Radiative Corrections to Democratic Lepton Mixing

A new ansatz of democratic lepton mixing is proposed at the GUT scale and the radiative corrections to its phenomenological consequences are calculated at the electroweak scale. We demonstrate that it is possible to obtain the experimentally favored results for both neutrino masses and lepton flavor mixing angles from this ansatz, provided the neutrino Yukawa coupling matrix takes a specific nontrivial pattern. The seesaw threshold effects play a significant role in the running of relevant physical quantities.Comment: 10 pages (1 table, 2 figures). More discussions added. Phys. Lett. B in pres

Existence Conditions of Super-Replication Cost in a Multinomial Model

This paper gives a theorem for the continuous time super-replication cost of European options in an unbounded multinomial market. An approximation multinomial scheme is put forward on a finite time interval [0,1] corresponding to a pure jump Levy model with unbounded jumps. Under the assumption that the expected underlying stock price at time 1 is bounded, the limit of the sequence of the super-replication cost in a multinomial model is proved to be greater than or equal to an optimal control problem. Furthermore, it is discussed that the existence conditions of a super-replication cost and a liquidity premium for the multinomial model. This paper concentrates on a multinomial tree with unbounded jumps, which can be seen as an extension of the work of(Xing, 2015). The super-replication cost and the liquidity premium under the variance gamma model and the normal inverse Gaussian model are calculated and illustrated

Liquidity Premiums in a Levy Market

This paper gives a theorem for the continuous time super-replication cost of European options where the stock price follows an exponential Levy process. Under a mild assumption on the legend transform of the trading cost function, the limit of the sequence of the discrete super-replication cost is proved to be greater than or equal to an optimal control problem. The main tool is an approximation multinomial scheme based on a discrete grid on a finite time interval [0,1] for a pure jump Levy model. This multinomial model is constructed similar to that proposed by (Szimayer & Maller, Stoch. Proce. & Their Appl., 117, 1422-1447, 2007). Furthermore, it is proved that the existence of a liquidity premium for the continuous-time model under a Levy process. This paper concentrates on the Levy processes with infinitely many jumps in any finite time interval. The approach overcomes some difficulties that can be encountered when the Levy process has infinite activity

Improving Image Restoration with Soft-Rounding

Several important classes of images such as text, barcode and pattern images have the property that pixels can only take a distinct subset of values. This knowledge can benefit the restoration of such images, but it has not been widely considered in current restoration methods. In this work, we describe an effective and efficient approach to incorporate the knowledge of distinct pixel values of the pristine images into the general regularized least squares restoration framework. We introduce a new regularizer that attains zero at the designated pixel values and becomes a quadratic penalty function in the intervals between them. When incorporated into the regularized least squares restoration framework, this regularizer leads to a simple and efficient step that resembles and extends the rounding operation, which we term as soft-rounding. We apply the soft-rounding enhanced solution to the restoration of binary text/barcode images and pattern images with multiple distinct pixel values. Experimental results show that soft-rounding enhanced restoration methods achieve significant improvement in both visual quality and quantitative measures (PSNR and SSIM). Furthermore, we show that this regularizer can also benefit the restoration of general natural images.Comment: 9 pages, 6 figure

Role of cytokines in experimental neurodegenerative and neuroinflammatory disorders

Altered expression of cytokines in response to body injury has diverse actions that can exacerbate, mediate, reduce or inhibit neuronal and myelin damage as well as influence the disease development in a variety of nervous system disorders, such as Alzheimer s disease (AD), multiple sclerosis and Guillain-Barré Syndrome (GBS). In these studies, we attempted to explore the possible roles of tumor necrosis factor (TNF)-α and interleukin (IL)-18 in experimental neurodegenerative and neuroinflammatory disorders. The role of TNF-α in kainic acid (KA)-induced excitotoxic neurodegeneration has been studied by comparing TNF receptor 1 (TNFR1) knockout (TNFR1-/-) mice with wild-type (WT) mice. After nasal application of KA, TNFR1-/- mice showed significantly severer seizures than WT mice. In addition, obvious neuronal damage, enhanced microglia activation and astrogliosis in hippocampus as well as increased locomotor activity were found in TNFR1-/- mice compared with WT controls. Moreover, CC chemokine receptor 3 expression on activated microglia was increased in TNFR1-/- mice after KA treatment as measured by flow cytometry. These data suggest that TNF-α may play a protective role via TNFR1 signalling in KA-induced neurodegeneration. Epidemiological studies concerning gender differences in AD support the higher prevalence and incidence of AD in women. The influence of age and gender on excitotoxic neurodegeneration has been investigated by treating C57BL/6 mice (aged females and males as well as adult females and males) with KA. The results showed that aged female mice were more sensitive to KA-induced excitotoxicity associated with severer seizure activity, increased locomotion and rearing in open-field test, prominent hippocampal neuronal damage, enhanced astrocyte proliferation compared with aged males, adult females and adult male mice, respectively. In addition, higher level of brain-derived neurotrophic factor in hippocampi of aged female mice was observed. These results denote that aged female mice are more sensitive to KA-induced excitotoxicity. IL-18 participates in the fundamental inflammatory processes, especially during aging. Based on the above results, we were interested in studying the role of IL-18 in KA-induced neurodegeneration in aged female C57BL/6 mice. We found that aged female IL-18-/- and WT mice showed similar responses to KA insult as demonstrated by comparable seizure activities, behavioral changes and neuronal cell death. However, aged female IL-18-/- mice failed to exhibit as strong microglial activation as WT mice. Interestingly, even though the number of activated microglia was less in KA-treated IL-18-/- mice than in KA-treated WT mice, the proportion of microglia that expressed the cytokines, TNF-α, IL-6 and IL-10 was higher in KA-treated IL-18-/- mice. Deficiency of IL-18 attenuates microglial activation after KA-induced excitotoxicity in aged brain, while the net effects of IL-18 deficiency are balanced by the enhancement of TNF-α, IL-6 and IL-10 production. To further explore the role of IL-18 in the neurodegeneration and neuroinflammation, another animal model - experimental autoimmune neuritis (EAN) was induced by immunization of mice (IL-18-/-) with P0 protein peptide 180-199. The clinical course was not significantly different between IL-18-/- and WT mice. The splenic mononuclear cell (MNC) proliferation was also similar in both animal groups. However, the percentages of interferon-γ, IL-10 and IL-12 positive cells were decreased among infiltrating MNC of cauda equina in IL-18-/- mice. This indicates that IL-18 deficiency inhibits the production of both Th1 and Th2 cytokines in the target organ of EAN. In summary, TNF-α may play a protective role via TNFR1 signalling in KA-induced neurodegeneration, while IL-18 may not be a key inflammatory cytokine in experimental neurodegenerative and neuroinflammatory disorders