Stanford, CA, United States

Stanford University

www.stanford.edu
Stanford, CA, United States

Leland Stanford Junior University, or more commonly Stanford University, is a private research university in Stanford, California, and one of the world's most prestigious institutions, with the highest undergraduate selectivity and the top position in numerous surveys and measures in the United States.Stanford was founded in 1885 by Leland Stanford, former governor of and U.S. senator from California and leading railroad tycoon, and his wife, Jane Lathrop Stanford, in memory of their only child, Leland Stanford, Jr., who had died of typhoid fever at age 15 the previous year. Stanford was opened on October 1, 1891 as a coeducational and non-denominational institution. Tuition was free until 1920. The university struggled financially after Leland Stanford's 1893 death and after much of the campus was damaged by the 1906 San Francisco earthquake. Following World War II, Provost Frederick Terman supported faculty and graduates' entrepreneurialism to build self-sufficient local industry in what would later be known as Silicon Valley. By 1970, Stanford was home to a linear accelerator, and was one of the original four ARPANET nodes .Stanford is located in northern Silicon Valley near Palo Alto, California. The University's academic departments are organized into seven schools, with several other holdings, such as laboratories and nature reserves, located outside the main campus. Its 8,180-acre campus is one of the largest in the United States. The University is also one of the top fundraising institutions in the country, becoming the first school to raise more than a billion dollars in a year.Stanford's undergraduate program is the most selective in the country with an acceptance rate of 5.07% for the 2018 Class. Students compete in 36 varsity sports, and the University is one of two private institutions in the Division I FBS Pacific-12 Conference. It has gained 105 NCAA team championships, the second-most for a university, 465 individual championships, the most in Division I, and has won the NACDA Directors' Cup, recognizing the university with the best overall athletic team achievement, every year since 1994-1995.Stanford faculty and alumni have founded many companies including Google, Hewlett-Packard, Nike, Sun Microsystems, and Yahoo!, and companies founded by Stanford alumni generate more than $2.7 trillion in annual revenue, equivalent to the 10th-largest economy in the world. Fifty-nine Nobel laureates have been affiliated with the University, and it is the alma mater of 30 living billionaires and 17 astronauts. Stanford has produced a total of 18 Turing Award laureates, the highest in the world for any one institution. It is also one of the leading producers of members of the United States Congress. Wikipedia.

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Patent
Stanford University | Date: 2017-03-29

Recombinant adeno-associated viral (AAV) capsid proteins are provided. Methods for generating the recombinant adeno-associated viral capsid proteins and a library from which the capsids are selected are also provided


Patent
Stanford University | Date: 2017-01-11

Administering an effective dose of glutenase to a Celiac or dermatitis herpetiformis patient reduces levels of toxic gluten oligopeptides, thereby attenuating or eliminating the damaging effects of gluten.


Patent
Greenlight Biosciences and Stanford University | Date: 2017-09-20

The embodiments described herein pertain to cells, and methods for preparing cells, that can be used as biocatalysts by altering enzymes that compete for a substrate or product of a pathway of interest such that the targeted enzyme is sensitive to a site-specific protease, which protease is expressed but relocated in the cell to a site where it is not in contact with the targeted enzyme in the intact cell. Upon cell lysis, the protease contacts the target enzyme, which is then inactivated by protease cleavage.


Methods and compositions are provided for displaying a protein of interest (POI) on the surface of a eukaryotic cell by fusing the POI to a signal polypeptide, a stalk polypeptide, and a surface anchor polypeptide to generate a surface accessible fusion protein. Nucleic acids are provided that include nucleotide sequences encoding a signal polypeptide, a stalk polypeptide, and a surface anchor polypeptide. In some cases, a subject nucleic acid includes and insertion site for the insertion of a POI. In some cases, a subject nucleic acid includes a nucleotide sequence that encodes a POI. In some cases a stalk polypeptide is a synthetic stalk polypeptide and various example synthetic stalk polypeptides are disclosed. In some cases, a surface anchor polypeptide is a glycosylphosphatidylinisotol (GPI) anchor domain, which can be synthetic. Kits are also provided for practicing the subject methods.


Menon V.,Stanford University
Trends in Cognitive Sciences | Year: 2013

The human brain undergoes protracted developmental changes during which it constructs functional networks that engender complex cognitive abilities. Understanding brain function ultimately depends on knowledge of how dynamic interactions between distributed brain regions mature with age to produce sophisticated cognitive systems. This review summarizes recent progress in our understanding of the ontogeny of functional brain networks. Here I describe how complementary methods for probing functional connectivity are providing unique insights into the emergence and maturation of distinct functional networks from childhood to adulthood. I highlight six emerging principles governing the development of large-scale functional networks and discuss how they inform cognitive and affective function in typically developing children and in children with neurodevelopmental disorders. © 2013 Elsevier Ltd.


Clarke L.E.,Stanford University | Barres B.A.,Stanford University
Nature Reviews Neuroscience | Year: 2013

Astrocytes are now emerging as key participants in many aspects of brain development, function and disease. In particular, new evidence shows that astrocytes powerfully control the formation, maturation, function and elimination of synapses through various secreted and contact-mediated signals. Astrocytes are also increasingly being implicated in the pathophysiology of many psychiatric and neurological disorders that result from synaptic defects. A better understanding of how astrocytes regulate neural circuit development and function in the healthy and diseased brain might lead to the development of therapeutic agents to treat these diseases. © 2013 Macmillan Publishers Limited. All rights reserved.


Fernald R.D.,Stanford University
Annual Review of Neuroscience | Year: 2012

In the course of evolution, social behavior has been a strikingly potent selective force in shaping brains to control action. Physiological, cellular, and molecular processes reflect this evolutionary force, particularly in the regulation of reproductive behavior and its neural circuitry. Typically, experimental analysis is directed at how the brain controls behavior, but the brain is also changed by behavior over evolution, during development, and through its ongoing function. Understanding how the brain is influenced by behavior offers unusual experimental challenges. General principles governing the social regulation of the brain are most evident in the control of reproductive behavior. This is most likely because reproduction is arguably the most important event in an animal's life and has been a powerful and essential selective force over evolution. Here I describe the mechanisms through which behavior changes the brain in the service of reproduction using a teleost fish model system. © 2012 by Annual Reviews. All rights reserved.


Menon V.,Stanford University
Trends in Cognitive Sciences | Year: 2011

The science of large-scale brain networks offers a powerful paradigm for investigating cognitive and affective dysfunction in psychiatric and neurological disorders. This review examines recent conceptual and methodological developments which are contributing to a paradigm shift in the study of psychopathology. I summarize methods for characterizing aberrant brain networks and demonstrate how network analysis provides novel insights into dysfunctional brain architecture. Deficits in access, engagement and disengagement of large-scale neurocognitive networks are shown to play a prominent role in several disorders including schizophrenia, depression, anxiety, dementia and autism. Synthesizing recent research, I propose a triple network model of aberrant saliency mapping and cognitive dysfunction in psychopathology, emphasizing the surprising parallels that are beginning to emerge across psychiatric and neurological disorders. © 2011 Elsevier Ltd.


Porteus M.,Stanford University
Annual Review of Pharmacology and Toxicology | Year: 2016

The ability to manipulate the genome with precise spatial and nucleotide resolution (genome editing) has been a powerful research tool. In the past decade, the tools and expertise for using genome editing in human somatic cells and pluripotent cells have increased to such an extent that the approach is now being developed widely as a strategy to treat human disease. The fundamental process depends on creating a site-specific DNA double-strand break (DSB) in the genome and then allowing the cell's endogenous DSB repair machinery to fix the break such that precise nucleotide changes are made to the DNA sequence. With the development and discovery of several different nuclease platforms and increasing knowledge of the parameters affecting different genome editing outcomes, genome editing frequencies now reach therapeutic relevance for a wide variety of diseases. Moreover, there is a series of complementary approaches to assessing the safety and toxicity of any genome editing process, irrespective of the underlying nuclease used. Finally, the development of genome editing has raised the issue of whether it should be used to engineer the human germline. Although such an approach could clearly prevent the birth of people with devastating and destructive genetic diseases, questions remain about whether human society is morally responsible enough to use this tool. Copyright © 2016 by Annual Reviews. All rights reserved.


Steinman L.,Stanford University
Annual Review of Immunology | Year: 2014

Eighty percent of individuals with multiple sclerosis (MS) initially develop a clinical pattern with periodic relapses followed by remissions, called relapsing-remitting MS (RRMS). This period of fluctuating disease may last for a decade or more. Clinical relapses reflect acute inflammation in the central nervous system (CNS), composed of the brain and spinal cord. Often, different anatomic areas in the CNS are involved each time a relapse occurs, resulting in varied clinical manifestations in each instance. Relapses are nearly always followed by some degree of remission, though recovery to baseline status before the flare is often incomplete. There are nine approved drugs for treatment of RRMS. The most potent drug for inhibiting relapses, the humanized anti-α4 integrin antibody known as Natalizumab, blocks homing of mononuclear cells to the CNS. The mechanisms of action of the approved drugs for RRMS provide a strong foundation for understanding the pathobiology of the relapse. Despite substantial progress in controlling relapses with the current armamentarium of medications, there is much to learn and ever more effective and safe therapies to develop. © 2014 by Annual Reviews. All rights reserved.

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