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The Johns Hopkins University is a private research university in Baltimore, Maryland. Founded in 1876, the university was named after its first benefactor, the American entrepreneur, abolitionist, and philanthropist Johns Hopkins. His $7 million bequest—of which half financed the establishment of The Johns Hopkins Hospital—was the largest philanthropic gift in the history of the United States at the time. Daniel Coit Gilman, who was inaugurated as the institution's first president on February 22, 1876, led the university to revolutionize higher education in the U.S. by integrating teaching and research.The first research university in the Western Hemisphere and one of the founding members of the American Association of Universities, Johns Hopkins has ranked among the world’s top universities throughout its history. The National Science Foundation has ranked the university #1 among U.S. academic institutions in total science, medical, and engineering research and development spending for 31 consecutive years. Johns Hopkins is also ranked #12 in the U.S. News and World Report undergraduate program rankings for 2014 and was also ranked 11th in the U.S. News and World Report Best Global University Rankings of 2014, outranking Princeton University, Yale University, University of Pennsylvania, and Cornell University.Over the course of almost 140 years, 36 Nobel Prize winners have been affiliated with Johns Hopkins . Founded in 1883, the Blue Jays men’s lacrosse team has captured 44 national titles and joined the Big Ten Conference as an affiliate member in 2014.Johns Hopkins is organized into ten divisions on campuses in Maryland and Washington, D.C. with international centers in Italy, China, and Singapore. The two undergraduate divisions, the Krieger School of Arts and science and the Whiting School of Engineering, are located on the Homewood campus in Baltimore's Charles Village neighborhood. The medical school, the nursing school, and the Bloomberg School of Public Health are located on the Medical Institutions campus in East Baltimore. The university also consists of the Peabody Institute, the Applied Physics Laboratory, the Paul H. Nitze School of Advanced International Studies, the education school, the Carey Business School, and various other facilities. Wikipedia.

Cutting G.R.,Johns Hopkins University
Nature Reviews Genetics | Year: 2015

The availability of the human genome sequence and tools for interrogating individual genomes provide an unprecedented opportunity to apply genetics to medicine. Mendelian conditions, which are caused by dysfunction of a single gene, offer powerful examples that illustrate how genetics can provide insights into disease. Cystic fibrosis, one of the more common lethal autosomal recessive Mendelian disorders, is presented here as an example. Recent progress in elucidating disease mechanism and causes of phenotypic variation, as well as in the development of treatments, demonstrates that genetics continues to play an important part in cystic fibrosis research 25 years after the discovery of the disease-causing gene. © 2014 Macmillan Publishers Limited. All rights reserved. Source

Corden J.L.,Johns Hopkins University
Chemical Reviews | Year: 2013

The RNA polymerase II (Pol II) C-terminal domain (CTD) is a repetitive disordered domain that extends from the catalytic core of the enzyme. This tail domain is heavily modified by phosphorylation, glycosylation, and proline isomerization. In addition to the enzymes that modify the tail a number of RNA processing factors and chromatin modification factors interact with the CTD. Thus, this domain acts as a tether to bring into close proximity the machinery necessary to synthesize and process Pol II transcripts. Gene-specific aspects of CTD function will be discussed in accompanying reviews by Jeronimo et al. and Eick and Geyer. To set the stage for discussing the CTD the evolution of this domain is also considered. Genetic and gene expression effects of altering the CTD will then be considered. Source

Pardoll D.M.,Johns Hopkins University
Nature Reviews Cancer | Year: 2012

Among the most promising approaches to activating therapeutic antitumour immunity is the blockade of immune checkpoints. Immune checkpoints refer to a plethora of inhibitory pathways hardwired into the immune system that are crucial for maintaining self-tolerance and modulating the duration and amplitude of physiological immune responses in peripheral tissues in order to minimize collateral tissue damage. It is now clear that tumours co-opt certain immune-checkpoint pathways as a major mechanism of immune resistance, particularly against T cells that are specific for tumour antigens. Because many of the immune checkpoints are initiated by ligand-receptor interactions, they can be readily blocked by antibodies or modulated by recombinant forms of ligands or receptors. Cytotoxic T-lymphocyte-associated antigen 4 (CTLA4) antibodies were the first of this class of immunotherapeutics to achieve US Food and Drug Administration (FDA) approval. Preliminary clinical findings with blockers of additional immune-checkpoint proteins, such as programmed cell death protein 1 (PD1), indicate broad and diverse opportunities to enhance antitumour immunity with the potential to produce durable clinical responses. © 2012 Macmillan Publishers Limited. All rights reserved. Source

HIV pre-exposure prophylaxis trials with antiretroviral drugs have been variably successful. Even trials demonstrating the best efficacy leave room for improvement. Pharmacological data illuminate several sources of outcome variability, especially the impact of poor adherence, which is critical to manage PrEP in the clinic and to develop the next generation of PrEP candidates. © 2013 Elsevier Inc. Source

Armanios M.,Johns Hopkins University
Nature reviews. Genetics | Year: 2012

There has been mounting evidence of a causal role for telomere dysfunction in a number of degenerative disorders. Their manifestations encompass common disease states such as idiopathic pulmonary fibrosis and bone marrow failure. Although these disorders seem to be clinically diverse, collectively they comprise a single syndrome spectrum defined by the short telomere defect. Here we review the manifestations and unique genetics of telomere syndromes. We also discuss their underlying molecular mechanisms and significance for understanding common age-related disease processes. Source

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