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Winston - Salem, NC, United States

Wake Forest University is a private, independent, nonprofit, non-sectarian, coeducational research university in Winston-Salem, North Carolina, founded in 1834. The university received its name from its original location in Wake Forest, north of Raleigh, North Carolina, the state capital. The Reynolda Campus, the university's main campus, has been located north of downtown Winston-Salem since the university moved there in 1956. The Wake Forest Baptist Medical Center campus is located near the Ardmore neighborhood in central Winston-Salem. The University also occupies lab space at Biotech Plaza, at the downtown Piedmont Research Park, and at the Center for Nanotechnology and Molecular Materials. The University's Babcock Graduate School of Management maintains a presence on the main campus in Winston-Salem and in Charlotte, North Carolina. In the 2014 U.S. News America's Best Colleges report, Wake Forest ranked 11th in terms of "Best Undergraduate Teaching" and 27th overall among national universities. Wikipedia.

Holmes R.P.,Wake forest University
Molecular Aspects of Medicine | Year: 2012

Seven members of the aquaporin (AQP) family are expressed in different regions of the kidney. AQP1-4 are localized in plasma membranes of renal epithelial cells and are intimately involved in water reabsorption by the kidney. AQP7 is also localized in the plasma membrane and may facilitate glycerol transport. AQP6 and AQP11 are localized within the cell, with AQP6 involved in anion transport and AQP11 water transport. Mutations in AQP2 can result in diabetes insipidus, whereas mutations in other AQPs have not yet been shown to be disease-associated. Genetic polymorphisms may contribute to the susceptibility to defects in urine concentrating mechanisms associated with some diseases. Most of the AQPs are subject to transcriptional regulation and post-translational modifications by a range of biological modifiers. As a result a number of chronic kidney and systemic diseases produce changes in the abundance of AQPs. The more recent developments in this field are reviewed. © 2012 Elsevier Ltd. All rights reserved.

Loeser R.F.,Wake forest University
Current Opinion in Rheumatology | Year: 2013

Purpose of Review: Aging is a primary risk factor for the development of osteoarthritis and the understanding of how aging processes contribute to the development of osteoarthritis is an important area of active research. The most recent literature in this area was reviewed in order to update investigators on the status of the field. Recent Findings: The field is beginning to move beyond a cartilage focus to include other joint tissues relevant to osteoarthritis such as ligaments, meniscus, and bone. Synovitis also appears to play a role in osteoarthritis but has not been a focus of aging studies. Studies in small animals, including mice and rats, demonstrate age-related changes that can contribute to osteoarthritis and show that animal age is a key factor to be considered in interpreting the results of studies using surgically induced models of osteoarthritis. There is accumulating evidence that cellular processes such as damage-induced cell senescence contribute to osteoarthritis and a growing body of literature on the role of epigenetic regulation of gene expression in aging and osteoarthritis. Summary: Not all osteoarthritis is due to aging processes in joint tissues, but the age-related changes being discovered certainly could play a major contributing role. Copyright © 2012 Lippincott Williams & Wilkins.

Nunez M.,Wake forest University
Hepatology | Year: 2010

Highly active antiretroviral therapy (HAART)-related hepatotoxicity complicates the management of patients infected with human immunodeficiency virus (HIV), increases medical costs, alters the prescription patterns, and affects the guideline recommendations. Among the clinical consequences derived from HAART-related liver toxicity, hypersensitivity reactions and lactic acidosis are recognized as acute events with potential to evolve into fatal cases, whereas there seems to be other syndromes not as well characterized but of equal concern as possible long-term liver complications. Belonging to the latter category of syndrome, HAART-related nonalcoholic steatohepatitis, liver fibrosis, portal hypertension, and nodular regenerative hyperplasia are discussed in this review. Updated information on liver toxicity of current antiretroviral drugs, including the most recently licensed, is provided. Management and prevention of liver toxicity among HIV-infected patients treated with HAARTare reviewed as well. Copyright © 2010 by the American Association for the Study of Liver Diseases.

Hegde A.N.,Wake forest University
Learning and Memory | Year: 2010

Proteolysis by the ubiquitin-proteasome pathway (UPP) has emerged as a new molecular mechanism that controls wide-ranging functions in the nervous system, including fine-tuning of synaptic connections during development and synaptic plasticity in the adult organism. In the UPP, attachment of a small protein, ubiquitin, tags the substrates for degradation by a multisubunit complex called the proteasome. Linkage of ubiquitin to protein substrates is highly specific and occurs through a series of well-orchestrated enzymatic steps. The UPP regulates neurotransmitter receptors, protein kinases, synaptic proteins, transcription factors, and other molecules critical for synaptic plasticity. Accumulating evidence indicates that the operation of the UPP in neurons is not homogeneous and is subject to tightly managed local regulation in different neuronal subcompartments. Investigations on both invertebrate and vertebrate model systems have revealed local roles for enzymes that attach ubiquitin to substrate proteins, as well as for enzymes that remove ubiquitin from substrates. The proteasome also has been shown to possess disparate functions in different parts of the neuron. Here I give a broad overview of the role of the UPP in synaptic plasticity and highlight the local roles and regulation of the proteolytic pathway in neurons. © 2010 Cold Spring Harbor Laboratory Press.

We investigated the predictive value of geriatric assessment (GA) on overall survival (OS) for older adults with acute myelogenous leukemia (AML). Consecutive patients ≥ 60 years with newly diagnosed AML and planned intensive chemotherapy were enrolled at a single institution. Pretreatment GA included evaluation of cognition, depression, distress, physical function (PF) (self-reported and objectively measured), and comorbidity. Objective PF was assessed using the Short Physical Performance Battery (SPPB, timed 4-m walk, chair stands, standing balance) and grip strength. Cox proportional hazards models were fit for each GA measure as a predictor of OS. Among 74 patients, the mean age was 70 years, and 78.4% had an Eastern Cooperative Oncology Group (ECOG) score ≤ 1. OS was significantly shorter for participants who screened positive for impairment in cognition and objectively measured PF. Adjusting for age, gender, ECOG score, cytogenetic risk group, myelodysplastic syndrome, and hemoglobin, impaired cognition (Modified Mini-Mental State Exam < 77) and impaired objective PF (SPPB < 9) were associated with worse OS. GA methods, with a focus on cognitive and PF, improve risk stratification and may inform interventions to improve outcomes for older AML patients.

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