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  • 1
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2023-02-02
    Description: The global coronavirus pandemic has highlighted the paramount importance of immune health and the nutrient status of peoples worldwide. Vitamins C and D have important roles in both the innate and adaptive immune systems and are known to support healthy immune function. Both vitamins C and D have gene regulatory roles with the ability to up- and down-regulate thousands of genes, thus playing pleotropic roles in human health and disease. People from low- and middle-income countries tend to have inadequate micronutrient intakes and status, as do specific subgroups from high-income countries. This can affect their resistance to both communicable and non-communicable diseases and the severity of these diseases. In this Special Issue, we have compiled review articles and research papers (both observational and interventional studies) that explore the role of vitamins C and D in numerous aspects of global and population health.
    Keywords: immune system ; viral infection ; influenza ; COVID-19 ; micronutrients ; vitamins ; omega-3 fatty acids ; minerals ; vitamin C ; vitamin D ; vitamin C status ; vitamin C deficiency ; global health ; dietary intake ; obesity ; smoking ; communicable disease ; infection ; noncommunicable disease ; hypovitaminosis C ; low and middle income ; LMIC ; supplement ; non-communicable disease ; Vitamin C status ; energy ; well-being ; kiwifruit ; mood ; SARS-CoV-2 ; coronavirus ; ascorbate ; colds ; pneumonia ; sepsis ; immunonutrition ; supplementation ; dietary surveys ; trends ; descriptive studies ; United States ; fruit juice ; fruit ; vegetables ; psychology ; mental health ; nutrition ; healthy adults ; ethnicity ; Māori ; Pasifika ; Pacific ; Asian ; ascorbic acid ; post-viral fatigue ; lack of concentration ; sleep disturbances ; depression ; frailty ; elderly ; hospitalisation ; serum 25-hydroxyvitamin D ; first-generation immigrants ; melanin ; long COVID ; immunisation ; immune support ; body weight ; vitamin C intake ; plasma ascorbate concentrations ; vitamin C requirements ; dietary vitamin C ; hyperglycaemia ; South Africa ; vitamin D receptor ; vitamin D-binding protein ; n/a ; bic Book Industry Communication::G Reference, information & interdisciplinary subjects::GP Research & information: general ; bic Book Industry Communication::P Mathematics & science::PS Biology, life sciences ; bic Book Industry Communication::J Society & social sciences::JF Society & culture: general::JFC Cultural studies::JFCV Food & society
    Language: English
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  • 2
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2023-01-05
    Description: The purpose of the Special Issue was to collect the results of research and experience on the consequences of the COVID-19 pandemic for the energy sector and the energy market, broadly understood, that were visible after a year. In particular, the impact of COVID-19 on the energy sector in the EU, including Poland, and the US was examined. The topics concerned various issues, e.g., the situation of energy companies, including those listed on the stock exchange, mining companies, and those dealing with renewable energy. The topics related to the development of electromobility, managerial competences, energy expenditure of local government units, sustainable development of energy, and energy poverty during a pandemic were also discussed.
    Keywords: energy manager ; competences ; labor market ; energy industry ; COVID-19 ; decarbonizing transport ; energy efficiency ; electrify transport ; zero-emissions vehicles ; sustainable transport ; electric car charging points ; novel coronavirus pandemic ; alternative energy ; stock market sectors ; stock market companies ; energy ; energy company ; efficiency ; financial analysis ; pandemic ; environmental protection ; environmental problems ; greenhouse gas ; particulate matter (PM) ; renewable energy ; corruption ; electromobility ; companies in the Transport-Shipping-Logistics Sector ; pandemic-COVID-19 ; development ; self-government units ; energy consumption ; monitoring ; energy consumption effectiveness ; sustainable energy development ; households ; OPEC ; crude price ; volatility ; storage crisis ; futures ; shale ; electric vehicles market and policy ; electric vehicles ; purchase intention ; e-mobility ; consumers preferences ; consumer decision making ; social values ; delay discounting ; cultural factors ; economic factors ; machine learning methods ; sustainability ; energy poverty ; economic uncertainty ; energy policy ; policy measures ; reducing energy intensity ; ranking of countries’ energy intensity ; multi-criteria analysis ; sectors of the economy ; economic effects of the pandemic ; social effects of the pandemic ; countries of Western Europe ; countries of Central and Eastern Europe ; mining sector ; initiatives and adaptation measures ; economic situation ; COVID-19 pandemic ; fossil fuel energy ; carbon dioxide emissions ; nonlinear autoregressive distributed lag model ; frequency domain causality test ; Markow switching regression ; photovoltaics ; pandemics ; changes in energetic balance due to COVID-19 ; renewable sources of energy during pandemics ; United States ; energy sector ; fossil fuel ; emissions ; expenditures ; bic Book Industry Communication::G Reference, information & interdisciplinary subjects::GP Research & information: general ; bic Book Industry Communication::P Mathematics & science::PH Physics
    Language: English
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  • 3
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2024-03-27
    Description: “Advances in Transboundary Aquifer Assessment” features studies of transboundary aquifers, particularly at the border shared by Mexico and the United States, a semi-arid to arid region experiencing significant population growth and changing climate conditions. Aquifer assessment in a transboundary setting requires the cooperation of multiple jurisdictions, sometimes with different languages and cultures. The papers in this Special Issue represent a broad array of investigations of complex physical aquifer systems and related institutional settings, including identification and prioritization of needs and strategies for sustainable groundwater development and use; characterization of the physical framework of the aquifer, stressors on the aquifer system, and how those stressors influence the availability of groundwater in terms of its quantity and quality; and the incorporation of stakeholder input and prioritization directly into the process of aquifer assessment and model building.
    Keywords: transboundary aquifers ; United States ; Mexico ; assessment ; agreements ; groundwater management ; self-potential ; temperature ; conductivity ; surface water ; groundwater ; groundwater and surface water interactions ; rivers ; resistivity ; streamflow ; Santa Cruz River ; climate change ; water resources ; transboundary aquifer ; transboundary aquifer assessment ; Arizona ; Sonora ; groundwater storage ; groundwater use ; multilevel governance ; agreement ; transboundary basins ; retrospective analysis ; Canada ; groundwater depletion ; binational resource management ; serious games ; stakeholder cooperation ; transboundary waters ; US–Mexico ; water governance ; science production ; bidirectionality ; human and natural systems ; system dynamics modeling ; transboundary ; aquifers ; border ; Hueco Bolson ; MODFLOW ; Rio Grande ; Transboundary Aquifer Assessment Program ; collaboration ; trust ; power ; risk ; U.S./Mexico border ; ethnography ; salinization ; geothermal ; international water supplies ; water quality ; upflow ; vertical groundwater flow ; heat transport ; thermal modeling ; conceptual model ; hydrogeology ; geochemistry ; Santa Cruz River Aquifer ; water balance model ; climate uncertainty ; isotopes ; transboundary aquifers assessment ; Mesilla Basin ; Conejos-Médanos/Mesilla aquifer ; hydrogeomorphology ; recharge ; discharge ; aquifer assessment ; stakeholder involvement ; United States–Mexico border ; United States–Canada border ; thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general
    Language: English
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  • 4
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2023-04-05
    Description: Dietary patterns are evolving, and we are increasingly aware of the contribution of food and food systems to community and planetary health. To be responsive to these changes and to promote dietary patterns that enhance the health and wellbeing of populations and protect against climate change, nutrition professionals and researchers need to monitor evolving dietary patterns and trial comprehensive, multiaction solutions. Countries are pushing back on corporate and climate change disruptions to food systems and are looking for ways to strengthen community involvement in food systems, so that healthy and environmentally friendly food choices are easier to make. To achieve this, policymakers need access to the latest evidence on evolving dietary patterns and on effective solutions, and this Special Issue on Progress in Community Nutrition: Dietary Patterns and Planetary Health provides some of this evidence.
    Keywords: dietary guidelines ; dietary patterns ; evidence synthesis ; evidence translation ; qualitative research ; vegetable ; variety ; habitual ; dietary records ; capture proportion ; waste pickers ; nutritional status ; dietary intake ; dietary diversity ; South Africa ; red/processed meat dishes ; plant-based foods ; long-grain white rice ; nutrients to limit ; Canadian population ; plant-based diet ; planetary health ; human health ; sustainability ; chronic disease prevention ; food security ; culture ; food sovereignty ; monitoring ; Pacific Islands ; Māori ; Melanesian ; Micronesian ; Polynesian ; diet ; influencing factors ; Chinese ; immigrants ; review ; Canada ; United States ; food-based dietary guidelines ; messages ; images ; pre-testing ; Tanzania ; nutrition education ; schoolchildren ; fruit and vegetables ; community nutrition ; nutrition interventions ; health promotion ; validation ; short dietary questionnaire ; food groups ; dietary practices ; children ; Vietnam ; n/a ; bic Book Industry Communication::G Reference, information & interdisciplinary subjects::GP Research & information: general ; bic Book Industry Communication::P Mathematics & science::PS Biology, life sciences ; bic Book Industry Communication::J Society & social sciences::JF Society & culture: general::JFC Cultural studies::JFCV Food & society
    Language: English
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  • 5
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2022-11-17
    Description: Rarely has scientific research been as solicited as societies struggle to cope with the coronavirus. The questions raised by COVID-19 are germane to the medical and the social sciences. From an international relations perspective, COVID-19 gets to the heart of what comprises the global commons. From a public policy perspective, COVID-19 is the wicked policy problem par excellence, requiring inter-agency collaboration. From a comparative politics perspective, COVID-19 provides a vast living dataset to engage in multi-level comparisons and real-time experiments. In the medical research field, the pandemic has provided advancements in medical science that would not have been possible without access to a living laboratory. The reprint addresses the transnational and transdisciplinary challenges posed by the COVID-19 pandemic. Responding to existential dilemmas, the COVID-19 pandemic calls for a major transdisciplinary research effort that necessarily combines several levels of empirical analysis and methodological tools and bridges distinct academic and scientific traditions. The main sections of the reprint provide specific insights from medical and social sciences, health and well-being, politics and society and international relations. Though the chapters are framed in terms of distinct disciplinary perspectives and traditions, the overarching spirit of the book to open up received wisdoms and paradigms to challenges from scholars working in different academic disciplines and traditions.
    Keywords: COVID-19 ; coronavirus disease ; physiological effects ; psychological effects ; psychophysiological effects ; exercise ; physical activity ; n/a ; preventive behaviors ; physical activity (PA) ; fruit and vegetable consumption (FVC) ; depression ; loneliness ; older adults ; China ; behavioral response ; mental response ; pandemic ; social welfare ; trust ; transparency ; adult social care ; UK ; political trust ; social trust ; transnational ; transdisciplinary ; United States ; European Union ; Xi Jinping ; Donald Trump ; Joe Biden ; critical juncture ; (dis)trust ; health diplomacy ; facemasks ; racism ; bic Book Industry Communication::M Medicine::MB Medicine: general issues::MBN Public health & preventive medicine
    Language: English
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  • 6
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2024-04-01
    Description: This book investigates the impact of the United Nations General Assembly’s 2010 resolution that elevated rights to water and sanitation are stand-alone international human rights. A major goal of creating this new human right was to incentivize governments to prioritize and pursue policies to improve access to affordable, potable water to the more than 750 million people worldwide who lacked access, as well as to provide the more than 2.5 billion people with inadequate sanitation. The book’s chapters use a variety of methodological approaches including qualitative case studies and quantitative studies that draw on data from around the world. The chapters reveal how the global human right to water and sanitation was created, how it has been used in rights struggles around the world, and the extent to which it has improved access to water and sanitation for the world’s most marginalized people.
    Keywords: Cape Town Day Zero ; water rights ; water scarcity ; water-justice ; water-governance ; inequality ; South Africa ; right to water ; courts ; vulnerable groups ; UN resolutions ; water ; sanitation ; human rights ; human right to water and sanitation ; HRtWS ; natural language processing ; machine learning ; text analysis ; constitutional reform ; legal opportunity structure ; water legal framework ; socioeconomic rights ; Brazil ; Peru ; Colombia ; social movements ; political cost ; advocacy ; activism ; social movement ; socio-economic rights ; United States ; political opportunity ; coalition-building ; collective action ; human rights from below ; human rights to water and sanitation ; water access ; constitutionalisation ; norm diffusion ; opportunity structures ; impact and efficacy of human rights ; human right to water ; drinking water ; irrigation ; marginalised groups ; indigenous communities ; social and economic rights ; human rights critiques ; right to life ; right to environment ; global rights ; evolution of rights ; construction of rights ; Latin America ; South Asia ; Europe ; Africa ; USA ; thema EDItEUR::N History and Archaeology::NH History ; thema EDItEUR::J Society and Social Sciences::JB Society and culture: general::JBF Social and ethical issues
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  • 7
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2024-04-02
    Description: This volume enquires about how racialization shapes European societies and the lives of people affected by it in myriad ways. It provides a powerful collection of new publications by scholars who, through their research, contribute to placing race and racialization studies at the forefront of European academia.
    Keywords: European Muslims ; inequalities ; gender ; youth of migrant origin ; knowledge production ; anti-racism ; intersectionality ; EU anti-racism action plan 2020–2025 ; activism ; border externalization ; West Africa ; migration ; illegalization ; politics of belonging ; narratives ; black youth ; gender ideologies ; Spain ; racialization ; aporophobia ; class ; discrimination ; immigration ; Roma ; Ciganos/Roma ; racism ; social inequalities ; COVID-19 pandemic ; Portugal ; integration ; race ; Europe ; United States ; Charnegroes ; Black Africans ; Catalonia ; national identity ; Africanness ; antigypsyism ; hate speech ; racial discrimination ; symbolic violence ; EU Roma framework ; Spanish politics ; colorblindness ; diversity ; multiracial ; interculturalism ; diversity management ; post-racial ; whiteness ; colorblind ; European colonialism ; thema EDItEUR::N History and Archaeology::NH History ; thema EDItEUR::J Society and Social Sciences::JB Society and culture: general::JBF Social and ethical issues ; thema EDItEUR::J Society and Social Sciences::JH Sociology and anthropology::JHM Anthropology::JHMC Social and cultural anthropology
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  • 8
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2024-04-02
    Description: Sustainability is an urgent developmental task for our society and is attracting increasing attention. Therefore, higher education institutions (HEIs) are also called upon to deal theoretically, conceptually, methodically, critically, and reflectively with the associated challenges and the processes and conditions of transformation in order to contribute to sustainable development. How can complex organisations such as HEIs succeed in initiating and maintaining the process of sustainable development within their own institutions and make it a permanent responsibility? How can as many protagonists as possible be persuaded to get involved in sustainable development? This book deals with the promotion of sustainable university development and provides an overview of how universities can be organised sustainably and how sustainable development can be implemented in their various functional areas. In the sense of a “whole-institution approach”, which encompasses entire HEIs, the focus is not only on the core areas of teaching (higher education for sustainable development) and research (sustainability in research) but, also, on the operational management of HEIs. In addition, this book focuses on sustainability governance and transfer for sustainable development at HEIs as cross-disciplinary issues.
    Keywords: higher education institutions ; implementation ; organisational factors ; sustainable development ; interpretative structural modelling (ISM) ; higher education institutions (HEIs) ; cross-sector collaboration ; multi-professional collaboration ; transdisciplinary research ; narrative analysis ; sensemaking ; whole institution approach ; organizational networks ; constant comparative analysis ; athletic departments ; higher education ; sustainability ; loose coupling ; shared governance ; United States ; intellectual capital ; performance ; quality of life ; sustainability assessment ; environmental management performance ; German-speaking countries ; survey ; whole-institution approach ; competencies ; knowledge ; values ; case study ; discourse analysis ; environment ; Global South ; Sustainable Development Goals ; universities’ transformation ; sustainability assessment tool ; sustainability governance ; systems theory ; governance equalizer ; politics ; profession ; organization ; public ; organizational culture ; Germany ; sustainability in science ; transformative science ; grammar of responsibility ; ethics of knowledge ; universities as echo chambers of society ; catalytic science ; universities ; organizational change ; higher education for sustainable development (HESD) ; sustainability transitions ; SD ; alliances ; university ; transfer ; practitioner–university partnership ; societal impact ; education for sustainable development ; higher education development ; sustainable university development ; systemic development ; inter-organizational networks ; worldviews ; societal transformation ; systemic transformation ; thema EDItEUR::N History and Archaeology::NH History ; thema EDItEUR::J Society and Social Sciences::JN Education
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  • 9
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2024-04-09
    Description: What are the causes and consequences of species diversity in forested ecosystems, and how is this species diversity being affected by rapid environmental and climatic change, movement of invertebrate and vertebrate herbivores into new biogeographic regions, and expanding human populations and associated shifts in land-use patterns? In this book, we explore these questions for assemblages of forest trees, shrubs, and understory herbs at spatial scales ranging from small plots to large forest dynamics plots, at temporal scales ranging from seasons to centuries, in both temperate and tropical regions, and across rural-to-urban gradients in land use.
    Keywords: G1-922 ; Q1-390 ; gamma diversity ; tree species ; Climatic change ; individual species-area relationship ; woody species ; TILD ; trees ; Pseudotsuga menziesii ; windthrow ; precipitation ; species conservation ; spatial analysis ; codispersion analysis ; variation partitioning ; herbaceous perennial species ; northern hardwood forests ; climate change ; stand development ; potential habitats ; Smithsonian ForestGEO ; tree regeneration ; forest conversion ; Biodiversity Exploratories ; trunk breakage ; topography ; questionnaire survey ; mid-domain effect ; assemblage lineage diversity ; Salicaceae ; salvaging ; temperate forests ; Shannon diversity ; USDA Forest Service ; tree species diversity ; Bray-Curtis ; species-area relationship ; Ericaceae ; legacies ; Picea abies ; herbaceous layer ; spatial patterns ; mountains ; United States ; wind damage ; abundance ; Hubbard Brook ; elevational shifts ; uprooting ; species diversity ; evolutionary diversity ; Pinus sylvestris ; natural disturbance-based silviculture ; Vietnam ; diversity ; Maxent ; human footprint ; productivity ; China ; microarthropod ; phylogenetic diversity ; temperature ; household respondents ; succession ; biodiversity ; tornado ; salvage logging ; excess nitrogen ; climate ; forest management ; understory plant communities ; Simpson diversity ; species richness ; landscape scale ; structural complexity ; tropical evergreen mixed forest ; seasonal variations ; disturbance severity ; competition and facilitation ; canopy structure ; Fagus sylvatica ; thema EDItEUR::R Earth Sciences, Geography, Environment, Planning::RG Geography
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  • 10
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2023-12-20
    Description: Mike Mosher’s “Some Aspects of Californian Cyberpunk” vividly reminds us of the influence of West Coast counterculture on cyberpunks, with special emphasis on 1960s theoretical gurus such as Timothy Leary and Marshall McLuhan, who explored the frontiers of inner space as well as the global village. Frenchy Lunning’s “Cyberpunk Redux: Dérives in the Rich Sight of Post-Anthropocentric Visuality” examines how the heritage of Ridley Scott’s techno-noir film
    Keywords: PN1993-1999 ; NX1-820 ; n/a ; virtual reality ; Tobi Hirotaka ; collage ; cyberpunk ; co-productions ; virtual worlds ; European cinema ; reception history ; Metropia ; transnational cinema ; layers ; manga ; cinematism ; Lo Tek ; audience ; 2000s ; techno-Orientalism ; outlaw technologist ; YLEM artists using science and technology ; animation ; Masaki Gor? ; “rich sight” ; Germany ; extraterritorial ; proscenium views ; care ; Japanese science fiction ; United States ; post-utopia ; comics ; flattened screens ; William Gibson ; science fiction ; animatism ; post-apocalyptic narrative ; genre ; SCAN ; HyperCard ; bOING bOING ; nostalgia ; global capitalism ; virtual idol ; MONDO 2000 ; Timothy Leary ; Walter Benjamin ; visuality ; fractal space ; Marshall McLuhan ; Renaissance ; Hyperart Thomasson ; Pattern Recognition ; dystopia ; Kowloon Walled City ; participatory aesthetics ; Guerrilla Games ; translation ; intertextuality ; nuclear politics ; end of history ; Horizon: Zero Dawn ; detritus ; Blade Runner ; bic Book Industry Communication::A The arts::AP Film, TV & radio::APF Films, cinema
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  • 11
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2024-04-08
    Description: The articles in this volume present a variety of theoretical and historical cases to enlarge our understanding of religious conflict and coexistence. Seven out of the ten articles discuss cases of major religions in Korea, including Shamanism, Buddhism, Taoism, Confucianism, and Christianity. They explore the particularity of Korean religions in seeking theological and philosophical inclusiveness, playing a positive role in society and building stable interreligious relations. The other three articles cover non-Korean themes including religious conflict of interfaith families, a biblical analysis of particularism and universalism and a new interpretation of Paul’s letter to the Romans. All of these articles are aimed at identifying major causes of religious conflict and finding some effective solutions drawn from various theoretical and practical domains.
    Keywords: early Korean Catholicism ; Confucianism ; women and Catholicism ; Catholic saints ; particularism ; universalism ; intolerance ; purity ; Leviticus ; colonialism ; anti-Semitism ; Korean Buddhism ; Jinul ; sudden enlightenment ; gradual cultivation ; Korean Seon ; Zen ; potentiality and actuality ; Aristotelian metaphysics ; religious conflicts ; coexistence of religions ; Korean religions ; Jeju Island ; Buddhism ; syncretism ; harmonization (hoetong) ; Unified Silla (668–935) ; Goryeo (918–1392) ; New Testament ; the letter to Romans ; Paul ; sect ; cult ; anti-Jewish discourses ; Jews and gentiles ; unity ; second temple Judaism ; Roman empire ; Suun Choe Je-u ; Joseon dynasty ; Donghak ; religious pluralism ; mysticism ; ethics ; perennial philosophy ; enlightenment ; morality books ; spirit-writing ; Kwanwang shrines ; Thearch Kwan (Kwanje/Guandi) ; Three Sages ; Late Chosŏn ; Korea Christian Action Organization for Urban Industrial Mission (Saseon) ; Korean Protestantism ; Korean Catholicism ; social justice ; solidarity ; interfaith families ; public ; Christian ; Jewish ; gender ; United States ; n/a ; bic Book Industry Communication::H Humanities::HR Religion & beliefs ; thema EDItEUR::Q Philosophy and Religion::QR Religion and beliefs
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  • 12
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2024-03-27
    Description: Next year (2018), we will be celebrating the 15th anniversary of the International Journal of Environmental Research and Public Health—IJERPH (ISSN 1660-4601). Hence, we are currently organizing a Special Issue to commemorate this important milestone. Founded in 2004, IJERPH has experienced a tremendous growth in terms of the number and quality of scientific publications. With a 2016 impact factor of 2.101, IJERPH now ranks among the top international journals in the emerging field of environmental research and public health. As described on our website (https://www.mdpi.com/journal/ijerph), IJERPH is a peer-reviewed journal that focuses on the publication of scientific and technical information on the impacts of natural phenomena and anthropogenic factors on the quality of our environment, the interrelationships between environmental health and the quality of life, as well as the socio-cultural, political, economic, and legal considerations related to environmental stewardship and public health. Its primary areas of research interests include: Gene-environment interactions Environmental genomics and proteomics Environmental toxicology, mutagenesis and carcinogenesis Environmental epidemiology and disease control Health risk assessment and management Ecotoxicology, and ecological risk assessment and management Natural resources damage assessment Environmental chemistry and computational modeling Environmental policy and management Environmental engineering and biotechnology Emerging issues in environmental health and diseases Environmental education and public health To help celebrate the 15th anniversary, you are kindly invited to submit original articles, critical reviews, research notes, and short communications on any of the above-listed topics. Please also encourage any of our colleagues who may be interested to submit manuscripts. We expect that this issue will attract considerable attention, as we prepare to celebrate the excellent scientific contributions and socio-economic impacts of IJERPH over the past 15 years.
    Keywords: transportation noise ; MTNR1B gene ; rs10830963 ; diabetes ; glycosylated hemoglobin ; circadian sleep-wake cycle ; gene-environment interactions ; adults ; cohort study ; metal mobility ; soil flushing ; soil reclamation ; agricultural soil ; EDDS deficiency ; child sexual abuse ; adolescents ; girls ; boys ; gender differences ; legal proceedings ; child-friendly justice ; prevention ; cervical Arabin pessary ; cerclage ; second trimester of pregnancy ; sepiolite ; adsorption ; potentially toxic elements ; modification ; regeneration ; Xiangjiang River ; air pollution ; neighborhood deprivation index ; preterm birth ; spatial approach ; participatory research ; second hand smoking ; communication media ; vulnerable populations ; migrants ; health care research ; quality assurance ; hospital management ; health inequities ; environmental vulnerability ; multi-criteria spatial analysis ; risk management tool ; hazardous substance ; road accidents ; online hate ; hate speech ; bystander ; perpetrator ; online disinhibition ; online discrimination ; cyber aggression ; Bothrops lanceolatus ; envenomation ; snakebite ; bacteria ; infection ; antibiotic susceptibility ; ADL ; disability ; health ; home ; usability ; parenting desire ; lesbian ; gay ; minority stress ; mediation ; demographic factor ; EQ-5D ; health-related quality of life ; depression ; family planning ; Bayesian ; spatial ; RDHS ; Rwanda ; suicide ; premature mortality ; young men ; Greenland ; Denmark ; head injury ; incidence ; national health insurance ; population-based study ; mortality ; traumatic brain injury ; polycystic ovary syndrome ; self-efficacy ; optimism ; acceptance of illness ; September 11 terrorist attacks ; pilot aircraft-assisted suicide ; copycat effect ; obesity ; endoscopy ; Helicobacter pylori ; BMI ; Saudi patients ; urban lake ; comprehensive nutrition status Index ; heavy metals ; health risk ; fuzzy comprehensive method ; physical fitness ; Mediterranean diet ; body composition ; dementia ; health services ; resource utilization ; dementia care ; informal care ; formal care ; cognitive disorder ; physical activity in pregnancy ; PPAQ ; quality of life ; WHOQoL-Bref ; pregnant women ; food availability ; eating away from home ; household food spending ; trace elements ; concentration ; microwave digester ; Wuhan ; soil contamination ; ecological risk ; tuberculosis ; screening for tuberculosis ; public health ; immigrants ; health impact assessments ; premature death ; equity impact ; health impact ; reduction of air pollution ; environmental inequalities ; spatial analysis ; small area ; AirQ ; traffic congestion ; activity-travel patterns ; real-time traffic data ; the uncertain geographic context problem (UGCoP) ; the neighborhood effect averaging problem (NEAP) ; evaluation ; method ; policy ; strategy ; social ; trend ; winter tourism ; climate change ; snow abundance index ; meteorological suitability index ; copula function ; spatial suitability assessment ; oral surgery ; oral medicine ; leucoplakia ; hyperkeratosis ; laser ; electronic waste ; informal recycling ; PBDEs ; soil ; dust ; Nigeria ; aerobic capacity ; attrition ; change-of-direction speed ; deputy sheriff ; graduation ; high-intensity running ; police ; strength endurance ; tactical ; roadside exposure ; inflammation biomarker ; Nepal ; PM2.5 ; oily sludge ; incineration ; kinetic ; modeling ; differential/integral method ; engineering ; curriculum proposals ; arbuscular mycorrhizal fungi ; global change ; grassland ecosystem ; stoichiometry ; phosphorus limitation ; unsafe behavior ; targeted intervention ; coal miners ; safety management ; bioaerosols ; influenza virus ; ferret animal model ; aerosol chamber ; dengue fever ; Aedes albopictus ; living environment ; logistic regression analysis ; China ; human capital ; multilevel linear regression ; self-rated mental health ; social capital ; groundwater ; iron and manganese removal ; biofilter ; food contamination ; gastrointestinal diseases ; morbidity ; deep neural networks ; evolutionary learning ; health literacy ; adolescent health ; Mexico ; health disparities ; motivation ; videogaming ; psychopathology ; adverse childhood experiences (ACEs) ; Hungarian representative adult sample ; opinion poll ; ACE Score Calculator ; influenza vaccination ; pneumonia ; population-based case-control study ; adolescent ; risk factors ; psychosocial ; socio-environmental ; behavior ; United States ; Latinos ; physical education ; social and emotional learning ; sport education model ; subjective well-being ; trait emotional intelligence ; social anxiety ; thema EDItEUR::G Reference, Information and Interdisciplinary subjects::GP Research and information: general
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  • 13
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    MDPI - Multidisciplinary Digital Publishing Institute
    Publication Date: 2024-04-14
    Description: This book is a collection of papers for the Special Issue “Quantitative Methods for Economics and Finance” of the journal Mathematics. This Special Issue reflects on the latest developments in different fields of economics and finance where mathematics plays a significant role. The book gathers 19 papers on topics such as volatility clusters and volatility dynamic, forecasting, stocks, indexes, cryptocurrencies and commodities, trade agreements, the relationship between volume and price, trading strategies, efficiency, regression, utility models, fraud prediction, or intertemporal choice.
    Keywords: academic cheating ; tax evasion ; informality ; pairs trading ; hurst exponent ; financial markets ; long memory ; co-movement ; cointegration ; risk ; delay ; decision-making process ; probability ; discount ; detection ; mean square error ; multicollinearity ; raise regression ; variance inflation factor ; derivation ; intertemporal choice ; decreasing impatience ; elasticity ; GARCH ; EGARCH ; VaR ; historical simulation approach ; peaks-over-threshold ; EVT ; student t-copula ; generalized Pareto distribution ; centered model ; noncentered model ; intercept ; essential multicollinearity ; nonessential multicollinearity ; commodity prices ; futures prices ; number of factors ; eigenvalues ; volatility cluster ; Hurst exponent ; FD4 approach ; volatility series ; probability of volatility cluster ; S&amp ; P500 ; Bitcoin ; Ethereum ; Ripple ; bitcoin ; deep learning ; deep recurrent convolutional neural networks ; forecasting ; asset pricing ; financial distress prediction ; unconstrained distributed lag model ; multiple periods ; Chinese listed companies ; cash flow management ; corporate prudential risk ; the financial accelerator ; financial distress ; induced risk aversion ; liquidity constraints ; liquidity risk ; macroeconomic propagation ; multiperiod financial management ; non-linear macroeconomic modelling ; Tobin’s q ; precautionary savings ; pharmaceutical industry ; scale economies ; profitability ; biotechnological firms ; non-parametric efficiency ; productivity ; DEA ; dispersion trading ; option arbitrage ; volatility trading ; correlation risk premium ; econometrics ; computational finance ; ensemble empirical mode decomposition (EEMD) ; autoregressive integrated moving average (ARIMA) ; support vector regression (SVR) ; genetic algorithm (GA) ; energy consumption ; cryptocurrency ; gold ; P 500 ; DCC ; copula ; copulas ; Markov Chain Monte Carlo simulation ; local optima vs. local minima ; SRA approach ; foreign direct investment ; bilateral investment treaties ; regional trade agreements ; structural gravity model ; policy uncertainty ; stock prices ; dynamically simulated autoregressive distributed lag (DYS-ARDL) ; threshold regression ; United States ; thema EDItEUR::W Lifestyle, Hobbies and Leisure::WC Antiques, vintage and collectables::WCF Collecting coins, banknotes, medals and other related items
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  • 14
    Publication Date: 2016-01-20
    Description: Massive open online courses (MOOCs) are often characterized as remedies to educational disparities related to social class. Using data from 68 MOOCs offered by Harvard and MIT between 2012 and 2014, we found that course participants from the United States tended to live in more-affluent and better-educated neighborhoods than the average U.S. resident. Among those who did register for courses, students with greater socioeconomic resources were more likely to earn a certificate. Furthermore, these differences in MOOC access and completion were larger for adolescents and young adults, the traditional ages where people find on-ramps into science, technology, engineering, and mathematics (STEM) coursework and careers. Our findings raise concerns that MOOCs and similar approaches to online learning can exacerbate rather than reduce disparities in educational outcomes related to socioeconomic status.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hansen, John D -- Reich, Justin -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1245-8. doi: 10.1126/science.aab3782. Epub 2015 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harvard Graduate School of Education, Harvard University, Cambridge, MA 02138, USA. john_hansen@mail.harvard.edu. ; Office of Digital Learning, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785488" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Career Choice ; Certification/*methods ; Education, Distance/*methods ; Engineering/education ; Humans ; Internet ; Learning ; Mathematics/education ; *Online Systems ; Science/education ; *Social Class ; Students ; Technology/education ; United States ; Young Adult
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1188-90. doi: 10.1126/science.350.6265.1188.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785475" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/blood/genetics/*physiology ; Animals ; Biological Clocks/genetics/*physiology ; Biomarkers/blood/metabolism ; DNA/genetics ; DNA Methylation ; Epigenesis, Genetic ; Humans ; Mice ; Rats ; Telomere Homeostasis
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  • 16
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheid, Johannes F -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1175. doi: 10.1126/science.aad7133.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital, Boston, MA 02114, USA. The Rockefeller University, New York, NY 10021, USA. fscheid@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785466" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/genetics/immunology/isolation & purification ; Antibodies, Neutralizing/genetics/*immunology/isolation & purification ; B-Lymphocytes/*immunology ; Cell Separation/methods ; HIV Antibodies/genetics/*immunology/isolation & purification ; HIV Infections/*blood ; Humans ; Immunologic Memory ; Mice ; env Gene Products, Human Immunodeficiency Virus/*immunology
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  • 17
    Publication Date: 2016-01-20
    Description: Mitochondrial morphology is shaped by fusion and division of their membranes. Here, we found that adult myocardial function depends on balanced mitochondrial fusion and fission, maintained by processing of the dynamin-like guanosine triphosphatase OPA1 by the mitochondrial peptidases YME1L and OMA1. Cardiac-specific ablation of Yme1l in mice activated OMA1 and accelerated OPA1 proteolysis, which triggered mitochondrial fragmentation and altered cardiac metabolism. This caused dilated cardiomyopathy and heart failure. Cardiac function and mitochondrial morphology were rescued by Oma1 deletion, which prevented OPA1 cleavage. Feeding mice a high-fat diet or ablating Yme1l in skeletal muscle restored cardiac metabolism and preserved heart function without suppressing mitochondrial fragmentation. Thus, unprocessed OPA1 is sufficient to maintain heart function, OMA1 is a critical regulator of cardiomyocyte survival, and mitochondrial morphology and cardiac metabolism are intimately linked.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wai, Timothy -- Garcia-Prieto, Jaime -- Baker, Michael J -- Merkwirth, Carsten -- Benit, Paule -- Rustin, Pierre -- Ruperez, Francisco Javier -- Barbas, Coral -- Ibanez, Borja -- Langer, Thomas -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):aad0116. doi: 10.1126/science.aad0116.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, University of Cologne, 50674 Cologne, Germany. Max-Planck-Institute for Biology of Aging, Cologne, Germany. ; Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain. ; Institute for Genetics, University of Cologne, 50674 Cologne, Germany. ; INSERM UMR 1141, Hopital Robert Debre, Paris, France. Universite Paris 7, Faculte de Medecine Denis Diderot, Paris, France. ; Centre for Metabolomics and Bioanalysis (CEMBIO), Faculty of Pharmacy, Universidad San Pablo CEU, Campus Monteprincipe, Boadilla del Monte, 28668 Madrid, Spain. ; Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain. Department of Cardiology, Instituto de Investigacion Sanitaria (IIS), Fundacion Jimenez Diaz Hospital, Madrid, Spain. thomas.langer@uni-koeln.de bibanez@cnic.es. ; Institute for Genetics, University of Cologne, 50674 Cologne, Germany. Max-Planck-Institute for Biology of Aging, Cologne, Germany. Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany. Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany. thomas.langer@uni-koeln.de bibanez@cnic.es.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785494" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cardiomyopathy, Dilated/genetics/metabolism/pathology ; Diet, High-Fat ; Embryonic Development ; Female ; GTP Phosphohydrolases ; Gene Deletion ; Heart/embryology ; Heart Failure/genetics/*metabolism/pathology ; Male ; Metalloendopeptidases/genetics ; Metalloproteases/genetics/metabolism ; Mice ; Mice, Knockout ; Mitochondria, Heart/*metabolism/ultrastructure ; *Mitochondrial Degradation ; *Mitochondrial Dynamics ; Mitochondrial Proteins/genetics/metabolism ; Muscle, Skeletal/enzymology ; Myocardium/*metabolism/pathology ; Myocytes, Cardiac/enzymology/pathology ; Proteolysis
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: Mitochondria generate adenosine 5'-triphosphate (ATP) and are a source of potentially toxic reactive oxygen species (ROS). It has been suggested that the gradual mitochondrial dysfunction that is observed to accompany aging could in fact be causal to the aging process. Here we review findings that suggest that age-dependent mitochondrial dysfunction is not sufficient to limit life span. Furthermore, mitochondrial ROS are not always deleterious and can even stimulate pro-longevity pathways. Thus, mitochondrial dysfunction plays a complex role in regulating longevity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Ying -- Hekimi, Siegfried -- MOP-114891/Canadian Institutes of Health Research/Canada -- MOP-123295/Canadian Institutes of Health Research/Canada -- MOP-97869/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1204-7. doi: 10.1126/science.aac4357.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. ; Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada. siegfried.hekimi@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785479" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/*metabolism ; Animals ; Caenorhabditis elegans Proteins/genetics ; Electron Transport/genetics ; Electron Transport Complex III/genetics ; Longevity/genetics/*physiology ; Mice ; Mice, Knockout ; Mitochondria/genetics/*metabolism ; Point Mutation ; Reactive Oxygen Species/*metabolism
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  • 19
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akiyama, Hiroko -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1135. doi: 10.1126/science.aad9386.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hiroko Akiyama is a professor at the Institute of Gerontology at the University of Tokyo, 7-3-1 Hongo, Bunkyoku, Tokyo, Japan. akiyama@iog.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785447" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Female ; Humans ; Japan ; *Longevity ; Retirement ; Social Security
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  • 20
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cleary, Allison S -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1174-5. doi: 10.1126/science.aad7103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pennsylvania State University College of Medicine, Hershey PA 17078, USA. acleary@hmc.psu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785463" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics/metabolism/*pathology ; Clone Cells/metabolism/pathology ; Female ; Mammary Neoplasms, Experimental/genetics/metabolism/*pathology ; Mice ; Neoplasms, Basal Cell/genetics/metabolism/pathology ; Wnt1 Protein/genetics/*metabolism ; ras Proteins/genetics/metabolism
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  • 21
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1186-7. doi: 10.1126/science.350.6265.1186.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785474" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/physiology ; Caenorhabditis elegans Proteins/genetics/physiology ; Caloric Restriction ; Death ; Humans ; Hydra/genetics/physiology ; Longevity/genetics/*physiology ; Mice ; Mutation ; Phosphatidylinositol 3-Kinases/genetics/physiology
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  • 22
    Publication Date: 2016-01-20
    Description: In developing hearts, changes in the cardiac metabolic milieu during the perinatal period redirect mitochondrial substrate preference from carbohydrates to fatty acids. Mechanisms responsible for this mitochondrial plasticity are unknown. Here, we found that PINK1-Mfn2-Parkin-mediated mitophagy directs this metabolic transformation in mouse hearts. A mitofusin (Mfn) 2 mutant lacking PINK1 phosphorylation sites necessary for Parkin binding (Mfn2 AA) inhibited mitochondrial Parkin translocation, suppressing mitophagy without impairing mitochondrial fusion. Cardiac Parkin deletion or expression of Mfn2 AA from birth, but not after weaning, prevented postnatal mitochondrial maturation essential to survival. Five-week-old Mfn2 AA hearts retained a fetal mitochondrial transcriptional signature without normal increases in fatty acid metabolism and mitochondrial biogenesis genes. Myocardial fatty acylcarnitine levels and cardiomyocyte respiration induced by palmitoylcarnitine were concordantly depressed. Thus, instead of transcriptional reprogramming, fetal cardiomyocyte mitochondria undergo perinatal Parkin-mediated mitophagy and replacement by mature adult mitochondria. Mitophagic mitochondrial removal underlies developmental cardiomyocyte mitochondrial plasticity and metabolic transitioning of perinatal hearts.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747105/" 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/PMC4747105/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gong, Guohua -- Song, Moshi -- Csordas, Gyorgy -- Kelly, Daniel P -- Matkovich, Scot J -- Dorn, Gerald W 2nd -- HL058493/HL/NHLBI NIH HHS/ -- HL108943/HL/NHLBI NIH HHS/ -- HL122124/HL/NHLBI NIH HHS/ -- HL128071/HL/NHLBI NIH HHS/ -- HL59888/HL/NHLBI NIH HHS/ -- R01 HL058493/HL/NHLBI NIH HHS/ -- R01 HL059888/HL/NHLBI NIH HHS/ -- R01 HL108943/HL/NHLBI NIH HHS/ -- R01 HL128071/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):aad2459. doi: 10.1126/science.aad2459. Epub 2015 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA. ; Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA. ; Center for Metabolic Origins of Disease, Cardiovascular Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL, USA. ; Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA. gdorn@dom.wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785495" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cellular Reprogramming ; GTP Phosphohydrolases/genetics/metabolism ; Heart/*embryology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria, Heart/metabolism/*physiology/ultrastructure ; Mitochondrial Degradation/genetics/*physiology ; Mitochondrial Dynamics ; Myocardium/*metabolism/ultrastructure ; Myocytes, Cardiac/metabolism/ultrastructure ; Protein Kinases/metabolism ; Ubiquitin-Protein Ligases/genetics/*metabolism
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  • 23
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: Research into stem cells and aging aims to understand how stem cells maintain tissue health, what mechanisms ultimately lead to decline in stem cell function with age, and how the regenerative capacity of somatic stem cells can be enhanced to promote healthy aging. Here, we explore the effects of aging on stem cells in different tissues. Recent research has focused on the ways that genetic mutations, epigenetic changes, and the extrinsic environmental milieu influence stem cell functionality over time. We describe each of these three factors, the ways in which they interact, and how these interactions decrease stem cell health over time. We are optimistic that a better understanding of these changes will uncover potential strategies to enhance stem cell function and increase tissue resiliency into old age.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodell, Margaret A -- Rando, Thomas A -- P01 AG036695/AG/NIA NIH HHS/ -- R01 AG047820/AG/NIA NIH HHS/ -- R01 AR062185/AR/NIAMS NIH HHS/ -- R37 AG023806/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1199-204. doi: 10.1126/science.aab3388.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cells and Regenerative Medicine Center, Center for Cell and Gene Therapy, and Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA. goodell@bcm.edu rando@stanford.edu. ; Glenn Center for the Biology of Aging and Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA, and Center for Regenerative Rehabilitation, Veterans Administration Palo Alto Health Care System, Palo Alto, CA 94304, USA. goodell@bcm.edu rando@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785478" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*physiology ; Aging/*physiology ; Animals ; Cell Aging ; Epigenesis, Genetic ; Genetic Drift ; *Health ; Humans ; Mice ; Mutation ; Organ Specificity ; Selection, Genetic
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gottlieb, Roberta A -- Bernstein, Daniel -- New York, N.Y. -- Science. 2015 Dec 4;350(6265):1162-3. doi: 10.1126/science.aad8222.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA. roberta.gottlieb@cshs.org. ; Department of Pediatrics, Stanford University, Palo Alto, CA 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26785456" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Heart/*embryology ; Heart Failure/*metabolism ; Male ; Mitochondria, Heart/*metabolism/*physiology ; Mitochondrial Degradation/*physiology ; *Mitochondrial Dynamics ; Myocardium/*metabolism ; Ubiquitin-Protein Ligases/*metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kupferschmidt, Kai -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1143. doi: 10.1126/science.351.6278.1143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965608" target="_blank"〉PubMed〈/a〉
    Keywords: Acinetobacter/*growth & development ; Animals ; *Death ; Humans ; Mice ; Moraxellaceae/*growth & development ; Rhizobiaceae/*growth & development ; Time Factors
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  • 26
    Publication Date: 2016-02-26
    Description: In most animal species, juvenile growth is marked by an exponential gain in body weight and size. Here we show that the microbiota of infant mice sustains both weight gain and longitudinal growth when mice are fed a standard laboratory mouse diet or a nutritionally depleted diet. We found that the intestinal microbiota interacts with the somatotropic hormone axis to drive systemic growth. Using monocolonized mouse models, we showed that selected lactobacilli promoted juvenile growth in a strain-dependent manner that recapitulated the microbiota's effect on growth and the somatotropic axis. These findings show that the host's microbiota supports juvenile growth. Moreover, we discovered that lactobacilli strains buffered the adverse effects of chronic undernutrition on the postnatal growth of germ-free mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwarzer, Martin -- Makki, Kassem -- Storelli, Gilles -- Machuca-Gayet, Irma -- Srutkova, Dagmar -- Hermanova, Petra -- Martino, Maria Elena -- Balmand, Severine -- Hudcovic, Tomas -- Heddi, Abdelaziz -- Rieusset, Jennifer -- Kozakova, Hana -- Vidal, Hubert -- Leulier, Francois -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):854-7. doi: 10.1126/science.aad8588.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genomique Fonctionnelle de Lyon, Universite de Lyon, Ecole Normale Superieure de Lyon, Centre National de la Recherche Scientifique, Universite Claude Bernard Lyon 1, Unite Mixte de Recherche 5242, 46 Allee d'Italie, 69364 Lyon Cedex 07, France. Laboratory of Gnotobiology, Institute of Microbiology of the Czech Academy of Sciences, v. v. i., Novy Hradek, Czech Republic. ; Institut de Genomique Fonctionnelle de Lyon, Universite de Lyon, Ecole Normale Superieure de Lyon, Centre National de la Recherche Scientifique, Universite Claude Bernard Lyon 1, Unite Mixte de Recherche 5242, 46 Allee d'Italie, 69364 Lyon Cedex 07, France. Laboratoire CarMeN, Universite Lyon 1, Unite Mixte de Recherche INSERM U-1060 et INRA U-1397, Faculte de Medecine Lyon-Sud, Chemin du Grand Revoyet, 69600 Oullins, France. ; Institut de Genomique Fonctionnelle de Lyon, Universite de Lyon, Ecole Normale Superieure de Lyon, Centre National de la Recherche Scientifique, Universite Claude Bernard Lyon 1, Unite Mixte de Recherche 5242, 46 Allee d'Italie, 69364 Lyon Cedex 07, France. ; Laboratory of Gnotobiology, Institute of Microbiology of the Czech Academy of Sciences, v. v. i., Novy Hradek, Czech Republic. ; UMR203 BF2I, Biologie Fonctionnelle Insectes et Interactions, Universite de Lyon, INRA, INSA-Lyon, F-69621 Villeurbanne, France. ; Laboratoire CarMeN, Universite Lyon 1, Unite Mixte de Recherche INSERM U-1060 et INRA U-1397, Faculte de Medecine Lyon-Sud, Chemin du Grand Revoyet, 69600 Oullins, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912894" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Weight/*physiology ; Diet ; Femur/growth & development ; Gastrointestinal Microbiome/*physiology ; Lactobacillus plantarum/*physiology ; Malnutrition/*microbiology/*physiopathology ; Mice ; Mice, Inbred BALB C ; Weight Gain/*physiology
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  • 27
    Publication Date: 2016-01-23
    Description: Mono-ubiquitination of Fancd2 is essential for repairing DNA interstrand cross-links (ICLs), but the underlying mechanisms are unclear. The Fan1 nuclease, also required for ICL repair, is recruited to ICLs by ubiquitinated (Ub) Fancd2. This could in principle explain how Ub-Fancd2 promotes ICL repair, but we show that recruitment of Fan1 by Ub-Fancd2 is dispensable for ICL repair. Instead, Fan1 recruitment--and activity--restrains DNA replication fork progression and prevents chromosome abnormalities from occurring when DNA replication forks stall, even in the absence of ICLs. Accordingly, Fan1 nuclease-defective knockin mice are cancer-prone. Moreover, we show that a Fan1 variant in high-risk pancreatic cancers abolishes recruitment by Ub-Fancd2 and causes genetic instability without affecting ICL repair. Therefore, Fan1 recruitment enables processing of stalled forks that is essential for genome stability and health.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770513/" 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/PMC4770513/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lachaud, Christophe -- Moreno, Alberto -- Marchesi, Francesco -- Toth, Rachel -- Blow, J Julian -- Rouse, John -- WT096598MA/Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):846-9. doi: 10.1126/science.aad5634. Epub 2016 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Protein Phosphorylation and Ubiquitylation Unit, College of Life Sciences, Sir James Black Centre, University of Dundee, Dundee DD1 5EH, Scotland, UK. ; Centre for Gene Regulation and Expression, College of Life Sciences, Sir James Black Centre, University of Dundee, Dundee DD1 5EH, Scotland, UK. ; School of Veterinary Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Bearsden Road, Glasgow G61 1QH, UK. ; Medical Research Council Protein Phosphorylation and Ubiquitylation Unit, College of Life Sciences, Sir James Black Centre, University of Dundee, Dundee DD1 5EH, Scotland, UK. j.rouse@dundee.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26797144" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Chromosome Aberrations ; DNA Repair ; *DNA Replication ; Endodeoxyribonucleases/genetics/*metabolism ; Fanconi Anemia Complementation Group D2 Protein/genetics/*metabolism ; Female ; Gene Knock-In Techniques ; Genetic Predisposition to Disease ; Genomic Instability/*genetics ; Liver Neoplasms/genetics/pathology ; Lung Neoplasms/genetics/pathology ; Lymphoma/genetics/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Pancreatic Neoplasms/*genetics ; *Ubiquitination
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  • 28
    Publication Date: 2016-03-19
    Description: Maintaining energy homeostasis is crucial for the survival and health of organisms. The brain regulates feeding by responding to dietary factors and metabolic signals from peripheral organs. It is unclear how the brain interprets these signals. O-GlcNAc transferase (OGT) catalyzes the posttranslational modification of proteins by O-GlcNAc and is regulated by nutrient access. Here, we show that acute deletion of OGT from alphaCaMKII-positive neurons in adult mice caused obesity from overeating. The hyperphagia derived from the paraventricular nucleus (PVN) of the hypothalamus, where loss of OGT was associated with impaired satiety. These results identify O-GlcNAcylation in alphaCaMKII neurons of the PVN as an important molecular mechanism that regulates feeding behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817221/" 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/PMC4817221/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lagerlof, Olof -- Slocomb, Julia E -- Hong, Ingie -- Aponte, Yeka -- Blackshaw, Seth -- Hart, Gerald W -- Huganir, Richard L -- N01-HV-00240/HV/NHLBI NIH HHS/ -- P01 HL107153/HL/NHLBI NIH HHS/ -- P01HL107153/HL/NHLBI NIH HHS/ -- R01 DK061671/DK/NIDDK NIH HHS/ -- R01 NS036715/NS/NINDS NIH HHS/ -- R01DK6167/DK/NIDDK NIH HHS/ -- R01NS036715/NS/NINDS NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1293-6. doi: 10.1126/science.aad5494.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; National Institute on Drug Abuse + National Institutes of Health/Johns Hopkins University Graduate Partnership Program, Baltimore, MD 21224, USA. ; Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Intramural Research Program, Neuronal Circuits and Behavior Unit, National Institute on Drug Abuse, Baltimore, MD 21224, USA. ; Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; Solomon H. Snyder Department of Neuroscience, Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. rhuganir@jhmi.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989246" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylglucosamine/metabolism ; Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism ; Energy Metabolism/genetics/*physiology ; Feeding Behavior/*physiology ; Gene Deletion ; Homeostasis/genetics ; Hyperphagia/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; N-Acetylglucosaminyltransferases/genetics/*physiology ; Neurons/enzymology ; Obesity/genetics ; Paraventricular Hypothalamic Nucleus/cytology/enzymology/*physiology ; Protein Processing, Post-Translational ; Satiety Response/physiology
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Segal, Rosalind A -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1494. doi: 10.1126/science.351.6280.1494.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rosalind A. Segal is a neurobiology professor at Harvard Medical School and co-chair of cancer biology at the Dana-Farber Cancer Institute in Boston. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013735" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; Female ; Humans ; Neurobiology/manpower ; *Sexism ; *Women, Working
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  • 30
    Publication Date: 2016-04-23
    Description: Ecological character displacement is a process of morphological divergence that reduces competition for limited resources. We used genomic analysis to investigate the genetic basis of a documented character displacement event in Darwin's finches on Daphne Major in the Galapagos Islands: The medium ground finch diverged from its competitor, the large ground finch, during a severe drought. We discovered a genomic region containing the HMGA2 gene that varies systematically among Darwin's finch species with different beak sizes. Two haplotypes that diverged early in the radiation were involved in the character displacement event: Genotypes associated with large beak size were at a strong selective disadvantage in medium ground finches (selection coefficient s = 0.59). Thus, a major locus has apparently facilitated a rapid ecological diversification in the adaptive radiation of Darwin's finches.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamichhaney, Sangeet -- Han, Fan -- Berglund, Jonas -- Wang, Chao -- Almen, Markus Sallman -- Webster, Matthew T -- Grant, B Rosemary -- Grant, Peter R -- Andersson, Leif -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):470-4. doi: 10.1126/science.aad8786.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden. ; Department of Ecology and Evolutionary Biology, Princeton University, Princeton, NJ, USA. ; Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden. Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences, Uppsala, Sweden. Department of Veterinary Integrative Biosciences, Texas A&M University, College Station, TX, USA. leif.andersson@imbim.uu.se.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102486" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Beak/*anatomy & histology ; Body Size/genetics ; *Droughts ; Ecuador ; Female ; Finches/*anatomy & histology/classification/*genetics ; Genomics ; Genotype ; HMGA2 Protein/genetics ; Haplotypes ; Organ Size/genetics ; Phylogeny ; *Quantitative Trait Loci ; *Selection, Genetic
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  • 31
    Publication Date: 2016-02-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Claiborne, Anne B -- English, Rebecca A -- Kahn, Jeffrey P -- 10002265/PHS HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):668-70. doi: 10.1126/science.aaf3091. Epub 2016 Feb 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Medicine, U.S. National Academies of Sciences, Engineering, and Medicine, Washington, DC 20001, USA. aclaiborne@nas.edu. ; Institute of Medicine, U.S. National Academies of Sciences, Engineering, and Medicine, Washington, DC 20001, USA. ; Johns Hopkins Berman Institute of Bioethics, Johns Hopkins University, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26842937" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Nucleus/genetics ; DNA, Mitochondrial/genetics ; Ethics, Medical ; *Government Regulation ; Humans ; Mitochondrial Diseases/genetics/*prevention & control ; Mitochondrial Replacement Therapy/*ethics/*standards ; *Oocytes ; United States ; United States Food and Drug Administration ; *Zygote
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  • 32
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Servick, Kelly -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):15. doi: 10.1126/science.351.6268.15.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721984" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; California ; Cell Differentiation ; Clinical Trials as Topic ; Drug Industry ; Embryonic Stem Cells/cytology/*transplantation ; Financing, Organized ; Humans ; Photoreceptor Cells/physiology ; Rats ; Regenerative Medicine/*economics/*trends ; Retina/cytology/physiology ; Stem Cell Research/*economics
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  • 33
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cohen, Jon -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):16-9. doi: 10.1126/science.351.6268.16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomedical Research/*economics ; Communicable Disease Control/*economics ; Financial Management ; Humans ; National Institutes of Health (U.S.) ; United States ; Vaccines/*economics
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shanahan, Jesse -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):418. doi: 10.1126/science.351.6271.418.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jesse Shanahan is a master's student in astronomy at Wesleyan University in Middletown, Connecticut. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798017" target="_blank"〉PubMed〈/a〉
    Keywords: Astronomy/*education ; *Career Mobility ; Disabled Persons/*psychology/statistics & numerical data ; Fear ; *Hostility ; Humans ; Male ; United States
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  • 35
    Publication Date: 2016-02-27
    Description: Oocytes differentiate in diverse species by receiving organelles and cytoplasm from sister germ cells while joined in germline cysts or syncytia. Mouse primordial germ cells form germline cysts, but the role of cysts in oogenesis is unknown. We find that mouse germ cells receive organelles from neighboring cyst cells and build a Balbiani body to become oocytes, whereas nurselike germ cells die. Organelle movement, Balbiani body formation, and oocyte fate determination are selectively blocked by low levels of microtubule-dependent transport inhibitors. Membrane breakdown within the cyst and an apoptosis-like process are associated with organelle transfer into the oocyte, events reminiscent of nurse cell dumping in Drosophila We propose that cytoplasmic and organelle transport plays an evolutionarily conserved and functionally important role in mammalian oocyte differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lei, Lei -- Spradling, Allan C -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):95-9. doi: 10.1126/science.aad2156. Epub 2016 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute Research Laboratories, Department of Embryology, Carnegie Institution for Science, 3520 San Martin Drive, Baltimore, MD 21218, USA. spradling@ciwemb.edu leile@med.umich.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26917595" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Biological Evolution ; Cytoplasm/physiology/ultrastructure ; Female ; Giant Cells/*cytology ; Mice ; Microtubules/drug effects/physiology ; Oocytes/*cytology ; *Oogenesis ; Organelles/*physiology
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  • 36
    Publication Date: 2016-01-30
    Description: Cystic fibrosis (CF) is caused by mutations in the gene that encodes the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel. In humans and pigs, the loss of CFTR impairs respiratory host defenses, causing airway infection. But CF mice are spared. We found that in all three species, CFTR secreted bicarbonate into airway surface liquid. In humans and pigs lacking CFTR, unchecked H(+) secretion by the nongastric H(+)/K(+) adenosine triphosphatase (ATP12A) acidified airway surface liquid, which impaired airway host defenses. In contrast, mouse airways expressed little ATP12A and secreted minimal H(+); consequently, airway surface liquid in CF and non-CF mice had similar pH. Inhibiting ATP12A reversed host defense abnormalities in human and pig airways. Conversely, expressing ATP12A in CF mouse airways acidified airway surface liquid, impaired defenses, and increased airway bacteria. These findings help explain why CF mice are protected from infection and nominate ATP12A as a potential therapeutic target for CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shah, Viral S -- Meyerholz, David K -- Tang, Xiao Xiao -- Reznikov, Leah -- Abou Alaiwa, Mahmoud -- Ernst, Sarah E -- Karp, Philip H -- Wohlford-Lenane, Christine L -- Heilmann, Kristopher P -- Leidinger, Mariah R -- Allen, Patrick D -- Zabner, Joseph -- McCray, Paul B Jr -- Ostedgaard, Lynda S -- Stoltz, David A -- Randak, Christoph O -- Welsh, Michael J -- 5T32GM007337/GM/NIGMS NIH HHS/ -- DK054759/DK/NIDDK NIH HHS/ -- F30 HL123239/HL/NHLBI NIH HHS/ -- F30HL123239/HL/NHLBI NIH HHS/ -- HL091842/HL/NHLBI NIH HHS/ -- HL117744/HL/NHLBI NIH HHS/ -- HL51670/HL/NHLBI NIH HHS/ -- K08HL097071/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):503-7. doi: 10.1126/science.aad5589.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pathology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pediatrics University of Iowa, Iowa City, IA 52242, USA. ; Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Pediatrics University of Iowa, Iowa City, IA 52242, USA. Department of Microbiology, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Biomedical Engineering, College of Engineering, University of Iowa, Iowa City, IA 52242, USA. ; Department of Medicine, University of Iowa, Iowa City, IA 52242, USA. Department of Molecular Physiology and Biophysics, Pappajohn Biomedical Institute, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823428" target="_blank"〉PubMed〈/a〉
    Keywords: Acids/metabolism ; Animals ; Bicarbonates/metabolism ; Cystic Fibrosis/*metabolism/*microbiology ; H(+)-K(+)-Exchanging ATPase/genetics/*metabolism ; Humans ; Hydrogen-Ion Concentration ; Lung/*metabolism/*microbiology ; Mice ; Mice, Inbred CFTR/genetics/metabolism ; Mice, Transgenic ; Swine
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  • 37
    Publication Date: 2016-01-02
    Description: Several recent studies link parental environments to phenotypes in subsequent generations. In this work, we investigate the mechanism by which paternal diet affects offspring metabolism. Protein restriction in mice affects small RNA (sRNA) levels in mature sperm, with decreased let-7 levels and increased amounts of 5' fragments of glycine transfer RNAs (tRNAs). In testicular sperm, tRNA fragments are scarce but increase in abundance as sperm mature in the epididymis. Epididymosomes (vesicles that fuse with sperm during epididymal transit) carry RNA payloads matching those of mature sperm and can deliver RNAs to immature sperm in vitro. Functionally, tRNA-glycine-GCC fragments repress genes associated with the endogenous retroelement MERVL, in both embryonic stem cells and embryos. Our results shed light on sRNA biogenesis and its dietary regulation during posttesticular sperm maturation, and they also link tRNA fragments to regulation of endogenous retroelements active in the preimplantation embryo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sharma, Upasna -- Conine, Colin C -- Shea, Jeremy M -- Boskovic, Ana -- Derr, Alan G -- Bing, Xin Y -- Belleannee, Clemence -- Kucukural, Alper -- Serra, Ryan W -- Sun, Fengyun -- Song, Lina -- Carone, Benjamin R -- Ricci, Emiliano P -- Li, Xin Z -- Fauquier, Lucas -- Moore, Melissa J -- Sullivan, Robert -- Mello, Craig C -- Garber, Manuel -- Rando, Oliver J -- DP1ES025458/DP/NCCDPHP CDC HHS/ -- R01HD080224/HD/NICHD NIH HHS/ -- UL1 TR000161/TR/NCATS NIH HHS/ -- UL1 TR001453/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):391-6. doi: 10.1126/science.aad6780. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Obstetrics, Gynecology and Reproduction, Universite Laval, Centre Hospitalier Universitaire de Quebec Research Center, Quebec City, Quebec G1V 4G2, Canada. ; RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. RNAi Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. ; Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA. oliver.rando@umassmed.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/metabolism ; Diet, Protein-Restricted ; Epididymis/metabolism ; *Fertilization ; *Gene Expression Regulation ; Male ; Mice ; MicroRNAs/metabolism ; RNA, Transfer, Gly/*metabolism/*physiology ; Retroelements/genetics ; *Sperm Maturation ; Spermatozoa/*metabolism ; Testis/metabolism
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):13. doi: 10.1126/science.351.6268.13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721982" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA/chemistry/genetics/metabolism ; *Epigenesis, Genetic ; Male ; Metabolism/*genetics ; Mice ; RNA, Transfer/genetics/*metabolism ; *Spermatozoa
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  • 39
    Publication Date: 2016-02-26
    Description: Voltage-gated CaV1.2 channels (L-type calcium channel alpha1C subunits) are critical mediators of transcription-dependent neural plasticity. Whether these channels signal via the influx of calcium ion (Ca(2+)), voltage-dependent conformational change (VDeltaC), or a combination of the two has thus far been equivocal. We fused CaV1.2 to a ligand-gated Ca(2+)-permeable channel, enabling independent control of localized Ca(2+) and VDeltaC signals. This revealed an unexpected dual requirement: Ca(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for subsequent VDeltaC-mediated accumulation. Neither signal alone sufficed to activate transcription. Signal order was crucial: Efficiency peaked when Ca(2+) preceded VDeltaC by 10 to 20 seconds. CaV1.2 VDeltaC synergistically augmented signaling by N-methyl-d-aspartate receptors. Furthermore, VDeltaC mistuning correlated with autistic symptoms in Timothy syndrome. Thus, nonionic VDeltaC signaling is vital to the function of CaV1.2 in synaptic and neuropsychiatric processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Boxing -- Tadross, Michael R -- Tsien, Richard W -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):863-7. doi: 10.1126/science.aad3647.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. ; Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. tadrossm@janelia.hhmi.org. ; Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/chemistry/*metabolism ; *Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; *Gene Expression Regulation ; HEK293 Cells ; Hippocampus/cytology ; Humans ; Long QT Syndrome/genetics/metabolism ; Neuronal Plasticity/*genetics ; Neurons/drug effects/*metabolism ; Nimodipine/pharmacology ; Protein Conformation/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; Syndactyly/genetics/metabolism
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  • 40
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leslie, Mitch -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):21-3. doi: 10.1126/science.352.6281.21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034353" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*immunology ; Diabetes Mellitus, Type 1/immunology ; Infection/*immunology ; Inflammation/*immunology ; Lymph Nodes/cytology/*immunology ; Mice ; Pancreas/immunology ; T-Lymphocytes/*immunology
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):440-3. doi: 10.1126/science.351.6272.440.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823410" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Child, Preschool ; DNA Mutational Analysis ; DNA Repair/genetics ; Female ; *Genes, Neoplasm ; *Genetic Predisposition to Disease ; Humans ; Male ; Mutation ; Neoplasms/*genetics/mortality ; Pedigree ; Tumor Suppressor Protein p53/genetics
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  • 42
    Publication Date: 2016-02-27
    Description: Ebola virus disease in humans is highly lethal, with case fatality rates ranging from 25 to 90%. There is no licensed treatment or vaccine against the virus, underscoring the need for efficacious countermeasures. We ascertained that a human survivor of the 1995 Kikwit Ebola virus disease outbreak maintained circulating antibodies against the Ebola virus surface glycoprotein for more than a decade after infection. From this survivor we isolated monoclonal antibodies (mAbs) that neutralize recent and previous outbreak variants of Ebola virus and mediate antibody-dependent cell-mediated cytotoxicity in vitro. Strikingly, monotherapy with mAb114 protected macaques when given as late as 5 days after challenge. Treatment with a single human mAb suggests that a simplified therapeutic strategy for human Ebola infection may be possible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Corti, Davide -- Misasi, John -- Mulangu, Sabue -- Stanley, Daphne A -- Kanekiyo, Masaru -- Wollen, Suzanne -- Ploquin, Aurelie -- Doria-Rose, Nicole A -- Staupe, Ryan P -- Bailey, Michael -- Shi, Wei -- Choe, Misook -- Marcus, Hadar -- Thompson, Emily A -- Cagigi, Alberto -- Silacci, Chiara -- Fernandez-Rodriguez, Blanca -- Perez, Laurent -- Sallusto, Federica -- Vanzetta, Fabrizia -- Agatic, Gloria -- Cameroni, Elisabetta -- Kisalu, Neville -- Gordon, Ingelise -- Ledgerwood, Julie E -- Mascola, John R -- Graham, Barney S -- Muyembe-Tamfun, Jean-Jacques -- Trefry, John C -- Lanzavecchia, Antonio -- Sullivan, Nancy J -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1339-42. doi: 10.1126/science.aad5224. Epub 2016 Feb 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Research in Biomedicine, Universita della Svizzera Italiana, CH-6500 Bellinzona, Switzerland. Humabs BioMed SA, 6500 Bellinzona, Switzerland. ; Vaccine Research Center, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, MD 21702, USA. ; Institute for Research in Biomedicine, Universita della Svizzera Italiana, CH-6500 Bellinzona, Switzerland. ; Humabs BioMed SA, 6500 Bellinzona, Switzerland. ; National Institute for Biomedical Research, National Laboratory of Public Health, Kinshasa B.P. 1197, Democratic Republic of the Congo. ; Institute for Research in Biomedicine, Universita della Svizzera Italiana, CH-6500 Bellinzona, Switzerland. Institute of Microbiology, ETH Zurich, CH-8093 Zurich, Switzerland. ; Vaccine Research Center, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. njsull@mail.nih.gov.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26917593" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Antibodies, Monoclonal/*administration & dosage/immunology/isolation & ; purification ; Antibodies, Neutralizing/*administration & dosage/immunology/isolation & ; purification ; Antibodies, Viral/*administration & dosage/immunology/isolation & purification ; Clinical Trials as Topic ; Disease Outbreaks ; Ebolavirus/*immunology ; Female ; Hemorrhagic Fever, Ebola/epidemiology/*prevention & control ; Humans ; Macaca ; Male ; Molecular Sequence Data ; Survivors
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  • 43
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):284-7. doi: 10.1126/science.352.6283.284.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081051" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Female ; Fetal Diseases/*prevention & control ; Humans ; Osteogenesis Imperfecta/*prevention & control ; Pregnancy ; *Stem Cell Transplantation ; *Stem Cells
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  • 44
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):286. doi: 10.1126/science.352.6283.286.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081052" target="_blank"〉PubMed〈/a〉
    Keywords: Clinical Trials as Topic ; Female ; Fetal Growth Retardation/*therapy ; Gene Transfer Techniques ; Genetic Therapy/*methods ; Humans ; Placenta ; Pregnancy ; Uterine Artery ; Vascular Endothelial Growth Factor A/*genetics
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  • 45
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin-Frankel, Jennifer -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1126. doi: 10.1126/science.351.6278.1126.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965598" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cholesterol, HDL/*blood ; Coronary Disease/*blood/*genetics ; Female ; Humans ; Male ; Scavenger Receptors, Class B/*genetics
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  • 46
    Publication Date: 2016-01-02
    Description: CRISPR/Cas9-mediated genome editing holds clinical potential for treating genetic diseases, such as Duchenne muscular dystrophy (DMD), which is caused by mutations in the dystrophin gene. To correct DMD by skipping mutant dystrophin exons in postnatal muscle tissue in vivo, we used adeno-associated virus-9 (AAV9) to deliver gene-editing components to postnatal mdx mice, a model of DMD. Different modes of AAV9 delivery were systematically tested, including intraperitoneal at postnatal day 1 (P1), intramuscular at P12, and retro-orbital at P18. Each of these methods restored dystrophin protein expression in cardiac and skeletal muscle to varying degrees, and expression increased from 3 to 12 weeks after injection. Postnatal gene editing also enhanced skeletal muscle function, as measured by grip strength tests 4 weeks after injection. This method provides a potential means of correcting mutations responsible for DMD and other monogenic disorders after birth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760628/" 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/PMC4760628/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, Chengzu -- Amoasii, Leonela -- Mireault, Alex A -- McAnally, John R -- Li, Hui -- Sanchez-Ortiz, Efrain -- Bhattacharyya, Samadrita -- Shelton, John M -- Bassel-Duby, Rhonda -- Olson, Eric N -- DK-099653/DK/NIDDK NIH HHS/ -- HL-077439/HL/NHLBI NIH HHS/ -- HL-093039/HL/NHLBI NIH HHS/ -- HL-111665/HL/NHLBI NIH HHS/ -- R01 DK099653/DK/NIDDK NIH HHS/ -- R01 HL077439/HL/NHLBI NIH HHS/ -- R01 HL093039/HL/NHLBI NIH HHS/ -- R01 HL111665/HL/NHLBI NIH HHS/ -- U01 HL100401/HL/NHLBI NIH HHS/ -- U01-HL-100401/HL/NHLBI NIH HHS/ -- U54 HD 087351/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):400-3. doi: 10.1126/science.aad5725. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Sen. Paul D. Wellstone Muscular Dystrophy Cooperative Research Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Sen. Paul D. Wellstone Muscular Dystrophy Cooperative Research Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. eric.olson@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721683" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *CRISPR-Cas Systems ; Dependovirus ; Disease Models, Animal ; Dystrophin/*genetics ; Exons/genetics ; Female ; Forelimb/physiopathology ; Genetic Therapy/*methods ; Genome/genetics ; Hand Strength ; Male ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/metabolism ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Myocardium/metabolism
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  • 47
    Publication Date: 2016-01-23
    Description: Differentiated macrophages can self-renew in tissues and expand long term in culture, but the gene regulatory mechanisms that accomplish self-renewal in the differentiated state have remained unknown. Here we show that in mice, the transcription factors MafB and c-Maf repress a macrophage-specific enhancer repertoire associated with a gene network that controls self-renewal. Single-cell analysis revealed that, in vivo, proliferating resident macrophages can access this network by transient down-regulation of Maf transcription factors. The network also controls embryonic stem cell self-renewal but is associated with distinct embryonic stem cell-specific enhancers. This indicates that distinct lineage-specific enhancer platforms regulate a shared network of genes that control self-renewal potential in both stem and mature cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soucie, Erinn L -- Weng, Ziming -- Geirsdottir, Laufey -- Molawi, Kaaweh -- Maurizio, Julien -- Fenouil, Romain -- Mossadegh-Keller, Noushine -- Gimenez, Gregory -- VanHille, Laurent -- Beniazza, Meryam -- Favret, Jeremy -- Berruyer, Carole -- Perrin, Pierre -- Hacohen, Nir -- Andrau, J-C -- Ferrier, Pierre -- Dubreuil, Patrice -- Sidow, Arend -- Sieweke, Michael H -- P01AG036695/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):aad5510. doi: 10.1126/science.aad5510. Epub 2016 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Centre de Recherche en Cancerologie de Marseille, INSERM (U1068), CNRS (U7258), Universite Aix-Marseille (UM105), Marseille, France. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu. ; Department of Pathology, Stanford University, Stanford, CA 94305-5324, USA. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Max-Delbruck-Centrum fur Molekulare Medizin in der Helmholtz-Gemeinschaft, 10 Robert-Rossle-Strasse, 13125 Berlin, Germany. ; Broad Institute of Harvard University and MIT, Cambridge, MA 02142, USA. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Institut de Genetique Moleculaire de Montpellier, CNRS UMR 5535, 1919 Route de Mende, 34293 Montpellier, France. ; Centre de Recherche en Cancerologie de Marseille, INSERM (U1068), CNRS (U7258), Universite Aix-Marseille (UM105), Marseille, France. ; Department of Pathology, Stanford University, Stanford, CA 94305-5324, USA. Department of Genetics, Stanford University, Stanford, CA 94305, USA. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Max-Delbruck-Centrum fur Molekulare Medizin in der Helmholtz-Gemeinschaft, 10 Robert-Rossle-Strasse, 13125 Berlin, Germany. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26797145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/*genetics ; Cell Lineage/*genetics ; Cell Proliferation ; Cells, Cultured ; Down-Regulation ; Embryonic Stem Cells/*cytology ; Enhancer Elements, Genetic/*physiology ; *Gene Expression Regulation ; Gene Regulatory Networks ; Macrophages/*cytology ; MafB Transcription Factor/metabolism ; Mice ; Proto-Oncogene Proteins c-maf/metabolism ; Single-Cell Analysis ; Transcriptional Activation
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  • 48
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stevens, Beth -- Muthukumar, Allie K -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):813. doi: 10.1126/science.aaf2849.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, F. M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA. beth.stevens@childrens.harvard.edu. ; Department of Neurology, F. M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912878" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; Cerebellar Cortex/*cytology ; Female ; Hedgehog Proteins/*metabolism ; Male ; Neurons/*metabolism ; Receptors, G-Protein-Coupled/*metabolism
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  • 49
    Publication Date: 2016-04-02
    Description: Global climate change is a major threat to biodiversity. Large-scale analyses have generally focused on the impacts of climate change on the geographic ranges of species and on phenology, the timing of ecological phenomena. We used long-term monitoring of the abundance of breeding birds across Europe and the United States to produce, for both regions, composite population indices for two groups of species: those for which climate suitability has been either improving or declining since 1980. The ratio of these composite indices, the climate impact indicator (CII), reflects the divergent fates of species favored or disadvantaged by climate change. The trend in CII is positive and similar in the two regions. On both continents, interspecific and spatial variation in population abundance trends are well predicted by climate suitability trends.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, Philip A -- Mason, Lucy R -- Green, Rhys E -- Gregory, Richard D -- Sauer, John R -- Alison, Jamie -- Aunins, Ainars -- Brotons, Lluis -- Butchart, Stuart H M -- Campedelli, Tommaso -- Chodkiewicz, Tomasz -- Chylarecki, Przemyslaw -- Crowe, Olivia -- Elts, Jaanus -- Escandell, Virginia -- Foppen, Ruud P B -- Heldbjerg, Henning -- Herrando, Sergi -- Husby, Magne -- Jiguet, Frederic -- Lehikoinen, Aleksi -- Lindstrom, Ake -- Noble, David G -- Paquet, Jean-Yves -- Reif, Jiri -- Sattler, Thomas -- Szep, Tibor -- Teufelbauer, Norbert -- Trautmann, Sven -- van Strien, Arco J -- van Turnhout, Chris A M -- Vorisek, Petr -- Willis, Stephen G -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):84-7. doi: 10.1126/science.aac4858.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Conservation Ecology Group, School of Biological and Biomedical Sciences, Durham University, South Road, Durham DH1 3LE, UK. ; Royal Society for the Protection of Birds, Centre for Conservation Science, The Lodge, Sandy, Bedfordshire SG19 2DL, UK. ; Royal Society for the Protection of Birds, Centre for Conservation Science, The Lodge, Sandy, Bedfordshire SG19 2DL, UK. Conservation Science Group, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK. ; United States Geological Survey, Patuxent Wildlife Research Center, 12100 Beech Forest Road, Laurel, MD 20708, USA. ; Institute of Integrative Biology, University of Liverpool, Crown Street, Liverpool L69 3BX, UK. ; Faculty of Biology, University of Latvia, Jelgavas iela 1, Riga, LV-1004, Latvia. ; Center for Mediterranean Forest Research, Centre Tecnologic Forestal de Catalunya, InForest JRU, Solsona 25280, Spain. REAF, Cerdanyola del Valles 08193, Catalonia, Spain. CSIC, Cerdanyola del Valles 08193, Catalonia, Spain. ; Conservation Science Group, Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, UK. BirdLife International, The David Attenborough Building, Pembroke Street, Cambridge CB2 3QZ, UK. ; MITO2000 National Committee; c/o Dream Italia, Via Garibaldi 3, 52015, Pratovecchio-Stia, Arezzo, Italy. ; Ogolnopolskie Towarzystwo Ochrony Ptakow, Odrowaza 24,05-270 Marki, Poland. ; Museum and Institute of Zoology, Polish Academy of Sciences, Wilcza 64, 00-679 Warszawa, Poland. ; BirdWatch Ireland, Unit 20 Block D Bullford Business Campus, Kilcoole, County Wicklow, Ireland. ; Institute of Ecology and Earth Sciences, University of Tartu, Vanemuise Street 46, 51014 Tartu, Estonia. Estonian Ornithological Society, Veski 4, 51005 Tartu, Estonia. ; Sociedad Espanola de Ornitologia/BirdLife Melquiades Biencinto, 34, 28053 Madrid. Spain. ; European Bird Census Council, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Sovon Dutch Centre for Field Ornithology, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Department of Animal Ecology and Ecophysiology, Institute for Water and Wetland Research, Radboud University, Post Office Box 9010, 6500 GL Nijmegen, Netherlands. ; Dansk Ornitologisk Forening-BirdLife Denmark and University of Aarhus, Vesterbrogade 140, 1620 Kobenhavn V, Denmark. ; European Bird Census Council-Catalan Ornithological Institute, Natural History Museum of Barcelona, Placa Leonardo da Vinci 4-5, 08019 Barcelona, Catalonia, Spain. ; Section for Science, Nord University, 7600 Levanger, Norway. ; UMR7204 Sorbonne Universites-MNHN-CNRS-UPMC, CESCO, CRBPO, CP 135, 43 Rue Buffon, 75005 Paris, France. ; The Helsinki Lab of Ornithology, Finnish Museum of Natural History, Post Office Box 17, 00014 University of Helsinki, Finland. ; Biodiversity Unit, Department of Biology, Lund University, Ecology Building, S-223 62 Lund, Sweden. ; The British Trust for Ornithology, The Nunnery, Thetford, Norfolk IP24 2PU, UK. ; Natagora, Departement Etudes, Rue Nanon 98, B-5000 Namur, Belgium. ; Institute for Environmental Studies, Faculty of Science, Charles University in Prague, Czech Republic. Department of Zoology and Laboratory of Ornithology, Faculty of Science, Palacky University Olomouc, 17 Listopadu 50, 771 43 Olomouc, Czech Republic. ; Swiss Ornithological Institute, Seerose 1, 6204 Sempach, Switzerland. ; Institute of Environmental Sciences, University of Nyiregyhaza, Sostoi ut 31/b, 4400 Nyiregyhaza, Hungary. ; BirdLife Austria, Museumsplatz 1/10/8, A-1070 Vienna, Austria. ; Dachverband Deutscher Avifaunisten e.V. (Federation of German Avifaunists), An den Speichern 6, D-48157 Munster, Germany. ; Statistics Netherlands, Post Office Box 24500, 2490 HA The Hague, Netherlands. ; Sovon Dutch Centre for Field Ornithology, Post Office Box 6521, 6503 GA Nijmegen, Netherlands. Department of Animal Ecology and Ecophysiology, Institute for Water and Wetland Research, Radboud University, Post Office Box 9010, 6500 GL Nijmegen, Netherlands. ; Department of Zoology and Laboratory of Ornithology, Faculty of Science, Palacky University Olomouc, 17 Listopadu 50, 771 43 Olomouc, Czech Republic. Pan-European Common Bird Monitoring Scheme, Czech Society for Ornithology, Na Belidle 252/34, CZ-15000 Prague 5, Czech Republic.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034371" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Migration ; Animals ; Biodiversity ; *Birds ; Breeding ; *Climate Change ; Ecological Parameter Monitoring ; Europe ; Population Dynamics ; United States
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  • 50
    Publication Date: 2016-04-23
    Description: Tissue-resident memory T (Trm) cells permanently localize to portals of pathogen entry, where they provide immediate protection against reinfection. To enforce tissue retention, Trm cells up-regulate CD69 and down-regulate molecules associated with tissue egress; however, a Trm-specific transcriptional regulator has not been identified. Here, we show that the transcription factor Hobit is specifically up-regulated in Trm cells and, together with related Blimp1, mediates the development of Trm cells in skin, gut, liver, and kidney in mice. The Hobit-Blimp1 transcriptional module is also required for other populations of tissue-resident lymphocytes, including natural killer T (NKT) cells and liver-resident NK cells, all of which share a common transcriptional program. Our results identify Hobit and Blimp1 as central regulators of this universal program that instructs tissue retention in diverse tissue-resident lymphocyte populations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mackay, Laura K -- Minnich, Martina -- Kragten, Natasja A M -- Liao, Yang -- Nota, Benjamin -- Seillet, Cyril -- Zaid, Ali -- Man, Kevin -- Preston, Simon -- Freestone, David -- Braun, Asolina -- Wynne-Jones, Erica -- Behr, Felix M -- Stark, Regina -- Pellicci, Daniel G -- Godfrey, Dale I -- Belz, Gabrielle T -- Pellegrini, Marc -- Gebhardt, Thomas -- Busslinger, Meinrad -- Shi, Wei -- Carbone, Francis R -- van Lier, Rene A W -- Kallies, Axel -- van Gisbergen, Klaas P J M -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):459-63. doi: 10.1126/science.aad2035.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. Australian Research Council (ARC) Centre of Excellence in Advanced Molecular Imaging, University of Melbourne, Melbourne, Australia. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl. ; Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), Vienna, Austria. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. ; Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, AMC, University of Amsterdam, Amsterdam, Netherlands. ; Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. Department of Experimental Immunology, AMC, Amsterdam, Netherlands. ; Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Australia. Australian Research Council (ARC) Centre of Excellence in Advanced Molecular Imaging, University of Melbourne, Melbourne, Australia. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Computing and Information Systems, The University of Melbourne, Melbourne, Australia. ; The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl. ; Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Academic Medical Center (AMC), University of Amsterdam, Amsterdam, Netherlands. The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. Department of Medical Biology, The University of Melbourne, Melbourne, Australia. Department of Experimental Immunology, AMC, Amsterdam, Netherlands. lkmackay@unimelb.edu.au kallies@wehi.edu.au k.vangisbergen@sanquin.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102484" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gastrointestinal Tract/immunology ; *Gene Expression Regulation ; Genes, Regulator/genetics/*physiology ; Immunologic Memory/*genetics ; Kidney/immunology ; Killer Cells, Natural/*immunology ; Liver/immunology ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Natural Killer T-Cells/*immunology ; Skin/immunology ; Transcription Factors/genetics/*physiology ; Transcription, Genetic ; Up-Regulation
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  • 51
    Publication Date: 2016-03-19
    Description: Sanchez et al.'s textbook k-anonymization example does not prove, or even suggest, that location and other big-data data sets can be anonymized and of general use. The synthetic data set that they "successfully anonymize" bears no resemblance to modern high-dimensional data sets on which their methods fail. Moving forward, deidentification should not be considered a useful basis for policy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Montjoye, Yves-Alexandre -- Pentland, Alex Sandy -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1274. doi: 10.1126/science.aaf1578.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Harvard University, Institute for Quantitative Social Science, Cambridge, MA 02138, USA. yvesalexandre@demontjoye.com. ; Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989244" target="_blank"〉PubMed〈/a〉
    Keywords: *Commerce ; *Data Collection ; Female ; Humans ; *Information Dissemination ; Male ; *Privacy
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stone, Richard -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1138-40. doi: 10.1126/science.351.6278.1138.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965605" target="_blank"〉PubMed〈/a〉
    Keywords: Computer Simulation ; *Explosions ; *Forensic Sciences ; Humans ; *Nuclear Weapons ; United States
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  • 53
    Publication Date: 2016-02-26
    Description: T cell-mediated destruction of insulin-producing beta cells in the pancreas causes type 1 diabetes (T1D). CD4 T cell responses play a central role in beta cell destruction, but the identity of the epitopes recognized by pathogenic CD4 T cells remains unknown. We found that diabetes-inducing CD4 T cell clones isolated from nonobese diabetic mice recognize epitopes formed by covalent cross-linking of proinsulin peptides to other peptides present in beta cell secretory granules. These hybrid insulin peptides (HIPs) are antigenic for CD4 T cells and can be detected by mass spectrometry in beta cells. CD4 T cells from the residual pancreatic islets of two organ donors who had T1D also recognize HIPs. Autoreactive T cells targeting hybrid peptides may explain how immune tolerance is broken in T1D.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Delong, Thomas -- Wiles, Timothy A -- Baker, Rocky L -- Bradley, Brenda -- Barbour, Gene -- Reisdorph, Richard -- Armstrong, Michael -- Powell, Roger L -- Reisdorph, Nichole -- Kumar, Nitesh -- Elso, Colleen M -- DeNicola, Megan -- Bottino, Rita -- Powers, Alvin C -- Harlan, David M -- Kent, Sally C -- Mannering, Stuart I -- Haskins, Kathryn -- 1K01DK094941/DK/NIDDK NIH HHS/ -- 1R01DK081166/DK/NIDDK NIH HHS/ -- 5U01DK89572/DK/NIDDK NIH HHS/ -- DK104211/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):711-4. doi: 10.1126/science.aad2791.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Microbiology, University of Colorado School of Medicine, Denver, Anschutz Medical Campus, Aurora, CO 80045, USA. thomas.delong@ucdenver.edu katie.haskins@ucdenver.edu. ; Department of Immunology and Microbiology, University of Colorado School of Medicine, Denver, Anschutz Medical Campus, Aurora, CO 80045, USA. ; Pharmaceutical Sciences, University of Colorado School of Medicine, Aurora, CO 80045, USA. ; Immunology and Diabetes Unit, St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, Victoria 3065, Australia. ; Department of Medicine, Diabetes Division, Diabetes Center of Excellence, University of Massachusetts Medical School, Worcester, MA, USA. ; Institute of Cellular Therapeutics, Allegheny-Singer Research Institute, Allegheny Health Network, Pittsburgh, PA, USA. ; Division of Diabetes, Endocrinology, and Metabolism, Department of Medicine, and Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN, USA. VA Tennessee Valley Healthcare System, Nashville, TN, USA. ; Immunology and Diabetes Unit, St. Vincent's Institute of Medical Research, 9 Princes Street, Fitzroy, Victoria 3065, Australia. University of Melbourne, Department of Medicine, St. Vincent's Hospital, Fitzroy, Victoria 3065, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912858" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; C-Peptide/chemistry/*immunology ; CD4-Positive T-Lymphocytes/*immunology ; Clone Cells ; Diabetes Mellitus, Experimental/*immunology/pathology ; Diabetes Mellitus, Type 1/*immunology/pathology ; Epitopes/*immunology ; Immune Tolerance ; Insulin-Secreting Cells/*immunology/pathology ; Mice ; Mice, Inbred NOD ; Molecular Sequence Data ; Peptides/chemistry/immunology
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  • 54
    Publication Date: 2016-01-02
    Description: Frame-disrupting mutations in the DMD gene, encoding dystrophin, compromise myofiber integrity and drive muscle deterioration in Duchenne muscular dystrophy (DMD). Removing one or more exons from the mutated transcript can produce an in-frame mRNA and a truncated, but still functional, protein. In this study, we developed and tested a direct gene-editing approach to induce exon deletion and recover dystrophin expression in the mdx mouse model of DMD. Delivery by adeno-associated virus (AAV) of clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 endonucleases coupled with paired guide RNAs flanking the mutated Dmd exon23 resulted in excision of intervening DNA and restored the Dmd reading frame in myofibers, cardiomyocytes, and muscle stem cells after local or systemic delivery. AAV-Dmd CRISPR treatment partially recovered muscle functional deficiencies and generated a pool of endogenously corrected myogenic precursors in mdx mouse muscle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tabebordbar, Mohammadsharif -- Zhu, Kexian -- Cheng, Jason K W -- Chew, Wei Leong -- Widrick, Jeffrey J -- Yan, Winston X -- Maesner, Claire -- Wu, Elizabeth Y -- Xiao, Ru -- Ran, F Ann -- Cong, Le -- Zhang, Feng -- Vandenberghe, Luk H -- Church, George M -- Wagers, Amy J -- 1DP2OD004345/OD/NIH HHS/ -- 5DP1-MH100706/DP/NCCDPHP CDC HHS/ -- 5PN2EY018244/EY/NEI NIH HHS/ -- 5R01DK097768-03/DK/NIDDK NIH HHS/ -- 5U01HL100402/HL/NHLBI NIH HHS/ -- P50 HG005550/HG/NHGRI NIH HHS/ -- T2GM007753/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):407-11. doi: 10.1126/science.aad5177. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA 02115, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. ; Biological and Biomedical Sciences Program, Harvard Medical School, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Genetics and Program in Genomics, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. McGovern Institute for Brain Research, Department of Brain and Cognitive Science, and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Grousbeck Gene Therapy Center, Schepens Eye Research Institute, and Massachusetts Eye and Ear Infirmary, 20 Staniford Street, Boston, MA 02114, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Stem Cell and Regenerative Biology, Harvard University, and Harvard Stem Cell Institute, Cambridge, MA 02138, USA. amy_wagers@harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; Dependovirus ; Disease Models, Animal ; Exons ; Frameshift Mutation ; Genetic Therapy/*methods ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/metabolism ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Myocardium/metabolism ; RNA, Messenger/genetics ; Satellite Cells, Skeletal Muscle/*metabolism ; Sequence Deletion ; Transduction, Genetic/*methods
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  • 55
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takamura, Noboru -- Orita, Makiko -- Yamashita, Shunichi -- Chhem, Rethy -- New York, N.Y. -- Science. 2016 May 6;352(6286):666. doi: 10.1126/science.352.6286.666-a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. takamura@nagasaki-u.ac.jp. ; Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. ; Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, 852-8523 Japan. Cambodia Development Resource Institute, Phnom Penh 622, Cambodia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27151855" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Radiation-Induced/*epidemiology ; *Disasters ; *Epidemics ; Female ; *Fukushima Nuclear Accident ; Humans ; Radiation Exposure/*adverse effects ; Thyroid Gland/*abnormalities/*pathology ; Thyroid Neoplasms/*epidemiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 56
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Devkota, Suzanne -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):452-3. doi: 10.1126/science.aaf1353.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA. suzanne.devkota@cshs.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823414" target="_blank"〉PubMed〈/a〉
    Keywords: Diabetes Mellitus, Type 2/*microbiology ; Female ; Gastrointestinal Microbiome/*drug effects/*physiology ; Humans ; Male ; Metformin/*pharmacology
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  • 57
    Publication Date: 2016-01-28
    Description: Genes encoding human beta-type globin undergo a developmental switch from embryonic to fetal to adult-type expression. Mutations in the adult form cause inherited hemoglobinopathies or globin disorders, including sickle cell disease and thalassemia. Some experimental results have suggested that these diseases could be treated by induction of fetal-type hemoglobin (HbF). However, the mechanisms that repress HbF in adults remain unclear. We found that the LRF/ZBTB7A transcription factor occupies fetal gamma-globin genes and maintains the nucleosome density necessary for gamma-globin gene silencing in adults, and that LRF confers its repressive activity through a NuRD repressor complex independent of the fetal globin repressor BCL11A. Our study may provide additional opportunities for therapeutic targeting in the treatment of hemoglobinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4778394/" 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/PMC4778394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masuda, Takeshi -- Wang, Xin -- Maeda, Manami -- Canver, Matthew C -- Sher, Falak -- Funnell, Alister P W -- Fisher, Chris -- Suciu, Maria -- Martyn, Gabriella E -- Norton, Laura J -- Zhu, Catherine -- Kurita, Ryo -- Nakamura, Yukio -- Xu, Jian -- Higgs, Douglas R -- Crossley, Merlin -- Bauer, Daniel E -- Orkin, Stuart H -- Kharchenko, Peter V -- Maeda, Takahiro -- R01 AI084905/AI/NIAID NIH HHS/ -- R01 HL032259/HL/NHLBI NIH HHS/ -- R56 DK105001/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):285-9. doi: 10.1126/science.aad3312.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. ; School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia. ; Medical Research Council, Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, Oxford University, Oxford, UK. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. ; Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Ibaraki, Japan. Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Children's Research Institute, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Division of Hematology/Oncology, Boston Children's Hospital, Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Department of Biomedical Informatics, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org. ; Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. peter.kharchenko@post.harvard.edu tmaeda@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816381" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Sickle Cell/genetics ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Line ; Chromatin/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Erythroblasts/cytology ; Erythropoiesis/genetics ; Fetal Hemoglobin/*genetics ; *Gene Silencing ; Humans ; Mice ; Mice, Knockout ; Nuclear Proteins/genetics/*metabolism ; Repressor Proteins/genetics/*metabolism ; Sequence Deletion ; Thalassemia/genetics ; Transcription Factors/genetics/*metabolism ; gamma-Globins/*genetics
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  • 58
    Publication Date: 2016-04-30
    Description: Wakefulness is driven by the widespread release of neuromodulators by the ascending arousal system. Yet, it is unclear how these substances orchestrate state-dependent, global changes in neuronal activity. Here, we show that neuromodulators induce increases in the extracellular K(+) concentration ([K(+)]e) in cortical slices electrically silenced by tetrodotoxin. In vivo, arousal was linked to AMPA receptor-independent elevations of [K(+)]e concomitant with decreases in [Ca(2+)]e, [Mg(2+)]e, [H(+)]e, and the extracellular volume. Opposite, natural sleep and anesthesia reduced [K(+)]e while increasing [Ca(2+)]e, [Mg(2+)]e, and [H(+)]e as well as the extracellular volume. Local cortical activity of sleeping mice could be readily converted to the stereotypical electroencephalography pattern of wakefulness by simply imposing a change in the extracellular ion composition. Thus, extracellular ions control the state-dependent patterns of neural activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Fengfei -- O'Donnell, John -- Xu, Qiwu -- Kang, Ning -- Goldman, Nanna -- Nedergaard, Maiken -- NS078167/NS/NINDS NIH HHS/ -- NS078304/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):550-5. doi: 10.1126/science.aad4821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. ; Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. ; Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA. Center for Basic and Translational Neuroscience, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark. nedergaard@urmc.rochester.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/analysis/metabolism ; Cations/analysis/*metabolism ; Cerebral Cortex/chemistry/drug effects/*physiology ; Electroencephalography ; Magnesium/analysis/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/drug effects/metabolism/physiology ; Neurotransmitter Agents/metabolism/pharmacology ; Potassium/*metabolism ; Receptors, AMPA/metabolism ; Sleep/drug effects/*physiology ; Sodium Channel Blockers/pharmacology ; Tetrodotoxin/pharmacology ; Wakefulness/drug effects/*physiology
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  • 59
    Publication Date: 2016-03-19
    Description: Systemic inflammation, which results from the massive release of proinflammatory molecules into the circulatory system, is a major risk factor for severe illness, but the precise mechanisms underlying its control are not fully understood. We observed that prostaglandin E2 (PGE2), through its receptor EP4, is down-regulated in human systemic inflammatory disease. Mice with reduced PGE2 synthesis develop systemic inflammation, associated with translocation of gut bacteria, which can be prevented by treatment with EP4 agonists. Mechanistically, we demonstrate that PGE2-EP4 signaling acts directly on type 3 innate lymphoid cells (ILCs), promoting their homeostasis and driving them to produce interleukin-22 (IL-22). Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic inflammation. Hence, the ILC-IL-22 axis is essential in protecting against gut barrier dysfunction, enabling PGE2-EP4 signaling to impede systemic inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841390/" 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/PMC4841390/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffin, Rodger -- O'Connor, Richard A -- Crittenden, Siobhan -- Forster, Thorsten -- Yu, Cunjing -- Zheng, Xiaozhong -- Smyth, Danielle -- Robb, Calum T -- Rossi, Fiona -- Skouras, Christos -- Tang, Shaohui -- Richards, James -- Pellicoro, Antonella -- Weller, Richard B -- Breyer, Richard M -- Mole, Damian J -- Iredale, John P -- Anderton, Stephen M -- Narumiya, Shuh -- Maizels, Rick M -- Ghazal, Peter -- Howie, Sarah E -- Rossi, Adriano G -- Yao, Chengcan -- 106122/Wellcome Trust/United Kingdom -- BB/K091121/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- DK37097/DK/NIDDK NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1333-8. doi: 10.1126/science.aad9903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. ; Institute for Immunology and Infection Research, The University of Edinburgh, Edinburgh EH9 3JT, UK. ; MRC Centre for Regenerative Medicine, The University of Edinburgh, Edinburgh EH16 4UU, UK. ; Department of Gastroenterology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China. ; Department of Veterans Affairs, Tennessee Valley Health Authority, Nashville, TN 37212, USA. Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA. ; Center for Innovation in Immunoregulative Technology and Therapeutics (AK Project), Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan. Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo 102-0075, Japan. ; Division of Pathway Medicine, Edinburgh Infectious Diseases, The University of Edinburgh, Edinburgh EH16 4SB, UK. Centre for Synthetic and Systems Biology (SynthSys), The University of Edinburgh, Edinburgh EH9 3JD, UK. ; Medical Research Council (MRC) Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. chengcan.yao@ed.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Infections/genetics/immunology ; Dinoprostone/*immunology ; Gene Expression ; Humans ; Immunity, Innate ; Inflammation/drug therapy/*immunology/microbiology ; Interleukins/*immunology ; Intestines/*immunology/microbiology ; Lymphocytes/*immunology ; Mice ; Receptors, Prostaglandin E, EP4 Subtype/antagonists & ; inhibitors/genetics/*immunology ; Signal Transduction
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  • 60
    Publication Date: 2016-03-05
    Description: During corticogenesis, excitatory neurons are born from progenitors located in the ventricular zone (VZ), from where they migrate to assemble into circuits. How neuronal identity is dynamically specified upon progenitor division is unknown. Here, we study this process using a high-temporal-resolution technology allowing fluorescent tagging of isochronic cohorts of newborn VZ cells. By combining this in vivo approach with single-cell transcriptomics in mice, we identify and functionally characterize neuron-specific primordial transcriptional programs as they dynamically unfold. Our results reveal early transcriptional waves that instruct the sequence and pace of neuronal differentiation events, guiding newborn neurons toward their final fate, and contribute to a road map for the reverse engineering of specific classes of cortical neurons from undifferentiated cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Telley, Ludovic -- Govindan, Subashika -- Prados, Julien -- Stevant, Isabelle -- Nef, Serge -- Dermitzakis, Emmanouil -- Dayer, Alexandre -- Jabaudon, Denis -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1443-6. doi: 10.1126/science.aad8361. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Neurosciences, University of Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. ; Department of Genetic Medicine and Development, University of Geneva, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. ; Department of Genetic Medicine and Development, University of Geneva, Switzerland. Biomedical Research Foundation Academy of Athens, Greece. Center of Excellence in Genomic Medicine Research, King Abdulaziz University, Saudi Arabia. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. ; Department of Basic Neurosciences, University of Geneva, Switzerland. Department of Psychiatry, Geneva University Hospital, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. ; Department of Basic Neurosciences, University of Geneva, Switzerland. Clinic of Neurology, Geneva University Hospital, Switzerland. Institute for Genetics and Genomics in Geneva (iGE3), University of Geneva, Switzerland. denis.jabaudon@unige.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Cerebral Ventricles/cytology/embryology ; DNA-Binding Proteins/genetics ; Female ; GPI-Linked Proteins/genetics ; Green Fluorescent Proteins/genetics ; Male ; Mice ; Neocortex/cytology/*embryology ; Nerve Tissue Proteins/genetics ; Neural Stem Cells/cytology ; Neurogenesis/*genetics ; Neurons/*cytology ; Neuropeptides/genetics ; SOXB1 Transcription Factors/genetics ; *Transcription, Genetic ; Transcriptome
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  • 61
    Publication Date: 2016-03-05
    Description: As tumors grow, they acquire mutations, some of which create neoantigens that influence the response of patients to immune checkpoint inhibitors. We explored the impact of neoantigen intratumor heterogeneity (ITH) on antitumor immunity. Through integrated analysis of ITH and neoantigen burden, we demonstrate a relationship between clonal neoantigen burden and overall survival in primary lung adenocarcinomas. CD8(+)tumor-infiltrating lymphocytes reactive to clonal neoantigens were identified in early-stage non-small cell lung cancer and expressed high levels of PD-1. Sensitivity to PD-1 and CTLA-4 blockade in patients with advanced NSCLC and melanoma was enhanced in tumors enriched for clonal neoantigens. T cells recognizing clonal neoantigens were detectable in patients with durable clinical benefit. Cytotoxic chemotherapy-induced subclonal neoantigens, contributing to an increased mutational load, were enriched in certain poor responders. These data suggest that neoantigen heterogeneity may influence immune surveillance and support therapeutic developments targeting clonal neoantigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGranahan, Nicholas -- Furness, Andrew J S -- Rosenthal, Rachel -- Ramskov, Sofie -- Lyngaa, Rikke -- Saini, Sunil Kumar -- Jamal-Hanjani, Mariam -- Wilson, Gareth A -- Birkbak, Nicolai J -- Hiley, Crispin T -- Watkins, Thomas B K -- Shafi, Seema -- Murugaesu, Nirupa -- Mitter, Richard -- Akarca, Ayse U -- Linares, Joseph -- Marafioti, Teresa -- Henry, Jake Y -- Van Allen, Eliezer M -- Miao, Diana -- Schilling, Bastian -- Schadendorf, Dirk -- Garraway, Levi A -- Makarov, Vladimir -- Rizvi, Naiyer A -- Snyder, Alexandra -- Hellmann, Matthew D -- Merghoub, Taha -- Wolchok, Jedd D -- Shukla, Sachet A -- Wu, Catherine J -- Peggs, Karl S -- Chan, Timothy A -- Hadrup, Sine R -- Quezada, Sergio A -- Swanton, Charles -- 12100/Cancer Research UK/United Kingdom -- 1R01CA155010-02/CA/NCI NIH HHS/ -- 1R01CA182461-01/CA/NCI NIH HHS/ -- 1R01CA184922-01/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1463-9. doi: 10.1126/science.aaf1490. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Francis Crick Institute, London WC2A 3LY, UK. Centre for Mathematics and Physics in the Life Sciences and Experimental Biology (CoMPLEX), University College London (UCL), London WC1E 6BT, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; Section for Immunology and Vaccinology, National Veterinary Institute, Technical University of Denmark, 1970 Frederiksberg C, Denmark. ; The Francis Crick Institute, London WC2A 3LY, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. ; The Francis Crick Institute, London WC2A 3LY, UK. ; Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. Department of Cellular Pathology, UCL, London WC1E 6BT, UK. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Dermatology, University Hospital, University Duisburg-Essen, 45147 Essen, Germany. German Cancer Consortium (DKTK), 69121 Heidelberg, Germany. ; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Hematology/Oncology Division, 177 Fort Washington Avenue, Columbia University, New York, NY 10032, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Department of Medicine, Harvard Medical School, Boston, MA 02115, USA. Department of Internal Medicine, Brigham and Woman's Hospital, Boston, MA 02115, USA. ; Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. Cancer Immunology Unit, UCL Cancer Institute, UCL, London WC1E 6BT, UK. s.quezada@ucl.ac.uk charles.swanton@crick.ac.uk. ; The Francis Crick Institute, London WC2A 3LY, UK. Cancer Research UK Lung Cancer Centre of Excellence, UCL Cancer Institute, London WC1E 6BT, UK. s.quezada@ucl.ac.uk charles.swanton@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940869" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/drug therapy/genetics/*immunology ; Aged ; Aged, 80 and over ; Antigens, Neoplasm/genetics/*immunology ; Antineoplastic Agents/therapeutic use ; CD4-Positive T-Lymphocytes/*immunology ; CTLA-4 Antigen/immunology ; Carcinoma, Non-Small-Cell Lung/genetics/immunology ; Cell Cycle Checkpoints/immunology ; Female ; Humans ; *Immunologic Surveillance ; Lung Neoplasms/drug therapy/genetics/*immunology ; Lymphocytes, Tumor-Infiltrating/immunology ; Male ; Melanoma/immunology ; Middle Aged ; Mutation ; Programmed Cell Death 1 Receptor/immunology ; Skin Neoplasms/immunology
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  • 62
    Publication Date: 2016-02-26
    Description: Transposable elements (TEs) are both a boon and a bane to eukaryotic organisms, depending on where they integrate into the genome and how their sequences function once integrated. We focus on two types of TEs: long interspersed elements (LINEs) and short interspersed elements (SINEs). LINEs and SINEs are retrotransposons; that is, they transpose via an RNA intermediate. We discuss how LINEs and SINEs have expanded in eukaryotic genomes and contribute to genome evolution. An emerging body of evidence indicates that LINEs and SINEs function to regulate gene expression by affecting chromatin structure, gene transcription, pre-mRNA processing, or aspects of mRNA metabolism. We also describe how adenosine-to-inosine editing influences SINE function and how ongoing retrotransposition is countered by the body's defense mechanisms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Elbarbary, Reyad A -- Lucas, Bronwyn A -- Maquat, Lynne E -- P30 AR061307/AR/NIAMS NIH HHS/ -- R37 GM074593/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):aac7247. doi: 10.1126/science.aac7247. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Center for RNA Biology, University of Rochester, Rochester, NY, USA. ; Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. Center for RNA Biology, University of Rochester, Rochester, NY, USA. Department of Oncology, Wilmot Cancer Institute, School of Medicine and Dentistry, University of Rochester, Rochester, NY, USA. lynne_maquat@urmc.rochester.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912865" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromatin/ultrastructure ; Disease/genetics ; Evolution, Molecular ; *Gene Expression Regulation ; Humans ; Long Interspersed Nucleotide Elements/genetics/*physiology ; Mice ; Protein Biosynthesis ; RNA Precursors/metabolism ; RNA Processing, Post-Transcriptional ; RNA Stability ; RNA, Messenger/metabolism ; Short Interspersed Nucleotide Elements/genetics/*physiology ; Transcription, Genetic
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  • 63
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McLaughlin, Kathleen -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):283. doi: 10.1126/science.352.6283.283.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kathleen McLaughlin is a writer in Beijing.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081050" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Aged, 80 and over ; Aging ; China/epidemiology ; *Family Relations ; Female ; Human Migration ; Humans ; Male ; Rural Population/*statistics & numerical data ; Sociology ; Suicide/*statistics & numerical data
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  • 64
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McNutt, Marcia -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):641. doi: 10.1126/science.aaf4014. Epub 2016 Feb 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Marcia McNutt Editor-in-Chief Science Journals.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912832" target="_blank"〉PubMed〈/a〉
    Keywords: Corrosion ; Federal Government ; Humans ; Michigan ; *Public Health ; Safety/*economics ; Trust ; United States ; United States Environmental Protection Agency ; Water Supply/*economics
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  • 65
    Publication Date: 2016-01-23
    Description: Oligodendrocytes myelinate axons in the central nervous system and develop from oligodendrocyte precursor cells (OPCs) that must first migrate extensively during brain and spinal cord development. We show that OPCs require the vasculature as a physical substrate for migration. We observed that OPCs of the embryonic mouse brain and spinal cord, as well as the human cortex, emerge from progenitor domains and associate with the abluminal endothelial surface of nearby blood vessels. Migrating OPCs crawl along and jump between vessels. OPC migration in vivo was disrupted in mice with defective vascular architecture but was normal in mice lacking pericytes. Thus, physical interactions with the vascular endothelium are required for OPC migration. We identify Wnt-Cxcr4 (chemokine receptor 4) signaling in regulation of OPC-endothelial interactions and propose that this signaling coordinates OPC migration with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tsai, Hui-Hsin -- Niu, Jianqin -- Munji, Roeben -- Davalos, Dimitrios -- Chang, Junlei -- Zhang, Haijing -- Tien, An-Chi -- Kuo, Calvin J -- Chan, Jonah R -- Daneman, Richard -- Fancy, Stephen P J -- 1P01 NS083513/NS/NINDS NIH HHS/ -- 1R01NS064517/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):379-84. doi: 10.1126/science.aad3839.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. ; Departments of Pharmacology and Neuroscience, University of California at San Diego (UCSD), San Diego, CA 92093, USA. ; Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. ; Division of Hematology, Department of Medicine, Stanford University, Stanford, CA 94305, USA. Department of Urology, Cleveland Clinic Foundation, Cleveland, OH 44195, USA. Howard Hughes Medical Institute (HHMI), Chevy Chase, MD 20815, USA. Duke University School of Medicine, Durham, NC 27710, USA. ; Department of Neurology, UCSF, San Francisco, CA 94158, USA. ; Department of Pediatrics, University of California at San Francisco (UCSF), San Francisco, CA 94158, USA. Department of Neurology, UCSF, San Francisco, CA 94158, USA. Division of Neonatology, UCSF, San Francisco, CA 94158, USA. Newborn Brain Research Institute, UCSF, San Francisco, CA 94158, USA. stephen.fancy@ucsf.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26798014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology/embryology ; *Cell Movement ; Cerebral Cortex/blood supply/*embryology ; Endothelium, Vascular/cytology ; Humans ; Mice ; Neural Stem Cells/cytology/*physiology ; *Neurogenesis ; Oligodendroglia/cytology/*physiology ; *Organogenesis ; Pericytes/cytology/physiology ; Receptors, CXCR4/metabolism ; Signal Transduction ; Spinal Cord/blood supply/cytology/*embryology ; Wnt Proteins/metabolism
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  • 66
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fahlgren, Noah -- Bart, Rebecca -- Herrera-Estrella, Luis -- Rellan-Alvarez, Ruben -- Chitwood, Daniel H -- Dinneny, Jose R -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):824. doi: 10.1126/science.351.6275.824-a. Epub 2016 Feb 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Donald Danforth Plant Science Center, St. Louis, MO 63132, USA. ; Nacional de Genomica para la Biodiversidad, Irapuato, 36821, Mexico. ; Donald Danforth Plant Science Center, St. Louis, MO 63132, USA. jdinneny@carnegiescience.edu dchitwood@danforthcenter.org. ; Carnegie Institution for Science, Stanford, CA 94305, USA. jdinneny@carnegiescience.edu dchitwood@danforthcenter.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912883" target="_blank"〉PubMed〈/a〉
    Keywords: China ; Food, Genetically Modified/*adverse effects ; Genetic Engineering/*utilization ; Health ; Humans ; Plants, Genetically Modified/*adverse effects/genetics ; United States ; Zea mays/genetics
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  • 67
    Publication Date: 2016-01-30
    Description: Infection elicits CD4(+) memory T lymphocytes that participate in protective immunity. Although memory cells are the progeny of naive T cells, it is unclear that all naive cells from a polyclonal repertoire have memory cell potential. Using a single-cell adoptive transfer and spleen biopsy method, we found that in mice, essentially all microbe-specific naive cells produced memory cells during infection. Different clonal memory cell populations had different B cell or macrophage helper compositions that matched effector cell populations generated much earlier in the response. Thus, each microbe-specific naive CD4(+) T cell produces a distinctive ratio of effector cell types early in the immune response that is maintained as some cells in the clonal population become memory cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776317/" 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/PMC4776317/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tubo, Noah J -- Fife, Brian T -- Pagan, Antonio J -- Kotov, Dmitri I -- Goldberg, Michael F -- Jenkins, Marc K -- F32 AI107995/AI/NIAID NIH HHS/ -- R01 AI039614/AI/NIAID NIH HHS/ -- R01 AI106791/AI/NIAID NIH HHS/ -- T32 HL007062/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):511-4. doi: 10.1126/science.aad0483.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Mediated Disease Therapy Group, Genzyme, a Sanofi Company, Framingham, MA 01701, USA. ; Department of Medicine, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Department of Medicine, MRC Laboratory of Molecular Biology, Cambridge, UK. ; Department of Microbiology and Immunology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. ; Department of Microbiology and Immunology, Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455, USA. jenki002@umn.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823430" target="_blank"〉PubMed〈/a〉
    Keywords: Adoptive Transfer ; Animals ; B-Lymphocytes/immunology ; Bacterial Toxins/immunology ; CD4-Positive T-Lymphocytes/*immunology/*microbiology ; Clone Cells/immunology ; Heat-Shock Proteins/immunology ; Hemolysin Proteins/immunology ; *Immunologic Memory ; Listeria monocytogenes/*immunology ; Listeriosis/*immunology ; Mice ; Mice, Inbred C57BL ; Receptors, CXCR5/genetics/immunology ; Single-Cell Analysis
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  • 68
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuting, Thomas -- de Visser, Karin E -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):145-6. doi: 10.1126/science.aaf7300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University Hospital Magdeburg, Magdeburg, Germany. ; Division of Immunology, The Netherlands Cancer Institute, Amsterdam, Netherlands. k.d.visser@nki.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bystander Effect ; Humans ; Immunotherapy/methods ; Leukocyte Count ; Mice ; Mice, Transgenic ; Neoplasm Metastasis/*immunology/*therapy ; Neoplasms, Experimental/immunology/pathology/therapy ; Neutrophils/*immunology/*pathology
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  • 69
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):799-800. doi: 10.1126/science.351.6275.799.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912871" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Brain Mapping/economics/*methods ; DNA/*analysis ; Financing, Organized ; Fluorescence ; Mice ; Nerve Net/physiology ; Neurons/*chemistry ; Neurosciences/economics/trends ; RNA/*analysis ; Synapses/*physiology
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  • 70
    Publication Date: 2016-03-26
    Description: Brazil has experienced an unprecedented epidemic of Zika virus (ZIKV), with ~30,000 cases reported to date. ZIKV was first detected in Brazil in May 2015, and cases of microcephaly potentially associated with ZIKV infection were identified in November 2015. We performed next-generation sequencing to generate seven Brazilian ZIKV genomes sampled from four self-limited cases, one blood donor, one fatal adult case, and one newborn with microcephaly and congenital malformations. Results of phylogenetic and molecular clock analyses show a single introduction of ZIKV into the Americas, which we estimated to have occurred between May and December 2013, more than 12 months before the detection of ZIKV in Brazil. The estimated date of origin coincides with an increase in air passengers to Brazil from ZIKV-endemic areas, as well as with reported outbreaks in the Pacific Islands. ZIKV genomes from Brazil are phylogenetically interspersed with those from other South American and Caribbean countries. Mapping mutations onto existing structural models revealed the context of viral amino acid changes present in the outbreak lineage; however, no shared amino acid changes were found among the three currently available virus genomes from microcephaly cases. Municipality-level incidence data indicate that reports of suspected microcephaly in Brazil best correlate with ZIKV incidence around week 17 of pregnancy, although this correlation does not demonstrate causation. Our genetic description and analysis of ZIKV isolates in Brazil provide a baseline for future studies of the evolution and molecular epidemiology of this emerging virus in the Americas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Faria, Nuno Rodrigues -- Azevedo, Raimunda do Socorro da Silva -- Kraemer, Moritz U G -- Souza, Renato -- Cunha, Mariana Sequetin -- Hill, Sarah C -- Theze, Julien -- Bonsall, Michael B -- Bowden, Thomas A -- Rissanen, Ilona -- Rocco, Iray Maria -- Nogueira, Juliana Silva -- Maeda, Adriana Yurika -- Vasami, Fernanda Giseli da Silva -- Macedo, Fernando Luiz de Lima -- Suzuki, Akemi -- Rodrigues, Sueli Guerreiro -- Cruz, Ana Cecilia Ribeiro -- Nunes, Bruno Tardeli -- Medeiros, Daniele Barbosa de Almeida -- Rodrigues, Daniela Sueli Guerreiro -- Nunes Queiroz, Alice Louize -- da Silva, Eliana Vieira Pinto -- Henriques, Daniele Freitas -- Travassos da Rosa, Elisabeth Salbe -- de Oliveira, Consuelo Silva -- Martins, Livia Caricio -- Vasconcelos, Helena Baldez -- Casseb, Livia Medeiros Neves -- Simith, Darlene de Brito -- Messina, Jane P -- Abade, Leandro -- Lourenco, Jose -- Carlos Junior Alcantara, Luiz -- de Lima, Maricelia Maia -- Giovanetti, Marta -- Hay, Simon I -- de Oliveira, Rodrigo Santos -- Lemos, Poliana da Silva -- de Oliveira, Layanna Freitas -- de Lima, Clayton Pereira Silva -- da Silva, Sandro Patroca -- de Vasconcelos, Janaina Mota -- Franco, Luciano -- Cardoso, Jedson Ferreira -- Vianez-Junior, Joao Lidio da Silva Goncalves -- Mir, Daiana -- Bello, Gonzalo -- Delatorre, Edson -- Khan, Kamran -- Creatore, Marisa -- Coelho, Giovanini Evelim -- de Oliveira, Wanderson Kleber -- Tesh, Robert -- Pybus, Oliver G -- Nunes, Marcio R T -- Vasconcelos, Pedro F C -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 095066/Wellcome Trust/United Kingdom -- 102427/Wellcome Trust/United Kingdom -- MR/L009528/1/Medical Research Council/United Kingdom -- R24 AT 120942/AT/NCCIH NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):345-9. doi: 10.1126/science.aaf5036. Epub 2016 Mar 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Para State, Brazil. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. ; Instituto Adolfo Lutz, University of Sao Paulo, Sao Paulo, Brazil. ; Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. Metabiota, San Francisco, CA 94104, USA. ; Oswaldo Cruz Foundation (FIOCRUZ), Salvador, Bahia, Brazil. ; Centre of Post Graduation in Collective Health, Department of Health, Universidade Estadual de Feira de Santana, Feira de Santana, Bahia, Brazil. ; Institute for Health Metrics and Evaluation, University of Washington, Seattle, WA 98121, USA. Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. ; Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. ; Laboratorio de AIDS and Imunologia Molecular, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brazil. ; Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada. Department of Medicine, Division of Infectious Diseases, University of Toronto, Toronto, Ontario, Canada. ; Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. ; Brazilian Ministry of Health, Brasilia, Brazil. ; Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. ; Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. Metabiota, San Francisco, CA 94104, USA. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br. ; Center for Technological Innovation, Evandro Chagas Institute, Ministry of Health, Ananindeua, PA 67030-000, Brazil. Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br. ; Department of Arbovirology and Hemorrhagic Fevers, Evandro Chagas Institute, Ministry of Health, Ananindeua, Para State, Brazil. oliver.pybus@zoo.ox.ac.uk marcionunesbrasil@yahoo.com.br pedrovasconcelos@iec.pa.gov.br.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013429" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/virology ; Americas/epidemiology ; Animals ; *Disease Outbreaks ; Female ; Genome, Viral/genetics ; Humans ; Incidence ; Insect Vectors/virology ; Microcephaly/*epidemiology/virology ; Molecular Epidemiology ; Molecular Sequence Data ; Mutation ; Pacific Islands/epidemiology ; Phylogeny ; Pregnancy ; RNA, Viral/genetics ; Sequence Analysis, RNA ; Travel ; Zika Virus/classification/*genetics/isolation & purification ; Zika Virus Infection/*epidemiology/transmission/*virology
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  • 71
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):116-9. doi: 10.1126/science.351.6269.116.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744391" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies/*therapeutic use ; Clinical Trials as Topic ; *Cortical Spreading Depression/drug effects/immunology/physiology ; Drug Design ; Drug Industry ; Female ; Humans ; Male ; Migraine Disorders/*immunology/physiopathology/*therapy ; Receptors, Calcitonin Gene-Related Peptide/*antagonists & inhibitors/immunology ; Sex Ratio
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  • 72
    Publication Date: 2016-02-26
    Description: Astrocytes are specialized and heterogeneous cells that contribute to central nervous system function and homeostasis. However, the mechanisms that create and maintain differences among astrocytes and allow them to fulfill particular physiological roles remain poorly defined. We reveal that neurons actively determine the features of astrocytes in the healthy adult brain and define a role for neuron-derived sonic hedgehog (Shh) in regulating the molecular and functional profile of astrocytes. Thus, the molecular and physiological program of astrocytes is not hardwired during development but, rather, depends on cues from neurons that drive and sustain their specialized properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farmer, W Todd -- Abrahamsson, Therese -- Chierzi, Sabrina -- Lui, Christopher -- Zaelzer, Cristian -- Jones, Emma V -- Bally, Blandine Ponroy -- Chen, Gary G -- Theroux, Jean-Francois -- Peng, Jimmy -- Bourque, Charles W -- Charron, Frederic -- Ernst, Carl -- Sjostrom, P Jesper -- Murai, Keith K -- FDN 143337/Canadian Institutes of Health Research/Canada -- MOP 111152/Canadian Institutes of Health Research/Canada -- MOP 123390/Canadian Institutes of Health Research/Canada -- MOP 126137/Canadian Institutes of Health Research/Canada -- NIA 288936/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):849-54. doi: 10.1126/science.aab3103.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, Brain Repair and Integrative Neuroscience Program, The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. ; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. McGill Group for Suicide Studies, Douglas Hospital, Montreal, Quebec, Canada. ; Molecular Biology of Neural Development, Institut de Recherches Cliniques de Montreal, Department of Medicine, University of Montreal, Montreal, Quebec, Canada. Department of Biology, McGill University, Montreal, Quebec, Canada. ; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. McGill Group for Suicide Studies, Douglas Hospital, Montreal, Quebec, Canada. Department of Human Genetics, McGill University, Montreal, Quebec, Canada. Douglas Hospital Research Institute, Verdun, Quebec, Canada. ; Centre for Research in Neuroscience, Department of Neurology and Neurosurgery, Brain Repair and Integrative Neuroscience Program, The Research Institute of the McGill University Health Centre, Montreal General Hospital, Montreal, Quebec, Canada. keith.murai@mcgill.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912893" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism ; Cerebellar Cortex/*cytology ; Female ; Gene Deletion ; Hedgehog Proteins/genetics/*metabolism ; Male ; Mice ; Mice, Mutant Strains ; Neurons/*metabolism ; Receptors, G-Protein-Coupled/genetics/*metabolism ; Signal Transduction
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  • 73
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, Jeffrey -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):115. doi: 10.1126/science.351.6269.115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744390" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Financing, Organized/*statistics & numerical data ; Humans ; Research Personnel ; Research Support as Topic/*statistics & numerical data ; *Sexism ; United States ; *Women, Working
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  • 74
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mervis, Jeffrey -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):10-1. doi: 10.1126/science.351.6268.10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉With reporting from Science's news staff.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721980" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/*economics ; Budgets ; Humans ; National Institutes of Health (U.S.)/*economics ; *Research Support as Topic ; United States ; United States National Aeronautics and Space Administration/economics
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  • 75
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Underwood, Emily -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):277-8. doi: 10.1126/science.352.6283.277.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081045" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain ; *Datasets as Topic ; European Union ; Humans ; International Cooperation ; Neurosciences/*trends ; United States
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  • 76
    Publication Date: 2016-01-02
    Description: Motivation for reward drives adaptive behaviors, whereas impairment of reward perception and experience (anhedonia) can contribute to psychiatric diseases, including depression and schizophrenia. We sought to test the hypothesis that the medial prefrontal cortex (mPFC) controls interactions among specific subcortical regions that govern hedonic responses. By using optogenetic functional magnetic resonance imaging to locally manipulate but globally visualize neural activity in rats, we found that dopamine neuron stimulation drives striatal activity, whereas locally increased mPFC excitability reduces this striatal response and inhibits the behavioral drive for dopaminergic stimulation. This chronic mPFC overactivity also stably suppresses natural reward-motivated behaviors and induces specific new brainwide functional interactions, which predict the degree of anhedonia in individuals. These findings describe a mechanism by which mPFC modulates expression of reward-seeking behavior, by regulating the dynamical interactions between specific distant subcortical regions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772156/" 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/PMC4772156/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferenczi, Emily A -- Zalocusky, Kelly A -- Liston, Conor -- Grosenick, Logan -- Warden, Melissa R -- Amatya, Debha -- Katovich, Kiefer -- Mehta, Hershel -- Patenaude, Brian -- Ramakrishnan, Charu -- Kalanithi, Paul -- Etkin, Amit -- Knutson, Brian -- Glover, Gary H -- Deisseroth, Karl -- 1F31MH105151_01/MH/NIMH NIH HHS/ -- P41 EB015891/EB/NIBIB NIH HHS/ -- R00 MH097822/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Jan 1;351(6268):aac9698. doi: 10.1126/science.aac9698.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. Neurosciences Program, Stanford University, Stanford, CA 94305, USA. ; Brain Mind Research Institute, Weill Cornell Medical College, New York, NY 10065, USA. ; Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA. ; Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. ; Department of Psychology, Stanford University, Stanford, CA 94305, USA. ; Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA 94305, USA. ; Department of Neurosurgery, Stanford University, Stanford, CA 94305, USA. ; Department of Radiology, Stanford University, Stanford, CA, 94305, USA. ; Department of Bioengineering, Stanford University, Stanford, CA 94305, USA. Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA. Howard Hughes Medical Institute, Stanford University, Stanford, CA, 94305, USA. deissero@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26722001" target="_blank"〉PubMed〈/a〉
    Keywords: Anhedonia/*physiology ; Animals ; Brain Mapping ; Corpus Striatum/cytology/drug effects/*physiology ; Depressive Disorder/physiopathology ; Dopamine/pharmacology ; Dopaminergic Neurons/drug effects/*physiology ; Female ; Magnetic Resonance Imaging ; Male ; Mesencephalon/cytology/drug effects/physiology ; *Motivation ; Nerve Net/physiology ; Oxygen/blood ; Prefrontal Cortex/cytology/drug effects/*physiology ; Rats ; Rats, Inbred LEC ; Rats, Sprague-Dawley ; *Reward ; Schizophrenia/physiopathology
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  • 77
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, Harold -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):123. doi: 10.1126/science.aaf7301.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harold Varmus is the Lewis Thomas University Professor at the Meyer Cancer Center, Weill Cornell Medicine, New York, NY; Senior Associate Member of the New York Genome Center, New York, NY; and former director of the U.S. National Cancer Institute. varmus@med.cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124426" target="_blank"〉PubMed〈/a〉
    Keywords: Federal Government ; Humans ; Information Dissemination ; *Leadership ; Medical Oncology/economics/*trends ; Neoplasms/diagnosis/drug therapy/prevention & control ; United States
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  • 78
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: Berkowitz et al. (Reports, 9 October 2015, p. 196) described a randomized field experiment testing whether a math app designed to increase parent-child interaction could also bring academic benefits. A reanalysis of the data suggests that this well-designed trial failed to find strong evidence for the efficacy of the intervention. In particular, there was no significant effect of the intervention on math performance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frank, Michael C -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1161. doi: 10.1126/science.aad8008. Epub 2016 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Stanford University, Stanford, CA, USA. mcfrank@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965619" target="_blank"〉PubMed〈/a〉
    Keywords: *Educational Status ; Female ; Humans ; *Intergenerational Relations ; Male ; Mathematics/*education ; *Parent-Child Relations ; Students/*psychology
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fu, He -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):486. doi: 10.1126/science.352.6284.486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉He Fu is a Ph.D. candidate in the Department of Microbiology at the University of Illinois, Urbana-Champaign. For more on life and careers, visit sciencecareers.org. Send your story to SciCareerEditor@aaas.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102487" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; China ; *International Educational Exchange ; Microbiology/*education ; United States
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  • 80
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Midorikawa, Sanae -- Suzuki, Satoru -- Ohtsuru, Akira -- New York, N.Y. -- Science. 2016 May 6;352(6286):666-7. doi: 10.1126/science.352.6286.666-c.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Radiation Medical Science Center, Fukushima Medical University, Fukushima, 960-1295, Japan. Department of Radiation Health Management, Fukushima Medical University, Fukushima, 960-1295, Japan. hana@fmu.ac.jp. ; Radiation Medical Science Center, Fukushima Medical University, Fukushima, 960-1295, Japan. Department of Thyroid and Endocrinology, Fukushima Medical University, Fukushima, 960-1295, Japan. ; Radiation Medical Science Center, Fukushima Medical University, Fukushima, 960-1295, Japan. Department of Radiation Health Management, Fukushima Medical University, Fukushima, 960-1295, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27151857" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Radiation-Induced/*epidemiology ; *Disasters ; *Epidemics ; Female ; *Fukushima Nuclear Accident ; Humans ; Radiation Exposure/*adverse effects ; Thyroid Gland/*abnormalities/*pathology ; Thyroid Neoplasms/*epidemiology
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  • 81
    Publication Date: 2016-03-19
    Description: Steroids regulate cell proliferation, tissue development, and cell signaling via two pathways: a nuclear receptor mechanism and genome-independent signaling. Sperm activation, egg maturation, and steroid-induced anesthesia are executed via the latter pathway, the key components of which remain unknown. Here, we present characterization of the human sperm progesterone receptor that is conveyed by the orphan enzyme alpha/beta hydrolase domain-containing protein 2 (ABHD2). We show that ABHD2 is highly expressed in spermatozoa, binds progesterone, and acts as a progesterone-dependent lipid hydrolase by depleting the endocannabinoid 2-arachidonoylglycerol (2AG) from plasma membrane. The 2AG inhibits the sperm calcium channel (CatSper), and its removal leads to calcium influx via CatSper and ensures sperm activation. This study reveals that progesterone-activated endocannabinoid depletion by ABHD2 is a general mechanism by which progesterone exerts its genome-independent action and primes sperm for fertilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Melissa R -- Mannowetz, Nadja -- Iavarone, Anthony T -- Safavi, Rojin -- Gracheva, Elena O -- Smith, James F -- Hill, Rose Z -- Bautista, Diana M -- Kirichok, Yuriy -- Lishko, Polina V -- 1S10OD020062-01/OD/NIH HHS/ -- R01 AR059385/AR/NIAMS NIH HHS/ -- R01AR059385/AR/NIAMS NIH HHS/ -- R01GM111802/GM/NIGMS NIH HHS/ -- R01HD068914/HD/NICHD NIH HHS/ -- R21HD081403/HD/NICHD NIH HHS/ -- S10RR025622/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):555-9. doi: 10.1126/science.aad6887. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. ; QB3/Chemistry Mass Spectrometry Facility, University of California, Berkeley, CA 94720, USA. ; Department of Cellular and Molecular Physiology; Department of Neuroscience, Program in Cellular Neuroscience, Neurodegeneration, and Repair (CNNR), Yale School of Medicine, Yale University, New Haven, CT 06536, USA. ; Department of Urology, University of California, San Francisco, CA 94143, USA. ; Department of Physiology, University of California, San Francisco, CA 94158, USA. ; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA. lishko@berkeley.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989199" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Arachidonic Acids/*deficiency ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling ; Cell Membrane/metabolism ; Endocannabinoids/*deficiency ; Fertilization ; Glycerides/*deficiency ; Humans ; Hydrolases/genetics/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Progesterone/*metabolism/pharmacology ; Rats ; Rats, Wistar ; Receptors, Progesterone/genetics/*metabolism ; Sperm Motility/drug effects/*physiology ; Spermatozoa/drug effects/metabolism/*physiology ; Young Adult
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  • 82
    Publication Date: 2016-04-23
    Description: Progression through the stages of lymphocyte development requires coordination of the cell cycle. Such coordination ensures genomic integrity while cells somatically rearrange their antigen receptor genes [in a process called variable-diversity-joining (VDJ) recombination] and, upon successful rearrangement, expands the pools of progenitor lymphocytes. Here we show that in developing B lymphocytes, the RNA-binding proteins (RBPs) ZFP36L1 and ZFP36L2 are critical for maintaining quiescence before precursor B cell receptor (pre-BCR) expression and for reestablishing quiescence after pre-BCR-induced expansion. These RBPs suppress an evolutionarily conserved posttranscriptional regulon consisting of messenger RNAs whose protein products cooperatively promote transition into the S phase of the cell cycle. This mechanism promotes VDJ recombination and effective selection of cells expressing immunoglobulin-mu at the pre-BCR checkpoint.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galloway, Alison -- Saveliev, Alexander -- Lukasiak, Sebastian -- Hodson, Daniel J -- Bolland, Daniel -- Balmanno, Kathryn -- Ahlfors, Helena -- Monzon-Casanova, Elisa -- Mannurita, Sara Ciullini -- Bell, Lewis S -- Andrews, Simon -- Diaz-Munoz, Manuel D -- Cook, Simon J -- Corcoran, Anne -- Turner, Martin -- Medical Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):453-9. doi: 10.1126/science.aad5978.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. Department of Haematology, University of Cambridge, The Clifford Allbutt Building, Cambridge Biomedical Campus, Hills Road, Cambridge CB2 0AH, UK. ; Laboratory of Nuclear Dynamics, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Signalling, The Babraham Institute, Cambridge CB22 3AT, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Cambridge CB22 3AT, UK. Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK. ; Bioinformatics Group, The Babraham Institute, Cambridge CB22 3AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27102483" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology ; Conserved Sequence ; Cyclins/metabolism ; G0 Phase/genetics/physiology ; G1 Phase/genetics/physiology ; Gene Expression Regulation ; Immunoglobulin mu-Chains/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nuclear Proteins/genetics/*physiology ; Pre-B Cell Receptors ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics/*physiology ; S Phase/genetics/*physiology ; Selection, Genetic ; Transcription, Genetic ; Tristetraprolin/genetics/*physiology ; V(D)J Recombination
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2016 Mar 11;351(6278):1123-4. doi: 10.1126/science.351.6278.1123.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26965596" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*abnormalities/*virology ; Female ; Humans ; Infant ; Microcephaly/*virology ; Pregnancy ; Pregnancy Complications, Infectious/*virology ; World Health Organization ; *Zika Virus ; Zika Virus Infection/*complications
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  • 84
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-05-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyazaki, Makoto -- Tanigawa, Koichi -- Murakami, Michio -- New York, N.Y. -- Science. 2016 May 6;352(6286):666. doi: 10.1126/science.352.6286.666-b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Health Management, Fukushima Medical University, Fukushima, 960-1295, Japan. ; Fukushima Global Medical Science Center, Fukushima Medical University, Fukushima, 960-1295, Japan. tanigawa@fmu.ac.jp. ; Department of Risk Communication, Fukushima Medical University, Fukushima, 960-1295, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27151856" target="_blank"〉PubMed〈/a〉
    Keywords: Abnormalities, Radiation-Induced/*epidemiology ; *Disasters ; *Epidemics ; Female ; *Fukushima Nuclear Accident ; Humans ; Radiation Exposure/*adverse effects ; Thyroid Gland/*abnormalities/*pathology ; Thyroid Neoplasms/*epidemiology
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  • 85
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, Gretchen -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):110-1. doi: 10.1126/science.351.6269.110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26744386" target="_blank"〉PubMed〈/a〉
    Keywords: Brazil/epidemiology ; Communicable Diseases, Emerging/*epidemiology/*virology ; *Disease Outbreaks ; Female ; Fetal Blood/virology ; Flavivirus/isolation & purification/physiology ; Flavivirus Infections/diagnosis/*epidemiology ; Humans ; Infant ; Infant, Newborn ; Microcephaly/diagnosis/*epidemiology/*virology ; Pregnancy ; Pregnancy Complications, Infectious/*virology ; Virus Activation
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  • 86
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-03-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1250-1. doi: 10.1126/science.351.6279.1250. Epub 2016 Mar 17.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989228" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asia ; Biological Evolution ; Bone and Bones ; DNA/genetics ; Europe ; Female ; Fossils ; Humans ; Male ; *Mating Preference, Animal ; Neanderthals/*genetics/*psychology ; *Sexual Behavior
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  • 87
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibbons, Ann -- Culotta, Elizabeth -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):503-4. doi: 10.1126/science.352.6285.503.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126016" target="_blank"〉PubMed〈/a〉
    Keywords: Anthropology ; Congresses as Topic ; Female ; Humans ; Male ; Research Personnel ; Sexual Harassment/*prevention & control
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  • 88
    Publication Date: 2016-03-05
    Description: Examining complete gene knockouts within a viable organism can inform on gene function. We sequenced the exomes of 3222 British adults of Pakistani heritage with high parental relatedness, discovering 1111 rare-variant homozygous genotypes with predicted loss of function (knockouts) in 781 genes. We observed 13.7% fewer homozygous knockout genotypes than we expected, implying an average load of 1.6 recessive-lethal-equivalent loss-of-function (LOF) variants per adult. When genetic data were linked to the individuals' lifelong health records, we observed no significant relationship between gene knockouts and clinical consultation or prescription rate. In this data set, we identified a healthy PRDM9-knockout mother and performed phased genome sequencing on her, her child, and control individuals. Our results show that meiotic recombination sites are localized away from PRDM9-dependent hotspots. Thus, natural LOF variants inform on essential genetic loci and demonstrate PRDM9 redundancy in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Narasimhan, Vagheesh M -- Hunt, Karen A -- Mason, Dan -- Baker, Christopher L -- Karczewski, Konrad J -- Barnes, Michael R -- Barnett, Anthony H -- Bates, Chris -- Bellary, Srikanth -- Bockett, Nicholas A -- Giorda, Kristina -- Griffiths, Christopher J -- Hemingway, Harry -- Jia, Zhilong -- Kelly, M Ann -- Khawaja, Hajrah A -- Lek, Monkol -- McCarthy, Shane -- McEachan, Rosie -- O'Donnell-Luria, Anne -- Paigen, Kenneth -- Parisinos, Constantinos A -- Sheridan, Eamonn -- Southgate, Laura -- Tee, Louise -- Thomas, Mark -- Xue, Yali -- Schnall-Levin, Michael -- Petkov, Petko M -- Tyler-Smith, Chris -- Maher, Eamonn R -- Trembath, Richard C -- MacArthur, Daniel G -- Wright, John -- Durbin, Richard -- van Heel, David A -- GM 099640/GM/NIGMS NIH HHS/ -- MR/M009017/1/Medical Research Council/United Kingdom -- R01 GM104371/GM/NIGMS NIH HHS/ -- R01GM104371/GM/NIGMS NIH HHS/ -- WT098051/Wellcome Trust/United Kingdom -- WT099769/Wellcome Trust/United Kingdom -- WT101597/Wellcome Trust/United Kingdom -- WT102627/Wellcome Trust/United Kingdom -- British Heart Foundation/United Kingdom -- Arthritis Research UK/United Kingdom -- Cancer Research UK/United Kingdom -- Department of Health/United Kingdom -- Chief Scientist Office/United Kingdom -- New York, N.Y. -- Science. 2016 Apr 22;352(6284):474-7. doi: 10.1126/science.aac8624. Epub 2016 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. ; Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. ; Bradford Institute for Health Research, Bradford Teaching Hospitals National Health Service (NHS) Foundation Trust, Bradford BD9 6RJ, UK. ; Center for Genome Dynamics, The Jackson Laboratory, Bar Harbor, ME 04609, USA. ; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA 02114, USA. Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. ; Diabetes and Endocrine Centre, Heart of England NHS Foundation Trust and University of Birmingham, Birmingham B9 5SS, UK. ; TPP, Mill House, Troy Road, Leeds LS18 5TN, UK. ; Aston Research Centre for Healthy Ageing, Aston University, Birmingham B4 7ET, UK. ; 10X Genomics, 7068 Koll Center Parkway, Suite 415, Pleasanton, CA 94566, USA. ; Farr Institute of Health Informatics Research, London NW1 2DA, UK. Institute of Health Informatics, University College London, London NW1 2DA, UK. ; School of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT, UK. ; Department of Medical Genetics, University of Cambridge and National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre, Box 238, Cambridge Biomedical Campus, Cambridge CB2 0QQ, UK. Cambridge University Hospitals NHS Foundation Trust, Cambridge Biomedical Campus, Cambridge CB2 0QQ, UK. ; Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. Faculty of Life Sciences and Medicine, King's College London, London SE1 1UL, UK. ; Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. rd@sanger.ac.uk d.vanheel@qmul.ac.uk. ; Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. rd@sanger.ac.uk d.vanheel@qmul.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26940866" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Consanguinity ; DNA Mutational Analysis ; Drug Prescriptions ; Exome/genetics ; Female ; Fertility ; Gene Knockout Techniques ; Genes, Lethal ; Genetic Loci ; Genome, Human ; Great Britain ; *Health ; Histone-Lysine N-Methyltransferase/*genetics ; Homologous Recombination ; Homozygote ; Humans ; Male ; Mothers ; Pakistan/ethnology ; Phenotype
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  • 89
    Publication Date: 2016-01-28
    Description: Muscle contraction depends on release of Ca(2+) from the sarcoplasmic reticulum (SR) and reuptake by the Ca(2+)adenosine triphosphatase SERCA. We discovered a putative muscle-specific long noncoding RNA that encodes a peptide of 34 amino acids and that we named dwarf open reading frame (DWORF). DWORF localizes to the SR membrane, where it enhances SERCA activity by displacing the SERCA inhibitors, phospholamban, sarcolipin, and myoregulin. In mice, overexpression of DWORF in cardiomyocytes increases peak Ca(2+) transient amplitude and SR Ca(2+) load while reducing the time constant of cytosolic Ca(2+) decay during each cycle of contraction-relaxation. Conversely, slow skeletal muscle lacking DWORF exhibits delayed Ca(2+) clearance and relaxation and reduced SERCA activity. DWORF is the only endogenous peptide known to activate the SERCA pump by physical interaction and provides a means for enhancing muscle contractility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Benjamin R -- Makarewich, Catherine A -- Anderson, Douglas M -- Winders, Benjamin R -- Troupes, Constantine D -- Wu, Fenfen -- Reese, Austin L -- McAnally, John R -- Chen, Xiongwen -- Kavalali, Ege T -- Cannon, Stephen C -- Houser, Steven R -- Bassel-Duby, Rhonda -- Olson, Eric N -- AR-063182/AR/NIAMS NIH HHS/ -- DK-099653/DK/NIDDK NIH HHS/ -- F30AR 067094/AR/NIAMS NIH HHS/ -- HL-077439,/HL/NHLBI NIH HHS/ -- HL-093039/HL/NHLBI NIH HHS/ -- HL-111665/HL/NHLBI NIH HHS/ -- R01 AR063182/AR/NIAMS NIH HHS/ -- U01-HL-100401/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):271-5. doi: 10.1126/science.aad4076.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA. Department of Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA. ; Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Department of Physiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. ; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. eric.olson@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816378" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Binding Proteins/metabolism ; Humans ; Mice ; Mice, Knockout ; *Muscle Contraction ; Muscle Proteins/metabolism ; Muscle, Skeletal/*metabolism ; Myocardial Contraction ; Myocytes, Cardiac/*metabolism ; Peptides/genetics/*metabolism ; Proteolipids/metabolism ; RNA, Long Noncoding/genetics/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/*metabolism ; Transcription, Genetic
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  • 90
    Publication Date: 2016-01-02
    Description: Duchenne muscular dystrophy (DMD) is a devastating disease affecting about 1 out of 5000 male births and caused by mutations in the dystrophin gene. Genome editing has the potential to restore expression of a modified dystrophin gene from the native locus to modulate disease progression. In this study, adeno-associated virus was used to deliver the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system to the mdx mouse model of DMD to remove the mutated exon 23 from the dystrophin gene. This includes local and systemic delivery to adult mice and systemic delivery to neonatal mice. Exon 23 deletion by CRISPR-Cas9 resulted in expression of the modified dystrophin gene, partial recovery of functional dystrophin protein in skeletal myofibers and cardiac muscle, improvement of muscle biochemistry, and significant enhancement of muscle force. This work establishes CRISPR-Cas9-based genome editing as a potential therapy to treat DMD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, Christopher E -- Hakim, Chady H -- Ousterout, David G -- Thakore, Pratiksha I -- Moreb, Eirik A -- Castellanos Rivera, Ruth M -- Madhavan, Sarina -- Pan, Xiufang -- Ran, F Ann -- Yan, Winston X -- Asokan, Aravind -- Zhang, Feng -- Duan, Dongsheng -- Gersbach, Charles A -- DP1-MH100706/DP/NCCDPHP CDC HHS/ -- DP2-OD008586/OD/NIH HHS/ -- P01HL112761/HL/NHLBI NIH HHS/ -- R01DK097768/DK/NIDDK NIH HHS/ -- R01HL089221/HL/NHLBI NIH HHS/ -- R01NS90634/NS/NINDS NIH HHS/ -- T32GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 22;351(6271):403-7. doi: 10.1126/science.aad5143. Epub 2015 Dec 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biomedical Engineering, Duke University, Durham, NC, USA. Center for Genomic and Computational Biology, Duke University, Durham, NC, USA. ; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, USA. ; Gene Therapy Center, Departments of Genetics, Biochemistry and Biophysics, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Society of Fellows, Harvard University, Cambridge, MA, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. Graduate Program in Biophysics, Harvard Medical School, Boston, MA, USA. Harvard-MIT Division of Health Sciences and Technology, Harvard Medical School, Boston, MA, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA, USA. McGovern Institute for Brain Research, Massachusetts Institute of Technology, Cambridge, MA, USA. Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA. ; Department of Molecular Microbiology and Immunology, University of Missouri, Columbia, MO, USA. Department of Neurology, University of Missouri, Columbia, MO, USA. ; Department of Biomedical Engineering, Duke University, Durham, NC, USA. Center for Genomic and Computational Biology, Duke University, Durham, NC, USA. Department of Orthopaedic Surgery, Duke University Medical Center, Durham, NC, USA. charles.gersbach@duke.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26721684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *CRISPR-Cas Systems ; Clustered Regularly Interspaced Short Palindromic Repeats ; Dependovirus ; Disease Models, Animal ; Dystrophin/*genetics ; Exons/*genetics ; Genetic Therapy/*methods ; Male ; Mice ; Mice, Inbred mdx ; Muscle, Skeletal/*metabolism ; Muscular Dystrophy, Duchenne/genetics/*therapy ; Sequence Deletion
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  • 91
    Publication Date: 2016-03-19
    Description: Postnatal colonization of the body with microbes is assumed to be the main stimulus to postnatal immune development. By transiently colonizing pregnant female mice, we show that the maternal microbiota shapes the immune system of the offspring. Gestational colonization increases intestinal group 3 innate lymphoid cells and F4/80(+)CD11c(+) mononuclear cells in the pups. Maternal colonization reprograms intestinal transcriptional profiles of the offspring, including increased expression of genes encoding epithelial antibacterial peptides and metabolism of microbial molecules. Some of these effects are dependent on maternal antibodies that potentially retain microbial molecules and transmit them to the offspring during pregnancy and in milk. Pups born to mothers transiently colonized in pregnancy are better able to avoid inflammatory responses to microbial molecules and penetration of intestinal microbes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gomez de Aguero, Mercedes -- Ganal-Vonarburg, Stephanie C -- Fuhrer, Tobias -- Rupp, Sandra -- Uchimura, Yasuhiro -- Li, Hai -- Steinert, Anna -- Heikenwalder, Mathias -- Hapfelmeier, Siegfried -- Sauer, Uwe -- McCoy, Kathy D -- Macpherson, Andrew J -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1296-302. doi: 10.1126/science.aad2571.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Maurice Muller Laboratories (DKF), Universitatsklinik fur Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, 3010 Bern, Switzerland. ; Institute of Molecular Systems Biology, Swiss Federal Institute of Technology (ETH) Zurich, 8093 Zurich, Switzerland. ; Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany. ; Institute for Infectious Diseases, University of Bern, 3010 Bern, Switzerland. ; Maurice Muller Laboratories (DKF), Universitatsklinik fur Viszerale Chirurgie und Medizin Inselspital, Murtenstrasse 35, University of Bern, 3010 Bern, Switzerland. andrew.macpherson@insel.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989247" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies/immunology ; Escherichia coli/immunology ; Female ; Gastrointestinal Microbiome/*immunology ; Germ-Free Life ; Immune System/*growth & development/*microbiology ; Immunity, Innate/genetics/*immunology ; Immunity, Maternally-Acquired/genetics/*immunology ; Intestines/*immunology ; Lymphocytes/immunology ; Mice ; Mice, Inbred C57BL ; Pregnancy ; Symbiosis ; Transcription, Genetic
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  • 92
    Publication Date: 2016-04-16
    Description: Drug resistance compromises control of malaria. Here, we show that resistance to a commonly used antimalarial medication, atovaquone, is apparently unable to spread. Atovaquone pressure selects parasites with mutations in cytochrome b, a respiratory protein with low but essential activity in the mammalian blood phase of the parasite life cycle. Resistance mutations rescue parasites from the drug but later prove lethal in the mosquito phase, where parasites require full respiration. Unable to respire efficiently, resistant parasites fail to complete mosquito development, arresting their life cycle. Because cytochrome b is encoded by the maternally inherited parasite mitochondrion, even outcrossing with wild-type strains cannot facilitate spread of resistance. Lack of transmission suggests that resistance will be unable to spread in the field, greatly enhancing the utility of atovaquone in malaria control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodman, Christopher D -- Siregar, Josephine E -- Mollard, Vanessa -- Vega-Rodriguez, Joel -- Syafruddin, Din -- Matsuoka, Hiroyuki -- Matsuzaki, Motomichi -- Toyama, Tomoko -- Sturm, Angelika -- Cozijnsen, Anton -- Jacobs-Lorena, Marcelo -- Kita, Kiyoshi -- Marzuki, Sangkot -- McFadden, Geoffrey I -- AI031478/AI/NIAID NIH HHS/ -- RR00052/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 15;352(6283):349-53. doi: 10.1126/science.aad9279.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. gim@unimelb.edu.au deang@unimelb.edu.au. ; School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia. Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ; School of BioSciences, University of Melbourne, Melbourne, VIC 3010, Australia. ; Johns Hopkins University Bloomberg School of Public Health, Department of Molecular Microbiology and Immunology, Malaria Research Institute, Baltimore, MD 21205, USA. ; Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia. Department of Parasitology, Faculty of Medicine, Hasanuddin University, Jalan Perintis Kemerdekaan Km10, Makassar 90245, Indonesia. ; Division of Medical Zoology, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Tochigi 329-0498, Japan. ; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. ; Department of Biomedical Chemistry, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. School of Tropical Medicine and Global Health, Nagasaki University, Sakamoto, Nagasaki 852-8523, Japan. ; Eijkman Institute for Molecular Biology, JI Diponegoro no. 69, Jakarta, 10430, Indonesia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27081071" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles/*parasitology ; Antimalarials/*pharmacology/therapeutic use ; Atovaquone/*pharmacology/therapeutic use ; Cell Line ; Cytochromes b/*genetics ; Drug Resistance/*genetics ; Genes, Mitochondrial/genetics ; Humans ; Life Cycle Stages/drug effects/genetics ; Malaria/drug therapy/*parasitology/transmission ; Male ; Mice ; Mitochondria/*genetics ; Mutation ; Plasmodium berghei/*drug effects/genetics/growth & development ; Selection, Genetic
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  • 93
    Publication Date: 2016-04-02
    Description: Accurate sequence and assembly of genomes is a critical first step for studies of genetic variation. We generated a high-quality assembly of the gorilla genome using single-molecule, real-time sequence technology and a string graph de novo assembly algorithm. The new assembly improves contiguity by two to three orders of magnitude with respect to previously released assemblies, recovering 87% of missing reference exons and incomplete gene models. Although regions of large, high-identity segmental duplications remain largely unresolved, this comprehensive assembly provides new biological insight into genetic diversity, structural variation, gene loss, and representation of repeat structures within the gorilla genome. The approach provides a path forward for the routine assembly of mammalian genomes at a level approaching that of the current quality of the human genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gordon, David -- Huddleston, John -- Chaisson, Mark J P -- Hill, Christopher M -- Kronenberg, Zev N -- Munson, Katherine M -- Malig, Maika -- Raja, Archana -- Fiddes, Ian -- Hillier, LaDeana W -- Dunn, Christopher -- Baker, Carl -- Armstrong, Joel -- Diekhans, Mark -- Paten, Benedict -- Shendure, Jay -- Wilson, Richard K -- Haussler, David -- Chin, Chen-Shan -- Eichler, Evan E -- HG002385/HG/NHGRI NIH HHS/ -- HG003079/HG/NHGRI NIH HHS/ -- HG007234/HG/NHGRI NIH HHS/ -- HG007635/HG/NHGRI NIH HHS/ -- HG007990/HG/NHGRI NIH HHS/ -- R01 HG002385/HG/NHGRI NIH HHS/ -- U41 HG007635/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2016 Apr 1;352(6281):aae0344. doi: 10.1126/science.aae0344.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA. Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA. ; Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA. ; Genomics Institute, University of California Santa Cruz and Howard Hughes Medical Institute, Santa Cruz, CA 95064, USA. ; McDonnell Genome Institute, Department of Medicine, Department of Genetics, Washington University School of Medicine, St. Louis, MO 63108, USA. ; Pacific Biosciences of California, Menlo Park, CA 94025, USA. ; Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA 98195, USA. Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA. eee@gs.washington.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27034376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Contig Mapping ; Evolution, Molecular ; Expressed Sequence Tags ; Female ; Genetic Variation ; Genome, Human ; Genomics ; Gorilla gorilla/*genetics ; Humans ; Sequence Alignment ; Sequence Analysis, DNA/*methods
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  • 94
    Publication Date: 2016-04-30
    Description: Recent studies in human populations and mouse models reveal notable congruences in gut microbial taxa whose abundances are partly regulated by host genotype. Host genes associating with these taxa are related to diet sensing, metabolism, and immunity. These broad patterns are further validated in similar studies of nonmammalian microbiomes. The next generation of genome-wide association studies will expand the size of the data sets and refine the microbial phenotypes to fully capture these intriguing signatures of host-microbiome coevolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodrich, Julia K -- Davenport, Emily R -- Waters, Jillian L -- Clark, Andrew G -- Ley, Ruth E -- R01 DK093595/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2016 Apr 29;352(6285):532-5. doi: 10.1126/science.aad9379.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. ; Department of Molecular Biology and Genetics, Cornell University, Ithaca NY, USA. Department of Microbiology, Cornell University, Ithaca NY, USA. Department of Microbiome Science, Max Planck Institute for Developmental Biology, Tubingen, Germany. rel222@cornell.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27126034" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/*classification/genetics ; Diet ; *Genome-Wide Association Study ; Genotype ; Humans ; Mice ; Microbiota/genetics/*physiology ; Phenotype ; *Quantitative Trait Loci ; Species Specificity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
    Publication Date: 2016-03-26
    Description: Cell assembly sequences during learning are "replayed" during hippocampal ripples and contribute to the consolidation of episodic memories. However, neuronal sequences may also reflect preexisting dynamics. We report that sequences of place-cell firing in a novel environment are formed from a combination of the contributions of a rigid, predominantly fast-firing subset of pyramidal neurons with low spatial specificity and limited change across sleep-experience-sleep and a slow-firing plastic subset. Slow-firing cells, rather than fast-firing cells, gained high place specificity during exploration, elevated their association with ripples, and showed increased bursting and temporal coactivation during postexperience sleep. Thus, slow- and fast-firing neurons, although forming a continuous distribution, have different coding and plastic properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grosmark, Andres D -- Buzsaki, Gyorgy -- MH102840/MH/NIMH NIH HHS/ -- MH54671/MH/NIMH NIH HHS/ -- NS075015/NS/NINDS NIH HHS/ -- R01 MH107396/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 25;351(6280):1440-3. doi: 10.1126/science.aad1935.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Columbia University Medical Center, New York, NY 10019, USA. The Neuroscience Institute, School of Medicine, New York University, New York, NY 10016, USA. ; The Neuroscience Institute, School of Medicine, New York University, New York, NY 10016, USA. Center for Neural Science, New York University, New York, NY 10016, USA. gyorgy.buzsaki@nyumc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27013730" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Hippocampus/cytology/*physiopathology ; Learning/*physiology ; Male ; Maze Learning ; Neuronal Plasticity ; Pyramidal Cells/*physiology ; Rats ; Rats, Inbred LEC ; Sleep/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-01-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alberts, Bruce -- New York, N.Y. -- Science. 2016 Jan 15;351(6270):207. doi: 10.1126/science.aaf2001.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bruce Alberts is the Chancellor's Leadership Chair in Biochemistry and Biophysics for Science and Education at the University of California, San Francisco, CA, and emeritus editor-in-chief of Science. Bruce.Alberts@ucsf.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26816352" target="_blank"〉PubMed〈/a〉
    Keywords: *Career Choice ; *Faculty ; Humans ; Leadership ; Policy Making ; *Power (Psychology) ; Schools/*manpower/trends ; Teaching/*manpower/methods/trends ; United States
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  • 97
    Publication Date: 2016-03-19
    Description: Expansions of a hexanucleotide repeat (GGGGCC) in the noncoding region of the C9orf72 gene are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Decreased expression of C9orf72 is seen in expansion carriers, suggesting that loss of function may play a role in disease. We found that two independent mouse lines lacking the C9orf72 ortholog (3110043O21Rik) in all tissues developed normally and aged without motor neuron disease. Instead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of engorged macrophage-like cells. C9orf72 expression was highest in myeloid cells, and the loss of C9orf72 led to lysosomal accumulation and altered immune responses in macrophages and microglia, with age-related neuroinflammation similar to C9orf72 ALS but not sporadic ALS human patient tissue. Thus, C9orf72 is required for the normal function of myeloid cells, and altered microglial function may contribute to neurodegeneration in C9orf72 expansion carriers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Rourke, J G -- Bogdanik, L -- Yanez, A -- Lall, D -- Wolf, A J -- Muhammad, A K M G -- Ho, R -- Carmona, S -- Vit, J P -- Zarrow, J -- Kim, K J -- Bell, S -- Harms, M B -- Miller, T M -- Dangler, C A -- Underhill, D M -- Goodridge, H S -- Lutz, C M -- Baloh, R H -- GM085796/GM/NIGMS NIH HHS/ -- NS069669/NS/NINDS NIH HHS/ -- NS078398/NS/NINDS NIH HHS/ -- NS087351/NS/NINDS NIH HHS/ -- UL1TR000124/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1324-9. doi: 10.1126/science.aaf1064.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. ; The Jackson Laboratory, Bar Harbor, ME, USA. ; Division of Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. ; Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. ; Board of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. Department of Neurology, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989253" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/immunology ; Amyotrophic Lateral Sclerosis/genetics/*immunology ; Animals ; Frontotemporal Dementia/genetics/*immunology ; Gene Knockdown Techniques ; Guanine Nucleotide Exchange Factors/genetics/*physiology ; Heterozygote ; Humans ; Lymphatic Diseases/genetics/immunology ; Macrophages/*immunology ; Mice ; Mice, Knockout ; Microglia/*immunology ; Myeloid Cells/*immunology ; Proteins/genetics/*physiology ; Rats ; Splenomegaly/genetics/immunology
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  • 98
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-04-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paluck, Elizabeth Levy -- New York, N.Y. -- Science. 2016 Apr 8;352(6282):147. doi: 10.1126/science.aaf5207. Epub 2016 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology and Public and International Affairs, Princeton University, Princeton, NJ 08544, USA. epaluck@princeton.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27124440" target="_blank"〉PubMed〈/a〉
    Keywords: Female ; Homophobia/*prevention & control ; Humans ; Male ; *Politics ; *Transgender Persons
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  • 99
    Publication Date: 2016-01-30
    Description: The mammalian Y chromosome is considered a symbol of maleness, as it encodes a gene driving male sex determination, Sry, as well as a battery of other genes important for male reproduction. We previously demonstrated in the mouse that successful assisted reproduction can be achieved when the Y gene contribution is limited to only two genes, Sry and spermatogonial proliferation factor Eif2s3y. Here, we replaced Sry by transgenic activation of its downstream target Sox9, and Eif2s3y, by transgenic overexpression of its X chromosome-encoded homolog Eif2s3x. The resulting males with no Y chromosome genes produced haploid male gametes and sired offspring after assisted reproduction. Our findings support the existence of functional redundancy between the Y chromosome genes and their homologs encoded on other chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamauchi, Yasuhiro -- Riel, Jonathan M -- Ruthig, Victor A -- Ortega, Egle A -- Mitchell, Michael J -- Ward, Monika A -- HD072380/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 29;351(6272):514-6. doi: 10.1126/science.aad1795.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Biogenesis Research, John A. Burns School of Medicine, University of Hawaii, 1960 East-West Road, Honolulu, HI 96822, USA. ; Aix-Marseille Universite, INSERM, GMGF UMR_S 910, 13385 Marseille, France. ; Institute for Biogenesis Research, John A. Burns School of Medicine, University of Hawaii, 1960 East-West Road, Honolulu, HI 96822, USA. mward@hawaii.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26823431" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Eukaryotic Initiation Factor-2/*genetics ; Female ; Gene Dosage ; Haploidy ; Male ; Mice ; Mice, Transgenic ; Reproductive Techniques, Assisted ; SOX9 Transcription Factor/*genetics ; Sex-Determining Region Y Protein/*genetics ; Spermatogenesis/*genetics ; Spermatogonia/cytology/metabolism ; X Chromosome/*genetics ; Y Chromosome/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2016-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pennisi, Elizabeth -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):802. doi: 10.1126/science.351.6275.802.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912873" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Child Development ; Child, Preschool ; *Gastrointestinal Microbiome ; Germ-Free Life ; Growth Disorders/*microbiology/*therapy ; Humans ; Infant ; Malnutrition/*therapy ; Mice ; Muscle Development ; Osteogenesis ; Translational Medical Research
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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