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Author

Li Su

Other affiliations: Southwest University, University of Cambridge, Brown University  ...read more
Bio: Li Su is an academic researcher from Harvard University. The author has contributed to research in topics: Lung cancer & Medicine. The author has an hindex of 60, co-authored 348 publications receiving 13027 citations. Previous affiliations of Li Su include Southwest University & University of Cambridge.


Papers
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Journal ArticleDOI
TL;DR: A Matlab toolbox for representational similarity analysis is introduced, designed to help integrate a wide range of computational models into the analysis of multichannel brain-activity measurements as provided by modern functional imaging and neuronal recording techniques.
Abstract: Neuronal population codes are increasingly being investigated with multivariate pattern-information analyses. A key challenge is to use measured brain-activity patterns to test computational models of brain information processing. One approach to this problem is representational similarity analysis (RSA), which characterizes a representation in a brain or computational model by the distance matrix of the response patterns elicited by a set of stimuli. The representational distance matrix encapsulates what distinctions between stimuli are emphasized and what distinctions are de-emphasized in the representation. A model is tested by comparing the representational distance matrix it predicts to that of a measured brain region. RSA also enables us to compare representations between stages of processing within a given brain or model, between brain and behavioral data, and between individuals and species. Here, we introduce a Matlab toolbox for RSA. The toolbox supports an analysis approach that is simultaneously data- and hypothesis-driven. It is designed to help integrate a wide range of computational models into the analysis of multichannel brain-activity measurements as provided by modern functional imaging and neuronal recording techniques. Tools for visualization and inference enable the user to relate sets of models to sets of brain regions and to statistically test and compare the models using nonparametric inference methods. The toolbox supports searchlight-based RSA, to continuously map a measured brain volume in search of a neuronal population code with a specific geometry. Finally, we introduce the linear-discriminant t value as a measure of representational discriminability that bridges the gap between linear decoding analyses and RSA. In order to demonstrate the capabilities of the toolbox, we apply it to both simulated and real fMRI data. The key functions are equally applicable to other modalities of brain-activity measurement. The toolbox is freely available to the community under an open-source license agreement (http://www.mrc-cbu.cam.ac.uk/methods-and-resources/toolboxes/license/).

779 citations

Journal ArticleDOI
TL;DR: The LCS6 variant allele in a KRAS miRANA complementary site is significantly associated with increased risk for NSCLC among moderate smokers and represents a new paradigm for let-7 miRNAs in lung cancer susceptibility.
Abstract: Lung cancer is the leading cause of cancer deaths worldwide, yet few genetic markers of lung cancer risk useful for screening exist. The let-7 family-of-microRNAs (miRNA) are global genetic regulators important in controlling lung cancer oncogene expression by binding to the 3' untranslated regions of their target mRNAs. The purpose of this study was to identify single nucleotide polymorphisms (SNP) that could modify let-7 binding and to assess the effect of such SNPs on target gene regulation and risk for non-small cell lung cancer (NSCLC). let-7 complementary sites (LCS) were sequenced in the KRAS 3' untranslated region from 74 NSCLC cases to identify mutations and SNPs that correlated with NSCLC. The allele frequency of a previously unidentified SNP at LCS6 was characterized in 2,433 people (representing 46 human populations). The frequency of the variant allele is 18.1% to 20.3% in NSCLC patients and 5.8% in world populations. The association between the SNP and the risk for NSCLC was defined in two independent case-control studies. A case-control study of lung cancer from New Mexico showed a 2.3-fold increased risk (confidence interval, 1.1-4.6; P = 0.02) for NSCLC cancer in patients who smoked <40 pack-years. This association was validated in a second independent case-control study. Functionally, the variant allele results in KRAS overexpression in vitro. The LCS6 variant allele in a KRAS miRANA complementary site is significantly associated with increased risk for NSCLC among moderate smokers and represents a new paradigm for let-7 miRNAs in lung cancer susceptibility.

664 citations

Journal ArticleDOI
James D. McKay1, Rayjean J. Hung2, Younghun Han3, Xuchen Zong2, Robert Carreras-Torres1, David C. Christiani4, Neil E. Caporaso5, Mattias Johansson1, Xiangjun Xiao3, Yafang Li3, Jinyoung Byun3, Alison M. Dunning6, Karen A. Pooley6, David C. Qian3, Xuemei Ji3, Geoffrey Liu2, Maria Timofeeva1, Stig E. Bojesen7, Stig E. Bojesen8, Stig E. Bojesen9, Xifeng Wu10, Loic Le Marchand11, Demetrios Albanes5, Heike Bickeböller12, Melinda C. Aldrich13, William S. Bush14, Adonina Tardón15, Gad Rennert16, M. Dawn Teare17, John K. Field18, Lambertus A. Kiemeney19, Philip Lazarus20, Aage Haugen21, Stephen Lam22, Matthew B. Schabath, Angeline S. Andrew3, Hongbing Shen23, Yun Chul Hong24, Jian-Min Yuan25, Pier Alberto Bertazzi26, Angela Cecilia Pesatori26, Yuanqing Ye10, Nancy Diao4, Li Su4, Ruyang Zhang4, Yonathan Brhane2, Natasha B. Leighl27, Jakob S Johansen7, Anders Mellemgaard7, Walid Saliba16, Christopher A. Haiman28, Lynne R. Wilkens11, Ana Fernández-Somoano15, Guillermo Fernández-Tardón15, Henricus F. M. van der Heijden19, Jin Hee Kim29, Juncheng Dai23, Zhibin Hu23, Michael P.A. Davies18, Michael W. Marcus18, Hans Brunnström30, Jonas Manjer30, Olle Melander30, David C. Muller31, Kim Overvad32, Antonia Trichopoulou, Rosario Tumino33, Jennifer A. Doherty, Matt P Barnett34, Chu Chen34, Gary E. Goodman, Angela Cox17, Fiona Taylor17, Penella J. Woll17, Irene Brüske, H-Erich Wichmann35, H-Erich Wichmann36, Judith Manz, Thomas Muley37, Angela Risch, Albert Rosenberger12, Kjell Grankvist38, Mikael Johansson38, Frances A. Shepherd27, Ming-Sound Tsao27, Susanne M. Arnold39, Eric B. Haura, Ciprian Bolca, Ivana Holcatova40, Vladimir Janout41, Milica Kontic42, Jolanta Lissowska, Anush Mukeria, Simona Ognjanovic, Tadeusz M Orlowski, Ghislaine Scelo1, Beata Swiatkowska43, David Zaridze, Per Bakke44, Vidar Skaug21, Shanbeh Zienolddiny21, Eric J. Duell, Lesley M. Butler25, Woon-Puay Koh45, Yu-Tang Gao, Richard S. Houlston46, John McLaughlin, Victoria L. Stevens47, Philippe Joubert, Maxime Lamontagne, David C. Nickle48, Ma'en Obeidat49, Wim Timens50, Bin Zhu5, Lei Song5, Linda Kachuri2, María Soler Artigas51, María Soler Artigas52, Martin D. Tobin52, Martin D. Tobin51, Louise V. Wain51, Louise V. Wain52, Thorunn Rafnar53, Thorgeir E. Thorgeirsson53, Gunnar W Reginsson53, Kari Stefansson53, Dana B. Hancock54, Laura J. Bierut55, Margaret R. Spitz56, Nathan C. Gaddis54, Sharon M. Lutz57, Fangyi Gu5, Eric O. Johnson54, Ahsan Kamal3, Claudio W. Pikielny3, Dakai Zhu3, Sara Lindstroem58, Xia Jiang4, Rachel F. Tyndale59, Rachel F. Tyndale60, Georgia Chenevix-Trench61, Jonathan Beesley61, Yohan Bossé62, Stephen J. Chanock5, Paul Brennan1, Maria Teresa Landi5, Christopher I. Amos3 
International Agency for Research on Cancer1, Lunenfeld-Tanenbaum Research Institute2, Dartmouth College3, Harvard University4, National Institutes of Health5, University of Cambridge6, Copenhagen University Hospital7, Gentofte Hospital8, University of Copenhagen9, University of Texas MD Anderson Cancer Center10, University of Hawaii11, University of Göttingen12, Vanderbilt University Medical Center13, Case Western Reserve University14, University of Oviedo15, Technion – Israel Institute of Technology16, University of Sheffield17, University of Liverpool18, Radboud University Nijmegen19, Washington State University Spokane20, National Institute of Occupational Health21, BC Cancer Agency22, Nanjing Medical University23, New Generation University College24, University of Pittsburgh25, University of Milan26, Princess Margaret Cancer Centre27, University of Southern California28, Sejong University29, Lund University30, Imperial College London31, Aarhus University32, Prevention Institute33, Fred Hutchinson Cancer Research Center34, Ludwig Maximilian University of Munich35, Technische Universität München36, University Hospital Heidelberg37, Umeå University38, University of Kentucky39, Charles University in Prague40, University of Ostrava41, University of Belgrade42, Nofer Institute of Occupational Medicine43, University of Bergen44, National University of Singapore45, Institute of Cancer Research46, American Cancer Society47, Merck & Co.48, University of British Columbia49, University Medical Center Groningen50, University of Leicester51, National Institute for Health Research52, Amgen53, Research Triangle Park54, Washington University in St. Louis55, Baylor College of Medicine56, Anschutz Medical Campus57, University of Washington58, Centre for Addiction and Mental Health59, University of Toronto60, QIMR Berghofer Medical Research Institute61, Laval University62
TL;DR: 18 susceptibility loci achieving genome-wide significance are identified, including 10 new loci linked with lung cancer overall and six loci associated with lung adenocarcinoma, highlighting the striking heterogeneity in genetic susceptibility across the histological subtypes of lung cancer.
Abstract: Although several lung cancer susceptibility loci have been identified, much of the heritability for lung cancer remains unexplained. Here 14,803 cases and 12,262 controls of European descent were genotyped on the OncoArray and combined with existing data for an aggregated genome-wide association study (GWAS) analysis of lung cancer in 29,266 cases and 56,450 controls. We identified 18 susceptibility loci achieving genome-wide significance, including 10 new loci. The new loci highlight the striking heterogeneity in genetic susceptibility across the histological subtypes of lung cancer, with four loci associated with lung cancer overall and six loci associated with lung adenocarcinoma. Gene expression quantitative trait locus (eQTL) analysis in 1,425 normal lung tissue samples highlights RNASET2, SECISBP2L and NRG1 as candidate genes. Other loci include genes such as a cholinergic nicotinic receptor, CHRNA2, and the telomere-related genes OFBC1 and RTEL1. Further exploration of the target genes will continue to provide new insights into the etiology of lung cancer.

405 citations

Journal ArticleDOI
TL;DR: It is found that several potentially modifiable risk factors for damage accrual are identified and an integrated strategy to address these may improve long-term outcomes.
Abstract: We studied damage accrual and factors determining development and progression of damage in an international cohort of systemic lupus erythematosus (SLE) patients.

379 citations

Journal ArticleDOI
TL;DR: Despite current standard of care, nephritis was associated with ESRD and death, and renal insufficiency was linked to lower health-related quality of life.
Abstract: Objective. To determine nephritis outcomes in a prospective multi-ethnic/racial SLE inception cohort. Methods. Patients in the Systemic Lupus International Collaborating Clinics inception cohort (≤15 months of SLE diagnosis) were assessed annually for estimated glomerular filtration rate (eGFR), proteinuria and end-stage renal disease (ESRD). Health-related quality of life was measured by the Short Form (36 questions) health survey questionnaire (SF-36) subscales, mental and physical component summary scores. Results. There were 1827 patients, 89% females, mean (s.d.) age 35.1 (13.3) years. The mean (s.d.) SLE duration at enrolment was 0.5 (0.3) years and follow-up 4.6 (3.4) years. LN occurred in 700 (38.3%) patients: 566/700 (80.9%) at enrolment and 134/700 (19.1%) during follow-up. Patients with nephritis were younger, more frequently men and of African, Asian and Hispanic race/ethnicity. The estimated overall 10-year incidence of ESRD was 4.3% (95% CI: 2.8%, 5.8%), and with nephritis was 10.1% (95% CI: 6.6%, 13.6%). Patients with nephritis had a higher risk of death (HR = 2.98, 95% CI: 1.48, 5.99; P = 0.002) and those with eGFR <30 ml/min at diagnosis had lower SF-36 physical component summary scores (P < 0.01) and lower Physical function, Physical role and Bodily pain scores. Over time, patients with abnormal eGFR and proteinuria had lower SF-36 mental component summary (P ≤ 0.02) scores compared to patients with normal values. Conclusion. LN occurred in 38.3% of SLE patients, frequently as the initial presentation, in a large multi-ethnic inception cohort. Despite current standard of care, nephritis was associated with ESRD and death, and renal insufficiency was linked to lower health-related quality of life. Further advances are required for the optimal treatment of LN.

332 citations


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TL;DR: The 11th edition of Harrison's Principles of Internal Medicine welcomes Anthony Fauci to its editorial staff, in addition to more than 85 new contributors.
Abstract: The 11th edition of Harrison's Principles of Internal Medicine welcomes Anthony Fauci to its editorial staff, in addition to more than 85 new contributors. While the organization of the book is similar to previous editions, major emphasis has been placed on disorders that affect multiple organ systems. Important advances in genetics, immunology, and oncology are emphasized. Many chapters of the book have been rewritten and describe major advances in internal medicine. Subjects that received only a paragraph or two of attention in previous editions are now covered in entire chapters. Among the chapters that have been extensively revised are the chapters on infections in the compromised host, on skin rashes in infections, on many of the viral infections, including cytomegalovirus and Epstein-Barr virus, on sexually transmitted diseases, on diabetes mellitus, on disorders of bone and mineral metabolism, and on lymphadenopathy and splenomegaly. The major revisions in these chapters and many

6,968 citations

01 Mar 2007
TL;DR: An initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI is described.
Abstract: Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

5,467 citations

01 Jan 2016
TL;DR: The modern applied statistics with s is universally compatible with any devices to read, and is available in the digital library an online access to it is set as public so you can download it instantly.
Abstract: Thank you very much for downloading modern applied statistics with s. As you may know, people have search hundreds times for their favorite readings like this modern applied statistics with s, but end up in harmful downloads. Rather than reading a good book with a cup of coffee in the afternoon, instead they cope with some harmful virus inside their laptop. modern applied statistics with s is available in our digital library an online access to it is set as public so you can download it instantly. Our digital library saves in multiple countries, allowing you to get the most less latency time to download any of our books like this one. Kindly say, the modern applied statistics with s is universally compatible with any devices to read.

5,249 citations

Journal ArticleDOI
TL;DR: This research framework seeks to create a common language with which investigators can generate and test hypotheses about the interactions among different pathologic processes (denoted by biomarkers) and cognitive symptoms and envision that defining AD as a biological construct will enable a more accurate characterization and understanding of the sequence of events that lead to cognitive impairment that is associated with AD.
Abstract: In 2011, the National Institute on Aging and Alzheimer's Association created separate diagnostic recommendations for the preclinical, mild cognitive impairment, and dementia stages of Alzheimer's disease. Scientific progress in the interim led to an initiative by the National Institute on Aging and Alzheimer's Association to update and unify the 2011 guidelines. This unifying update is labeled a "research framework" because its intended use is for observational and interventional research, not routine clinical care. In the National Institute on Aging and Alzheimer's Association Research Framework, Alzheimer's disease (AD) is defined by its underlying pathologic processes that can be documented by postmortem examination or in vivo by biomarkers. The diagnosis is not based on the clinical consequences of the disease (i.e., symptoms/signs) in this research framework, which shifts the definition of AD in living people from a syndromal to a biological construct. The research framework focuses on the diagnosis of AD with biomarkers in living persons. Biomarkers are grouped into those of β amyloid deposition, pathologic tau, and neurodegeneration [AT(N)]. This ATN classification system groups different biomarkers (imaging and biofluids) by the pathologic process each measures. The AT(N) system is flexible in that new biomarkers can be added to the three existing AT(N) groups, and new biomarker groups beyond AT(N) can be added when they become available. We focus on AD as a continuum, and cognitive staging may be accomplished using continuous measures. However, we also outline two different categorical cognitive schemes for staging the severity of cognitive impairment: a scheme using three traditional syndromal categories and a six-stage numeric scheme. It is important to stress that this framework seeks to create a common language with which investigators can generate and test hypotheses about the interactions among different pathologic processes (denoted by biomarkers) and cognitive symptoms. We appreciate the concern that this biomarker-based research framework has the potential to be misused. Therefore, we emphasize, first, it is premature and inappropriate to use this research framework in general medical practice. Second, this research framework should not be used to restrict alternative approaches to hypothesis testing that do not use biomarkers. There will be situations where biomarkers are not available or requiring them would be counterproductive to the specific research goals (discussed in more detail later in the document). Thus, biomarker-based research should not be considered a template for all research into age-related cognitive impairment and dementia; rather, it should be applied when it is fit for the purpose of the specific research goals of a study. Importantly, this framework should be examined in diverse populations. Although it is possible that β-amyloid plaques and neurofibrillary tau deposits are not causal in AD pathogenesis, it is these abnormal protein deposits that define AD as a unique neurodegenerative disease among different disorders that can lead to dementia. We envision that defining AD as a biological construct will enable a more accurate characterization and understanding of the sequence of events that lead to cognitive impairment that is associated with AD, as well as the multifactorial etiology of dementia. This approach also will enable a more precise approach to interventional trials where specific pathways can be targeted in the disease process and in the appropriate people.

5,126 citations