Van Der Stoep Research Articles

Numerical techniques for the Heston collocated volatility model

In the collocating volatility (CLV) model, the stochastic collocation technique is used as a convenient representation of the terminal distribution of the market option prices. A specific dynamic is added in the form of a stochastic driver process, which allows more control over the prices of forward starting options. This is reminiscent of the Markov functional models. (Grzelak uses a single-factor Ornstein–Uhlenbeck process as the driver for the CLV model, and Fries uses a single-factor Wiener process with time-dependent volatility in his equity Markov functional model. Van der Stoep et al consider a Heston stochastic volatility driver process and show that it offers more flexibility to capture the forward smile in the context of foreign exchange options.) In this paper, we discuss all aspects of derivative pricing under the Heston– CLV model: calibration with an efficient Fourier method; a Monte Carlo simulation with second-order convergence; and accurate partial differential equation pricing through implicit and explicit finite-difference methods.

Telepsychiatry intervention is better for ADHD symptoms than usual treatment augmented by telemedicine consultation

ABSTRACT FROM: Myers K, Vander Stoep A, Zhou C, et al . Effectiveness of a telehealth service delivery model for treating attention-deficit/hyperactivity disorder: a community-based randomized controlled trial. J Am...

Methods to explore productive behaviors in personal and extrapersonal space.

Methods to explore productive behaviors in personal and extrapersonal space.

Homologous Elements hs3a and hs3b in the 3′ Regulatory Region of the Murine Immunoglobulin Heavy Chain (Igh) Locus Are Both Dispensable for Class-switch Recombination

Immunoglobulin heavy chain (IgH) genes are formed, tested, and modified to yield diverse, specific, and high affinity antibody responses to antigen. The processes involved must be regulated, however, to avoid unintended damage to chromosomes. The 3' regulatory region of the Igh locus plays a major role in regulating class-switch recombination (CSR), the process by which antibody effector functions are modified during an immune response. Loss of all known enhancer-like elements in this region dramatically impairs CSR, but individual element deletions have no effect on this process. In the present study, we explored the hypothesis that an underlying functional redundancy in the homologous elements hs3a and hs3b was masking the importance of either element to CSR. Several transgenic mouse lines were generated, each carrying a bacterial artificial chromosome transgene that mimicked Igh locus structure but in which hs3a was missing and hs3b was flanked by loxP sites. Matings to Cyclization Recombination Enzyme-expressing mice established "pairs" of lines that differed only in the presence or absence of hs3b. Remarkably, CSR remained robust in the absence of both hs3a and hs3b, suggesting that the remaining two elements of the 3' regulatory region, hs1.2 and hs4, although individually dispensable for CSR, are, together, sufficient to support CSR.

Mancala Games and Their Suitability for Players with Visual Impairments

The main barrier to access to competitive board games by players with visual impairments (that is, those who are blind or have low vision) is their physical design, which also implies a certain mode of In chess, a quick observation of the board is sufficient for masters to recognize, analyze, and remember a position (Gobet, de Voogt, & Retschitzki, 2004). This situation suggests a competitive disadvantage for players with limited or no vision. Indeed, people who are visually impaired are not found among the world's masters of board games. Some competitive board games feature play. In blindfold play, a player sits with his or her back to the board and communicates the moves to an opponent through a notation system. Without seeing the board, the player instructs moves to be played on the board and is then informed verbally about the opponent's countermoves. This particular skill has been shown for a series of games, including chess, mancala (the generic name for all games that are played on rows of holes with identical player counters) and checkers (de Voogt, 2005; Keessen & van der Stoep, 1986; Steinkohl, 1992). But in all cases of blindfold play, the performers were at an advanced level before they even attempted this skill. This article reports on a study that identified one group of competitive board games for which immediate visual perception, as in chess, is largely not needed. We contend that mancala board games are immediately suitable for players with visual impairments. In addition, the results of an experiment show that it is possible for blindfolded novice players who are allowed to touch the board and playing pieces to make basic but extensive calculations that are necessary to perform well in competitive mancala. RULES OF MANCALA Mancala games are found from South, Central, and Southeast Asia to the Middle East and from all over Africa to the Caribbean and parts of South America. Their physical appearance and playing rules vary widely across the world (see also ). The best way to learn mancala is to play with a teacher or an interactive program, rather than to read the rules; Internet and cell phone applications have been instrumental in the popularity of mancala games in the Western world. The following version of mancala is played mainly in Southeast Asia and is known under different names, such as Ohvalhu, Sungka, and Dakon--local names for a specific variant of mankala that uses end holes as a necessary part of the game and two rows of holes (De la Cruz, Cage, & Lian, 2000; Donkers, de Voogt, & Uiterwijk, 2000)--with little variation in rules. The game has been played on a high level (Donkers et al., 2000), and even the mathematics of the game has attracted attention (Manansala, 1995). It can be played on different sizes of boards. We use Ohvalhu, as it is played on the Maldive Islands, which commonly has two rows of eight holes, for the following explanation: * A playing board consisting of two rows of eight holes plus two end holes (enlarged holes at the far ends of a mancala board that are used to gather the captured counters) is placed sideways between two players (see Figure 1). * Each smaller hole contains eight counters (playing pieces used in mancala, commonly seeds, shells, or stones). * The players own the row nearest to them, as well as the end hole located toward the left of their row (see Figure 1). [FIGURE 1 OMITTED] The object of the game is to accumulate as many counters as possible in one's end hole. The starting player takes all the counters from one of his or her eight holes and puts one counter in each hole directly to the left. Thus, all the counters are taken out and placed one at a time in consecutive holes in a clockwise direction around the board. If the players run into their opponent's end hole, they skip it. If they run into their own end hole, they play into it (see Figure 1). …

Sarcoidosis During Anti-Tumor Necrosis Factor-α Therapy: No Relapse After Rechallenge

To the Editor: Anti-tumor necrosis factor (TNF)-α agents such as infliximab, adalimumab, and etanercept are more and more widely used. With this we see a growing number of case reports describing adverse events that occur during anti-TNF-α therapy. One adverse event that has been reported increasingly is the development of sarcoidosis1. This raises many questions. TNF-α plays an important role in the formation of granulomas. Based on this, specific anti-TNF-α agents are supposed to be effective in the treatment of granulomatous diseases such as Crohn’s disease and sarcoidosis. Although current evidence supports the efficacy of infliximab in Crohn’s disease, data regarding anti-TNF-α in sarcoidosis have been conflicting2,3. We describe 2 cases in which sarcoidosis occurred during respectively adalimumab and etanercept treatment, both for rheumatoid arthritis. After cure/stabilization of the sarcoidosis both patients were rechallenged with the anti-TNF-α agent they took originally. The first patient was a 55-year-old woman with rheumatoid arthritis (RA) for 5 years. Eight months after treatment with adalimumab 40 mg every 2 weeks, she developed erythema nodosum-like lesions … Address correspondence to D. van der Stoep. E-mail: dfvanderstoep{at}gmail.com

Arrests of Adolescent Clients of a Public Mental Health System During Adolescence and Young Adulthood

This study examined the relationship of age and gender with risk of arrest among adolescents and young adults who were intensive adolescent users of public mental health services. Data were obtained from the Massachusetts Department of Mental Health (DMH) and juvenile and criminal courts. Participants were youths receiving DMH adolescent case management services sometime in 1994-1996 who were born between 1976 and 1979 (781 males and 738 females). They were cross-matched to document arrests between age seven and 25. The study examined age at first arrest, age-specific risk, and the relationship between arrest history and arrest risk by gender and age. Most males (69%) and almost half the females (46%) were arrested by age 25. First arrest was most common before age 18. As in the general population, males' arrest patterns were more concerning than those of females, although patterns were of concern in both groups. Most female arrestees had multiple arrests, many as adults. No gender differences were observed for several factors, including risk of first arrest over age 18. Risk was far greater for those arrested in the previous year than for those never arrested. Findings justify concerns of public mental health systems regarding justice system involvement of adolescent clients. Risk of first arrest was significant from early adolescence through age 24, indicating a need for arrest prevention into young adulthood. The heightened arrest risk at all ages among those who were recently arrested demarcates a population in need of immediate intervention.

Loading of the Nonhomologous End Joining Factor, Ku, on Protein-occluded DNA Ends

The nonhomologous end joining pathway for DNA double strand break repair requires Ku to bind DNA ends and subsequently recruit other nonhomologous end joining factors, including the DNA-dependent protein kinase catalytic subunit and the XRCC4-Ligase IV complex, to the break site. Ku loads at a break by threading the DNA ends through a circular channel in its structure. This binding mechanism explains both the high specificity of Ku for ends and its ability to translocate along DNA once loaded. However, DNA in cells is typically coated with other proteins (e.g. histones), which might be expected to block the ability of Ku to load in this manner. Here we address how the nature of a protein obstruction dictates how Ku interacts with a DNA end. Ku is unable to access the ends within an important intermediate in V(D)J recombination (a complex of RAG proteins bound to cleaved recombination targeting signals), but Ku readily displaces the linker histone, H1, from DNA. Ku also retains physiological affinity for nucleosome-associated ends. Loading onto nucleosome-associated ends still occurs by threading the end through its channel, but rather than displacing the nucleosome, Ku peels as much as 50 bp of DNA away from the histone octamer surface. We suggest a model where Ku utilizes an unusual characteristic of its three-dimensional structure to recognize certain protein-occluded ends without the extensive remodeling of chromatin structure required by other DNA repair pathways.

Lesion Macrophages Are a Key Target for the Antiatherogenic Effects of LXR Agonists

The Liver X Receptors (LXRα and LXRβ) are members of the nuclear hormone receptor superfamily.1 These sterol-responsive transcription factors regulate the expression of a number of genes involved in intestinal cholesterol absorption, conversion of cholesterol to bile acids, and reverse cholesterol transport. Activation of LXRs blocks cholesterol absorption and induces cholesterol efflux from lipid-loaded cells such as macrophages. Because increased cholesterol efflux is predicted to limit the transformation of macrophages into atherosclerotic foam cells, LXR activity is predicted to be antiatherogenic. This hypothesis is supported by several studies using mice genetically deficient in LXR expression. Previous work from Tangirala and colleagues established that selective elimination of macrophage LXRα and LXRβ expression in the bone marrow compartment results in accelerated disease in both the spontaneous (ApoE−/−) and Western-diet inducible (LDLR−/−) models of atherosclerosis.2 Furthermore, LXRαβ double knockout mice fed a normal chow diet exhibit increased cholesterol accumulation in the macrophages of their arterial walls.2,3 In addition to their effects on cholesterol metabolism, activation of the LXRs by synthetic agonists has an inhibitory effect on inflammatory gene expression in macrophages, pointing to a second potential antiatherogenic mechanism of these receptors.4 Finally, recent studies suggest that the ability of microbial infections to modify the development of atherosclerosis may be accomplished in part through interference with the LXR signaling pathway and macrophage cholesterol metabolism.5 See page 135 Collectively, these studies point to LXRs as potential therapeutic targets for the treatment or prevention of atherosclerosis. However, it …

Reply: CIITA methylation and decreased levels of HLA-DR in tumour progression

Reply: CIITA methylation and decreased levels of HLA-DR in tumour progression

Ku70 is required for late B cell development and immunoglobulin heavy chain class switching.

Immunoglobulin (Ig) heavy chain (HC) class switch recombination (CSR) is a late B cell process that involves intrachromosomal DNA rearrangement. Ku70 and Ku80 form a DNA end-binding complex required for DNA double strand break repair and V(D)J recombination. Ku70(-/-) (K70T) mice, like recombination activating gene (RAG)-1- or RAG-2-deficient (R1T or R2T) mice, have impaired B and T cell development at an early progenitor stage, which is thought to result at least in part from defective V(D)J recombination (Gu, Y., K.J. Seidl, G.A. Rathbun, C. Zhu, J.P. Manis, N. van der Stoep, L. Davidson, H.L. Cheng, J.M. Sekiguchi, K. Frank, et al. 1997. Immunity. 7:653-665; Ouyang, H., A. Nussenzweig, A. Kurimasa, V.C. Soares, X. Li, C. Cordon-Cardo, W. Li, N. Cheong, M. Nussenzweig, G. Iliakis, et al. 1997. J. Exp. Med. 186:921-929). Therefore, to examine the potential role of Ku70 in CSR, we generated K70T mice that carry a germline Ig HC locus in which the JH region was replaced with a functionally rearranged VH(D)JH and Ig lambda light chain transgene (referred to as K70T/HL mice). Previously, we have shown that B cells from R1T or R2T mice carrying these rearranged Ig genes (R1T/HL or R2T/HL mice) can undergo CSR to IgG isotypes (Lansford, R., J. Manis, E. Sonoda, K. Rajewsky, and F. Alt. 1998. Int. Immunol. 10:325-332). K70T/HL mice had significant numbers of peripheral surface IgM+ B cells, which generated serum IgM levels similar to those of R2T/HL mice. However, in contrast to R2T/HL mice, K70T/HL mice had no detectable serum IgG isotypes. In vitro culture of K70T/HL B cells with agents that induce CSR in normal or R2T/HL B cells did lead to the induction of germline CH transcripts, indicating that initial signaling pathways for CSR were intact in K70T/HL cells. However, treatment with such agents did not lead to detectable CSR by K70T/HL B cells, and instead, led to cell death within 72 h. We conclude that Ku70 is required for the generation of B cells that have undergone Ig HC class switching. Potential roles for Ku70 in the CSR process are discussed.