On optimal dividends with penalty payments in the Cramer-Lundberg model

In this paper we study the optimal dividend problem where the surplus process of an insurance company is modeled by a Cramer-Lundberg model. As distinguished from classical models, we assume that the insurer can continue doing business although the surplus becomes negative, but penalty payments occur, depending on the level of the surplus. The higher the surplus level, the lower the penalty payments. The penalty payments are rather technical and necessary to avoid that losses can rise above any number. Nevertheless, the concept can also be reasonable in practice. For example, penalty payments can occur if the insurer needs to borrow money. The aim is to determine a dividend strategy that maximizes the difference between the expected discounted dividend and penalty payments. We show that the optimal strategy is a barrier strategy. As examples, exponential and linear penalty payments are considered

Minimisation of penalty payments by investments and reinsurance

This paper considers an optimal investment and reinsurance problem for an insurance company, where the surplus follows a linear diffusion. Contrary to classical models the insurer can continue doing business even if the surplus becomes negative, but penalty payments occur depending on the level of the current surplus. The insurer can invest in n risky assets and reduce the insurance risk either by excess of loss or by proportional reinsurance. The aim is to find an optimal investment and reinsurance strategy which minimises the penalty payments. We consider various penalty functions and derive closed form solutions

On optimal dividends with exponential and linear penalty payments

We study the optimal dividend problem where the surplus process of an insurance company is modelled by a diffusion process. The insurer is not ruined when the surplus becomes negative, but penalty payments occur, depending on the level of the surplus. The penalty payments shall avoid that losses can rise above any number and can be seen as a preference measure or costs for negative capital. As examples, exponential and linear penalty payments are considered. It turns out that a barrier dividend strategy is optimal. (C) 2016 Elsevier B.V. All rights reserved

High efficient difference frequency generation of tunable visible light in a self-controlled process

Generating the difference frequency of a frequency-doubled, widely tunable Ti:Al2O3 laser and a Nd:YAG laser provides tunable laser radiation in the visible spectrum range. The generated wavelength region closes the spectral gap between the fundamental and the second harmonic of the Ti:Sapphire laser. A prototype has being developed with a fully automated wavelength tuning, i.e. the wavelength tuning of the Ti:Sapphire laser, the angel tuning of the nonlinear crystals and the tuning of the temporal delay between the Ti:Sapphire and the Nd:YAG laser operate self-controlled. Design, theoretical modeling and experimental characterization of the system are closely discussed. At a repetition rate of one kilohertz, the frequency-doubled Ti:Sapphire laser provides pulses of approximately 20 ns, a spectral line width of 20 GHz. a nearly diffraction limited beam quality and pulse energies of up to 850 J. The tuning range reaches from 340 nm to 510 nm. For the three wave interact ion process in a 8 mm long BBO crystal the Ti:Sapphire pulses (pump wave) are mixed with 3.5 mJ pulses of a Nd:YAG laser (signal wave). The generated idler wave has pulse energies of up to 280 J and pulse durations of approximately 10 ns in the spectral range between 510 nm and 680 nm. This yields to a conversion efficiency of about 33% and a quantum conversion efficiency of more than 50%. To our knowledge, this clearly exceeds the values that has been obtained with comparable setups so far. Further increase of the efficiency is currently under investigation

Synchronous Onset of Breast and Pancreatic Cancers: Results of Germline and Somatic Genetic Analysis

Background: Synchronous cancers have occasionally been detected at initial diagnosis among patients with breast and ovarian cancer. However, simultaneous coexistence and diagnosis of breast and pancreas cancer has not previously been reported. Case Report: Paternal transmission of a germline BRCA2 mutation to a patient who was diagnosed at age 40 with locally advanced breast and pancreas cancer is presented. Somatic genomic analysis of both cancers with next-generation DNA sequencing confirmed the germline result and reported a variety of variants of unknown significance alterations, of which two were present in both the breast and pancreas cancers. Discussion: The possibility that genomic alterations could have been responsible for modulating the phenotypic or clinical expression of this rare presentation is considered. The authors call attention to the practice of privatizing the clinicogenetic information gained from genetic testing and call for health policy that will facilitate sharing in order to advance the outcomes of patients diagnosed with hereditary cancers

Using gene expression in patients with endometrial intraepithelial neoplasia to assess the risk of cancer

Patients diagnosed with an endometrial cancer precursor lesion on biopsy may be found to have endometrial cancer at the time of subsequent surgery. The current study seeks to identify patients with endometrial intraepithelial neoplasia (EIN) on biopsy that may be harboring an occult carcinoma. Immunohistochemical stains for gene loss of expression (LOE) for 6 genes, PTEN, ARID1A, MSH6, MSH2, MLH1, and PMS2, were performed on 113 biopsy specimens with EIN. For the 95 patients with follow-up histology, 40 patients had cancer, 41 had EIN, and 14 had normal endometrium. PTEN LOE was found frequently in both EIN and endometrial cancer, and therefore had low positive predictive value. All specimens with ARID1A, MSH6, MSH2, MLH1, or PMS2 LOE on biopsy were subsequently found to have cancer. LOE of any gene was associated with modest sensitivity (0.78) in identifying patients with endometrial cancer who had EIN on biopsy. Further investigation is warranted to determine if gene LOE is a useful clinical tool when evaluating patients with EIN on biopsy. Keywords: Endometrial intraepithelial neoplasia, Endometrial cancer, Gene expression, PTEN, ARID1A, Mismatch repair gene