Website: http://pharmacy.unc.edu/research/labs/kim-brouwer-lab
Email: kbrouwer@unc.edu
Voice: (919) 962-7030
Research in the Brouwer laboratory is focused on: (1) hepatobiliary xenobiotic disposition, including mechanisms of hepatic uptake, translocation and biliary excretion; (2) development/refinement of in vitro model systems to predict in vivo hepatobiliary disposition, drug interactions, and hepatotoxicity; (3) hepatic drug transport; and (4) pharmacokinetics, including aberrant gastrointestinal drug absorption phenomena.
]]>Email: pwatkins@thehamner.org
]]>Email: hunter.sid@epa.gov
Our research focuses on determining the mechanisms responsible for craniofacial birth defects. We use the whole embryo culture system to expose mouse conceptuses to toxicants and evaluate morphological, molecular (Affy arrays) and protein changes. Antisense morpholinos and adenoviruses are used to modulate gene expression and determine phenotypic effects. We are using embryonic stem cells as a model to evaluate the effects of environmental chemicals on differentiation. Using molecular markers to identify differentiation may provide critical information to identify developmental toxicants.
]]>Website: http://www.med.unc.edu/kaufmannlab
Email: william.kaufmann@pathology.unc.edu
Voice: (919) 966-8209
Research in the Kaufmann laboratory is concerned with determining the mechanisms whereby cell cycle checkpoints suppress human cancer development. We are focused on two checkpoints that help to stabilize the genome. The decatenation G2 checkpoint delays mitosis until daughter chromatids are sufficiently disentangled by topoisomerase II. This checkpoint is regulated by the breast cancer susceptibility gene BRCA1. The intra-S checkpoint regulates DNA synthesis by controlling the rates of replicon initiation and DNA chain elongation. This checkpoint is regulated by two proteins, Timeless and Tipin, that mediate signaling at stalled replication forks. A program project is studying how the Timeless-Tipin replication fork protection complex protects against UV-induced chromosomal damage and sunlight-induced melanoma.
]]>Website: http://www.niehs.nih.gov/research/atniehs/labs/lrb/enviro-gen/index.cfm
Email: kleeber1@niehs.nih.gov
Voice: (919) 541-3540
Genetic determinants of environmental lung diseases.
]]>Website:
Email: jmacdona@med.unc.edu
Voice: (919) 843-5154
Dr. Macdonald is the Founder and Scientific Director of the new Metabolomic Facility and Co-Scientific Director of the joint UNC/NCSU/NOAA Marine MRI facility at Pivers Island near Beaufort NC. Dr. Macdonald's research goal is to combine metabolomics and tissue engineering and apply these tools to quantitative biosystem analysis.
]]>Website:
Email: madden.michael@epa.gov
Voice: (919) 966-6257
Research description: Exposure to ambient air particulate matter(PM) has been associated with increased human deaths and cardiopulmonary morbidity, such as lung infections and increased asthma symptoms. I am investigating some types of PM and associated gases (such as aldehydes) that may be associated with those health effects so that the US EPA may be able to better regulate or manage the sources of the PM that are identified as playing a role in the adverse health outcomes. I am currently focusing on the effects of diesel exhaust using a variety of approaches ranging from exposing cultured human cells to the exhaust, to studying responses of humans exposed out in traffic. The EPA rules for diesel exhaust from large trucks implemented in 2007 and 2010 will drastically change the type of emissions, and I am currently designing and implementing testing strategies to assess the toxicity of the future types of diesel emissions. Additionally some of my research effort attempts to identify what populations are more sensitive to the effects of air pollutants, and the genetic and environmental reasons behind the increased sensitivity.
]]>Website: http://www.med.unc.edu/pathology/faculty/biosketch-of-dr-maeda
Email: nobuyo@med.unc.edu
Voice: (919) 966-6914
Our research is focused on the genetics and molecular pathology of complex multi-factorial conditions in humans - obesity, diabetes, hypercholesterolemia, insulin resistance, and hypertension. These conditions underlie cardiovascular diseases, including atherosclerosis, the major cause of death and disabilities in North America. Our approach consists of experiments with mice carrying modifications in various genes important for the maintenance of vascular function, antioxidant defense, and metabolism. We dissect how gene-gene and gene-environment interaction influences the pathogenesis of these common human conditions and their complications.
]]>Website: http://www.med.unc.edu/cellbio/faculty-research/deshmukh
Email: mohanish@med.unc.edu
We study how mammalian cells activate the programmed cell death pathway and die by apoptosis. We have focused our work on identifying unique mechanisms by which this pathway is regulated in postmitotic cells such as neurons, cardiomyocytes, and myotubes, as well as cancer, senescent, and stem cells. Excessive cell death is seen in many pathological conditions such as after stroke, neurodegeneration or cardiovascular diseases. In contrast, reduced cell death is a hallmark of cancers. Therefore, discovering the mechanism by which mammalian cells regulate cell death has significant therapeutic implications.
]]>Email: ramabhadran.ram@epa.gov
Voice: (919) 541-3558
1) Using cellular stress signaling pathways to develop in vitro assays in human cells to rapidly ascertain the toxic potential of a wide range of environmental compounds including nanoparticles used in commerce. This research draws extensively on signaling pathways in cells and on high throughput methods including robotics and developing methods for data analysis. 2) Design molecular studies to ascertain the mode of action of environmental compounds of potential concern. This research employs the use of gene over expression and suppression (RNAi) in established and primary cell cultures. 3) Development of alternate species assays for in vivo rapid screening of environmental compounds using normal and transgenic zebrafish.
]]>Website: http://www.sph.unc.edu/?option=com_profiles&profileAction=ProfDetail&pid=702665970
Email: iir@unc.edu
Voice: (919) 843-2596
Our laboratory applies molecular, biochemical, genetic and genomics approaches to understanding the mechanisms of environmental agent-related organ injury and carcinogenesis. Specifically, we are interested in nuclear receptor-mediated pathways in chemical carcinogenesis, oxidative DNA damage and repair, the role that alcohol and diet play in cancer, and the genetic determinants of the susceptibility to toxicant-induced liver injury. Through a combination of in vivo animal studies and experiments that utilize cellular and molecular models, we aim to better understand why certain chemicals cause cancer or organ damage in rodents and whether humans in general, or any susceptible sub-population in particular, are at risk from similar exposures.
]]>Email: samet.james@epa.gov
Voice: (919) 966-0665
Our laboratory is interested in the cellular and molecular mechanisms that control inflammatory responses induced by inhalation of ambient air pollutants. Projects focus on early events that result in the disregulation of signaling processes that regulate mediator expression. Approaches include real-time molecular imaging of human lung cells exposed in vitro and ex-vivo.
]]>Website: http://www.sph.unc.edu/?option=com_profiles&Itemid=1900&profileAction=ProfDetail&pid=700156018
Email: styblo@med.unc.edu
Voice: (919) 966-5721
Research interests involve metabolic interactions of essential microelements, especially trace metals, with toxic metals and metalloids that contaminate food chain and drinking water reservoirs. Research topics include: the interactions between selenium, an essential micronutrient, and arsenic, an environmental contaminant and human carcinogen; the enzymes and co-factors involved in the metabolism of arsenic and selenium; the mechanisms of arsenic- induced diabetes; and, the role of nutritional antioxidants and antioxidant enzymes in responses to the oxidative stress induced by exposure to environmental toxins, by viral infections or nutritional deficiencies.
]]>Website: http://www.sph.unc.edu/?option=com_profiles&Itemid;=1891&profileAction;=ProfDetail&pid;=704283985
Email: james_swenberg@unc.edu
Voice: (919) 966-6139
My laboratory focuses on understanding mechanisms of carcinogenesis, with emphasis on the role of DNA damage and repair. During the last few years, we have developed ultra-sensitive and highly specific mass spectrometry methods for measuring the DNA and hemoglobin adducts of vinyl chloride, crotonaldehyde, ethylene oxide, propylene oxide, styrene oxide, butadiene, malondialdehyde, cis-platin and O6-methyldeoxy-guanosine, as well as slotblot methods for AP sites and oxidative DNA damage. These methods have been applied to understanding critical mechanisms in carcinogenesis, as well as undertaking molecular epidemiology studies of workers in the butadiene and reinforced plastics industries. We are also examining changes in gene expression associated with oxidative stress and environmental chemical exposure.
]]>Website: http://www.med.unc.edu/biochem/people/faculty/joint/wilson
Email: emw@med.unc.edu
Voice: (919) 966-5168
Our research focus is on mechanisms of action of the androgen receptor (AR), a ligand-dependent transcriptional regulatory protein that mediates the effects of testosterone and dihydrotestosterone. Studies seek to identify and characterize AR coregulatory proteins and their regulation by phosphorylation and the cell cycle. Areas of interest include male sex development, the androgen insensitivity syndrome, and AR action in the ovary, endometrium and prostate cancer. Melanoma antigen gene protein-11 (MAGE-11) was identified as an AR coregulatory protein that belongs to the MAGE gene family of cancer-germline antigens. The MAGE-11 gene is located on the human X chromosome and is exclusively expressed in human and nonhuman primates, providing a gain-of- function to AR. Mechanisms whereby MAGE-11 regulates AR transcriptional activity through its interaction with the AR NH2-terminal FXXLF motif and cell cycle regulatory proteins are being investigated. Our objective is to understand how AR regulates gene transcription and cell proliferation in the human male and female reproductive tracts. Keywords: androgen receptor, MAGE-11, male reproduction, female reproduction, prostate cancer, transcription regulation, FXXLF motifs
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