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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.

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. Source

Ganz T.,University of California at Los Angeles
Blood | Year: 2011

Under evolutionary pressure to counter the toxicity of iron and to maintain adequate iron supply for hemoglobin synthesis and essential metabolic functions, humans and other vertebrates have effective mechanisms to conserve iron and to regulate its concentration, storage, and distribution in tissues. The iron-regulatory hormone hepcidin, first described 10 years ago, and its receptor and iron channel ferroportin control the dietary absorption, storage, and tissue distribution of iron. Hepcidin causes ferroportin internalization and degradation, thereby decreasing iron transfer into blood plasma from the duodenum, from macrophages involved in recycling senescent erythrocytes, and from iron-storing hepatocytes. Hepcidin is feedback regulated by iron concentrations in plasma and the liver and by erythropoietic demand for iron. Genetic malfunctions affecting the hepcidinferroportin axis are a main cause of iron overload disorders but can also cause iron-restricted anemias. Modulation of hepcidin and ferroportin expression during infection and inflammation couples iron metabolism to host defense and decreases iron availability to invading pathogens. This response also restricts the iron supply to erythropoietic precursors and may cause or contribute to the anemia associated with infections and inflammatory disorders. © 2011 by The American Society of Hematology. Source

Shapley A.E.,University of California at Los Angeles
Annual Review of Astronomy and Astrophysics | Year: 2011

The epoch of galaxy assembly from 2≤â(c)1/2z≤â(c)1/24 marks a critical stage during the evolution of today's galaxy population. During this period, the star-formation activity in the Universe was at its peak level, and the structural patterns observed among galaxies in the local Universe were not yet in place. A variety of novel techniques have been employed over the past decade to assemble multiwavelength observations of galaxies during this important epoch. In this primarily observational review, I present a census of the methods used to find distant galaxies and the empirical constraints on their multiwavelength luminosities and colors. I then discuss what is known about the stellar content and past histories of star formation in high-redshift galaxies; their interstellar contents including dust, gas, and heavy elements; and their structural and dynamical properties. I conclude by considering some of the most pressing and open questions regarding the physics of high-redshift galaxies, which are to be addressed with future facilities. © 2011 by Annual Reviews. All rights reserved. Source

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.). Source

Clarke S.G.,University of California at Los Angeles
Trends in Biochemical Sciences | Year: 2013

Methylated lysine and arginine residues in histones represent a crucial part of the histone code, and recognition of these methylated residues by protein interaction domains modulates transcription. Although some methylating enzymes appear to be histone specific, many can modify histone and non-histone substrates and an increasing number are specific for non-histone substrates. Some of the non-histone substrates can also be involved in transcription, but a distinct subset of protein methylation reactions occurs at residues buried deeply in ribosomal proteins that may function in protein-RNA interactions rather than protein-protein interactions. Additionally, recent work has identified enzymes that catalyze protein methylation reactions at new sites in ribosomal and other proteins. These reactions include modifications of histidine and cysteine residues as well as the N terminus. © 2013 Elsevier Ltd. Source

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