TY  - JOUR
A1  - Tucker, Marlee A.
A1  - Boehning-Gaese, Katrin
A1  - Fagan, William F.
A1  - Fryxell, John M.
A1  - Van Moorter, Bram
A1  - Alberts, Susan C.
A1  - Ali, Abdullahi H.
A1  - Allen, Andrew M.
A1  - Attias, Nina
A1  - Avgar, Tal
A1  - Bartlam-Brooks, Hattie
A1  - Bayarbaatar, Buuveibaatar
A1  - Belant, Jerrold L.
A1  - Bertassoni, Alessandra
A1  - Beyer, Dean
A1  - Bidner, Laura
A1  - van Beest, Floris M.
A1  - Blake, Stephen
A1  - Blaum, Niels
A1  - Bracis, Chloe
A1  - Brown, Danielle
A1  - de Bruyn, P. J. Nico
A1  - Cagnacci, Francesca
A1  - Calabrese, Justin M.
A1  - Camilo-Alves, Constanca
A1  - Chamaille-Jammes, Simon
A1  - Chiaradia, Andre
A1  - Davidson, Sarah C.
A1  - Dennis, Todd
A1  - DeStefano, Stephen
A1  - Diefenbach, Duane
A1  - Douglas-Hamilton, Iain
A1  - Fennessy, Julian
A1  - Fichtel, Claudia
A1  - Fiedler, Wolfgang
A1  - Fischer, Christina
A1  - Fischhoff, Ilya
A1  - Fleming, Christen H.
A1  - Ford, Adam T.
A1  - Fritz, Susanne A.
A1  - Gehr, Benedikt
A1  - Goheen, Jacob R.
A1  - Gurarie, Eliezer
A1  - Hebblewhite, Mark
A1  - Heurich, Marco
A1  - Hewison, A. J. Mark
A1  - Hof, Christian
A1  - Hurme, Edward
A1  - Isbell, Lynne A.
A1  - Janssen, Rene
A1  - Jeltsch, Florian
A1  - Kaczensky, Petra
A1  - Kane, Adam
A1  - Kappeler, Peter M.
A1  - Kauffman, Matthew
A1  - Kays, Roland
A1  - Kimuyu, Duncan
A1  - Koch, Flavia
A1  - Kranstauber, Bart
A1  - LaPoint, Scott
A1  - Leimgruber, Peter
A1  - Linnell, John D. C.
A1  - Lopez-Lopez, Pascual
A1  - Markham, A. Catherine
A1  - Mattisson, Jenny
A1  - Medici, Emilia Patricia
A1  - Mellone, Ugo
A1  - Merrill, Evelyn
A1  - Mourao, Guilherme de Miranda
A1  - Morato, Ronaldo G.
A1  - Morellet, Nicolas
A1  - Morrison, Thomas A.
A1  - Diaz-Munoz, Samuel L.
A1  - Mysterud, Atle
A1  - Nandintsetseg, Dejid
A1  - Nathan, Ran
A1  - Niamir, Aidin
A1  - Odden, John
A1  - Oliveira-Santos, Luiz Gustavo R.
A1  - Olson, Kirk A.
A1  - Patterson, Bruce D.
A1  - de Paula, Rogerio Cunha
A1  - Pedrotti, Luca
A1  - Reineking, Bjorn
A1  - Rimmler, Martin
A1  - Rogers, Tracey L.
A1  - Rolandsen, Christer Moe
A1  - Rosenberry, Christopher S.
A1  - Rubenstein, Daniel I.
A1  - Safi, Kamran
A1  - Said, Sonia
A1  - Sapir, Nir
A1  - Sawyer, Hall
A1  - Schmidt, Niels Martin
A1  - Selva, Nuria
A1  - Sergiel, Agnieszka
A1  - Shiilegdamba, Enkhtuvshin
A1  - Silva, Joao Paulo
A1  - Singh, Navinder
A1  - Solberg, Erling J.
A1  - Spiegel, Orr
A1  - Strand, Olav
A1  - Sundaresan, Siva
A1  - Ullmann, Wiebke
A1  - Voigt, Ulrich
A1  - Wall, Jake
A1  - Wattles, David
A1  - Wikelski, Martin
A1  - Wilmers, Christopher C.
A1  - Wilson, John W.
A1  - Wittemyer, George
A1  - Zieba, Filip
A1  - Zwijacz-Kozica, Tomasz
A1  - Mueller, Thomas
T1  - Moving in the Anthropocene
BT  - global reductions in terrestrial mammalian movements
JF  - Science
N2  - Animal movement is fundamental for ecosystem functioning and species survival, yet the effects of the anthropogenic footprint on animal movements have not been estimated across species. Using a unique GPS-tracking database of 803 individuals across 57 species, we found that movements of mammals in areas with a comparatively high human footprint were on average one-half to one-third the extent of their movements in areas with a low human footprint. We attribute this reduction to behavioral changes of individual animals and to the exclusion of species with long-range movements from areas with higher human impact. Global loss of vagility alters a key ecological trait of animals that affects not only population persistence but also ecosystem processes such as predator-prey interactions, nutrient cycling, and disease transmission.
Y1  - 2018
U6  - https://doi.org/10.1126/science.aam9712
SN  - 0036-8075
SN  - 1095-9203
VL  - 359
IS  - 6374
SP  - 466
EP  - 469
PB  - American Assoc. for the Advancement of Science
CY  - Washington
ER  - 
TY  - GEN
A1  - Patil, Kaustubh R.
A1  - Haider, Peter
A1  - Pope, Phillip B.
A1  - Turnbaugh, Peter J.
A1  - Morrison, Mark
A1  - Scheffer, Tobias
A1  - McHardy, Alice C.
T1  - Taxonomic metagenome sequence assignment with structured output models
T2  - Nature methods : techniques for life scientists and chemists
Y1  - 2011
U6  - https://doi.org/10.1038/nmeth0311-191
SN  - 1548-7091
VL  - 8
IS  - 3
SP  - 191
EP  - 192
PB  - Nature Publ. Group
CY  - London
ER  - 
TY  - JOUR
A1  - Tang, Alan T.
A1  - Sullivan, Katie Rose
A1  - Hong, Courtney C.
A1  - Goddard, Lauren M.
A1  - Mahadevan, Aparna
A1  - Ren, Aileen
A1  - Pardo, Heidy
A1  - Peiper, Amy
A1  - Griffin, Erin
A1  - Tanes, Ceylan
A1  - Mattei, Lisa M.
A1  - Yang, Jisheng
A1  - Li, Li
A1  - Mericko-Ishizuka, Patricia
A1  - Shen, Le
A1  - Hobson, Nicholas
A1  - Girard, Romuald
A1  - Lightle, Rhonda
A1  - Moore, Thomas
A1  - Shenkar, Robert
A1  - Polster, Sean P.
A1  - Roedel, Claudia Jasmin
A1  - Li, Ning
A1  - Zhu, Qin
A1  - Whitehead, Kevin J.
A1  - Zheng, Xiangjian
A1  - Akers, Amy
A1  - Morrison, Leslie
A1  - Kim, Helen
A1  - Bittinger, Kyle
A1  - Lengner, Christopher J.
A1  - Schwaninger, Markus
A1  - Velcich, Anna
A1  - Augenlicht, Leonard
A1  - Abdelilah-Seyfried, Salim
A1  - Min, Wang
A1  - Marchuk, Douglas A.
A1  - Awad, Issam A.
A1  - Kahn, Mark L.
T1  - Distinct cellular roles for PDCD10 define a gut-brain axis in cerebral cavernous malformation
JF  - Science Translational Medicine
N2  - Cerebral cavernous malformation (CCM) is a genetic, cerebrovascular disease. Familial CCM is caused by genetic mutations in KRIT1, CCM2, or PDCD10. Disease onset is earlier and more severe in individuals with PDCD10 mutations. Recent studies have shown that lesions arise from excess mitogen-activated protein kinase kinase kinase 3 (MEKK3) signaling downstream of Toll-like receptor 4 (TLR4) stimulation by lipopolysaccharide derived from the gut microbiome. These findings suggest a gut-brain CCM disease axis but fail to define it or explain the poor prognosis of patients with PDCD10 mutations. Here, we demonstrate that the gut barrier is a primary determinant of CCM disease course, independent of microbiome configuration, that explains the increased severity of CCM disease associated with PDCD10 deficiency. Chemical disruption of the gut barrier with dextran sulfate sodium augments CCM formation in a mouse model, as does genetic loss of Pdcd10, but not Krit1, in gut epithelial cells. Loss of gut epithelial Pdcd10 results in disruption of the colonic mucosal barrier. Accordingly, loss of Mucin-2 or exposure to dietary emulsifiers that reduce the mucus barrier increases CCM burden analogous to loss of Pdcd10 in the gut epithelium. Last, we show that treatment with dexamethasone potently inhibits CCM formation in mice because of the combined effect of action at both brain endothelial cells and gut epithelial cells. These studies define a gut-brain disease axis in an experimental model of CCM in which a single gene is required for two critical components: gut epithelial function and brain endothelial signaling.
Y1  - 2019
U6  - https://doi.org/10.1126/scitranslmed.aaw3521
SN  - 1946-6234
SN  - 1946-6242
VL  - 11
IS  - 520
PB  - American Assoc. for the Advancement of Science
CY  - Washington
ER  -