Admissible strategies in semimartingale portfolio selection

The choice of admissible trading strategies in mathematical modelling of financial markets is a delicate issue, going back to Harrison and Kreps [HK79]. In the context of optimal portfolio selection with expected utility preferences this question has been the focus of considerable attention over the last twenty years. We propose a novel notion of admissibility that has many pleasant features { admissibility is characterized purely under the objective measure P; each admissible strategy can be approximated by simple strategies using finite number of trading dates; the wealth of any admissible strategy is a supermartingale under all pricing measures; local boundedness of the price process is not required; neither strict monotonicity, strict concavity nor differentiability of the utility function are necessary; the definition encompasses both the classical mean-variance preferences and the monotone expected utility. For utility functions finite on R, our class represents a minimal set containing simple strategies which also contains the optimizer, under conditions that are milder than the celebrated reasonable asymptotic elasticity condition on the utility function

Weak localization effects in granular metals

The weak localization correction to the conductivity of a granular metal is calculated using the diagrammatic technique in the reciprocal grain lattice representation. The properties of this correction are very similar to that one in disordered metal, with the replacement of the electron mean free path $\ell$ by the grain diameter $d$ and the dimensionless conductance $g$ by the tunnelling dimensionless conductance $g_{T}$. In particular, we demonstrate that at zero temperature no conducting phase can exist for dimensions $D\leq 2$. We also analyze the WL correction to magnetoconductivity in the weak field limit.Comment: 4 pages, 3 figures; minor corrections adde

Local risk-minimization under the benchmark approach

© 2014, Springer-Verlag Berlin Heidelberg. We study the pricing and hedging of derivatives in incomplete financial markets by considering the local risk-minimization method in the context of the benchmark approach, which will be called benchmarked local risk-minimization. We show that the proposed benchmarked local risk-minimization allows to handle under extremely weak assumptions a much richer modeling world than the classical methodology

Parameters for a Super-Flavor-Factory

A Super Flavor Factory, an asymmetric energy e+e- collider with a luminosity of order 10^36 cm-2s-1, can provide a sensitive probe of new physics in the flavor sector of the Standard Model. The success of the PEP-II and KEKB asymmetric colliders in producing unprecedented luminosity above 10^34 cm-2s-1 has taught us about the accelerator physics of asymmetric e+e- colliders in a new parameter regime. Furthermore, the success of the SLAC Linear Collider and the subsequent work on the International Linear Collider allow a new Super-Flavor collider to also incorporate linear collider techniques. This note describes the parameters of an asymmetric Flavor-Factory collider at a luminosity of order 10^36 cm-2s-1 at the Upsilon(4S) resonance and about 10^35 cm-2s-1 at the Tau production threshold. Such a collider would produce an integrated luminosity of about 10,000 fb-1 (10 ab-1) in a running year (10^7 sec) at the Upsilon(4S) resonance.Comment: Flavor Physics & CP Violation Conference, Vancouver, 200

Association of a homozygous GCK missense mutation with mild diabetes

Background: Homozygous inactivating GCK mutations have been repeatedly reported to cause severe hyperglycemia, presenting as permanent neonatal diabetes mellitus (PNDM). Conversely, only two cases of GCK homozygous mutations causing mild hyperglycemia have been so far described. We here report a novel GCK mutation (c.1116G>C, p.E372D), in a family with one homozygous member showing mild hyperglycemia. Methods: GCK mutational screening was carried out by Sanger sequencing. Computational analyses to investigate pathogenicity and molecular dynamics (MD) were performed for GCK-E372D and for previously described homozygous mutations associated with mild (n = 2) or severe (n = 1) hyperglycemia, used as references. Results: Of four mildly hyperglycemic family-members, three were heterozygous and one, diagnosed in the adulthood, was homozygous for GCK-E372D. Two nondiabetic family members carried no mutations. Fasting glucose (p = 0.016) and HbA1c (p = 0.035) correlated with the number of mutated alleles (0–2). In-silico predicted pathogenicity was not correlated with the four mutations’ severity. At MD, GCK-E372D conferred protein structure flexibility intermediate between mild and severe GCK mutations. Conclusions: We present the third case of homozygous GCK mutations associated with mild hyperglycemia, rather than PNDM. Our in-silico analyses support previous evidences suggesting that protein stability plays a role in determining clinical severity of GCK mutations

Editorial: Endocrine modulators of neurological processes: potential treatment targets of pediatric neurological diseases.

Editorial on the Research Topic Endocrine Modulators of Neurological Processes: Potential Treatment Targets of Pediatric Neurological Diseases

Antiepileptogenic effects of trilostane in the kainic acid model of temporal lobe epilepsy

Objective: Epileptogenesis after status epilepticus (SE) has a faster onset in rats treated to reduce brain levels of the anticonvulsant neurosteroid allopregnanolone with the 5α-reductase inhibitor finasteride; however, it still has to be evaluated whether treatments aimed at increasing allopregnanolone levels could result in the opposite effect of delaying epileptogenesis. This possibility could be tested using the peripherally active inhibitor of 3β-hydroxysteroid dehydrogenase/Δ5-4 isomerase trilostane, which has been shown repeatedly to increase allopregnanolone levels in the brain. Methods: Trilostane (50 mg/kg) was administered subcutaneously once daily for up to six consecutive days, starting 10 min after intraperitoneal administration of kainic acid (15 mg/kg). Seizures were evaluated by video-electrocorticographic recordings for 70 days maximum, and endogenous neurosteroid levels were assessed by liquid chromatography–electrospray tandem mass spectrometry. Immunohistochemical staining was performed to evaluate the presence of brain lesions. Results: Trilostane did not alter the latency of kainic acid-induced SE onset or its overall duration. When compared to the vehicle-treated group, rats receiving six daily trilostane injections presented a remarkable delay of the first spontaneous electrocorticographic seizure and subsequent tonic–clonic spontaneous recurrent seizures (SRSs). Conversely, rats treated with only the first trilostane injection during SE did not differ from vehicle-treated rats in developing the SRSs. Notably, trilostane did not modify neuronal cell densities or the overall damage in the hippocampus. In comparison to the vehicle group, repeated administration of trilostane significantly decreased the activated microglia morphology in the subiculum. As expected, allopregnanolone and other neurosteroid levels were remarkably increased in the hippocampus and neocortex of rats treated for 6 days with trilostane, but pregnanolone was barely detectable. Neurosteroids returned to basal levels after a week of trilostane washout.. Significance: Overall, these results suggest that trilostane led to a remarkable increase in allopregnanolone brain levels, which was associated with protracted effects on epileptogenesis