Baltimore, MD, United States
Baltimore, MD, United States

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.


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Patent
Johns Hopkins University and Cardioxyl Pharmaceuticals | Date: 2017-02-01

The invention relates to N-hydroxysulfonamide derivatives that donate nitroxyl (HNO) under physiological conditions and are useful in treating and/or preventing the onset and/or development of diseases or conditions that are responsive to nitroxyl therapy, including heart failure and ischemia/reperfusion injury. Novel N-hydroxysulfonamide derivatives release NHO at a controlled rate under physiological conditions, and the rate of HNO release is modulated by varying the nature and location of functional groups on the N-hydroxysulfonamide derivatives.


Patent
Johns Hopkins University | Date: 2017-01-11

AmexinA2 (ANXA2), a member of the Annexin family of calcium-dependent, phospholipid binding proteins, is one of a panel of identified antigens recognized by the post-vaccination sera of patients who demonstrated prolonged disease-free survival following multiple vaccinations. AnnexinA2 is abundantly expressed in pancreatic adenocarcinomas and cell surface/membrane AnnexinA2 increases with the progression from premalignant lesions to invasive pancreatic adenocarcinomas. The cytoplasmic to cell surface translocation of AnnexinA2 expression is critical for pancreatic cancer cell invasion. In addition, phosphorylation of AnnexinA2 at Tyrosine 23 is important for its localization to the cell surface and for the invasion of pancreatic cancer cells. Finally, loss of AnnexinA2 leads to the loss of the Epithelial-Mesenchymal Transition.


Patent
Seoul National University and Johns Hopkins University | Date: 2017-02-15

The present disclosure relates to a pharmaceutical composition for preventing or treating neurodegenerative diseases, the pharmaceutical composition including a graphene nanostructure as an active ingredient.


The invention provides methods and compositions for administration of allogeneic lymphocytes as an an exogenous source of CD4+ T cell help for endogenous, tumor-reactive CD8+ T cells. Depletion of CD8+ T cells from the donor lymphocyte infusion reduces the risk of sustained engraftment and graft-versus-host disease. Removal of regulatory T cells from the infused population may augment the ability of non-regulatory T cells to provide help for endogenous effectors of anti-tumor immunity. Allogeneic T cell therapy is typically given in the context of allogeneic stem cell transplantation, in which the patient receives highly immunosuppressive conditioning followed by an infusion of a stem cell graft containing unselected populations of mature T cells. In the treatment described here, the graft is engineered to minimize the possibility of sustained donor cell engraftment, and the anti-tumor effector T cells derive from the host.


Patent
Johns Hopkins University | Date: 2017-02-03

Methods and systems for enabling human-machine collaborations include a generalizable framework that supports dynamic adaptation and reuse of robotic capability representations and human-machine collaborative behaviors. Specifically, a method of feedback-enabled user-robot collaboration includes obtaining a robot capability that models a robots functionality for performing task actions, specializing the robot capability with an information kernel that encapsulates task-related parameters associated with the task actions, and providing an instance of the specialized robot capability as a robot capability element that controls the robots functionality based on the task-related parameters. The method also includes obtaining, based on the robot capability elements user interaction requirements, user interaction capability elements, via which the robot capability element receives user input and provides user feedback, controlling, based on the task-related parameters, the robots functionality to perform the task actions in collaboration with the user input; and providing the user feedback including task-related information generated by the robot capability element in association with the task actions.


Patent
Johns Hopkins University | Date: 2017-01-31

Described are uses of A_(2a )adenosine receptor antagonists and agonists to provide long term modulation of immune responses. A_(2a )receptor antagonists in particular are provided to enhance immune responses by reducing T-cell mediated tolerance to antigenic stimuli and agonists are provided to enhance effectiveness of immunosuppressive agents. The application provides methods of treatment and prevention based on the long term effects of the compounds on T cell responses.


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.


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.


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.


Xing M.,Johns Hopkins University
Nature Reviews Cancer | Year: 2013

Thyroid cancer is a common endocrine malignancy. There has been exciting progress in understanding its molecular pathogenesis in recent years, as best exemplified by the elucidation of the fundamental role of several major signalling pathways and related molecular derangements. Central to these mechanisms are the genetic and epigenetic alterations in these pathways, such as mutation, gene copy-number gain and aberrant gene methylation. Many of these molecular alterations represent novel diagnostic and prognostic molecular markers and therapeutic targets for thyroid cancer, which provide unprecedented opportunities for further research and clinical development of novel treatment strategies for this cancer.© 2013 Macmillan Publishers Limited. All rights reserved.

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