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The Blair Lab Members

Ian A. Blair, Ph.D.


Ian Blair, Ph.D. Research in the Blair laboratory is heavily involved in the use of mass spectrometry for proteomics and DNA analysis.

Oxidative stress, carcinogenesis, and cardiovascular disease

The reactive oxygen species superoxide, peroxide, and hydroxyl radical, are generated constantly in vivo from ground state triplet oxygen. This occurs by a variety of endogenous processes including, normal mitochondrial aerobic respiration, phagocytosis of bacteria or virus-containing cells, and peroxisomal-mediated degradation of fatty acids. Catechols, which arise in vivo through the metabolism of drugs, environmental chemicals, and endogenous hormones, generate reactive oxygen species through redox cycling.

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Luis Gil De Gomez, Ph.D.

  Luis Gil de Gomez joined the Blair Lab in September, 2015 as a postdoc. He obtained his Ph.D. in 2013 under the supervision of Dr. Jesus Balsinde at University of Valladolid, Spain. His Ph.D. research focused on investigating arachidonic acid turnover in relation to inflammation processes. Based on a lipidomic profiling by LC/MS, characterization of specific phospholipid species was followed by evaluation of their biological roles in order to identify possible lipid mediators involved in innate immune response. Last 2-years work experience in Biocross has focused on the development of a diagnosis method for Alzheimer's disease by identifying alterations in plasma metabolites that persist throughout the continuum Alzheimer´s disease pathophysiology. In the Blair Lab, Luis is currently involved in identifying specific biomarkers for several diseases.

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Clementina Mesaros, Ph.D.


Clementina Mesaros joined the Blair lab in September 2004. She received her Ph. D. in organic chemistry from CASE University, Cleveland. Her graduate research in Prof. Robert Salomon's lab, involved the total synthesis of several oxidized phosphoplipids and mechanistic studies of lipids oxidation. During her three years of post-doctoral training in the Blair lab, she worked on the synthesis of reactive bifunctional electrophiles derived from AA. Clementina was also involved in identification of a novel 4-oxo-2(E)-nonenal adduct with glutathione (TOG) as a biomarker of oxidative stress using LC/MS approaches. She developed an LC/MS method for quantification of epoxy-eicosatrienoic acids and dihyrdroxy eicosatrienoic acids in biological samples. Clementina is now a Senior Investigator in the Blair lab and she is working on developing LC/MS assays for urinary biomarkers of oxidative stress.

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Lili Guo, Ph.D.


Lili Guo joined the Blair lab in February, 2014. She received her Ph.D. in cell and molecular biology from the University of Pennsylvania in 2013. Under the supervision of Dr. Xiaolu Yang, her Ph.D. research focused on protein post-translational modifications (PTMs) and their roles in regulating misfolded proteins in neurodegenerative diseases. In the Blair Lab, Lili utilizes LS/MS/MS approaches to study the mechanistic effects of anti-cancer drugs on metabolic pathways, PTMs, and cellular bioenergetics with the aim of improving existing therapies and elucidating new therapeutic targets.  She is also involved in developing and improving LC/MS approaches to quantify protein biomarkers for several diseases.

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Qingqing Wang, Ph.D.

  Qingqing Wang joined the Blair lab in September 2013 as a visiting associate professor. She received her Ph.D. in pharmaceutical analysis from Beijing Institute of Pharmacology in China. Her Ph.D. research focused on quantification and drug-drug interaction of acetylcholinesterase (AChE) inhibitors. She then joined the pharmacology and toxicology lab in the Beijing Institute of Radiation Medicine. There she developed and tested LC/MS and ELISA based methods for quantitative and qualitative determinations of peptides, antisense oligonucleotides, siRNA, amino acids and small molecular drugs in complex biological fluids. Qingqing is currently working on developing pre-ionized derivative based stable isotope dilution methods for quantification of estrogens and androgens. She is also involved in developing LC/MS approaches for non-invasive serum biomarkers of oxidative stress

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Liwei Weng, Ph.D.


Liwei Weng joined the Blair Lab in March, 2015 as a postdoc. She obtained her Ph.D. in 2014 under the supervision of Dr. Marc Greenberg in Johns Hopkins University. Her Ph.D. research mainly focused on investigating how the interactions between histone tails and nucleosomal DNA affect the reactivity of an abasic site. To gain insight into such interactions, she also developed a new DNA-protein cross-linking (DPC) method by taking advantage of the reaction between a modified electrophilic nucleotide and the nucleophilic residues in histone tails. In the Blair Lab, Liwei is currently involved in developing specific biomarkers for patients with mesothelioma and people exposed to asbestos.

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Lisa Bottalico

  Lisa Bottalico joined the Blair Lab in October 2012. She is a doctoral candidate in the Pharmacology Graduate Group and a student in the Certificate Program in Environmental Health Sciences. Lisa graduated with honors from La Salle University (Philadelphia, PA) in 2005 with a B.A. in Biology and English. She subsequently held a three year internship at the US Army Medical Research Center for Chemical Defense (APG, MD). In the Blair Lab, Lisa will work to develop a breast cancer risk model based on estrogen metabolomics.

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Dylan Marchione


Dylan joined the Blair lab in the summer of 2015. He is a doctoral candidate in the Pharmacology Graduate Group and a student in the Graduate Training in Medical Science Certificate Program. He graduated from The University of Alabama in 2014 with a B.S. and an M.S. in Biological Sciences. Under the supervision of Dr. Stevan Marcus, his M.S. research involved characterization of a novel mitochondrial stress response in the fission yeast S. pombe induced by a tumor-inhibitory triterpenoid saponin from the desert plant Acacia victoriae. In the Blair lab, Dylan is involved in the development of LC/MS-based approaches for assessing the efficacy of therapeutic interventions in Friedreich’s ataxia.

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