volatility of all four S&P 500 cash, futures, index option and futures option markets simultaneously. Synchronous half-hourly observations are sampled from transaction data. Special classes of extended simultaneous volatility systems (ESVL) are estimated and used to generate out-of-sample hedge ratios. In a hypothetical dynamic hedging scheme, ESVLbased hedge ratios, which incorporate incremental information in the implied volatilities of the two S&P 500 option markets, generate profits from interim rebalancing of the futures hedging position that are incremental over competing hedge ratios. In addition, ESVL-based hedge ratios are the only hedge ratios that manage to generate sufficient profit during the hedging period to cover losses incurred by the physical portfolio .volatility transmission, dynamic hedging, optimal hedge ratio, S&P 500

The role of signal transducer and activator of transcription 3 (STAT3) and its targeted inhibition in hematological malignancies

© 2018 by the authors. Licensee MDPI, Basel, Switzerland. Signal transducer and activator of transcription 3 (STAT3), a member of the STAT protein family, can be phosphorylated by receptor-associated Janus kinases (JAKs) in response to stimulation by cytokines and growth factors. It forms homo-or heterodimers that can translocate to the cell nucleus where they act as transcription activators. Constitutive activation of STAT3 has been found to be associated with initiation and progression of various cancers. It can exert proliferative as well as anti-apoptotic effects. This review focuses on the role of STAT3 in pathogenesis i.e., proliferation, differentiation, migration, and apoptosis of hematological malignancies viz. leukemia, lymphoma and myeloma, and briefly highlights the potential therapeutic approaches developed against STAT3 activation pathway

Unequal Intra-layer Coupling in a Bilayer Driven Lattice Gas

The system under study is a twin-layered square lattice gas at half-filling, being driven to non-equilibrium steady states by a large, finite `electric' field. By making intra-layer couplings unequal we were able to extend the phase diagram obtained by Hill, Zia and Schmittmann (1996) and found that the tri-critical point, which separates the phase regions of the stripped (S) phase (stable at positive interlayer interactions J_3), the filled-empty (FE) phase (stable at negative J_3) and disorder (D), is shifted even further into the negative J_3 region as the coupling traverse to the driving field increases. Many transient phases to the S phase at the S-FE boundary were found to be long-lived. We also attempted to test whether the universality class of D-FE transitions under a drive is still Ising. Simulation results suggest a value of 1.75 for the exponent gamma but a value close to 2.0 for the ratio gamma/nu. We speculate that the D-FE second order transition is different from Ising near criticality, where observed first-order-like transitions between FE and its "local minimum" cousin occur during each simulation run.Comment: 29 pages, 19 figure

Lipid profiles and outcomes of patients with prior cancer and subsequent myocardial infarction or stroke

Patients with cancer are at increased risk of myocardial infarction (MI) and stroke. Guidelines do not address lipid profile targets for these patients. Within the lipid profiles, we hypothesized that patients with cancer develop MI or stroke at lower low density lipoprotein cholesterol (LDL-C) concentrations than patients without cancer and suffer worse outcomes. We linked nationwide longitudinal MI, stroke and cancer registries from years 2007-2017. We identified 42,148 eligible patients with MI (2421 prior cancer; 39,727 no cancer) and 43,888 eligible patients with stroke (3152 prior cancer; 40,738 no cancer). Median LDL-C concentration was lower in the prior cancer group than the no cancer group at incident MI [2.43 versus 3.10 mmol/L, adjusted ratio 0.87 (95% CI 0.85-0.89)] and stroke [2.81 versus 3.22 mmol/L, adjusted ratio 0.93, 95% CI 0.91-0.95)]. Similarly, median triglyceride and total cholesterol concentrations were lower in the prior cancer group, with no difference in high density lipoprotein cholesterol. Prior cancer was associated with higher post-MI mortality [adjusted hazard ratio (HR) 1.48, 95% CI 1.37-1.59] and post-stroke mortality (adjusted HR 1.95, 95% CI 1.52-2.52). Despite lower LDL-C concentrations, patients with prior cancer had worse post-MI and stroke mortality than patients without cancer

Using vortex generators for flow separation control on tidal turbine profiles and blades

Tidal energy can play an important role in the Net Zero transition. Increasing tidal turbine performance through innovation is crucial if the cost of tidal energy is to become competitive compared to other sources of energy. The present investigation is a proof-of-concept study for the application of Vortex Generators (VGs) on tidal turbines in view of increasing their performance. The more mature wind energy industry uses passive VGs either as a retrofit or in the blade design process to reduce separation at the inboard part of wind turbine blades. Tidal turbine blades also experience flow separation and here we examine whether passive vane VGs can be used to reduce or suppress that separated flow. First, a wind tunnel investigation is performed to assess the performance of VGs on a 20% thick profile from the blade. Then, the VG effect on the 2D-profile is modelled in a Reynolds Averaged Navier-Stokes in-house solver. Results show that low profile VGs, i.e. VGs shorter than the local boundary layer, can increase the performance of the blade profile and successfully reduce flow separation. The VG effect on blade performance is examined in model scale and in full-size. VGs successfully suppress separation in both cases and it is shown that full-size information should be used for the placement of VGs. A maximum power coefficient increase of 1.05% is observed at a tip speed ratio of λ=3. The present proof-of-concept study demonstrates for the first time the potential of passive VGs to be included either in the design process of a tidal turbine blade or as a retrofit solution

Стимулирование инновационной активности персонала компании НГК

Объектом исследования выступает публичное акционерное общество "Газпром" и его дочернее общество с ограниченной ответственность "Газпром трансгаз Томск". Актуальность объясняется тем, что в настоящее время остаются открытыми вопросы привлечения ненаучного персонала предприятий нефтегазового комплекса к участию в инновационной деятельности. Целью работы является разработка способов стимулирования персонала предприятия нефтегазового комплекса к проявлению инновационной и рационализаторской активности. В исследовании проводился анализ применяемых способов мотивации и поощрения инновационных сотрудников предприятия нефтегазового комплекса. При проведении анализа выявляются ключевые проблемы стимулирования и предлагаются возможные решения.The object of the study is PJSC "Gazprom" and OOO "Gazprom transgaz Tomsk". The relevance is explained by the fact that at present the issues of attracting non-scientific personnel of oil and gas enterprises to participate in innovation remain open. The aim of the work is to develop ways to stimulate the personnel of the oil and gas complex to participate in innovation and rationalization activities. The study analyzed the methods used to motivate and encourage innovative employees of the oil and gas industry. The analysis identifies key incentive problems and suggests possible solutions

Pacritinib (SB1518), a JAK2/FLT3 inhibitor for the treatment of acute myeloid leukemia

FMS-like tyrosine kinase 3 (FLT3) is the most commonly mutated gene found in acute myeloid leukemia (AML) patients and its activating mutations have been proven to be a negative prognostic marker for clinical outcome. Pacritinib (SB1518) is a tyrosine kinase inhibitor (TKI) with equipotent activity against FLT3 (IC50=22 n) and Janus kinase 2 (JAK2, IC50=23 n). Pacritinib inhibits FLT3 phosphorylation and downstream STAT, MAPK and PI3 K signaling in FLT3-internal-tandem duplication (ITD), FLT3-wt cells and primary AML blast cells. Oral administration of pacritinib in murine models of FLT3-ITD-driven AML led to significant inhibition of primary tumor growth and lung metastasis. Upregulation of JAK2 in FLT3-TKI-resistant AML cells was identified as a potential mechanism of resistance to selective FLT3 inhibition. This resistance could be overcome by the combined FLT3 and JAK2 activities of pacritinib in this cellular model. Our findings provide a rationale for the clinical evaluation of pacritinib in AML including patients resistant to FLT3-TKI therapy