The role of surface roughness, albedo, and Bowen ratio on ecosystem energy balance in the Eastern United States

Land cover and land use influence surface climate through differences in biophysical surface properties, including partitioning of sensible and latent heat (e.g., Bowen ratio), surface roughness, and albedo. Clusters of closely spaced eddy covariance towers (e.g., \u3c10 \u3ekm) over a variety of land cover and land use types provide a unique opportunity to study the local effects of land cover and land use on surface temperature. We assess contributions albedo, energy redistribution due to differences in surface roughness and energy redistribution due to differences in the Bowen ratio using two eddy covariance tower clusters and the coupled (land-atmosphere) Variable-Resolution Community Earth System Model. Results suggest that surface roughness is the dominant biophysical factor contributing to differences in surface temperature between forested and deforested lands. Surface temperature of open land is cooler (−4.8 °C to −0.05 °C) than forest at night and warmer (+0.16 °C to +8.2 °C) during the day at northern and southern tower clusters throughout the year, consistent with modeled calculations. At annual timescales, the biophysical contributions of albedo and Bowen ratio have a negligible impact on surface temperature, however the higher albedo of snow-covered open land compared to forest leads to cooler winter surface temperatures over open lands (−0.4 °C to −0.8 °C). In both the models and observation, the difference in mid-day surface temperature calculated from the sum of the individual biophysical factors is greater than the difference in surface temperature calculated from radiative temperature and potential temperature. Differences in measured and modeled air temperature at the blending height, assumptions about independence of biophysical factors, and model biases in surface energy fluxes may contribute to daytime biases

Phage inducible islands in the gram-positive cocci

The SaPIs are a cohesive subfamily of extremely common phage-inducible chromosomal islands (PICIs) that reside quiescently at specific att sites in the staphylococcal chromosome and are induced by helper phages to excise and replicate. They are usually packaged in small capsids composed of phage virion proteins, giving rise to very high transfer frequencies, which they enhance by interfering with helper phage reproduction. As the SaPIs represent a highly successful biological strategy, with many natural Staphylococcus aureus strains containing two or more, we assumed that similar elements would be widespread in the Gram-positive cocci. On the basis of resemblance to the paradigmatic SaPI genome, we have readily identified large cohesive families of similar elements in the lactococci and pneumococci/streptococci plus a few such elements in Enterococcus faecalis. Based on extensive ortholog analyses, we found that the PICI elements in the four different genera all represent distinct but parallel lineages, suggesting that they represent convergent evolution towards a highly successful lifestyle. We have characterized in depth the enterococcal element, EfCIV583, and have shown that it very closely resembles the SaPIs in functionality as well as in genome organization, setting the stage for expansion of the study of elements of this type. In summary, our findings greatly broaden the PICI family to include elements from at least three genera of cocci

Depicting the tree of life in museums: guiding principles from psychological research

The Tree of Life is revolutionizing our understanding of life on Earth, and, accordingly, evolutionary trees are increasingly important parts of exhibits on biodiversity and evolution. The authors argue that in using these trees to effectively communicate evolutionary principles, museums need to take into account research results from cognitive, developmental, and educational psychology while maintaining a focus on visitor engagement and enjoyment. Six guiding principles for depicting evolutionary trees in museum exhibits distilled from this research literature were used to evaluate five current or recent museum trees. One of the trees was then redesigned in light of the research while preserving the exhibit’s original learning goals. By attending both to traditional factors that influence museum exhibit design and to psychological research on how people understand diagrams in general and Tree of Life graphics in particular, museums can play a key role in fostering 21st century scientific literacy

Perceptions and experiences of interventions to prevent postnatal depression: a systematic review and qualitative evidence synthesis

Background More women experience depressive symptoms antenatally than postnatally. Supporting women through the antenatal period is recognised as important in mitigating negative outcomes and in preventing postnatal depression (PND). A systematic review was conducted which aimed to provide a detailed service user and service provider perspective on the uptake, acceptability, and perception of harms of antenatal interventions and postnatal interventions for preventing PND. Methods A comprehensive literature search was conducted in 12 major bibliographic databases in November 2012 and updated in December 2014. Studies were included if they contained qualitative evidence on the perspectives and attitudes of pregnant women and postnatal women who had taken part in, or healthcare professionals (HCPs) involved in delivering, preventive interventions for PND. Results Twenty-two studies were included. Support and empowerment through education were identified as particularly helpful to women as intervention components, across all intervention types. Implications for accessing the service, understanding the remit of the service and women's preferences for group and individual care also emerged. Limitations The majority of the included studies were of moderate or low quality, which may result in a lack of rich data consistently across all studies, limiting to some degree interpretations that can be made. Conclusion The synthesis demonstrated important considerations for devising new interventions or adapting existing interventions. Specifically, it is important that individual or group interventions are carefully tailored to women's needs or preferences and women are aware of the remit of the HCPs role to ensure they feel able to access the support required

Ligand and Receptor Dynamics Contribute to the Mechanism of Graded PPARγ Agonism

SummaryLigand binding to proteins is not a static process, but rather involves a number of complex dynamic transitions. A flexible ligand can change conformation upon binding its target. The conformation and dynamics of a protein can change to facilitate ligand binding. The conformation of the ligand, however, is generally presumed to have one primary binding mode, shifting the protein conformational ensemble from one state to another. We report solution nuclear magnetic resonance (NMR) studies that reveal peroxisome proliferator-activated receptor γ (PPARγ) modulators can sample multiple binding modes manifesting in multiple receptor conformations in slow conformational exchange. Our NMR, hydrogen/deuterium exchange and docking studies reveal that ligand-induced receptor stabilization and binding mode occupancy correlate with the graded agonist response of the ligand. Our results suggest that ligand and receptor dynamics affect the graded transcriptional output of PPARγ modulators

CMT2N-causing aminoacylation domain mutants enable Nrp1 interaction with AlaRS

Through dominant mutations, aminoacyl-tRNA synthetases constitute the largest protein family linked to Charcot-Marie-Tooth disease (CMT). An example is CMT subtype 2N (CMT2N), caused by individual mutations spread out in AlaRS, including three in the aminoacylation domain, thereby suggesting a role for a tRNA-charging defect. However, here we found that two are aminoacylation defective but that the most widely distributed R329H is normal as a purified protein in vitro and in unfractionated patient cell samples. Remarkably, in contrast to wild-type (WT) AlaRS, all three mutant proteins gained the ability to interact with neuropilin 1 (Nrp1), the receptor previously linked to CMT pathogenesis in GlyRS. The aberrant AlaRS-Nrp1 interaction is further confirmed in patient samples carrying the R329H mutation. However, CMT2N mutations outside the aminoacylation domain do not induce the Nrp1 interaction. Detailed biochemical and biophysical investigations, including X-ray crystallography, small-angle X-ray scattering, hydrogen-deuterium exchange (HDX), switchSENSE hydrodynamic diameter determinations, and protease digestions reveal a mutation-induced structural loosening of the aminoacylation domain that correlates with the Nrp1 interaction. The b1b2 domains of Nrp1 are responsible for the interaction with R329H AlaRS. The results suggest Nrp1 is more broadly associated with CMT-associated members of the tRNA synthetase family. Moreover, we revealed a distinct structural loosening effect induced by a mutation in the editing domain and a lack of conformational impact with C-Ala domain mutations, indicating mutations in the same protein may cause neuropathy through different mechanisms. Our results show that, as with other CMT-associated tRNA synthetases, aminoacylation per se is not relevant to the pathology

CMT2N-causing aminoacylation domain mutants enable Nrp1 interaction with AlaRS.

Through dominant mutations, aminoacyl-tRNA synthetases constitute the largest protein family linked to Charcot-Marie-Tooth disease (CMT). An example is CMT subtype 2N (CMT2N), caused by individual mutations spread out in AlaRS, including three in the aminoacylation domain, thereby suggesting a role for a tRNA-charging defect. However, here we found that two are aminoacylation defective but that the most widely distributed R329H is normal as a purified protein in vitro and in unfractionated patient cell samples. Remarkably, in contrast to wild-type (WT) AlaRS, all three mutant proteins gained the ability to interact with neuropilin 1 (Nrp1), the receptor previously linked to CMT pathogenesis in GlyRS. The aberrant AlaRS-Nrp1 interaction is further confirmed in patient samples carrying the R329H mutation. However, CMT2N mutations outside the aminoacylation domain do not induce the Nrp1 interaction. Detailed biochemical and biophysical investigations, including X-ray crystallography, small-angle X-ray scattering, hydrogen-deuterium exchange (HDX), switchSENSE hydrodynamic diameter determinations, and protease digestions reveal a mutation-induced structural loosening of the aminoacylation domain that correlates with the Nrp1 interaction. The b1b2 domains of Nrp1 are responsible for the interaction with R329H AlaRS. The results suggest Nrp1 is more broadly associated with CMT-associated members of the tRNA synthetase family. Moreover, we revealed a distinct structural loosening effect induced by a mutation in the editing domain and a lack of conformational impact with C-Ala domain mutations, indicating mutations in the same protein may cause neuropathy through different mechanisms. Our results show that, as with other CMT-associated tRNA synthetases, aminoacylation per se is not relevant to the pathology

Disentangling the role of photosynthesis and stomatal conductance on rising forest water-use efficiency

Multiple lines of evidence suggest that plant water-use efficiency (WUE) -the ratio of carbon assimilation to water loss- has increased in recent decades. Although rising atmospheric CO2 has been proposed as the principal cause, the underlying physiological mechanisms are still being debated, and implications for the global water cycle remain uncertain. Here, we addressed this gap using 30-y tree ring records of carbon and oxygen isotope measurements and basal area increment from 12 species in 8 North American mature temperate forests. Our goal was to separate the contributions of enhanced photosynthesis and reduced stomatal conductance to WUE trends and to assess consistency between multiple commonly used methods for estimating WUE. Our results show that tree ring-derived estimates of increases in WUE are consistent with estimates from atmospheric measurements and predictions based on an optimal balancing of carbon gains and water costs, but are lower than those based on ecosystemscale flux observations. Although both physiological mechanisms contributed to rising WUE, enhanced photosynthesis was widespread, while reductions in stomatal conductance were modest and restricted to species that experienced moisture limitations. This finding challenges the hypothesis that rising WUE in forests is primarily the result of widespread, CO2-induced reductions in stomatal conductance

Blocking of interferon regulatory factor 1 reduces tumor necrosis factor α–induced interleukin‐18 bioactivity in rheumatoid arthritis synovial fibroblasts by induction of interleukin‐18 binding protein a: Role of the nuclear interferon regulatory factor 1–NF‐κB–c‐jun complex

Objective To examine the role of interferon regulatory factor 1 (IRF‐1) in tumor necrosis factor α (TNFα)–induced interleukin‐18 binding protein a (IL‐18BPa) expression in rheumatoid arthritis synovial fibroblasts (RASFs). Methods TNFα‐induced IRF‐1 expression was assessed by real‐time quantitative polymerase chain reaction and Western blotting. The effect of TNFα on IRF‐1 was assessed using nuclear and cytoplasmic extracts, Western blots, and immunofluorescence. Chemical inhibitors of NF‐κB or MAP kinases were used to analyze the signaling pathways of TNFα‐induced IRF‐1 expression and IRF‐1 nuclear translocation. Control and IRF‐1 small interfering RNA (siRNA) were used to analyze the effect of IRF‐1 down‐regulation on TNFα‐induced IL‐18BP expression. IL‐18BPa expression was assessed by enzyme‐linked immunosorbent assay, and IL‐18 was assessed at the transcription and bioactivity levels using KG‐1 cells. Results TNFα induced RASF IRF‐1 expression at the messenger RNA and protein levels, with a maximal effect at 2 hours ( P < 0.05; n ≥ 3). Furthermore, TNFα induced nuclear translocation of IRF‐1, with maximal translocation at 2 hours (∼6 fold‐induction) ( P < 0.05; n = 4). Blocking of the NF‐κB or JNK‐2 pathways reduced TNFα‐induced IRF‐1 nuclear translocation by 35% and 50%, respectively ( P < 0.05; n ≥ 4). Using siRNA to knock down IRF‐1, we observed reduced IL‐18BPa expression. Additionally, IL‐18 bioactivity was higher when siRNA was used to knock down IRF‐1 expression. Conclusion These results show that IRF‐1 is a key regulator of IL‐18BPa expression and IL‐18 bioactivity in RASFs. Regulation of IRF‐1 will be a new therapeutic target in RA.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/88092/1/30583_ftp.pd

Insulin-Regulated Trafficking of GLUT4 Requires Ubiquitination

A major consequence of insulin binding its receptor on fat and muscle cells is translocation of the facilitative glucose transporter GLUT4 from an intracellular store to the cell surface where it serves to clear glucose from the bloodstream. Sorting of GLUT4 into its insulin-sensitive store requires the GGA [Golgi-localized, γ-ear-containing, ADP ribosylation factor (ARF)-binding] adaptor proteins, but the signal on GLUT4 to direct this sorting step is unknown. Here, we have identified a role for ubiquitination of GLUT4 in this process. We demonstrate that GLUT4 is ubiquitinated in 3T3-L1 adipocytes, and that a ubiquitin-resistant version fails to translocate to the cell surface of these cells in response to insulin. Our data support a model in which ubiquitination acts as a signal for the trafficking of GLUT4 from the endosomal/trans-Golgi network (TGN) system into its intracellular storage compartment, from where it is mobilized to the cell surface in response to insulin