@article{TiegsCostelloIskenetal.2019, author = {Tiegs, Scott D. and Costello, David M. and Isken, Mark W. and Woodward, Guy and McIntyre, Peter B. and Gessner, Mark O. and Chauvet, Eric and Griffiths, Natalie A. and Flecker, Alex S. and Acuna, Vicenc and Albarino, Ricardo and Allen, Daniel C. and Alonso, Cecilia and Andino, Patricio and Arango, Clay and Aroviita, Jukka and Barbosa, Marcus V. M. and Barmuta, Leon A. and Baxter, Colden V. and Bell, Thomas D. C. and Bellinger, Brent and Boyero, Luz and Brown, Lee E. and Bruder, Andreas and Bruesewitz, Denise A. and Burdon, Francis J. and Callisto, Marcos and Canhoto, Cristina and Capps, Krista A. and Castillo, Maria M. and Clapcott, Joanne and Colas, Fanny and Colon-Gaud, Checo and Cornut, Julien and Crespo-Perez, Veronica and Cross, Wyatt F. and Culp, Joseph M. and Danger, Michael and Dangles, Olivier and de Eyto, Elvira and Derry, Alison M. and Diaz Villanueva, Veronica and Douglas, Michael M. and Elosegi, Arturo and Encalada, Andrea C. and Entrekin, Sally and Espinosa, Rodrigo and Ethaiya, Diana and Ferreira, Veronica and Ferriol, Carmen and Flanagan, Kyla M. and Fleituch, Tadeusz and Shah, Jennifer J. Follstad and Frainer, Andre and Friberg, Nikolai and Frost, Paul C. and Garcia, Erica A. and Lago, Liliana Garcia and Garcia Soto, Pavel Ernesto and Ghate, Sudeep and Giling, Darren P. and Gilmer, Alan and Goncalves, Jose Francisco and Gonzales, Rosario Karina and Graca, Manuel A. S. and Grace, Mike and Grossart, Hans-Peter and Guerold, Francois and Gulis, Vlad and Hepp, Luiz U. and Higgins, Scott and Hishi, Takuo and Huddart, Joseph and Hudson, John and Imberger, Samantha and Iniguez-Armijos, Carlos and Iwata, Tomoya and Janetski, David J. and Jennings, Eleanor and Kirkwood, Andrea E. and Koning, Aaron A. and Kosten, Sarian and Kuehn, Kevin A. and Laudon, Hjalmar and Leavitt, Peter R. and Lemes da Silva, Aurea L. and Leroux, Shawn J. and Leroy, Carri J. and Lisi, Peter J. and MacKenzie, Richard and Marcarelli, Amy M. and Masese, Frank O. and Mckie, Brendan G. and Oliveira Medeiros, Adriana and Meissner, Kristian and Milisa, Marko and Mishra, Shailendra and Miyake, Yo and Moerke, Ashley and Mombrikotb, Shorok and Mooney, Rob and Moulton, Tim and Muotka, Timo and Negishi, Junjiro N. and Neres-Lima, Vinicius and Nieminen, Mika L. and Nimptsch, Jorge and Ondruch, Jakub and Paavola, Riku and Pardo, Isabel and Patrick, Christopher J. and Peeters, Edwin T. H. M. and Pozo, Jesus and Pringle, Catherine and Prussian, Aaron and Quenta, Estefania and Quesada, Antonio and Reid, Brian and Richardson, John S. and Rigosi, Anna and Rincon, Jose and Risnoveanu, Geta and Robinson, Christopher T. and Rodriguez-Gallego, Lorena and Royer, Todd V. and Rusak, James A. and Santamans, Anna C. and Selmeczy, Geza B. and Simiyu, Gelas and Skuja, Agnija and Smykla, Jerzy and Sridhar, Kandikere R. and Sponseller, Ryan and Stoler, Aaron and Swan, Christopher M. and Szlag, David and Teixeira-de Mello, Franco and Tonkin, Jonathan D. and Uusheimo, Sari and Veach, Allison M. and Vilbaste, Sirje and Vought, Lena B. M. and Wang, Chiao-Ping and Webster, Jackson R. and Wilson, Paul B. and Woelfl, Stefan and Xenopoulos, Marguerite A. and Yates, Adam G. and Yoshimura, Chihiro and Yule, Catherine M. and Zhang, Yixin X. and Zwart, Jacob A.}, title = {Global patterns and drivers of ecosystem functioning in rivers and riparian zones}, series = {Science Advances}, volume = {5}, journal = {Science Advances}, number = {1}, publisher = {American Assoc. for the Advancement of Science}, address = {Washington}, issn = {2375-2548}, doi = {10.1126/sciadv.aav0486}, pages = {8}, year = {2019}, abstract = {River ecosystems receive and process vast quantities of terrestrial organic carbon, the fate of which depends strongly on microbial activity. Variation in and controls of processing rates, however, are poorly characterized at the global scale. In response, we used a peer-sourced research network and a highly standardized carbon processing assay to conduct a global-scale field experiment in greater than 1000 river and riparian sites. We found that Earth's biomes have distinct carbon processing signatures. Slow processing is evident across latitudes, whereas rapid rates are restricted to lower latitudes. Both the mean rate and variability decline with latitude, suggesting temperature constraints toward the poles and greater roles for other environmental drivers (e.g., nutrient loading) toward the equator. These results and data set the stage for unprecedented "next-generation biomonitoring" by establishing baselines to help quantify environmental impacts to the functioning of ecosystems at a global scale.}, language = {en} } @article{AbdrakhmatovWalkerCampbelletal.2016, author = {Abdrakhmatov, Kanatbek E. and Walker, R. T. and Campbell, G. E. and Carr, A. S. and Elliott, A. and Hillemann, Christian and Hollingsworth, J. and Landgraf, Angela and Mackenzie, D. and Mukambayev, A. and Rizza, M. and Sloan, R. A.}, title = {Multisegment rupture in the 11 July 1889 Chilik earthquake (M-w 8.0-8.3), Kazakh Tien Shan, interpreted from remote sensing, field survey, and paleoseismic trenching}, series = {Journal of geophysical research : Solid earth}, volume = {121}, journal = {Journal of geophysical research : Solid earth}, publisher = {American Geophysical Union}, address = {Washington}, issn = {2169-9313}, doi = {10.1002/2015JB012763}, pages = {4615 -- 4640}, year = {2016}, abstract = {The 11 July 1889 Chilik earthquake (M-w 8.0-8.3) forms part of a remarkable sequence of large earthquakes in the late nineteenth and early twentieth centuries in the northern Tien Shan. Despite its importance, the source of the 1889 earthquake remains unknown, though the macroseismic epicenter is sited in the Chilik valley, similar to 100 km southeast of Almaty, Kazakhstan (similar to 2 million population). Several short fault segments that have been inferred to have ruptured in 1889 are too short on their own to account for the estimated magnitude. In this paper we perform detailed surveying and trenching of the similar to 30 km long Saty fault, one of the previously inferred sources, and find that it was formed in a single earthquake within the last 700 years, involving surface slip of up to 10 m. The scarp-forming event, likely to be the 1889 earthquake, was the only surface-rupturing event for at least 5000 years and potentially for much longer. From satellite imagery we extend the mapped length of fresh scarps within the 1889 epicentral zone to a total of similar to 175 km, which we also suggest as candidate ruptures from the 1889 earthquake. The 175 km of rupture involves conjugate oblique left-lateral and right-lateral slip on three separate faults, with step overs of several kilometers between them. All three faults were essentially invisible in the Holocene geomorphology prior to the last slip. The recurrence interval between large earthquakes on any of these faults, and presumably on other faults of the Tien Shan, may be longer than the timescale over which the landscape is reset, providing a challenge for delineating sources of future hazard.}, language = {en} } @article{MorrisKassamBerczetal.2019, author = {Morris, Mackenzie C. and Kassam, Farzaan and Bercz, Aron and Beckmann, Nadine and Schumacher, Fabian and Gulbins, Erich and Makley, Amy T. and Goodman, Michael D.}, title = {The Role of Chemoprophylactic Agents in Modulating Platelet Aggregability After Traumatic Brain Injury}, series = {Journal of surgical research}, volume = {244}, journal = {Journal of surgical research}, publisher = {Elsevier}, address = {San Diego}, issn = {0022-4804}, doi = {10.1016/j.jss.2019.06.022}, pages = {1 -- 8}, year = {2019}, abstract = {Background: The pathophysiology behind the subacute but persistent hypercoagulable state after traumatic brain injury (TBI) is poorly understood but contributes to morbidity induced by venous thromboembolism. Because platelets and their microvesicles have been hypothesized to play a role in post-traumatic hypercoagulability, administration of commonly used agents may ameliorate this coagulability. We hypothesized that utilization of aspirin, ketorolac, amitriptyline, unfractionated heparin, or enoxaparin would modulate the platelet aggregation response after TBI. Methods: Concussive TBI was induced by weight drop. Mice were then randomized to receive aspirin, ketorolac, amitriptyline, heparin, enoxaparin, or saline control at 2 and 8 h after TBI. Mice were sacrificed at 6 or 24 h after injury to determine coagulability by rotational thromboelastometry (ROTEM), platelet function testing with impedance aggregometry, and microvesicle enumeration. Platelet sphingolipid metabolites were analyzed by mass spectrometry. Results: ROTEM demonstrated increased platelet contribution to maximum clot firmness at 6 h after TBI in mice that received aspirin or amitriptyline, but this did not persist at 24 h. By contrast, adenosine diphosphate- and arachidonic acid-induced platelet aggregation at 6 h was significantly lower in mice receiving ketorolac, aspirin, and amitriptyline compared with mice receiving saline at 6 h after injury and only arachidonic acid-initiated platelet aggregation was decreased by aspirin at 24 h. There were no differences in microvesicle production at either time point. Platelet sphingosine-1-phosphate levels were decreased at 6 h in the group receiving amitriptyline and increased at 24 h along with platelet ceramide levels at 24 h in the amitriptyline group. Conclusion: After TBI, amitriptyline decreased platelet aggregability and increased contribution to clot in a manner similar to aspirin. The amitriptyline effects on platelet function and sphingolipid metabolites may represent a possible role of the acid sphingomyelinase in the hypercoagulability observed after injury. In addition, inhibition of platelet reactivity may be an underappreciated benefit of low molecular weight heparins, such as enoxaparin. (C) 2019 Elsevier Inc. All rights reserved.}, language = {en} }