54 research outputs found

    Pelagic microbial heterotrophy in response to a highly productive bloom of <i>Phaeocystis antarctica</i> in the Amundsen Sea Polynya, Antarctica

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    Abstract Heterotrophic bacteria play a key role in marine carbon cycling, and understanding their activities in polar systems is important for considering climate change impacts there. One goal of the ASPIRE project was to examine the relationship between the phytoplankton bloom and bacterial heterotrophy in the Amundsen Sea Polynya (ASP). Bacterial abundance, production (BP), respiration, growth efficiency, and extracellular enzyme activity (EEA) were compared to nutrient and organic matter inventories, chlorophyll a (Chl a), viral and microzooplankton abundance, and net primary production (NPP). Bacterial production and respiration clearly responded (0.04–4.0 and 10–53 µg C L−1 d−1, respectively) to the buildup of a massive Phaeocystis antarctica bloom (Chl a: 0.2–22 µg L−1), with highest rates observed in the central polynya where Chl a and particulate organic carbon (POC) were greatest. The highest BP rates exceeded those reported for the Ross Sea or any other Antarctic coastal system, yet the BP:NPP ratio (2.1–9.4%) was relatively low. Bacterial respiration was also high, and growth efficiency (2–27%; median = 10%) was similar to oligotrophic systems. Thus, the integrated bacterial carbon demand (0.8–2.8 g C m−2 d−1) was a high fraction (25–128%; median = 43%) of NPP during bloom development. During peak bloom, activity was particle-associated: BP and EEA correlated well with POC, and size fractionation experiments showed that the larger size fraction (> 3 µm) accounted for a majority (∼ 75%) of the BP. The community was psychrophilic, with a 5x reduction in BP when warmed to 20°C. In deeper waters, respiration remained relatively high, likely fueled by the significant downward particle flux in the region. A highly active, particle-associated, heterotrophic microbial community clearly responded to the extraordinary phytoplankton bloom in the ASP, likely limiting biological pump efficiency during the early season

    Is a reduction in the individual vigilance of mothers a key evolutionary driver of group formation in white rhinos?

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    A key benefit and evolutionary driver of group living is reduced predation risk. In white rhinos, groups comprise adult females, their calves and one to six unrelated subadults. Subadults benefit from group living through exposure to novel areas, and protection from territorial males (i.e. ‘buddy system’). In contrast, it is unclear whether mothers benefit from group living. To determine if they benefit, or if there is simply no cost, we recorded the vigilance of white rhino mothers in different-sized groups. We predicted that as group size increased, calves would have lower predation risk and mothers would reduce their vigilance. In contrast, we found that vigilance did not decrease as group size increased. Our findings thus indicate that decreased vigilance is not a benefit that white rhino mothers gain from living in groups. Also, costs of group formation are minimal for mothers as their large body size and ability to feed on a wide range of grasses reduces competition with other group members. As a result, we suggest that the benefits obtained by subadults, coupled with the lack of costs to adult females, are the main drivers of group formation in white rhinos.We thank Ezemvelo KZN Wildlife and the staff of the Hluhluwe-iMfolozi Park for permission to undertake the study. We acknowledge funds made available by the University of Pretoria (P.W.B), and the National Research Foundation (NRF) (A.M.S.). Any opinion, findings and conclusions or recommendations expressed are those of the authors and therefore the NRF does not accept any liability in regard thereto. The experimental procedure was purely observational and noninvasive, and consistent with the University of Pretoria and South African animal ethic protocols. Finally, we thank Graham Kerley and an anonymous reviewer for their valuable comments.http://africanzoology.journals.ac.za/am2013ab201

    A comparison of specialist rehabilitation and care assistant support with specialist rehabilitation alone and usual care for people with Parkinson's living in the community: study protocol for a randomised controlled trial

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    <p>Abstract</p> <p>Background</p> <p>Parkinson's Disease is a degenerative neurological condition that causes movement problems and other distressing symptoms. People with Parkinson's disease gradually lose their independence and strain is placed on family members. A multidisciplinary approach to rehabilitation for people with Parkinson's is recommended but has not been widely researched. Studies are needed that investigate cost-effective community-based service delivery models to reduce disability and dependency and admission to long term care, and improve quality of life.</p> <p>Methods</p> <p>A pragmatic three parallel group randomised controlled trial involving people with Parkinson's Disease and live-in carers (family friends or paid carers), and comparing: management by a specialist multidisciplinary team for six weeks, according to a care plan agreed between the professionals and the patient and carer (Group A); multidisciplinary team management and additional support for four months from a trained care assistant (Group B); usual care, no coordinated team care planning or ongoing support (Group C). Follow up will be for six months to determine the impact and relative cost-effectiveness of the two interventions, compared to usual care. The primary outcomes are disability (patients) and strain (carers). Secondary outcomes include patient mobility, falls, speech, pain, self efficacy, health and social care use; carer general health; patient and carer social functioning, psychological wellbeing, health related quality of life. Semi structured interviews will be undertaken with providers (team members, care assistants), service commissioners, and patients and carers in groups A and B, to gain feedback about the acceptability of the interventions. A cost - effectiveness evaluation is embedded in the trial.</p> <p>Discussion</p> <p>The trial investigates components of recent national policy recommendations for people with long term conditions, and Parkinson's Disease in particular, and will provide guidance to inform local service planning and commissioning.</p> <p>Trial registration</p> <p>ISRCTN: <a href="http://www.controlled-trials.com/ISRCTN44577970">ISRCTN44577970</a></p

    Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

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    Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction

    Genome-Wide Association Study for Coronary Artery Calcification With Follow-Up in Myocardial Infarction

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    Coronary artery calcification (CAC) detected by computed tomography is a non-invasive measure of coronary atherosclerosis, that underlies most cases of myocardial infarction (MI). We aimed to identify common genetic variants associated with CAC and further investigate their associations with MI

    Genetic loci associated with prevalent and incident myocardial infarction and coronary heart disease in the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium

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    No funding sources had a role in the design of the study or the analysis or interpretation of the data. Infrastructure for the CHARGE Consortium is supported in part by the National Heart, Lung and Blood Institute (NHLBI) grant R01HL105756. JH, ACM and PSdeV were supported by NIH NHLBI R01HL141291. PSdV was additionally supported by American Heart Association grant number 18CDA34110116. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the NHLBI; the National Institutes of Health; or the U.S. Department of Health and Human Services. The Age, Gene, Environment, Susceptibility Study (AGES) study has been funded by NIH contracts N01-AG-1-2100 and HHSN271201200022C, the NIA Intramural Research Program, Hjartavernd (the Icelandic Heart Association), and the Althingi (the Icelandic Parliament). The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services (contract numbers HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I and HHSN268201700005I). Funding support for “Building on GWAS for NHLBI-diseases: the U.S. CHARGE consortium” was provided by the NIH through the American Recovery and Reinvestment Act of 2009 (ARRA) (5RC2HL102419). Cardiovascular Health Study (CHS) research was supported by NHLBI contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086; and NHLBI grants U01HL080295, R01HL087652, R01HL105756, R01HL103612, R01HL120393, and U01HL130114 with additional contribution from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided through R01AG023629 from the National Institute on Aging (NIA). A full list of principal CHS investigators and institutions can be found at https://chsnhlbi.org/. The provision of genotyping data was supported in part by the National Center for Advancing Translational Sciences, CTSI grant UL1TR001881, and the National Institute of Diabetes and Digestive and Kidney Disease Diabetes Research Center (DRC) grant DK063491 to the Southern California Diabetes Endocrinology Research Center. The Family Heart Study (FamHS) was supported by the grant R01-HL-117078 from the National Heart, Lung, and Blood Institute, and grant R01-DK-089256 from the National Institute of Diabetes and Digestive and Kidney Diseases. The Framingham Heart Study (FHS) The National Heart, Lung and Blood Institute’s Framingham Heart Study is supported by contract N01-HC-25195. GeneSTAR was supported by grants from the National Institutes of Health/National Heart, Lung and Blood Institute (HL49762, HL59684, HL071025, HL58625, U01 HL72518, HL089474, HL092165, HL099747, K23HL105897, K23HL094747, HL11006, and HL112064), National Institute of Nursing Research (NR0224103, NR008153), National Institute of Neurological Disorders and Stroke (NS062059), and by a grant from the National Center for Research Resources (M01-RR000052) to the Johns Hopkins General Clinical Research Center. Genotyping services were provided through the RS&G Service by the Northwest Genomics Center at the University of Washington, Department of Genome Sciences, under U.S. Federal Government contract number HHSN268201100037C from the National Heart, Lung, and Blood Institute. MESA and the MESA SHARe projects are conducted and supported by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with MESA investigators. Support for MESA is provided by contracts 75N92020D00001, HHSN268201500003I, N01-HC-95159, 75N92020D00005, N01-HC-95160, 75N92020D00002, N01-HC-95161, 75N92020D00003, N01-HC-95162, 75N92020D00006, N01-HC-95163, 75N92020D00004, N01-HC-95164, 75N92020D00007, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, UL1-TR-000040, UL1-TR-001079, UL1-TR-001420. Also supported in part by the National Center for Advancing Translational Sciences, CTSI grant UL1TR001881, and the National Institute of Diabetes and Digestive and Kidney Disease Diabetes Research Center (DRC) grant DK063491 to the Southern California Diabetes Endocrinology Research Center. For the Rotterdam Study, the work was supported by the Erasmus Medical Center and Erasmus University, Rotterdam; The Netherlands Organisation for the Health Research and Development (ZonMw); the Research Institute for Diseases in the Elderly (014-93-015, RIDE2); the Ministry of Education, Culture and Science; the Ministry for Health, Welfare and Sports; the European Commission (DG XII); the Municipality of Rotterdam; The Netherlands Organisation of Scientific Research (NWO) (175.010.2005.011, 911-03-012); the Netherlands Genomics Initiative (NGI) (NWO 050-060-810), the Netherlands Organisation for Scientific Research (NWO) (veni 916.12.154). SHIP is supported by the German Federal Ministry of Education and Research (Bundesministerium für Bildung und Forschung (BMBF); grants 01ZZ9603, 01ZZ0103, and 01ZZ0403) and the German Research Foundation (Deutsche Forschungsgemeinschaft (DFG); grant GR 1912/5-1). The Study of Health in Pomerania (SHIP) and SHIP-TREND are part of the Community Medicine Research net (CMR) of the Ernst-Moritz-Arndt University Greifswald (EMAU) which is funded by the BMBF as well as the Ministry for Education, Science and Culture and the Ministry of Labor, Equal Opportunities, and Social Affairs of the Federal State of Mecklenburg-West Pomerania. The CMR encompasses several research projects that share data from SHIP. The EMAU is a member of the Center of Knowledge Interchange (CKI) program of the Siemens AG. SNP typing of SHIP and SHIP-TREND using the Illumina Infinium HumanExome BeadChip (version v1.0) was supported by the BMBF (grant 03Z1CN22). The Women’s Genome Health Study (WGHS) is supported by the National Heart, Lung, and Blood Institute (HL043851, HL080467, HL099355) and the National Cancer Institute (CA047988 and UM1CA182913), with collaborative scientific support and funding for genotyping provided by Amgen. There was no additional external funding received for this study. Publisher Copyright: Copyright: This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.Background Genome-wide association studies have identified multiple genomic loci associated with coronary artery disease, but most are common variants in non-coding regions that provide limited information on causal genes and etiology of the disease. To overcome the limited scope that common variants provide, we focused our investigation on low-frequency and rare sequence variations primarily residing in coding regions of the genome. Methods and results Using samples of individuals of European ancestry from ten cohorts within the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, both cross-sectional and prospective analyses were conducted to examine associations between genetic variants and myocardial infarction (MI), coronary heart disease (CHD), and all-cause mortality following these events. For prevalent events, a total of 27,349 participants of European ancestry, including 1831 prevalent MI cases and 2518 prevalent CHD cases were used. For incident cases, a total of 55,736 participants of European ancestry were included (3,031 incident MI cases and 5,425 incident CHD cases). There were 1,860 all-cause deaths among the 3,751 MI and CHD cases from six cohorts that contributed to the analysis of all-cause mortality. Single variant and gene-based analyses were performed separately in each cohort and then meta-analyzed for each outcome. A low-frequency intronic variant (rs988583) in PLCL1 was significantly associated with prevalent MI (OR = 1.80, 95% confidence interval: 1.43, 2.27; P = 7.12 × 10−7). We conducted gene-based burden tests for genes with a cumulative minor allele count (cMAC) > 5 and variants with minor allele frequency (MAF) < 5%. TMPRSS5 and LDLRAD1 were significantly associated with prevalent MI and CHD, respectively, and RC3H2 and ANGPTL4 were significantly associated with incident MI and CHD, respectively. No loci were significantly associated with all-cause mortality following a MI or CHD event. Conclusion This study identified one known locus (ANGPTL4) and four new loci (PLCL1, RC3H2, TMPRSS5, and LDLRAD1) associated with cardiovascular disease risk that warrant further investigation.Peer reviewe

    Is a reduction in the individual vigilance of mothers a key evolutionary driver of group formation in white rhinos?

    No full text
    A key benefit and evolutionary driver of group living is reduced predation risk. In white rhinos, groups comprise adult females, their calves and one to six unrelated subadults. Subadults benefit from group living through exposure to novel areas, and protection from territorial males (i.e. ‘buddy system’). In contrast, it is unclear whether mothers benefit from group living. To determine if they benefit, or if there is simply no cost, we recorded the vigilance of white rhino mothers in different-sized groups. We predicted that as group size increased, calves would have lower  predation risk and mothers would reduce their vigilance. In contrast, we found that vigilance did not decrease as group size increased. Our findings thus indicate that decreased vigilance is not a benefit that white rhino mothers gain from living in groups. Also, costs of group formation are minimal for mothers as their large body size and ability to feed on a wide range of grasses reduces competition with other group members. As a result, we suggest that the benefits obtained by subadults, coupled with the lack of costs to adult females, are the main drivers of group formation in white rhinos.Keywords: buddy system, Ceratotherium simum, group formation, vigilance, white rhinoceros

    Is a reduction in the individual vigilance of mothers a key evolutionary driver of group formation in white rhinos?

    No full text
    A key benefit and evolutionary driver of group living is reduced predation risk. In white rhinos, groups comprise adult females, their calves and one to six unrelated subadults. Subadults benefit from group living through exposure to novel areas, and protection from territorial males (i.e. 'buddy system'). In contrast, it is unclear whether mothers benefit from group living. To determine if they benefit, or if there is simply no cost, we recorded the vigilance of white rhino mothers in different-sized groups. We predicted that as group size increased, calves would have lower predation risk and mothers would reduce their vigilance. In contrast, we found that vigilance did not decrease as group size increased. Our findings thus indicate that decreased vigilance is not a benefit that white rhino mothers gain from living in groups. Also, costs of group formation are minimal for mothers as their large body size and ability to feed on a wide range of grasses reduces competition with other group members. As a result, we suggest that the benefits obtained by subadults, coupled with the lack of costs to adult females, are the main drivers of group formation in white rhinos
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