Network analysis of sea turtle movements and connectivity: A tool for conservation prioritization

Aim: Understanding the spatial ecology of animal movements is a critical element in conserving long-lived, highly mobile marine species. Analyzing networks developed from movements of six sea turtle species reveals marine connectivity and can help prioritize conservation efforts. Location: Global. Methods: We collated telemetry data from 1235 individuals and reviewed the literature to determine our dataset's representativeness. We used the telemetry data to develop spatial networks at different scales to examine areas, connections, and their geographic arrangement. We used graph theory metrics to compare networks across regions and species and to identify the role of important areas and connections. Results: Relevant literature and citations for data used in this study had very little overlap. Network analysis showed that sampling effort influenced network structure, and the arrangement of areas and connections for most networks was complex. However, important areas and connections identified by graph theory metrics can be different than areas of high data density. For the global network, marine regions in the Mediterranean had high closeness, while links with high betweenness among marine regions in the South Atlantic were critical for maintaining connectivity. Comparisons among species-specific networks showed that functional connectivity was related to movement ecology, resulting in networks composed of different areas and links. Main conclusions: Network analysis identified the structure and functional connectivity of the sea turtles in our sample at multiple scales. These network characteristics could help guide the coordination of management strategies for wide-ranging animals throughout their geographic extent. Most networks had complex structures that can contribute to greater robustness but may be more difficult to manage changes when compared to simpler forms. Area-based conservation measures would benefit sea turtle populations when directed toward areas with high closeness dominating network function. Promoting seascape connectivity of links with high betweenness would decrease network vulnerability.Fil: Kot, Connie Y.. University of Duke; Estados UnidosFil: Åkesson, Susanne. Lund University; SueciaFil: Alfaro Shigueto, Joanna. Universidad Cientifica del Sur; Perú. University of Exeter; Reino Unido. Pro Delphinus; PerúFil: Amorocho Llanos, Diego Fernando. Research Center for Environmental Management and Development; ColombiaFil: Antonopoulou, Marina. Emirates Wildlife Society-world Wide Fund For Nature; Emiratos Arabes UnidosFil: Balazs, George H.. Noaa Fisheries Service; Estados UnidosFil: Baverstock, Warren R.. The Aquarium and Dubai Turtle Rehabilitation Project; Emiratos Arabes UnidosFil: Blumenthal, Janice M.. Cayman Islands Government; Islas CaimánFil: Broderick, Annette C.. University of Exeter; Reino UnidoFil: Bruno, Ignacio. Instituto Nacional de Investigaciones y Desarrollo Pesquero; ArgentinaFil: Canbolat, Ali Fuat. Hacettepe Üniversitesi; Turquía. Ecological Research Society; TurquíaFil: Casale, Paolo. Università degli Studi di Pisa; ItaliaFil: Cejudo, Daniel. Universidad de Las Palmas de Gran Canaria; EspañaFil: Coyne, Michael S.. Seaturtle.org; Estados UnidosFil: Curtice, Corrie. University of Duke; Estados UnidosFil: DeLand, Sarah. University of Duke; Estados UnidosFil: DiMatteo, Andrew. CheloniData; Estados UnidosFil: Dodge, Kara. New England Aquarium; Estados UnidosFil: Dunn, Daniel C.. University of Queensland; Australia. The University of Queensland; Australia. University of Duke; Estados UnidosFil: Esteban, Nicole. Swansea University; Reino UnidoFil: Formia, Angela. Wildlife Conservation Society; Estados UnidosFil: Fuentes, Mariana M. P. B.. Florida State University; Estados UnidosFil: Fujioka, Ei. University of Duke; Estados UnidosFil: Garnier, Julie. The Zoological Society of London; Reino UnidoFil: Godfrey, Matthew H.. North Carolina Wildlife Resources Commission; Estados UnidosFil: Godley, Brendan J.. University of Exeter; Reino UnidoFil: González Carman, Victoria. Instituto National de Investigación y Desarrollo Pesquero; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Harrison, Autumn Lynn. Smithsonian Institution; Estados UnidosFil: Hart, Catherine E.. Grupo Tortuguero de las Californias A.C; México. Investigacion, Capacitacion y Soluciones Ambientales y Sociales A.C; MéxicoFil: Hawkes, Lucy A.. University of Exeter; Reino UnidoFil: Hays, Graeme C.. Deakin University; AustraliaFil: Hill, Nicholas. The Zoological Society of London; Reino UnidoFil: Hochscheid, Sandra. Stazione Zoologica Anton Dohrn; ItaliaFil: Kaska, Yakup. Dekamer—Sea Turtle Rescue Center; Turquía. Pamukkale Üniversitesi; TurquíaFil: Levy, Yaniv. University Of Haifa; Israel. Israel Nature And Parks Authority; IsraelFil: Ley Quiñónez, César P.. Instituto Politécnico Nacional; MéxicoFil: Lockhart, Gwen G.. Virginia Aquarium Marine Science Foundation; Estados Unidos. Naval Facilities Engineering Command; Estados UnidosFil: López-Mendilaharsu, Milagros. Projeto TAMAR; BrasilFil: Luschi, Paolo. Università degli Studi di Pisa; ItaliaFil: Mangel, Jeffrey C.. University of Exeter; Reino Unido. Pro Delphinus; PerúFil: Margaritoulis, Dimitris. Archelon; GreciaFil: Maxwell, Sara M.. University of Washington; Estados UnidosFil: McClellan, Catherine M.. University of Duke; Estados UnidosFil: Metcalfe, Kristian. University of Exeter; Reino UnidoFil: Mingozzi, Antonio. Università Della Calabria; ItaliaFil: Moncada, Felix G.. Centro de Investigaciones Pesqueras; CubaFil: Nichols, Wallace J.. California Academy Of Sciences; Estados Unidos. Center For The Blue Economy And International Environmental Policy Program; Estados UnidosFil: Parker, Denise M.. Noaa Fisheries Service; Estados UnidosFil: Patel, Samir H.. Coonamessett Farm Foundation; Estados Unidos. Drexel University; Estados UnidosFil: Pilcher, Nicolas J.. Marine Research Foundation; MalasiaFil: Poulin, Sarah. University of Duke; Estados UnidosFil: Read, Andrew J.. Duke University Marine Laboratory; Estados UnidosFil: Rees, ALan F.. University of Exeter; Reino Unido. Archelon; GreciaFil: Robinson, David P.. The Aquarium and Dubai Turtle Rehabilitation Project; Emiratos Arabes UnidosFil: Robinson, Nathan J.. Fundación Oceanogràfic; EspañaFil: Sandoval-Lugo, Alejandra G.. Instituto Politécnico Nacional; MéxicoFil: Schofield, Gail. Queen Mary University of London; Reino UnidoFil: Seminoff, Jeffrey A.. Noaa National Marine Fisheries Service Southwest Regional Office; Estados UnidosFil: Seney, Erin E.. University Of Central Florida; Estados UnidosFil: Snape, Robin T. E.. University of Exeter; Reino UnidoFil: Sözbilen, Dogan. Dekamer—sea Turtle Rescue Center; Turquía. Pamukkale University; TurquíaFil: Tomás, Jesús. Institut Cavanilles de Biodiversitat I Biologia Evolutiva; EspañaFil: Varo Cruz, Nuria. Universidad de Las Palmas de Gran Canaria; España. Ads Biodiversidad; España. Instituto Canario de Ciencias Marinas; EspañaFil: Wallace, Bryan P.. University of Duke; Estados Unidos. Ecolibrium, Inc.; Estados UnidosFil: Wildermann, Natalie E.. Texas A&M University; Estados UnidosFil: Witt, Matthew J.. University of Exeter; Reino UnidoFil: Zavala Norzagaray, Alan A.. Instituto politecnico nacional; MéxicoFil: Halpin, Patrick N.. University of Duke; Estados Unido

Loss Of Non-Coding Rna, Snord116, Attenuates Chronic Pathological Cardiac Remodeling And Protects Cardiomyocyte Contraction And Relaxation Kinetics During Ischemia.

Physiological cardiac remodeling is a beneficial process by which the heart becomes more efficient. To investigate mechanisms regulating cardiac remodeling, we assayed gene expression of epicardial cells after running exercise, which induces physiological cardiac remodeling. We identified Snord116 and FoxG1 as the most differentially expressed gene and transcription factor, respectively, (both increased) in running animals, compared with healthy, non-running controls. Snord116 is a maternally-imprinted locus containing sequences for small nucleolar RNAs (snoRNAs) and 116hg, a long noncoding RNA (lncRNA). The 116hg lncRNA was reported to regulate the rhythmic diurnal methylation of thousands of genes with epigenetic, metabolic, and circadian functions. FoxG1 controls the proliferation of neural progenitor cells. In cultured epicardial cells, shRNA-mediated FoxG1 knockdown reduced proliferation and Snord116 expression; this indicated a potential role for FoxG1 in epicardial-based cardiac remodeling. Although paternal Snord116 deletion causes Prader Willi Syndrome, a complex disorder with neurologic, metabolic, and cardiovascular pathologies, the role of Snord116 in cardiac cells is poorly understood. To investigate the impact of Snord116 expression on pathological cardiac remodeling, we obtained Snord116 paternal deletion (Snord116p-) mice and monitored cardiac structure and function during aging and after myocardial infarction (MI). We found that Snord116p- mice did not undergo age-induced ventricular wall thickening as was observed in wildtype littermates (WT LM). At 8 weeks post-MI, compared with WT LM, Snord116p- mice had reduced remodeling and scar tissue formation, as well as improved cardiac function. Of note, we demonstrated increased left ventricular levels of beta-hydroxybutyrate dehydrogenase (BDH1), concurrent with elevated 3-hydroxybutyrate (β-OHB) in the blood of Snord116p- animals compared with WT LM, indicating increased myocardial ketone body use. These data suggest Snord116 expression impacts chronic cardiac remodeling potentially through the regulation of myocardial metabolism. To determine whether Snord116 expression affected the cardiomyocyte response to ischemia, we developed a model of ischemia and reperfusion using living myocardial slices. We monitored cardiomyocyte function in slices derived from Snord116p- and WT LM mice of both sexes at baseline, after ischemia, and after a recovery period. We found that loss of Snord116 protected cardiomyocytes from ischemia-induced prolongation of systole and delayed diastolic elongation. Importantly, we found that tissue derived from female animals demonstrated a greater increase in end diastolic force, compared with tissue from males. This work establishes the utility of myocardial slices to investigate sex- and genetic-based regulation of cardiomyocyte function. Our studies established that loss of Snord116 expression reduced pathological cardiac remodeling. One mechanism by which Snord116 expression exerted change on the progression of pathological remodeling was by increasing the ability of cardiomyocytes to withstand ischemic stress. Further work to define the mechanism(s) by which Snord116 loss or inhibition benefits cardiac remodeling could lead to new therapeutics for the treatment of cardiovascular disease

Obstetric shift-to-shift handover in Kerala, India: A cross-sectional mixed method study.

IntroductionBeyond the provision of services, quality of care and patient safety measures such as optimal clinical handover at shift changes determine maternity outcomes. We aimed to establish the proportion of women handed over and the content of clinical handovers and communication between shifts within 3 diverse obstetrics units in Kerala, India, and to describe the handover environment.MethodsA cross sectional study was conducted for six weeks during February and March 2015at three hospitals in Kerala, India, during nurses obstetric handover in one tertiary private, one tertiary government and one secondary government hospital. Nursing handovers in obstetric post-operative, in-patient and labour wards were sampled. An SBAR-based (situation, background, assessment and recommendation) data schedule was completed whilst observing handover at nursing shift changes. Since obstetricians had no scheduled handover, qualitative interviews were conducted with obstetricians in two hospitals to establish how they acquire information when beginning a shift.ResultsData was obtained on 258 patients handed over, within 67 shift changes. The median percentage of women handed over was 100% in two of the hospitals and 27.6% in the other. The median number of information items included out of a possible 25 was 11, 5 and 4,and did not change significantly for women with high-risk status. Important items regarding assessment and recommendation for care were often missed, including high-risk status. The median number of environment items achieved was good at 7 out of 10 in all hospitals. Obstetricians sought information in various ways when required. All supported the development of structured tools, face-to-face and team handovers.ConclusionsMaternity unit handovers for doctors and nurses were inadequate. Ensuring handover of all women and including critical information, between shifts as well as between doctors, needs to be improved to increase patient safety

The Neural Progenitor Cell-Associated Transcription Factor FoxG1 Regulates Cardiac Epicardial Cell Proliferation

The epicardium is a layer of mesothelial cells that covers the surface of the heart. During development, epicardial cells undergo epithelial-to-mesenchymal transition (EMT) to form multipotent precursors that migrate into the heart and contribute to the coronary vasculature by differentiating into adventitial fibroblasts, smooth muscle cells, and endothelial cells. Epicardial cells also provide paracrine signals to cardiac myocytes that are required for appropriate heart growth. In adult hearts, a similar process of epicardial cell EMT, migration, and differentiation occurs after myocardial infarction (MI, heart attack). Pathological cardiac hypertrophy is associated with fibrosis, negative remodeling, and reduced cardiac function. In contrast, aerobic exercises such as swimming and running promote physiological (i.e., beneficial) hypertrophy, which is associated with angiogenesis and improved cardiac function. As epicardial cell function(s) during physiological hypertrophy are poorly understood, we analyzed and compared the native epicardial cells isolated directly from the hearts of running-exercised mice and age-matched, nonrunning littermates. To obtain epicardial cells, we enzymatically digested the surfaces of whole hearts and performed magnetic-activated cell sorting (MACS) with antibodies against CD104 (integrin β4). By cDNA microarray assays, we identified genes with increased transcription in epicardial cells after running exercise; these included FoxG1, a transcription factor that controls neural progenitor cell proliferation during brain development and Snord116, a small noncoding RNA that coordinates expression of genes with epigenetic, circadian, and metabolic functions. In cultured epicardial cells, shRNA-mediated FoxG1 knockdown significantly decreased cell proliferation, as well as Snord116 expression. Our results demonstrate that FoxG1 regulates epicardial proliferation, and suggest it may affect cardiac remodeling

Sex differences in long-term survival after intensive care unit treatment for sepsis: A cohort study

Objective To determine the effect of sex on sepsis-related ICU admission and survival for up to 3-years. Methods Retrospective cohort study of adults admitted to Australian ICUs between 2018 and 2020. Men and women with a primary diagnosis of sepsis were included. The primary outcome of time to death for up to 3-years was examined using Kaplan Meier plots. Secondary outcomes included the duration of ICU and hospital stay. Results Of 523,576 admissions, there were 63,039 (12·0%) sepsis-related ICU admissions. Of these, there were 50,956 patients (43·4% women) with 3-year survival data. Men were older (mean age 66·5 vs 63·6 years), more commonly received mechanical ventilation (27·4% vs 24·7%) and renal replacement therapy (8·2% vs 6·8%) and had worse survival (Hazard Ratio [HR] 1·11; 95% Confidence Interval [CI] 1·07 to 1·14, PConclusion Men are more likely to be admitted to ICU with sepsis and have worse survival for up to 3-years. Understanding causal mechanisms of sex differences may facilitate the development of targeted sepsis strategies

Sex differences in long-term survival after intensive care unit treatment for sepsis: A cohort study.

ObjectiveTo determine the effect of sex on sepsis-related ICU admission and survival for up to 3-years.MethodsRetrospective cohort study of adults admitted to Australian ICUs between 2018 and 2020. Men and women with a primary diagnosis of sepsis were included. The primary outcome of time to death for up to 3-years was examined using Kaplan Meier plots. Secondary outcomes included the duration of ICU and hospital stay.ResultsOf 523,576 admissions, there were 63,039 (12·0%) sepsis-related ICU admissions. Of these, there were 50,956 patients (43·4% women) with 3-year survival data. Men were older (mean age 66·5 vs 63·6 years), more commonly received mechanical ventilation (27·4% vs 24·7%) and renal replacement therapy (8·2% vs 6·8%) and had worse survival (Hazard Ratio [HR] 1·11; 95% Confidence Interval [CI] 1·07 to 1·14, PConclusionMen are more likely to be admitted to ICU with sepsis and have worse survival for up to 3-years. Understanding causal mechanisms of sex differences may facilitate the development of targeted sepsis strategies