Lineage, Sex, and Wealth as Moderators of Kin Investment

Supporting Hamilton’s inclusive fitness theory, archival analyses of inheritance patterns in wills have revealed that people invest more of their estates in kin of closer genetic relatedness. Recent classroom experiments have shown that this genetic relatedness effect is stronger for relatives of direct lineage (children, grandchildren) than for relatives of collateral lineage (siblings, nieces, nephews). In the present research, multilevel modeling of more than 1,000 British Columbian wills revealed a positive effect of genetic relatedness on proportions of estates allocated to relatives. This effect was qualified by an interaction with lineage, such that it was stronger for direct than for collateral relatives. Exploratory analyses of the moderating role of benefactors’ sex and estate values showed the genetic relatedness effect was stronger among female and wealthier benefactors. The importance of these moderators to understanding kin investment in modern humans is discussed.     

Epitope mapping of function‐blocking monoclonal antibody CM6 suggests a “weak” integrin binding site on the laminin‐332 LG2 domain

Laminin‐332 (Ln‐332) is an extracellular matrix molecule that regulates cell adhesion, spreading, and migration by interaction with cell surface receptors such as α3β1 and α6β4. Previously, we developed a function‐blocking monoclonal antibody against rat Ln‐332, CM6, which blocks hemidesmosome assembly induced by Ln‐332‐α6β4 interactions. However, the location of its epitope on Ln‐332 has remained unclear. In this study, we show that the CM6 epitope is located on the laminin G‐like (LG)2 module of the Ln‐332 α3 chain. To specify the residues involved in this epitope, we produced a series of GST‐fused α3 LG2 mutant proteins in which rat‐specific acids were replaced with human acids by a site‐directed mutagenesis strategy. CM6 reactivity against these proteins showed that CM6 binds to the ¹⁰⁸⁹NERSVR¹⁰⁹⁴ sequence of rat Ln‐332 LG2 module. In a structural model, this sequence maps to an LG2 loop sequence that is exposed to solvent according to predictions, consistent with its accessibility to antibody. CM6 inhibits integrin‐dependent cell adhesion on Ln‐332 and inhibits cell spreading on both Ln‐332 and recombinant LG2 (rLG2; but not rLG3), suggesting the presence of an α3β1 binding site on LG2. However, we were unable to show that rLG2 supports adhesion in standard assays, suggesting that LG2 may contain a “weak” integrin binding site, only detectable in spreading assays that do not require washes. These results, together with our previous findings, indicate that binding sites for α3β1 and α6β4 are closely spaced in the Ln‐332 LG domains where they regulate alternative cell functions, namely adhesion/migration or hemidesmosome anchoring. J. Cell. Physiol. 223:541–548, 2010. © 2010 Wiley‐Liss, Inc.     

Curing “Moral Disability”: Brain Trauma and Self-Control in Victorian Science and Fiction

While, historically, the disabled body has appeared in literature as “monstrous,” burgeoning psychological theories of the Victorian period predicated an unusual shift. In a culture of sexual anxiety and fears of devolution and moral decay, the physically disabled and “weak” are portrayed as strangely free from moral corruption. Unlike the cultural link between deviance and disability witnessed in the medical literature and eugenic approach to generation, authors of narrative fiction—particularly Charles Dickens, but Wilkie Collins, Charlotte Yonge, and others as well—portray disabled characters as “purified,” and trauma itself as potentially sanitizing. This present paper argues that such constructions were made possible by developments in the treatment of insanity. “Curing ‘Moral Disability’: Brain Trauma and Self-Control in Victorian Fiction,” examines the concept of trauma-as-cure. Throughout the Victorian period, case studies on brain trauma appeared in widely circulated journals like the Lancet, concurrently with burgeoning theories about psychological disturbance and “moral insanity.” While not widely practiced until the early twentieth century, attempts at surgical “cures” aroused curiosity and speculation—the traumatic event that could free sufferers from deviance. This work provides a unique perspective on representations of disability as cure in the nineteenth century as a means of giving voice to the marginalized, disabled, and disempowered.     

Environmental drivers of habitat use by common bottlenose dolphins (Tursiops truncatus) in the Indian River Lagoon,Florida, USA

Anthropogenic impacts in estuarine systems can influence marine mammal habitat use, population dynamics, fitness, and mortality events. The objective was to examine habitat use among the resident common bottlenose dolphin (Tursiops truncatus) population inhabiting the Indian River Lagoon, Florida, and the influences of variation in environmental factors and prey availability in 2003–2015. We utilized photo-identification surveys, stratified random samples of prey, and environmental variables collected monthly. Kernel density estimation was used to determine the magnitude-per-unit area of dolphins across the IRL by wet and dry seasons each year, the values were used as a response variable in classification and regression tree analyses with fish community and environmental variables as predictors. Spatial patterns in dolphin density in the IRL were associated with salinity and dissolved oxygen levels, which are in part associated with freshwater discharges of nutrient and algae laden waters from the region's storm water management system. These findings isolate locations of concern for management of dolphin habitat, and anthropogenic drivers of dolphin distributions requiring further research.     

Generation and characterization of a rabbit monoclonal antibody site-specific for tau O-GlcNAcylated at serine 400

Aggregation of tau into paired helical filaments is a pathological process leading to neurotoxicity in Alzheimer’s disease and other tauopathies. Tau is posttranslationally modified by O-linked N-acetylglucosamine (O-GlcNAc), and increasing tau O-GlcNAcylation may protect against its aggregation. Research tools to study the relationship between tau aggregation and tau O-GlcNAcylation have not been widely available. Here we describe the generation of a rabbit monoclonal antibody specific for tau O-GlcNAcylated at Ser400 (O-tau(S400)). We show the utility of this antibody for in vitro and in vivo experiments to investigate the function of O-GlcNAc modifications of tau at Ser400.