A relatively simple architectural space was modeled and used to compare the effects of spatial training in simulations versus training in the real world. Thirty-five subjects were trained in one of the following conditions: real world (RW), virtual environment (VE), nonimmersive virtual environment (NVE), and model (Mod). The VE condition made use of a head-mounted display to view the simulated environment, while the NVE condition used a desktop monitor. In the Mod condition, the subject viewed and could manipulate a 3-D model of the space, viewed from a desktop display. The training-transfer tasks, performed after brief unstructured exposure to the actual space or to one of the simulations, consisted of estimating the bearing and range to various targets in the real space from various spatially distributed stations, each such pair of estimates constituting a subtask of the overall transfer task. Results obtained from each of the four training conditions proved to be roughly the same. Training in any one of the simulations was comparable to training in the real world. Independent of training condition, there was a strong tendency among subjects to underestimate range. Variability in range errors was dominated by differences among subjects, whereas variability in bearing errors was dominated by differences among subtasks. These results are discussed in the context of plans for future work. IntroductionAs evidenced both in this special issue of Presence and in a recent past special issue (Vol. 7, No. 2), considerable attention is being given to the use of virtual environment technology for training spatial behavior.In our research program, we are primarily concerned with the use of VE technology to train individuals' spatial behavior in the real world. We are interested in spatial behavior in virtual worlds only to the extent that it relates to behavior in the real world. More specifically, our focus is on transfer from experiences in the virtual world to behavior in the real world. Furthermore, within this general domain, we are concerned with two distinct but related sets of objectives. The first set focuses on the use of VE technology for familiarizing individuals with specific spaces. The second set focuses on the use of VE technology to improve an individual's spatial behavior in general. In this paper, attention is confined entirely to the first set.

Autophagy plays a critical role in the maintenance of cellular homeostasis by degrading proteins, lipids and organelles. Autophagy is activated in response to stress, but its regulation in the context of other stress response pathways, such as those mediated by heat shock factor 1 (HSF1) and nuclear factor-erythroid 2 p45-related factor 2 (NRF2), is not well understood. We found that the Michael acceptor bis(2-hydoxybenzylidene)acetone (HBB2), a dual activator of NRF2 and HSF1, protects against the development of UV irradiation-mediated cutaneous squamous cell carcinoma in mice. We further show that HBB2 is an inducer of autophagy. In cells, HBB2 increases the levels of the autophagy-cargo protein p62/sequestosome 1, and the lipidated form of microtubule-associated protein light chain 3 isoform B. Activation of autophagy by HBB2 is impaired in NRF2-deficient cells, which have reduced autophagic flux and low basal and induced levels of p62. Conversely, HSF1-deficient cells have increased autophagic flux under both basal as well as HBB2-induced conditions, accompanied by increased p62 levels. Our findings suggest that NRF2 and HSF1 have opposing roles during autophagy, and illustrate the existence of tight mechanistic links between the cellular stress responses.

Isolated syndactyly is a common limb malformation with limited known genetic etiology. We used exome sequencing to discover a novel heterozygous missense variant c.2915G > C: p.Arg972Pro in AFF3 on chromosome 2q11.2 in a family with isolated syndactyly in hands and feet. AFF3 belongs to a family of nuclear transcription activating factors and is involved in limb dorsoventral patterning. The variant Arg972Pro is located near the C terminus, a region that is yet to be associated with human disorders. Functional studies did not show a difference in the stability or subcellular localization of the mutant and wild type proteins. Instead, overexpression in zebrafish embryos suggests that Arg972Pro is a loss‐of‐function allele. These results suggest that variants in the C terminus of AFF3 may cause a phenotype distinct from previously characterized AFF3 variants.