Los Angeles, CA, United States

University of California at Los Angeles

Los Angeles, CA, United States

The University of California, Los Angeles , is a public research university located in the Westwood neighborhood of Los Angeles, California, United States. Founded in 1919, it became the University of California Southern Branch in 1927, making it the second-oldest undergraduate campus of the ten-campus system after the original University of California campus at Berkeley . It offers 337 undergraduate and graduate degree programs in a wide range of disciplines. With an approximate enrollment of 30,000 undergraduate and 12,000 graduate students, UCLA is the university with the largest enrollment in the state of California and the most applied to university in the United States with over 112,000 applications for Fall 2015.The university is organized into five undergraduate colleges, seven professional schools, and four professional health science schools. The undergraduate colleges are the College of Letters and Science; Henry Samueli School of Engineering and Applied Science ; School of the Arts and Architecture; School of Theater, Film, and Television; and School of Nursing. Fifteen Nobel laureates, one Fields Medalist, and three Turing Award winners have been faculty, researchers, or alumni. Among the current faculty members, 52 have been elected to the National Academy of science, 28 to the National Academy of Engineering, 39 to the Institute of Medicine, and 124 to the American Academy of Arts and science. The university was elected to the Association of American Universities in 1974.UCLA student-athletes compete as the Bruins in the Pacific-12 Conference. The Bruins have won 125 national championships, including 112 NCAA team championships. UCLA student-athletes have won 250 Olympic medals: 125 gold, 65 silver and 60 bronze. The Bruins have competed in every Olympics since 1920 with one exception , and have won a gold medal in every Olympics that the United States has participated in since 1932. Wikipedia.

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University of California at Los Angeles | Date: 2017-01-19

Methods and compositions are provided for treating neuropsychiatric disorders such as schizophrenia, depression, attention deficit disorder, mild cognitive impairment, dementia, and bipolar disorder. The methods entail administering to a patient diagnosed as having a neuropsychiatric disorder (e.g., schizophrenia, depression, attention deficit disorder, mild cognitive impairment, dementia bipolar disorder, etc.) or as at risk for a neuropsychiatric disorder a benzoic acid, benzoic acid salt, and/or benzoic acid derivative, and/or a sorbic acid, sorbic acid salt, and/or sorbic acid derivative, in combination with a neuropharmacological agent (e.g., an antipsychotic, an antidepressant, medications for attention deficit and hyperactivity disorder, cognitive impairment, or dementia, etc.) where the benzoic acid, benzoic acid salt, or benzoic acid derivative, and/or a sorbic acid, sorbic acid salt, and/or sorbic acid derivative, is in an amount sufficient to increase the efficacy of the neuropharmacological agent.

University of Notre Dame and University of California at Los Angeles | Date: 2016-09-14

Systems and methods are provided for identifying markers for inflammation in a tissue image. The tissue image is captured as an image of a histology slide. Subcellular structures in the tissue image are segmented via a first automated process to identify at least one variety of immune cells within the image. Glands and vilii are identified within the tissue image via a second automated process. Neutrophils are identified within the tissue image via a third automated process. An output representing the identified glands, villi, neutrophils, and other immune cells is provided to a human operator.

University of California at Los Angeles | Date: 2016-06-13

A Candida albicans bloodstream infections cause significant morbidity and mortality in hospitalized patients. Filament formation and adherence to host cells are critical virulence factors of C. albicans. Multiple filamentation regulatory pathways have been discovered, however the downstream effectors of these regulatory pathways remain unknown. The cell surface proteins in the ALS group are downstream effectors of the filamentation regulatory pathway. Particularly, Als1p mediates adherence to endothelial cells in vitro and is required for virulence. The blocking of adherence by the organism is described resulting from the use of a composition and method disclosed herein. Specifically, a pharmaceutical composition comprised of a gene, gene product, or specific antibody to the ALS gene family is administered as a vaccine to generate an immune response capable of blocking adherence of the organism.

Colwell C.S.,University of California at Los Angeles
Nature Reviews Neuroscience | Year: 2011

Neurons in the suprachiasmatic nucleus (SCN) function as part of a central timing circuit that drives daily changes in our behaviour and underlying physiology. A hallmark feature of SCN neuronal populations is that they are mostly electrically silent during the night, start to fire action potentials near dawn and then continue to generate action potentials with a slow and steady pace all day long. Sets of currents are responsible for this daily rhythm, with the strongest evidence for persistent Na + currents, L-type Ca 2+ currents, hyperpolarization-activated currents (I H), large-conductance Ca 2+ activated K + (BK) currents and fast delayed rectifier (FDR) K + currents. These rhythms in electrical activity are crucial for the function of the circadian timing system, including the expression of clock genes, and decline with ageing and disease. This article reviews our current understanding of the ionic and molecular mechanisms that drive the rhythmic firing patterns in the SCN. © 2011 Macmillan Publishers Limited. All rights reserved.

Burda J.E.,University of California at Los Angeles | Sofroniew M.V.,University of California at Los Angeles
Neuron | Year: 2014

The CNS is prone to heterogeneous insults of diverse etiologies that elicit multifaceted responses. Acute and focal injuries trigger wound repair with tissue replacement. Diffuse and chronic diseases provoke gradually escalating tissue changes. The responses to CNS insults involve complex interactions among cells of numerous lineages and functions, including CNS intrinsic neural cells, CNS intrinsic nonneural cells, and CNS extrinsic cells that enter from the circulation. The contributions of diverse nonneuronal cell types to outcome after acute injury, or to the progression of chronic disease, are of increasing interest as the push toward understanding and ameliorating CNS afflictions accelerates. In some cases, considerable information is available, in others, comparatively little, as examined and reviewed here. © 2014 Elsevier Inc.

Geschwind D.H.,University of California at Los Angeles
Trends in Cognitive Sciences | Year: 2011

Characterized by a combination of abnormalities in language, social cognition and mental flexibility, autism is not a single disorder but a neurodevelopmental syndrome commonly referred to as autism spectrum disorder (ASD). Several dozen ASD susceptibility genes have been identified in the past decade, collectively accounting for 10-20% of ASD cases. These findings, although demonstrating that ASD is etiologically heterogeneous, provide important clues about its pathophysiology. Diverse genetic and genomic approaches provide evidence converging on disruption of key biological pathways, many of which are also implicated in other allied neurodevelopmental disorders. Knowing the genes involved in ASD provides us with a crucial tool to probe both the specificity of ASD and the shared neurobiological and cognitive features across what are considered clinically distinct disorders, with the goal of linking gene to brain circuits to cognitive function. © 2011 Elsevier Ltd.

Eisenberger N.I.,University of California at Los Angeles
Nature Reviews Neuroscience | Year: 2012

Experiences of social rejection, exclusion or loss are generally considered to be some of the most 'painful' experiences that we endure. Indeed, many of us go to great lengths to avoid situations that may engender these experiences (such as public speaking). Why is it that these negative social experiences have such a profound effect on our emotional well-being? Emerging evidence suggests that experiences of social pain-the painful feelings associated with social disconnection-rely on some of the same neurobiological substrates that underlie experiences of physical pain. Understanding the ways in which physical and social pain overlap may provide new insights into the surprising relationship between these two types of experiences. © 2012 Macmillan Publishers Limited. All rights reserved.

Slamon D.,University of California at Los Angeles
The New England journal of medicine | Year: 2011

Trastuzumab improves survival in the adjuvant treatment of HER-positive breast cancer, although combined therapy with anthracycline-based regimens has been associated with cardiac toxicity. We wanted to evaluate the efficacy and safety of a new nonanthracycline regimen with trastuzumab. We randomly assigned 3222 women with HER2-positive early-stage breast cancer to receive doxorubicin and cyclophosphamide followed by docetaxel every 3 weeks (AC-T), the same regimen plus 52 weeks of trastuzumab (AC-T plus trastuzumab), or docetaxel and carboplatin plus 52 weeks of trastuzumab (TCH). The primary study end point was disease-free survival. Secondary end points were overall survival and safety. At a median follow-up of 65 months, 656 events triggered this protocol-specified analysis. The estimated disease-free survival rates at 5 years were 75% among patients receiving AC-T, 84% among those receiving AC-T plus trastuzumab, and 81% among those receiving TCH. Estimated rates of overall survival were 87%, 92%, and 91%, respectively. No significant differences in efficacy (disease-free or overall survival) were found between the two trastuzumab regimens, whereas both were superior to AC-T. The rates of congestive heart failure and cardiac dysfunction were significantly higher in the group receiving AC-T plus trastuzumab than in the TCH group (P<0.001). Eight cases of acute leukemia were reported: seven in the groups receiving the anthracycline-based regimens and one in the TCH group subsequent to receiving an anthracycline outside the study. The addition of 1 year of adjuvant trastuzumab significantly improved disease-free and overall survival among women with HER2-positive breast cancer. The risk-benefit ratio favored the nonanthracycline TCH regimen over AC-T plus trastuzumab, given its similar efficacy, fewer acute toxic effects, and lower risks of cardiotoxicity and leukemia. (Funded by Sanofi-Aventis and Genentech; BCIRG-006 ClinicalTrials.gov number, NCT00021255.).

Sofroniew M.V.,University of California at Los Angeles
Nature Reviews Neuroscience | Year: 2015

Astrocytes form borders (glia limitans) that separate neural from non-neural tissue along perivascular spaces, meninges and tissue lesions in the CNS. Transgenic loss-of-function studies reveal that astrocyte borders and scars serve as functional barriers that restrict the entry of inflammatory cells into CNS parenchyma in health and disease. Astrocytes also have powerful pro-inflammatory potential. Thus, astrocytes are emerging as pivotal regulators of CNS inflammatory responses. This Review discusses evidence that astrocytes have crucial roles in attracting and restricting CNS inflammation, with important implications for diverse CNS disorders. © 2015 Macmillan Publishers Limited. All rights reserved.

Ganz T.,University of California at Los Angeles
Physiological Reviews | Year: 2013

The iron hormone hepcidin and its receptor and cellular iron exporter ferroportin control the major fluxes of iron into blood plasma: intestinal iron absorption, the delivery of recycled iron from macrophages, and the release of stored iron from hepatocytes. Because iron losses are comparatively very small, iron absorption and its regulation by hepcidin and ferroportin determine total body iron content. Hepcidin is in turn feedback-regulated by plasma iron concentration and iron stores, and negatively regulated by the activity of erythrocyte precursors, the dominant consumers of iron. Hepcidin and ferroportin also play a role in host defense and inflammation, and hepcidin synthesis is induced by inflammatory signals including interleukin-6 and activin B. This review summarizes and discusses recent progress in molecular characterization of systemic iron homeostasis and its disorders, and identifies areas for further investigation. © 2013.

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