Institution
Columbia University
Education•New York, New York, United States•
About: Columbia University is a education organization based out in New York, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 95695 authors who have published 224027 publications receiving 12838453 citations. The organization is also known as: Columbia University in the City of New York & King's College of New York.
Topics: Population, Poison control, Health care, Mental health, Public health
Papers published on a yearly basis
Papers
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TL;DR: DNMT3L recognizes histone H3 tails that are unmethylated at lysine 4 and induces de novo DNA methylation by recruitment or activation of DNMT3A2, and substitution of key residues in the binding site eliminated the H3 tail–DN MT3L interaction.
Abstract: Mammals use DNA methylation for the heritable silencing of retrotransposons and imprinted genes and for the inactivation of the X chromosome in females. The establishment of patterns of DNA methylation during gametogenesis depends in part on DNMT3L, an enzymatically inactive regulatory factor that is related in sequence to the DNA methyltransferases DNMT3A and DNMT3B1,2. The main proteins that interact in vivo with the product of an epitope-tagged allele of the endogenous Dnmt3L gene were identified by mass spectrometry as DNMT3A2, DNMT3B and the four core histones. Peptide interaction assays showed that DNMT3L specifically interacts with the extreme amino terminus of histone H3; this interaction was strongly inhibited by methylation at lysine 4 of histone H3 but was insensitive to modifications at other positions. Crystallographic studies of human DNMT3L showed that the protein has a carboxy-terminal methyltransferase-like domain and an N-terminal cysteine-rich domain. Cocrystallization of DNMT3L with the tail of histone H3 revealed that the tail bound to the cysteine-rich domain of DNMT3L, and substitution of key residues in the binding site eliminated the H3 tail-DNMT3L interaction. These data indicate that DNMT3L recognizes histone H3 tails that are unmethylated at lysine 4 and induces de novo DNA methylation by recruitment or activation of DNMT3A2.
1,450 citations
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09 Feb 2010TL;DR: This book discusses microaggressive impact in the Workplace and Employment, Race, Gender, and Sexual-Orientation Microaggressions, and its applications in education, employment, and health practice.
Abstract: Foreword Preface Acknowledgments About the Author SECTION ONE: PSYCHOLOGICAL MANIFESTATION AND DYNAMICS OFMICROAGGRESSIONS CHAPTER ONE: The Manifestation of Racial, Gender, andSexual-Orientation Microaggressions CHAPTER TWO: Taxonomy of Microaggressions CHAPTER THREE: The Psychological Dilemmas and Dynamics ofMicroaggressions SECTION TWO: MICROAGGRESSIVE IMPACT ON TARGETS ANDPERPETRATORS CHAPTER FOUR: The Microaggression Process Model: From Beginningto End CHAPTER FIVE: Microaggressive Stress: Impact on Physical andMental Health CHAPTER SIX: Microaggressive Perpetrators and Oppression: TheNature of the Beast SECTION THREE: GROUP-SPECIFIC MICROAGGRESSIONS: RACE, GENDER,AND SEXUAL ORIENTATION CHAPTER SEVEN: Racial/Ethnic Microaggressions and Racism CHAPTER EIGHT: Gender Microaggressions and Sexism CHAPTER NINE: Sexual-Orientation Microaggressions andHeterosexism SECTION FOUR: MICROAGGRESSIONS IN EMPLOYMENT, EDUCATION, ANDMENTAL HEALTH PRACTICE CHAPTER TEN: Microaggressive Impact in the Workplace andEmployment CHAPTER ELEVEN: Microaggressive Impact on Education andTeaching: Facilitating Diffi cult Dialogues on Race in theClassroom CHAPTER TWELVE: Microaggressive Impact on Mental HealthPractice References Index
1,449 citations
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TL;DR: This book argues that a new conceptualization is needed in order to come to terms with the experience and consciousness of this new migrant population, called “transnationalism,” and describes the new type of migrants as transmigrants.
Abstract: Our earlier conceptions of immigrant and migrant n o longer suffice. The word immigrant evokes images of permanent rupture, of the uprooted, the abandonment of old patterns and the painful learning of a new language and culture. Now, a new kind of migrating population is emerging, composed of those whose networks, activities and patterns of life encompass both their host and home societies. Their lives cut across national boundaries and bring two societies into a single social field. In this book we argue that a new conceptualization is needed in order to come to terms with the experience and consciousness of this new migrant population. We call this new conceptualization, “transnationalism,” and describe the new type of migrants as transmigrants. We have defined transnationalism as the processes by which immigrants build social fields that link together their country of origin and their country of settlement. Immigrants who build such social fields are designated “transmigrants.” Transmigrants develop and maintain multiple relationsfamilial, economic, social, organizational, religious, and political that span borders. Transmigrants take actions, make decisions, and feel concerns, and develop identities within social net-
1,448 citations
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TL;DR: The potential use of phosphorothioate oligos as inhibitors of viral replication is highlighted and these are examples of oligos that are being considered for clinical therapeutic trials and meet some, but not all, of these criteria.
Abstract: Because of the specificity of Watson-Crick base pairing, attempts are now being made to use oligodeoxynucleotides (oligos) in the therapy of human disease. However, for a successful outcome, the oligo must meet at least six criteria: (i) the oligos can be synthesized easily and in bulk; (ii) the oligos must be stable in vivo; (iii) the oligos must be able to enter the target cell; (iv) the oligos must be retained by the target cell; (v) the oligos must be able to interact with their cellular targets; and (vi) the oligos should not interact in a non-sequence-specific manner with other macromolecules. Phosphorothioate oligos are examples of oligos that are being considered for clinical therapeutic trials and meet some, but not all, of these criteria. The potential use of phosphorothioate oligos as inhibitors of viral replication is highlighted.
1,447 citations
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Copenhagen University Hospital1, French Institute of Health and Medical Research2, St George's, University of London3, University of Gothenburg4, The Catholic University of America5, University of Western Australia6, Columbia University7, University of Milan8, New York University9, Forest Research Institute10, University of Amsterdam11, Hacettepe University12, University of Copenhagen13
TL;DR: The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated LP(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD.
Abstract: AIMS: The aims of the study were, first, to critically evaluate lipoprotein(a) [Lp(a)] as a cardiovascular risk factor and, second, to advise on screening for elevated plasma Lp(a), on desirable levels, and on therapeutic strategies. METHODS AND RESULTS: The robust and specific association between elevated Lp(a) levels and increased cardiovascular disease (CVD)/coronary heart disease (CHD) risk, together with recent genetic findings, indicates that elevated Lp(a), like elevated LDL-cholesterol, is causally related to premature CVD/CHD. The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels. Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both. We advise that Lp(a) be measured once, using an isoform-insensitive assay, in subjects at intermediate or high CVD/CHD risk with premature CVD, familial hypercholesterolaemia, a family history of premature CVD and/or elevated Lp(a), recurrent CVD despite statin treatment, ≥3% 10-year risk of fatal CVD according to European guidelines, and/or ≥10% 10-year risk of fatal + non-fatal CHD according to US guidelines. As a secondary priority after LDL-cholesterol reduction, we recommend a desirable level for Lp(a) <80th percentile (less than ∼50 mg/dL). Treatment should primarily be niacin 1-3 g/day, as a meta-analysis of randomized, controlled intervention trials demonstrates reduced CVD by niacin treatment. In extreme cases, LDL-apheresis is efficacious in removing Lp(a). CONCLUSION: We recommend screening for elevated Lp(a) in those at intermediate or high CVD/CHD risk, a desirable level <50 mg/dL as a function of global cardiovascular risk, and use of niacin for Lp(a) and CVD/CHD risk reduction.
1,446 citations
Authors
Showing all 96627 results
Name | H-index | Papers | Citations |
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Walter C. Willett | 334 | 2399 | 413322 |
Douglas G. Altman | 253 | 1001 | 680344 |
Yi Chen | 217 | 4342 | 293080 |
David J. Hunter | 213 | 1836 | 207050 |
Irving L. Weissman | 201 | 1141 | 172504 |
Rakesh K. Jain | 200 | 1467 | 177727 |
Robert M. Califf | 196 | 1561 | 167961 |
Lewis C. Cantley | 196 | 748 | 169037 |
Stephen V. Faraone | 188 | 1427 | 140298 |
Patrick W. Serruys | 186 | 2427 | 173210 |
Stuart H. Orkin | 186 | 715 | 112182 |
Eric R. Kandel | 184 | 603 | 113560 |
David L. Kaplan | 177 | 1944 | 146082 |
Richard B. Lipton | 176 | 2110 | 140776 |
David Haussler | 172 | 488 | 224960 |