Exploiting Spillovers to Forecast Crashes

We develop Hawkes models in which events are triggered through self‐excitation as well as cross‐excitation. We examine whether incorporating cross‐excitation improves the forecasts of extremes in asset returns compared to only self‐excitation. The models are applied to US stocks, bonds and dollar exchange rates. We predict the probability of crashes in the series and the value at risk (VaR) over a period that includes the financial crisis of 2008 using a moving window. A Lagrange multiplier test suggests the presence of cross‐excitation for these series. Out‐of‐sample, we find that the models that include spillover effects forecast crashes and the VaR significantly more accurately than the models without these effects. Copyright © 2016 John Wiley & Sons, Ltd.     

Distribution of the eastern woodrat ( Neotoma floridana campestris ) in southern Nebraska

The eastern woodrat ( Neotoma floridana ) occurs throughout eastern and central parts of the United States. In Nebraska, 3 of 9 subspecies inhabit the state, including N. f. campestris , N. f. attwateri , and N. f. baileyi . We determined distributional limits of N. f. campestris along 2 river systems in southern Nebraska. As observed with other mammalian species in the Great Plains, we suspected that the distribution of woodrats likely had expanded, reflecting continued regulation of rivers and the concomitant increase in forests along them. We documented N. f. campestris at 7 sites in 5 counties, including a recent (since the 1960s) eastward expansion along the Republican River. We observed little movement along the Platte River. The greatest concentration of houses constructed by woodrats occurred in a shelterbelt near the Republican River; otherwise, abundances of houses tended to be greater along the Platte River. We suspect that the distribution of woodrats will continue to change in Nebraska unless breaks exist or are established in riparian forests along the Platte and Republican rivers.     

Cbl-b regulates the CD28 dependence of T-cell activation

Whereas co-stimulation of the T-cell antigen receptor (TCR) and CD28 triggers T-cell activation, stimulation of the TCR alone may result in an anergic state or T-cell deletion, both possible mechanisms of tolerance induction. Here we show that T cells that are deficient in the adaptor molecule Cbl-b (ref. 3) do not require CD28 engagement for interleukin-2 production, and that the Cbl-b-null mutation (Cbl-b(-/-)) fully restores T-cell-dependent antibody responses in CD28-/- mice. The main TCR signalling pathways, such as tyrosine kinases Zap-70 and Lck, Ras/mitogen-activated kinases, phospholipase Cgamma-1 and Ca2+ mobilization, were not affected in Cbl-b(-/-) T cells. In contrast, the activation of Vav, a guanine nucleotide exchange factor for Rac1/Rho/CDC42, was significantly enhanced. Our findings indicate that Cbl-b may influence the CD28 dependence of T-cell activation by selectively suppressing TCR-mediated Vav activation. Mice deficient in Cbl-b are highly susceptible to experimental autoimmune encephalomyelitis, suggesting that the dysregulation of signalling pathways modulated by Cbl-b may also contribute to human autoimmune diseases such as multiple sclerosis.     

Antisense-mediated redirection of mRNA splicing

Antisense technology has been used to study basic biological processes, and to block these processes when they deleteriously lead to human disease. A separate, equally important application of antisense technology is to upregulate the gene expression lost in the diseased state by shifting alternative splicing of pre-messenger RNA. This strategy has commonly relied upon the use of antisense oligonucleotides; however, another approach is to use a plasmid construct to generate antisense RNA inside the cell. Antisense therapeutics based on expression vectors and viral vectors offers a gene therapy approach, whereas those based on oligonucleotides offers a more drug like approach.