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Durham, NC, United States

Duke University is a private research university located in Durham, North Carolina, United States. Founded by Methodists and Quakers in the present-day town of Trinity in 1838, the school moved to Durham in 1892. In 1924, tobacco and electric power industrialist James B. Duke established The Duke Endowment, at which time the institution changed its name to honor his deceased father, Washington Duke.The university's campus spans over 8,600 acres on three contiguous campuses in Durham as well as a marine lab in Beaufort. Duke's main campus—designed largely by African American architect Julian Abele—incorporates Gothic architecture with the 210-foot Duke Chapel at the campus' center and highest point of elevation. The first-year-populated East Campus contains Georgian-style architecture, while the main Gothic-style West Campus 1.5 miles away is adjacent to the Medical Center.Duke's research expenditures in the 2012 fiscal year were $1.01 billion, the seventh largest in the nation. Competing in the Atlantic Coast Conference, Duke's athletic teams, known as the Blue Devils, have captured 15 team national championships, including four by its high profile men's basketball team. Duke was ranked among the world's best universities by both THE and QS, while tying for 8th in the 2015 U.S. News & World Report "Best National Universities Rankings." In 2014, Thomson Reuters named 32 Duke professors to its list of Highly Cited Researchers. The only schools with more primary affiliations were Harvard, Stanford, and UC Berkeley. Wikipedia.


Haynes B.F.,Duke University
Current Opinion in Immunology | Year: 2015

Development of a safe and effective vaccine for HIV is a major global priority. However, to date, efforts to design an HIV vaccine with methods used for development of other successful viral vaccines have not succeeded due to HIV diversity, HIV integration into the host genome, and ability of HIV to consistently evade anti-viral immune responses. Recent success in isolation of potent broadly neutralizing antibodies (bnAbs), in discovery of mechanisms of bnAb induction, and in discovery of atypical mechanisms of CD8T cell killing of HIV-infected cells, have opened new avenues for strategies for HIV vaccine design. © 2015 Elsevier Ltd. Source


Jennings R.B.,Duke University
Circulation Research | Year: 2013

A selective history of the pathophysiological, structural, and metabolic changes found during an episode of severe myocardial ischemia in the canine heart is presented. The changes that cause ischemic injury to become irreversible are discussed in detail because these changes are the target of any successful therapy designed to prevent ischemic cell death. Of these, the disruption of the sarcolemma, an injury the development of which is accelerated in vivo by the contraction of viable tissue elsewhere in the heart traumatizing the ischemic area, plus the changes in high-energy phosphate and the total adenine nucleotide pool are considered to be the critical events leading to the development of irreversibility. The discovery of preconditioning with ischemia is discussed, together with a brief description of postconditioning. Finally, reperfusion injury is discussed in a summary fashion. The evidence for the fact that myocytes are salvaged by reperfusion is presented, as is the evidence that myocytes become unsalvageable by reperfusion as the duration of ischemia increases. The concept that some of the myocytes that die after successful reperfusion with arterial blood actually are killed by changes initiated by reperfusion, so-called lethal reperfusion injury, is attractive in that prevention of this change would lead to greater salvage; however, the prevalence of this phenomenon in clinical practice remains to be determined. © 2013 American Heart Association, Inc. Source


Cullen B.R.,Duke University
Genes and Development | Year: 2011

Analyses of small RNA expression profiles have revealed that several DNA viruses-including particularly, herpesviruses-express high levels of multiple viral microRNAs (miRNAs) in infected cells. Here, I review our current understanding of how viral miRNAs influence viral replication and pathogenesis and discuss how viruses reshape the pattern of cellular miRNA expression. Indeed, viruses are now known to both activate and repress the expression of specific cellular miRNAs, and disrupting this process can perturb the ability of viruses to replicate normally. In addition, it is now clear that virally encoded miRNAs play a key role in inhibiting antiviral innate immune responses and can also promote cell transformation in culture. While our understanding of how viruses interact with miRNAs remains somewhat rudimentary, it is nevertheless already clear that these interactions can play a critical role in mediating viral pathogenesis and therefore may represent novel and highly specific targets for therapeutic intervention. © 2011 by Cold Spring Harbor Laboratory Press. Source


Muir A.J.,Duke University
American Journal of Gastroenterology | Year: 2014

Hepatitis C virus (HCV) treatment took a major step forward at the end of 2013 with the approvals of the second-generation protease inhibitor simeprevir (Olysio) and the nucleotide polymerase inhibitor sofosbuvir (Sovaldi). The interferon-free regimen of sofosbuvir and ribavirin is now available for genotype 2 and 3 patients. This regimen for 12 weeks is highly effective for genotype 2, whereas genotype 3 has proven to be more challenging and requires 24 weeks of therapy. Genotype 1 patients have reduced exposure to peginterferon-α with a 12-week regimen with sofosbuvir and a 24-week regimen with simeprevir. Genotype 4, 5, and 6 patients also respond well to the regimen of sofosbuvir, peginterferon-α, and ribavirin. In another landmark event, the initial approval of sofosbuvir included HCV/HIV-1 coinfected patients. Simeprevir and sofosbuvir also provide a window to the future with sustained virologic response (SVR) rates of >90% for genotype 1 when these agents are combined. Interferon-free regimens for genotype 1 patients have anticipated approvals in late 2014 or early 2015. Clinicians and patients will have the opportunity to discuss and select from current treatment options or await upcoming regimens. These potent new agents provide the tools to cure HCV for many patients. © 2014 by the American College of Gastroenterology. Source


Tedder T.F.,Duke University
Journal of Immunology | Year: 2015

B cells are commonly thought to enhance inflammatory immune responses. However, specific regulatory B cell subsets recently were identified that downregu-late adaptive and innate immunity, inflammation, and autoimmunity through diverse molecular mechanisms. In both mice and humans, a rare, but specific, subset of regulatory B cells is functionally characterized by its capacity to produce IL-10, a potent inhibitory cytokine. For clarity, this regulatory B cell subset has been labeled as B10 cells, because their ability to downregu-late immune responses and inflammatory disease is fully attributable to IL-10, and their absence or loss exacerbates disease symptoms in mouse models. This review preferentially focuses on what is known about mouse B10 cell development, phenotype, and effector function, as well as on mechanistic studies that demonstrated their functional importance during inflammation, autoimmune disease, and immune responses. Copyright © 2015 by The American Association of Immunologists, Inc. Source

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