Core networks for visual-concrete and abstract thought content: a brain electric microstate analysis

Commonality of activation of spontaneously forming and stimulus-induced mental representations is an often made but rarely tested assumption in neuroscience. In a conjunction analysis of two earlier studies, brain electric activity during visual-concrete and abstract thoughts was studied. The conditions were: in study 1, spontaneous stimulus-independent thinking (post-hoc, visual imagery or abstract thought were identified); in study 2, reading of single nouns ranking high or low on a visual imagery scale. In both studies, subjects' tasks were similar: when prompted, they had to recall the last thought (study 1) or the last word (study 2). In both studies, subjects had no instruction to classify or to visually imagine their thoughts, and accordingly were not aware of the studies' aim. Brain electric data were analyzed into functional topographic brain images (using LORETA) of the last microstate before the prompt (study 1) and of the word-type discriminating event-related microstate after word onset (study 2). Conjunction analysis across the two studies yielded commonality of activation of core networks for abstract thought content in left anterior superior regions, and for visual-concrete thought content in right temporal-posterior inferior regions. The results suggest that two different core networks are automatedly activated when abstract or visual-concrete information, respectively, enters working memory, without a subject task or instruction about the two classes of information, and regardless of internal or external origin, and of input modality. These core machineries of working memory thus are invariant to source or modality of input when treating the two types of information.

Footprint of recycled water subsidies downwind of Lake Michigan

Continental evaporation is a significant and dynamic flux within the atmospheric water budget, but few methods provide robust observational constraints on the large-scale hydroclimatological and hydroecological impacts of this ‘recycled-water' flux. We demonstrate a geospatial analysis that provides such information, using stable isotope data to map the distribution of recycled water in shallow aquifers downwind from Lake Michigan. The δ2H and δ18O values of groundwater in the study region decrease from south to north, as expected based on meridional gradients in climate and precipitation isotope ratios. In contrast, deuterium excess (d = δ2H − 8 × δ18O) values exhibit a significant zonal gradient and finer-scale spatially patterned variation. Local d maxima occur in the northwest and southwest corners of the Lower Peninsula of Michigan, where ‘lake-effect' precipitation events are abundant. We apply a published model that describes the effect of recycling from lakes on atmospheric vapor d values to estimate that up to 32% of recharge into individual aquifers may be derived from recycled Lake Michigan water. Applying the model to geostatistical surfaces representing mean d values, we estimate that between 10% and 18% of the vapor evaporated from Lake Michigan is re-precipitated within downwind areas of the Lake Michigan drainage basin. Our approach provides previously unavailable observational constraints on regional land-atmosphere water fluxes in the Great Lakes Basin and elucidates patterns in recycled-water fluxes that may influence the biogeography of the region. As new instruments and networks facilitate enhanced spatial monitoring of environmental water isotopes, similar analyses can be widely applied to calibrate and validate water cycle models and improve projections of regional hydroecological change involving the coupled lake-atmosphere-land system. Read More: http://www.esajournals.org/doi/abs/10.1890/ES12-00062.1

Distributed Atomic Polarizabilities of Amino Acids and their Hydrogen-Bonded Aggregates

With the purpose of rational design of optical materials, distributed atomic polarizabilities of amino acid molecules and their hydrogen-bonded aggregates are calculated in order to identify the most efficient functional groups, able to buildup larger electric susceptibilities in crystals. Moreover, we carefully analyze how the atomic polarizabilities depend on the one-electron basis set or the many-electron Hamiltonian, including both wave function and density functional theory methods. This is useful for selecting the level of theory that best combines high accuracy and low computational costs, very important in particular when using the cluster method to estimate susceptibilities of molecular-based materials.

Proteotoxic stress induces phosphorylation of p62/SQSTM1 by ULK1 to regulate selective autophagic clearance of protein aggregates.

Disruption of proteostasis, or protein homeostasis, is often associated with aberrant accumulation of misfolded proteins or protein aggregates. Autophagy offers protection to cells by removing toxic protein aggregates and injured organelles in response to proteotoxic stress. However, the exact mechanism whereby autophagy recognizes and degrades misfolded or aggregated proteins has yet to be elucidated. Mounting evidence demonstrates the selectivity of autophagy, which is mediated through autophagy receptor proteins (e.g. p62/SQSTM1) linking autophagy cargos and autophagosomes. Here we report that proteotoxic stress imposed by the proteasome inhibition or expression of polyglutamine expanded huntingtin (polyQ-Htt) induces p62 phosphorylation at its ubiquitin-association (UBA) domain that regulates its binding to ubiquitinated proteins. We find that autophagy-related kinase ULK1 phosphorylates p62 at a novel phosphorylation site S409 in UBA domain. Interestingly, phosphorylation of p62 by ULK1 does not occur upon nutrient starvation, in spite of its role in canonical autophagy signaling. ULK1 also phosphorylates S405, while S409 phosphorylation critically regulates S405 phosphorylation. We find that S409 phosphorylation destabilizes the UBA dimer interface, and increases binding affinity of p62 to ubiquitin. Furthermore, lack of S409 phosphorylation causes accumulation of p62, aberrant localization of autophagy proteins and inhibition of the clearance of ubiquitinated proteins or polyQ-Htt. Therefore, our data provide mechanistic insights into the regulation of selective autophagy by ULK1 and p62 upon proteotoxic stress. Our study suggests a potential novel drug target in developing autophagy-based therapeutics for the treatment of proteinopathies including Huntington's disease.