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 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.

California Institute of Technology, University of California at Los Angeles and University of Southern California | Date: 2015-12-28

A portion of a concentric bipolar microelectrode sensor is attached to an inflatable balloon of a catheter. Another portion of the concentric bipolar microelectrode sensor is also attached to a body of the catheter. The inflatable balloon is guided to become in proximity of a tissue. The inflatable balloon is then inflated. The inflation increases the likelihood of contact between microelectrodes of the concentric bipolar microelectrode sensor with the tissue. A voltage is supplied to the microelectrodes. The tissues impedance is accordingly measured over a frequency range. A disease of the tissue, such as a lesion, is diagnosed based on the measured impedance.

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.

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.

Hahn B.H.,University of California at Los Angeles
New England Journal of Medicine | Year: 2013

A 20-year-old woman was evaluated by her rheumatologist because she was disabled by flares of systemic lupus erythematosus (SLE). A diagnosis of SLE had been made 2 years earlier, on the basis of a photosensitive malar rash, oral ulcers, polyarthritis, pericarditis, and positive assays for antinuclear antibodies (ANA) and anti-double-stranded DNA (dsDNA) antibodies. Treatment with analgesics and hydroxychloroquine for 6 months was not beneficial; prednisone at a dose of 40 mg daily resulted in some improvement, but the patient gained 6.8 kg (15 lb) and required two hospitalizations for infections. SLE flares occurred when the prednisone dose was less than 30 mg daily. Trials of methotrexate, mycophenolate mofetil, and azathioprine either had unacceptable side effects or failed to control flares or permit prednisone tapering. On examination, she had cushingoid features with 20 swollen, tender joints and 3 oral ulcers. The ANA titer was positive, at 1:320. An assay for anti-dsDNA antibodies was negative, and the serum complement level was normal. The rheumatologist recommended a trial of belimumab. Copyright © 2013 Massachusetts Medical Society.

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.

Smale S.T.,University of California at Los Angeles
Cell | Year: 2010

An inflammatory response is initiated by the temporally controlled activation of genes encoding a broad range of regulatory and effector proteins. A central goal is to devise strategies for the selective modulation of proinflammatory gene transcription, to allow the suppression of genes responsible for inflammation-associated pathologies while maintaining a robust host response to microbial infection. Toward this goal, recent studies have revealed an unexpected level of diversity in the mechanisms by which chromatin structure and individual transcription factors contribute to the selective regulation of inflammatory genes. © 2010 Elsevier Inc.

Horvath S.,University of California at Los Angeles
Genome Biology | Year: 2013

Background: It is not yet known whether DNA methylation levels can be used to accurately predict age across a broad spectrum of human tissues and cell types, nor whether the resulting age prediction is a biologically meaningful measure.Results: I developed a multi-tissue predictor of age that allows one to estimate the DNA methylation age of most tissues and cell types. The predictor, which is freely available, was developed using 8,000 samples from 82 Illumina DNA methylation array datasets, encompassing 51 healthy tissues and cell types. I found that DNA methylation age has the following properties: first, it is close to zero for embryonic and induced pluripotent stem cells; second, it correlates with cell passage number; third, it gives rise to a highly heritable measure of age acceleration; and, fourth, it is applicable to chimpanzee tissues. Analysis of 6,000 cancer samples from 32 datasets showed that all of the considered 20 cancer types exhibit significant age acceleration, with an average of 36 years. Low age-acceleration of cancer tissue is associated with a high number of somatic mutations and TP53 mutations, while mutations in steroid receptors greatly accelerate DNA methylation age in breast cancer. Finally, I characterize the 353 CpG sites that together form an aging clock in terms of chromatin states and tissue variance.Conclusions: I propose that DNA methylation age measures the cumulative effect of an epigenetic maintenance system. This novel epigenetic clock can be used to address a host of questions in developmental biology, cancer and aging research. © 2013 Horvath; licensee BioMed Central Ltd.

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