ALBERT

Description: All orthobunyaviruses possess three genome segments of single-stranded negative sense RNA that are encapsidated with the virus-encoded nucleocapsid (N) protein to form a ribonucleoprotein (RNP) complex, which is uncharacterized at high resolution. We report the crystal structure of both the Bunyamwera virus (BUNV) N–RNA complex and the unbound Schmallenberg virus (SBV) N protein, at resolutions of 3.20 and 2.75 Å, respectively. Both N proteins crystallized as ring-like tetramers and exhibit a high degree of structural similarity despite classification into different orthobunyavirus serogroups. The structures represent a new RNA-binding protein fold. BUNV N possesses a positively charged groove into which RNA is deeply sequestered, with the bases facing away from the solvent. This location is highly inaccessible, implying that RNA polymerization and other critical base pairing events in the virus life cycle require RNP disassembly. Mutational analysis of N protein supports a correlation between structure and function. Comparison between these crystal structures and electron microscopy images of both soluble tetramers and authentic RNPs suggests the N protein does not bind RNA as a repeating monomer; thus, it represents a newly described architecture for bunyavirus RNP assembly, with implications for many other segmented negative-strand RNA viruses.

Description: The mechanism of IFN-β therapy in relapsing-remitting multiple sclerosis (RRMS) is not well understood, but induction of apoptosis in specific leukocyte subsets is likely to be important. Enhanced expression of TNFSF10 or TNF-related apoptosis-inducing ligand (TRAIL) mRNA in unseparated leukocytes has been put forward as a therapeutic response marker, but it is unclear which leukocyte subsets express TRAIL. We investigated the basis of TRAIL expression in response to IFN-β by studying activation of STATs 1, 3, and 5, p38 MAPK, and NF-κB in different leukocyte subsets of patients with RRMS. Monocytes, B cells, and T cells showed substantial differences in the activation of p38 and the STATs in response to i.m. injection of IFN-β1a or stimulation in vitro. Induction of cell-surface TRAIL, analyzed in nine leukocyte subsets, was observed only on monocytes and granulocytes and correlated with the activation of p38 and/or NF-κB in these subsets only, in agreement with previous work in fibroblasts showing that the induction of TRAIL in response to IFN-β depends on the activation of p38 and NF-κB as well as STATs 1 and 2. We propose that, in myeloid cells, the differential activation of p38 and NF-κB and induction of TRAIL, which sensitizes cells to apoptosis, can help to explain differences in responsiveness to IFN-β therapy among patients with RRMS and, furthermore, that such differential patterns of activation and expression may also be important in understanding the therapeutic responses to IFN-α/β in hepatitis and cancer.

Description: Bottle gourd (Lagenaria siceraria) was one of the first domesticated plants, and the only one with a global distribution during pre-Columbian times. Although native to Africa, bottle gourd was in use by humans in east Asia, possibly as early as 11,000 y ago (BP) and in the Americas by 10,000...

Description: Colonial breeding is widespread among animals. Some, such as eusocial insects, may use agonistic behavior to partition available foraging habitat into mutually exclusive territories; others, such as breeding seabirds, do not. We found that northern gannets, satellite-tracked from 12 neighboring colonies, nonetheless forage in largely mutually exclusive areas and that these colony-specific home ranges are determined by density-dependent competition. This segregation may be enhanced by individual-level public information transfer, leading to cultural evolution and divergence among colonies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wakefield, Ewan D -- Bodey, Thomas W -- Bearhop, Stuart -- Blackburn, Jez -- Colhoun, Kendrew -- Davies, Rachel -- Dwyer, Ross G -- Green, Jonathan A -- Gremillet, David -- Jackson, Andrew L -- Jessopp, Mark J -- Kane, Adam -- Langston, Rowena H W -- Lescroel, Amelie -- Murray, Stuart -- Le Nuz, Melanie -- Patrick, Samantha C -- Peron, Clara -- Soanes, Louise M -- Wanless, Sarah -- Votier, Stephen C -- Hamer, Keith C -- New York, N.Y. -- Science. 2013 Jul 5;341(6141):68-70. doi: 10.1126/science.1236077. Epub 2013 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biology, University of Leeds, Leeds, UK. e.d.wakefield@leeds.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23744776" target="_blank"〉PubMed〈/a〉

Description: In the open ocean ecosystem, climate and anthropogenic changes have driven biological change at both ends of the food chain. Understanding how the population dynamics of pelagic predators are simultaneously influenced by nutrient-driven processes acting from the “bottom-up” and predator-driven processes acting from the “top-down” is therefore considered an urgent task. Using a state-space demographic model, we evaluated the population trajectory of an oceanic predator, the macaroni penguin ( Eudyptes chrysolophus ), and numerically assessed the relative importance of bottom-up and top-down drivers acting through different demographic rates. The population trajectory was considerably more sensitive to changes in top-down control of survival compared to bottom-up control of survival or productivity. This study integrates a unique set of demographic and covariate data and highlights the benefits of using a single estimation framework to examine the links between covariates, demographic rates and population dynamics. This article is protected by copyright. All rights reserved.

Description: Germinal centre B-cell-like diffuse large B-cell lymphoma (GCB-DLBCL) is a common malignancy, yet the signalling pathways that are deregulated and the factors leading to its systemic dissemination are poorly defined. Work in mice showed that sphingosine-1-phosphate receptor-2 (S1PR2), a Galpha12 and Galpha13 coupled receptor, promotes growth regulation and local confinement of germinal centre B cells. Recent deep sequencing studies of GCB-DLBCL have revealed mutations in many genes in this cancer, including in GNA13 (encoding Galpha13) and S1PR2 (refs 5,6, 7). Here we show, using in vitro and in vivo assays, that GCB-DLBCL-associated mutations occurring in S1PR2 frequently disrupt the receptor's Akt and migration inhibitory functions. Galpha13-deficient mouse germinal centre B cells and human GCB-DLBCL cells were unable to suppress pAkt and migration in response to S1P, and Galpha13-deficient mice developed germinal centre B-cell-derived lymphoma. Germinal centre B cells, unlike most lymphocytes, are tightly confined in lymphoid organs and do not recirculate. Remarkably, deficiency in Galpha13, but not S1PR2, led to germinal centre B-cell dissemination into lymph and blood. GCB-DLBCL cell lines frequently carried mutations in the Galpha13 effector ARHGEF1, and Arhgef1 deficiency also led to germinal centre B-cell dissemination. The incomplete phenocopy of Galpha13- and S1PR2 deficiency led us to discover that P2RY8, an orphan receptor that is mutated in GCB-DLBCL and another germinal centre B-cell-derived malignancy, Burkitt's lymphoma, also represses germinal centre B-cell growth and promotes confinement via Galpha13. These findings identify a Galpha13-dependent pathway that exerts dual actions in suppressing growth and blocking dissemination of germinal centre B cells that is frequently disrupted in germinal centre B-cell-derived lymphoma.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267955/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267955/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muppidi, Jagan R -- Schmitz, Roland -- Green, Jesse A -- Xiao, Wenming -- Larsen, Adrien B -- Braun, Sterling E -- An, Jinping -- Xu, Ying -- Rosenwald, Andreas -- Ott, German -- Gascoyne, Randy D -- Rimsza, Lisa M -- Campo, Elias -- Jaffe, Elaine S -- Delabie, Jan -- Smeland, Erlend B -- Braziel, Rita M -- Tubbs, Raymond R -- Cook, J R -- Weisenburger, Dennis D -- Chan, Wing C -- Vaidehi, Nagarajan -- Staudt, Louis M -- Cyster, Jason G -- AI45073/AI/NIAID NIH HHS/ -- GM097261/GM/NIGMS NIH HHS/ -- R01 AI045073/AI/NIAID NIH HHS/ -- R01 GM097261/GM/NIGMS NIH HHS/ -- T32 CA128583/CA/NCI NIH HHS/ -- T32 CA1285835/CA/NCI NIH HHS/ -- T32 DK007636/DK/NIDDK NIH HHS/ -- UL1 TR000439/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2014 Dec 11;516(7530):254-8. doi: 10.1038/nature13765. Epub 2014 Sep 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Microbiology and Immunology, University of California, San Francisco, California, 94143, USA [2] Department of Medicine, University of California, San Francisco, California 94143, USA [3] Howard Hughes Medical Institute, University of California, San Francisco, California 94143, USA. ; Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Department of Microbiology and Immunology, University of California, San Francisco, California, 94143, USA [2] Howard Hughes Medical Institute, University of California, San Francisco, California 94143, USA [3] Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA. ; Division of Immunology, Beckman Research Institute of the City of Hope, Duarte, California 91010, USA. ; 1] Department of Microbiology and Immunology, University of California, San Francisco, California, 94143, USA [2] Howard Hughes Medical Institute, University of California, San Francisco, California 94143, USA. ; Department of Pathology, University of Wurzburg, 97080 Wurzburg, Germany. ; 1] Department of Clinical Pathology, Robert-Bosch-Krankenhaus, Auerbachstrasse 110, 70376 Stuttgart, Germany [2] Dr. Margarete Fischer-Bosch Institute for Clinical Pharmacology, 70376 Stuttgart, Germany. ; British Columbia Cancer Agency, Vancouver, British Columbia V5Z 1L3, Canada. ; Department of Pathology, University of Arizona, Tucson, Arizona 85724, USA. ; Hospital Clinic, University of Barcelona, 08036 Barcelona, Spain. ; Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Pathology Clinic, Rikshospitalet University Hospital, 0372 Oslo, Norway. ; 1] Institute for Cancer Research, Rikshospitalet University Hospital, University of Oslo, 0310 Oslo, Norway [2] Center for Cancer Biomedicine, Faculty Division of the Norwegian Radium Hospital, University of Oslo, 0310 Oslo, Norway. ; Oregon Health and Science University, Portland, Oregon 97239, USA. ; Cleveland Clinic Pathology and Laboratory Medicine Institute, Cleveland, Ohio 44195, USA. ; Department of Pathology, City of Hope National Medical Center, Duarte, California 91010, USA. ; 1] Department of Pathology, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA [2] Department of Microbiology, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25274307" target="_blank"〉PubMed〈/a〉

Description: To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943200/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bovine Genome Sequencing and Analysis Consortium -- Elsik, Christine G -- Tellam, Ross L -- Worley, Kim C -- Gibbs, Richard A -- Muzny, Donna M -- Weinstock, George M -- Adelson, David L -- Eichler, Evan E -- Elnitski, Laura -- Guigo, Roderic -- Hamernik, Debora L -- Kappes, Steve M -- Lewin, Harris A -- Lynn, David J -- Nicholas, Frank W -- Reymond, Alexandre -- Rijnkels, Monique -- Skow, Loren C -- Zdobnov, Evgeny M -- Schook, Lawrence -- Womack, James -- Alioto, Tyler -- Antonarakis, Stylianos E -- Astashyn, Alex -- Chapple, Charles E -- Chen, Hsiu-Chuan -- Chrast, Jacqueline -- Camara, Francisco -- Ermolaeva, Olga -- Henrichsen, Charlotte N -- Hlavina, Wratko -- Kapustin, Yuri -- Kiryutin, Boris -- Kitts, Paul -- Kokocinski, Felix -- Landrum, Melissa -- Maglott, Donna -- Pruitt, Kim -- Sapojnikov, Victor -- Searle, Stephen M -- Solovyev, Victor -- Souvorov, Alexandre -- Ucla, Catherine -- Wyss, Carine -- Anzola, Juan M -- Gerlach, Daniel -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Edgar, Robert C -- McEwan, John C -- Payne, Gemma M -- Raison, Joy M -- Junier, Thomas -- Kriventseva, Evgenia V -- Eyras, Eduardo -- Plass, Mireya -- Donthu, Ravikiran -- Larkin, Denis M -- Reecy, James -- Yang, Mary Q -- Chen, Lin -- Cheng, Ze -- Chitko-McKown, Carol G -- Liu, George E -- Matukumalli, Lakshmi K -- Song, Jiuzhou -- Zhu, Bin -- Bradley, Daniel G -- Brinkman, Fiona S L -- Lau, Lilian P L -- Whiteside, Matthew D -- Walker, Angela -- Wheeler, Thomas T -- Casey, Theresa -- German, J Bruce -- Lemay, Danielle G -- Maqbool, Nauman J -- Molenaar, Adrian J -- Seo, Seongwon -- Stothard, Paul -- Baldwin, Cynthia L -- Baxter, Rebecca -- Brinkmeyer-Langford, Candice L -- Brown, Wendy C -- Childers, Christopher P -- Connelley, Timothy -- Ellis, Shirley A -- Fritz, Krista -- Glass, Elizabeth J -- Herzig, Carolyn T A -- Iivanainen, Antti -- Lahmers, Kevin K -- Bennett, Anna K -- Dickens, C Michael -- Gilbert, James G R -- Hagen, Darren E -- Salih, Hanni -- Aerts, Jan -- Caetano, Alexandre R -- Dalrymple, Brian -- Garcia, Jose Fernando -- Gill, Clare A -- Hiendleder, Stefan G -- Memili, Erdogan -- Spurlock, Diane -- Williams, John L -- Alexander, Lee -- Brownstein, Michael J -- Guan, Leluo -- Holt, Robert A -- Jones, Steven J M -- Marra, Marco A -- Moore, Richard -- Moore, Stephen S -- Roberts, Andy -- Taniguchi, Masaaki -- Waterman, Richard C -- Chacko, Joseph -- Chandrabose, Mimi M -- Cree, Andy -- Dao, Marvin Diep -- Dinh, Huyen H -- Gabisi, Ramatu Ayiesha -- Hines, Sandra -- Hume, Jennifer -- Jhangiani, Shalini N -- Joshi, Vandita -- Kovar, Christie L -- Lewis, Lora R -- Liu, Yih-Shin -- Lopez, John -- Morgan, Margaret B -- Nguyen, Ngoc Bich -- Okwuonu, Geoffrey O -- Ruiz, San Juana -- Santibanez, Jireh -- Wright, Rita A -- Buhay, Christian -- Ding, Yan -- Dugan-Rocha, Shannon -- Herdandez, Judith -- Holder, Michael -- Sabo, Aniko -- Egan, Amy -- Goodell, Jason -- Wilczek-Boney, Katarzyna -- Fowler, Gerald R -- Hitchens, Matthew Edward -- Lozado, Ryan J -- Moen, Charles -- Steffen, David -- Warren, James T -- Zhang, Jingkun -- Chiu, Readman -- Schein, Jacqueline E -- Durbin, K James -- Havlak, Paul -- Jiang, Huaiyang -- Liu, Yue -- Qin, Xiang -- Ren, Yanru -- Shen, Yufeng -- Song, Henry -- Bell, Stephanie Nicole -- Davis, Clay -- Johnson, Angela Jolivet -- Lee, Sandra -- Nazareth, Lynne V -- Patel, Bella Mayurkumar -- Pu, Ling-Ling -- Vattathil, Selina -- Williams, Rex Lee Jr -- Curry, Stacey -- Hamilton, Cerissa -- Sodergren, Erica -- Wheeler, David A -- Barris, Wes -- Bennett, Gary L -- Eggen, Andre -- Green, Ronnie D -- Harhay, Gregory P -- Hobbs, Matthew -- Jann, Oliver -- Keele, John W -- Kent, Matthew P -- Lien, Sigbjorn -- McKay, Stephanie D -- McWilliam, Sean -- Ratnakumar, Abhirami -- Schnabel, Robert D -- Smith, Timothy -- Snelling, Warren M -- Sonstegard, Tad S -- Stone, Roger T -- Sugimoto, Yoshikazu -- Takasuga, Akiko -- Taylor, Jeremy F -- Van Tassell, Curtis P -- Macneil, Michael D -- Abatepaulo, Antonio R R -- Abbey, Colette A -- Ahola, Virpi -- Almeida, Iassudara G -- Amadio, Ariel F -- Anatriello, Elen -- Bahadue, Suria M -- Biase, Fernando H -- Boldt, Clayton R -- Carroll, Jeffery A -- Carvalho, Wanessa A -- Cervelatti, Eliane P -- Chacko, Elsa -- Chapin, Jennifer E -- Cheng, Ye -- Choi, Jungwoo -- Colley, Adam J -- de Campos, Tatiana A -- De Donato, Marcos -- Santos, Isabel K F de Miranda -- de Oliveira, Carlo J F -- Deobald, Heather -- Devinoy, Eve -- Donohue, Kaitlin E -- Dovc, Peter -- Eberlein, Annett -- Fitzsimmons, Carolyn J -- Franzin, Alessandra M -- Garcia, Gustavo R -- Genini, Sem -- Gladney, Cody J -- Grant, Jason R -- Greaser, Marion L -- Green, Jonathan A -- Hadsell, Darryl L -- Hakimov, Hatam A -- Halgren, Rob -- Harrow, Jennifer L -- Hart, Elizabeth A -- Hastings, Nicola -- Hernandez, Marta -- Hu, Zhi-Liang -- Ingham, Aaron -- Iso-Touru, Terhi -- Jamis, Catherine -- Jensen, Kirsty -- Kapetis, Dimos -- Kerr, Tovah -- Khalil, Sari S -- Khatib, Hasan -- Kolbehdari, Davood -- Kumar, Charu G -- Kumar, Dinesh -- Leach, Richard -- Lee, Justin C-M -- Li, Changxi -- Logan, Krystin M -- Malinverni, Roberto -- Marques, Elisa -- Martin, William F -- Martins, Natalia F -- Maruyama, Sandra R -- Mazza, Raffaele -- McLean, Kim L -- Medrano, Juan F -- Moreno, Barbara T -- More, Daniela D -- Muntean, Carl T -- Nandakumar, Hari P -- Nogueira, Marcelo F G -- Olsaker, Ingrid -- Pant, Sameer D -- Panzitta, Francesca -- Pastor, Rosemeire C P -- Poli, Mario A -- Poslusny, Nathan -- Rachagani, Satyanarayana -- Ranganathan, Shoba -- Razpet, Andrej -- Riggs, Penny K -- Rincon, Gonzalo -- Rodriguez-Osorio, Nelida -- Rodriguez-Zas, Sandra L -- Romero, Natasha E -- Rosenwald, Anne -- Sando, Lillian -- Schmutz, Sheila M -- Shen, Libing -- Sherman, Laura -- Southey, Bruce R -- Lutzow, Ylva Strandberg -- Sweedler, Jonathan V -- Tammen, Imke -- Telugu, Bhanu Prakash V L -- Urbanski, Jennifer M -- Utsunomiya, Yuri T -- Verschoor, Chris P -- Waardenberg, Ashley J -- Wang, Zhiquan -- Ward, Robert -- Weikard, Rosemarie -- Welsh, Thomas H Jr -- White, Stephen N -- Wilming, Laurens G -- Wunderlich, Kris R -- Yang, Jianqi -- Zhao, Feng-Qi -- 062023/Wellcome Trust/United Kingdom -- 077198/Wellcome Trust/United Kingdom -- BBS/B/13438/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/13446/Biotechnology and Biological Sciences Research Council/United Kingdom -- P30 DA018310/DA/NIDA NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273-04/HG/NHGRI NIH HHS/ -- U54 HG003273-04S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05/HG/NHGRI NIH HHS/ -- U54 HG003273-05S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05S2/HG/NHGRI NIH HHS/ -- U54 HG003273-06/HG/NHGRI NIH HHS/ -- U54 HG003273-06S1/HG/NHGRI NIH HHS/ -- U54 HG003273-06S2/HG/NHGRI NIH HHS/ -- U54 HG003273-07/HG/NHGRI NIH HHS/ -- U54 HG003273-08/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 24;324(5926):522-8. doi: 10.1126/science.1169588.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19390049" target="_blank"〉PubMed〈/a〉

Description: Author(s): C. Stock, E. E. Rodriguez, N. Lee, F. Demmel, P. Fouquet, M. Laver, Ch. Niedermayer, Y. Su, K. Nemkovski, M. A. Green, J. A. Rodriguez-Rivera, J. W. Kim, L. Zhang, and S.-W. Cheong CaFe 2 O 4 is an anisotropic S = 5 2 antiferromagnet with two competing A ( ↑ ↑ ↓ ↓ ) and B ( ↑ ↓ ↑ ↓ ) magnetic order parameters separated by static antiphase boundaries at low temperatures. Neutron diffraction and bulk susceptibility measurements, show that the spins near these boundaries are weakly correlated an... [Phys. Rev. Lett. 119, 257204] Published Fri Dec 22, 2017

Description: We present the results of our survey of 1612-MHz circumstellar OH maser emission from asymptotic giant branch (AGB) stars and red supergiants (RSGs) in the Large Magellanic Cloud (LMC). We have discovered four new circumstellar maser sources in the LMC, and increased the number of reliable wind speeds from infrared (IR) stars in the LMC from 5 to 13. Using our new wind speeds, as well as those from Galactic sources, we have derived an updated relation for dust-driven winds: v exp   ZL 0.4 . We compare the subsolar metallicity LMC OH/IR stars with carefully selected samples of more metal-rich OH/IR stars, also at known distances, in the Galactic Centre and Galactic bulge. We derive pulsation periods for eight of the bulge stars for the first time by using near-IR photometry from the Vista Variables in the Via Lactea survey. We have modelled our LMC OH/IR stars and developed an empirical method of deriving gas-to-dust ratios and mass-loss rates by scaling the models to the results from maser profiles. We have done this also for samples in the Galactic Centre and bulge and derived a new mass-loss prescription which includes luminosity, pulsation period, and gas-to-dust ratio $\dot{M} = 1.06^{+3.5}_{-0.8} \textrm{ }\times {\rm }10^{-5} (L/10^4\,{\textrm{L}}_{\odot })^{0.9\pm 0.1}(P/500\,{\rm {d}})^{0.75\pm 0.3} (r_{\rm gd}/200)^{-0.03\pm 0.07}$  M yr –1 . The tightest correlation is found between mass-loss rate and luminosity. We find that the gas-to-dust ratio has little effect on the mass-loss of oxygen-rich AGB stars and RSGs within the Galaxy and the LMC. This suggests that the mass-loss of oxygen-rich AGB stars and RSGs is (nearly) independent of metallicity between a half and twice solar.

Description: 〈title xmlns:mml="http://www.w3.org/1998/Math/MathML"〉Abstract〈/title〉〈p xmlns:mml="http://www.w3.org/1998/Math/MathML" xml:lang="en"〉The Gulf of Maine's lunar semidiurnal (M〈sub〉2〈/sub〉) ocean tide exhibits spatially coherent amplitude changes of ∼1–3 cm on interannual time scales, though no causative mechanism has been identified. Here we show, using a specially designed numerical modeling framework, that stratification changes account for 32%–48% (Pearson coefficient 0.58–0.69) of the observed M〈sub〉2〈/sub〉 variability at tide gauges from 1994 to 2019. Masking experiments and energy diagnoses reveal that the modeled variability is primarily driven by fluctuations in barotropic‐to‐baroclinic energy conversion on the continental slope south of the gulf's mouth, with a 1‐cm amplitude increase at Boston corresponding to a ∼7% (0.30 GW) drop in the area‐integrated conversion rate. Evidence is given for the same process to have caused the decade‐long M〈sub〉2〈/sub〉 amplitude decrease in the Gulf of Maine beginning in 1980/81. The study has implications for nuisance flooding predictions and space geodetic analyses seeking highest accuracies.〈/p〉

Description: Plain Language Summary: The height of the twice‐daily tide at Boston is about 135 cm, but researchers have long noted that this value fluctuates by about 1–3 cm from year to year. Here we show that the annual tidal height changes—seen in fact throughout the Gulf of Maine—are closely linked to how seawater density is distributed three‐dimensionally in the region. In particular, as tidal currents enter the gulf over steep underwater topography, the vertical distribution of density determines how much of the incoming wave energy is scattered back as internal tides into the deeper Northwest Atlantic. In years where this conversion of wave energy drops by 7% from its nominal value of 4 Gigawatt, the surface tide at Boston typically increases by 1 cm. Climate‐induced changes in ocean temperature and density may strengthen or weaken the conversion effect and thus slightly alter the role of tides in coastal flood events.〈/p〉

Description: Key Points〈: We propagate the M〈sub〉2〈/sub〉 tide through realistic, annually varying density structures (1993–2019) in a regional Gulf of Maine model. Stratification changes explain 32%–48% of the observed, cm‐level M〈sub〉2〈/sub〉 amplitude variability at coastal tide gauges from 1994 to 2019. Modeled M〈sub〉2〈/sub〉 changes mainly reflect fluctuations in the barotropic‐baroclinic energy conversion rate on the New England continental slope.

Description: Austrian Science Fund http://dx.doi.org/10.13039/501100002428

Description: Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659

Description: https://www.gesla.org/

Description: https://www.tpxo.net/global/tpxo9-atlas

Description: https://doi.pangaea.de/10.1594/PANGAEA.856844

Description: https://marine.copernicus.eu/access-data

Description: https://www.ncei.noaa.gov/products/northwest-atlantic-regional-climatology