Yon Rojanasakul

West Virginia University, Morgantown, West Virginia, United States

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Publications (185)606.81 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Despite the intriguing potential of carbon nanotubes (CNTs) for biomedical applications, their implementation is currently being hindered by many uncertainties regarding their toxicity and fate inside the biological systems. Several reports have shown that CNTs toxicity can be attributed to their length, surface chemistry, aggregation and metal impurities, just to name a few. However, due to the various types of CNTs being synthesized every day along with the different surface functionalization techniques, there is no fundamental understanding of the toxicological and pharmacological profiles of cellular systems exposed to CNTs with different physico-chemical properties. In this research, we provide a comprehensive analysis of the cellular behavior of human lung cells post exposure to CNTs using a combination of electronic and cell-based techniques. Our analyses rely on a non-invasive electronic cell impedance sensing (ECIS) platform to provide real-time measurements of cell adhesion, cell-cell interactions as well as changes in cellular morphology upon exposure to CNTs with user-defined physical and chemical properties. The approach is complemented by standard microscopy techniques as well as conventional in vitro cellular-based assays, such as cell cycle analysis, cell proliferation and viability, in order to derive structure-function relations associated with the cytotoxic and apoptotic events induced by exposure to CNTs. Our results correlated the different physico-chemical properties of CNTs with the various biological responses and provided mechanistic insights into their Cyto- and genotoxic effects. Out study help define a novel platform for nanomaterials toxicity analysis and thus could expand the biomedical applications of CNTs and other nanomaterials.
    14 AIChE Annual Meeting; 11/2014
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    ABSTRACT: Even though tremendous advances have been made in the treatment of cancers during the past decades, success rate among cancer patients is still dismal largely due to problems associated with chemo/radio-resistance and relapse. Emerging evidence has indicated that cancer stem cells (CSCs) are behind the resistance and recurrence problems, but our understanding of their regulation is limited. Rapid reversible changes of CSC-like cells within tumors may result from the effect of biological mediators found in tumor microenvironment. Here we show how nitric oxide (NO), a key cellular modulator whose level is elevated in many tumors, affects CSC-like phenotypes of human non-small-cell lung carcinoma (NSCLC) H292 and H460 cells. Exposure of NO gradually altered the cell morphology towards mesenchymal stem-like shape. NO exposure promoted CSC-like phenotype indicated by increased expression of known CSC markers, CD133 and ALDH1A1, in the exposed cells. This effect of NO on stemness was reversible after cessation of the NO treatment for 7 days. Furthermore, such effect was reproducible using another NO-donor, S-nitroso-N-acetylpenicillamine (SNAP). Importantly, inhibition of NO by known NO scavenger 2-(4-carboxy-phenyl)-4,4,5,5 tetramethylimidazoline-1-oxy-3-oxide (PTIO) strongly inhibited CSC-like aggressive cellular behavior and marker expression. Lastly, we unveiled the underlying mechanism of NO action through the activation of caveolin-1 (Cav-1) which is upregulated by NO and is responsible for the aggressive behavior of the cells, including anoikis resistance, anchorage-independent cell growth, and increased cell migration and invasion. These findings indicate a novel role of NO in CSC regulation and its importance in aggressive cancer behaviors through Cav-1 upregulation. Copyright © 2014, American Journal of Physiology - Cell Physiology.
    American journal of physiology. Cell physiology. 11/2014;
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    ABSTRACT: Chronic exposure to single-walled carbon nanotubes (SWCNT) has been reported to induce apoptosis resistance of human lung epithelial cells. Since resistance to apoptosis is a foundation of neoplastic transformation and cancer development, we evaluated the apoptosis resistance characteristic of the exposed lung cells to understand the pathogenesis mechanism. Passage control and SWCNT-transformed human lung epithelial cells were treated with known inducers of apoptosis via the intrinsic (antimycin A and CDDP) or extrinsic (FasL and TNF-α) pathway and analyzed for apoptosis by DNA fragmentation, annexin-V expression, and caspase activation assays. Whole genome microarray was performed to aid the analysis of apoptotic gene signaling network. The SWCNT-transformed cells exhibited defective death receptor pathway in association with c-FLIP overexpression. Knockdown or chemical inhibition of c-FLIP abrogated the apoptosis resistance of SWCNT-transformed cells. Whole genome expression signature analysis confirmed these findings. This study is the first to demonstrate carbon nanotube-induced defective death receptor pathway and the role of c-FLIP in the process. Published by Oxford University Press on behalf of the Society of Toxicology 2014. This work is written by US Government employees and is in the public domain in the US.
    Toxicological sciences : an official journal of the Society of Toxicology. 11/2014;
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    ABSTRACT: The unique intrinsic properties of carbon nanotubes (CNTs) make them potential candidates for a wide range of biomedical applications spanning bio-imaging, disease targeting, and delivery of genes and drugs. Therefore, in-depth analysis of their toxicity and fate inside biological systems is crucial prior to their application. Several reports have shown that CNTs toxicity can be attributed to their length, surface chemistry, aggregation or metal impurities to name a few. However, due to the various types of CNTs and the different surface functionalizing techniques, there are many discrepancies in literature and limited understanding of their toxicological and pharmacological profiles. In this research, we employed an electric cell impedance sensing device to provide a comprehensive analysis of the cellular behavior of human lung cells post exposure to CNTs with different physical and chemical properties. This non-invasive approach employs arrays with gold electrodes as immobilization platforms to provide real-time measurements of cellular adhesion, cell-cell interactions as well as changes in cellular morphology. Such measurements were further supplemented with microscopy and viability assays to derive structure-function relations associated with the cytotoxic and apoptotic events induced by cellular exposure to CNTs. Our real-time results provided new insights into the underlying cellular mechanisms associated with CNTs exposure and promise to extend such cellular-based studies to advance the biomedical applications of CNTs and other nanomaterials.
    14 AIChE Annual Meeting; 11/2014
  • [Show abstract] [Hide abstract]
    ABSTRACT: Despite the intriguing potential of carbon nanotubes (CNTs) for biomedical applications, their implementation is currently being hindered by many uncertainties regarding their toxicity and fate inside the biological systems. Several reports have shown that CNTs toxicity can be attributed to their length, surface chemistry, aggregation and metal impurities, just to name a few. However, due to the various types of CNTs being synthesized every day along with the different surface functionalization techniques, there is no fundamental understanding of the toxicological and pharmacological profiles of cellular systems exposed to CNTs with different physico-chemical properties. In this research, we provide a comprehensive analysis of the cellular behavior of human lung cells post exposure to CNTs using a combination of electronic and cell-based techniques. Our analyses rely on a non-invasive electronic cell impedance sensing (ECIS) platform to provide real-time measurements of cell adhesion, cell-cell interactions as well as changes in cellular morphology upon exposure to CNTs with user-defined physical and chemical properties. The approach is complemented by standard microscopy techniques as well as conventional in vitro cellular-based assays, such as cell cycle analysis, cell proliferation and viability, in order to derive structure-function relations associated with the cytotoxic and apoptotic events induced by exposure to CNTs. Our results correlated the different physico-chemical properties of CNTs with the various biological responses and provided mechanistic insights into their Cyto- and genotoxic effects. Out study help define a novel platform for nanomaterials toxicity analysis and thus could expand the biomedical applications of CNTs and other nanomaterials.
    14 AIChE Annual Meeting; 11/2014
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    ABSTRACT: Digitoxin is a naturally occurring cardiac glycoside, well known for its efficiency in the treatment of congestive heart failure and arrhythmias. Recently, several reports have shown that digitoxin exhibits anti-neoplastic effects against several types of cancer ranging from breast to colon cancer, and from leukemia to lung cancer, suggesting digitoxin’s potential as a chemotherapeutic agent. The anticancer potency of digitoxin lies in its trisaccharide moiety which could be synthetically manipulated to produce a library of analogues. In our research we used an electrical cell impedance sensing system (ECIS) as a proxy to assess the cellular behavior of immortalized and tumorigenic human lung cells (BEAS-2B and H460 respectively) upon exposure to digitoxin and a synthetic monosaccharide (D6-MA). Our highthroughput, non-invasive approach employed arrays with gold electrodes as immobilization platforms to measure the changes in cellular attachment, migration and cell-cell interactions in real time. The analysis was complemented by conventional microscopy techniques as well as cell-based assays to provide insights to the mechanistic anti-proliferative and pro-apoptotic signaling pathways activated by the drugs exposure. The results showed that both drugsselective anticancer mechanisms towards cancer cells and provided structure-function relationships that correlated the cellular dynamics with molecular pathways changes upon exposure. Our study provide novel means to investigate the underlying anticancer mechanism associated with natural or synthetic compounds and promises to help expedite the understanding of their anticancer mechanisms as well as facilitate their potential implementation as chemotherapeutic agent. Disclaimer These findings and conclusions are those of the authors and do not necessarily represent the views of the National Institute for Occupational Safety and Health.
    14 AIChE Annual Meeting; 11/2014
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    ABSTRACT: Epidemiological studies suggest that living near mountaintop coal mining (MTM) activities is one of the contributing factors for high lung cancer incidence. The purpose of this study was to investigate the long-term carcinogenic potential of MTM particulate matter (PMMTM) exposure on human bronchial epithelial cells. Our results show that chronic exposure (3 months) to noncytotoxic, physiological relevant concentration (1 μg/mL) of PMMTM, but not control particle PMCON, induced neoplastic transformation, accelerated cell proliferation, and enhanced cell migration of the exposed lung cells. Xenograft transplantation of the PMMTM-exposed cells in mice caused no apparent tumor formation, but promoted tumor growth of human lung carcinoma H460 cells, suggesting the tumor-promoting effect of PMMTM. Chronic exposure to the main inorganic chemical constituent of PMMTM, molybdenum but not silica, similarly induced cell transformation and tumor promotion, suggesting the contribution of molybdenum, at least in part, in the PMMTM effects. These results provide new evidence for the carcinogenic potential of PMMTM and support further risk assessment and implementation of exposure control for PMMTM.
    Environmental science & technology. 10/2014;
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    ABSTRACT: Adverse side effects and acquired resistance to conventional platinum based chemotherapy have become major impediments in ovarian cancer treatment, and drive the development of more selective anticancer drugs. Chaetoglobosin K (ChK) was shown to have a more potent growth inhibitory effect than cisplatin on two cisplatin-resistant ovarian cancer cell lines, OVCAR-3 and A2780/CP70, and was less cytotoxic to a normal ovarian cell line, IOSE-364, than to the cancer cell lines. Hoechst 33342 staining and Flow cytometry analysis indicated that ChK induced preferential apoptosis and G2 cell cycle arrest in both ovarian cancer cells respect to the normal ovarian cells. ChK induced apoptosis through a p53-dependent caspase-8 activation extrinsic pathway, and caused G2 cell cycle arrest via cyclin B1 by increasing p53 expression and p38 phosphorylation in OVCAR-3 and A2780/CP70 cells. DR5 and p21 might play an important role in determining the sensitivity of normal and malignant ovarian cells to ChK. Based on these results, ChK would be a potential compound for treating platinum- resistant ovarian cancer.
    Cancer letters 10/2014; · 5.02 Impact Factor
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    ABSTRACT: Toxicity of engineered nanomaterials is associated with their inherent properties, both physical and chemical. Recent studies have shown that exposure to multi-walled carbon nanotubes (MWCNTs) promotes tumors and tumor-associated pathologies in model in vivo systems and lead to carcinogenesis. Herein we examined the potential of purified MWCNTs to affect human lung epithelial cells when used at occupationally relevant exposure doses for particles not otherwise regulated. The uptake of the purified MWCNTs was evaluated using fluorescence activated cell sorting (FACS) while the effects on cell fate were assessed using 2- (4-iodophenyl) - 3- (4-nitrophenyl) - 5-(2, 4-disulfophenyl) -2H-tetrazolium salt colorimetric assay, cell cycle and nanointendation. Our results showed that exposure to MWCNTs reduced cell metabolic activity and induced cell cycle arrest. Our analysis further emphasized that MWCNT-induced cellular fate results from multiple types of interactions that could be analyzed by means of intracellular biomechanical changes and could be pivotal in understanding the underlying MWCNTs-induced cell transformation.
    Environ. Sci.: Nano. 08/2014;
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    ABSTRACT: Aberrant collagen production can lead to many diseases such as fibrosis. Current methods of collagen detection are insensitive, time-consuming and laborious. We have developed a rapid, sensitive assay using chemiluminescence-based reporter cell system. Stable 3T3/NIH-SMAD-luciferase cells were generated for detection of collagen expression through TGF-β signaling, a major fibrogenic pathway. We demonstrated that these reporter cells could be used as a rapid screening tool for detection of SMAD-dependent collagen production with higher sensitivity than existing assays. Flexibility of this cell-based assay in different detection platforms makes it attractive for high throughput screening of potential fibrogenic agents and drug candidates.
    Journal of Bioscience and Bioengineering 06/2014; · 1.74 Impact Factor
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    Amruta Manke, Sudjit Luanpitpong, Yon Rojanasakul
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    ABSTRACT: Given their remarkable properties, carbon nanotubes (CNTs) have made their way through various industrial and medicinal applications and the overall production of CNTs is expected to grow rapidly in the next few years, thus requiring an additional recruitment of workers. However, their unique applications and desirable properties are fraught with concerns regarding occupational exposure. The concern about worker exposure to CNTs arises from the results of recent animal studies. Short-term and sub-chronic exposure studies in rodents have shown consistent adverse health effects such as pulmonary inflammation, granulomas, fibrosis, genotoxicity and mesothelioma after inhalation or instillation of several types of CNTs. Furthermore, physicochemical properties of CNTs such as dispersion, functionalization and particle size can significantly affect their pulmonary toxicity. Risk estimates from animal studies necessitate implementation of protective measures to limit worker exposure to CNTs. Information on workplace exposure is very limited, however, studies have reported that CNTs can be aerosolized and attain respirable airborne levels during synthesis and processing activities in the workplace. Quantitative risk assessments from sub-chronic animal studies recommend the health-based need to reduce exposures below the recommended exposure limit of 1 μg/m3. Practice of prevention measures including the use of engineering controls, personal protective equipment, health surveillance program, safe handling and use, as well as worker training can significantly minimize worker exposure and improve worker health and safety.
    Occupational Medicine and Health Affairs. 06/2014; 2(3).
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    ABSTRACT: We developed a 3D fibroblastic nodule model for fibrogenicity testing of nanomaterials and investigated the role of fibroblast stem-like cells (FSCs) in the fibrogenic process. We showed that carbon nanotubes (CNTs) induced fibroblastic nodule formation in primary human lung fibroblast cultures resembling the fibroblastic foci in clinical fibrosis, and promoted FSCs which are highly fibrogenic and a potential driving force of fibrogenesis. This study provides a predictive 3D model and mechanistic insight on CNT fibrogenesis.
    Nano Letters 05/2014; · 13.03 Impact Factor
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    ABSTRACT: Carbon nanotubes (CNT) hold great promise to create new and better products for commercial and biomedical applications, but their long-term adverse health effects are a major concern. The objective of this study was to address human lung cancer risks associated with chronic pulmonary exposure to single-walled (SW) CNT through the fundamental understanding of cellular and molecular processes leading to carcinogenesis. We hypothesized that the acquisition of cancer stem cells (CSC), a subpopulation that drive tumor initiation and progression, may contribute to CNT carcinogenesis.
    Particle and Fibre Toxicology 05/2014; 11(1):22. · 9.18 Impact Factor
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    ABSTRACT: Cancer stem cells (CSCs) may represent targets for carcinogenic initiation by chemical and environmental agents. Recent studies have raised a concern over the potential carcinogenicity of carbon nanotubes (CNTs), one of the most commonly used engineered nanomaterials with asbestos-like properties. Here, we show that chronic (6-month) exposure of human lung epithelial cells to single-walled (SW) CNTs at the workplace-relevant concentration induced an emergence of lung CSCs, as indicated by the induction of CSC tumor spheres and side population (SP). These CSCs, which were found to overexpress tumor promoter caveolin-1 (Cav-1), displayed aggressive cancer phenotypes of apoptosis resistance and enhanced cell invasion and migration compared with their non-CSC counterpart. Using gene manipulation strategies, we reveal for the first time that Cav-1 plays an essential role in CSC regulation and aggressiveness of SWCNT-transformed cells partly through p53 dysregulation, consistent with their suggested role by microarray and gene ontology analysis. Cav-1 not only promoted tumorigenesis in a xenograft mouse model but also metastasis of the transformed cells to neighboring tissues. Since CSCs are crucial to the initiation and early development of carcinogenesis, our findings on CSC induction by SWCNTs and Cav-1 could aid in the early detection and risk assessment of the disease.
    Oncotarget 05/2014; · 6.64 Impact Factor
  • Sudjit Luanpitpong, Liying Wang, Yon Rojanasakul
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    ABSTRACT: Carbon nanotubes (CNTs) hold great promise to create new and better products, but their adverse health effect is a major concern. Human exposure to CNTs is primarily through inhalation and dermal contact, especially during the manufacturing and handling processes. Numerous animal studies have demonstrated the potential pulmonary and dermal hazards associated with CNT exposure, while in vitro studies have assessed the effects of CNT exposure on various cellular behaviors and have been used to perform mechanistic studies. In this review, we provide an overview of the pathological effects of CNTs and examine the acute and chronic effects of CNT exposure on lung and dermal cellular behaviors, beyond the generally discussed cytotoxicity. We then examine the linkage of cellular behaviors and disease pathogenesis, and discuss the pertinent mechanisms.
    Nanomedicine 05/2014; 9(6):895-912. · 5.26 Impact Factor
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    ABSTRACT: Given their extremely small size and light weight, carbon nanotubes (CNTs) can be readily inhaled by human lungs resulting in increased rates of pulmonary disorders, particularly fibrosis. Although the fibrogenic potential of CNTs is well established, there is a lack of consensus regarding the contribution of physicochemical attributes of CNTs on the underlying fibrotic outcome. We designed an experimentally validated in vitro fibroblast culture model aimed at investigating the effect of fiber length on single-walled CNT (SWCNT)-induced pulmonary fibrosis. The fibrogenic response to short and long SWCNTs was assessed via oxidative stress generation, collagen expression and transforming growth factor-beta (TGF-β) production as potential fibrosis biomarkers. Long SWCNTs were significantly more potent than short SWCNTs in terms of reactive oxygen species (ROS) response, collagen production and TGF-β release. Furthermore, our finding on the length-dependent in vitro fibrogenic response was validated by the in vivo lung fibrosis outcome, thus supporting the predictive value of the in vitro model. Our results also demonstrated the key role of ROS in SWCNT-induced collagen expression and TGF-β activation, indicating the potential mechanisms of length-dependent SWCNT-induced fibrosis. Together, our study provides new evidence for the role of fiber length in SWCNT-induced lung fibrosis and offers a rapid cell-based assay for fibrogenicity testing of nanomaterials with the ability to predict pulmonary fibrogenic response in vivo.
    International Journal of Molecular Sciences 04/2014; 15(5):7444-7461. · 2.46 Impact Factor
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    ABSTRACT: Death receptor (DR) ligation can lead to divergent signaling pathways causing either caspase- mediated cell death or cell proliferation and inflammation. These variations in cellular fate are determined by adaptor proteins that are recruited to the DR signaling complex. FLICE inhibitory protein (FLIP) is an established inhibitor of caspase-8-mediated apoptosis, and it is also involved in NF-κB activation. However, the molecular mechanism that regulates FLIP within this complex is unknown. In this study, we provide new evidence for the regulation of NF-κB by FLIP through S-nitrosylation, which involves covalent modification of the protein's cysteine thiol by nitric oxide to form S-nitrosothiol. Point mutations of FLIP at cysteine residues 254 and 259 prevent FLIP S-nitrosylation and its ability to activate NF-κB. The mechanism by which FLIP nitrosylation regulates NF-κB activity involves RIP1 binding and redistribution, whereas TRAF2 binding and distribution are unaffected. We further show that FLIP processing and cleavage is dependent on its nitrosylation status. Collectively, our study reveals a novel pathway for FLIP regulation of NF-κB through protein S-nitrosylation, which is a key posttranslational mechanism controlling DR-mediated cell death and survival. Since increased expression of FLIP and nitric oxide are frequently observed in chemotherapy-resistant tumors, S-nitrosylation of FLIP could be a key mechanism of chemoresistance and tumor growth.
    Cell cycle (Georgetown, Tex.) 04/2014; 13(12). · 5.24 Impact Factor
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    ABSTRACT: Digitoxin belongs to a naturally occurring class of cardiac glycosides (CG); the drug is clinically approved for heart failure and known for its anti-cancer effects against non-small lung cancer cells (NSCLC). However, rising concerns are associated with its narrow therapeutic index and its concentration-dependent mechanism of action. Thus, before digitoxin implementation in designing and developing safer and more effective CG-based anticancer therapies, its pharmacological and safety profiles need to be fully elucidated. In this research we used a combinatorial approach to evaluate the anticancer mechanisms of digitoxin in real time. Our pproach employed a non-invasive electric cell impedance sensing technique as a proxy to monitor NSCLC behavior post-exposure to toxic, therapeutic and sub-therapeutic concentrations of the drug. By developing structure-function combinatorial relations we showed that digitoxin targets cancer cells in a time and dose-dependant manner with activation of proapoptotic and anti-proliferative signaling cascades being a result of strengthening cellular adhesion by sequestering key regulatory proliferation protein CDK4 from the nucleus.
    Biosensors & Bioelectronics 03/2014; 59:192–199. · 6.45 Impact Factor
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    ABSTRACT: Given their extremely small size and light weight, carbon nanotubes (CNTs) can be readily inhaled by human lungs resulting in increased rates of pulmonary disorders, particularly fibrosis. Although the fibrogenic potential of CNTs is well established, there is a lack of consensus regarding the contribution of physicochemical attributes of CNTs on the underlying fibrotic outcome. We designed an experimentally validated in vitro fibroblast culture model aimed at investigating the effect of fiber length on single-walled CNT (SWCNT)-induced pulmonary fibrosis. The fibrogenic response to short and long SWCNTs was assessed via oxidative stress generation, collagen expression and transforming growth factor-beta (TGF-β) production as potential fibrosis biomarkers. Long SWCNTs were significantly more potent than short SWCNTs in terms of reactive oxygen species (ROS) response, collagen production and TGF-β release. Furthermore, our finding on the length-dependent in vitro fibrogenic response was validated by the in vivo lung fibrosis outcome, thus supporting the predictive value of the in vitro model. Our results also demonstrated the key role of ROS in SWCNT-induced collagen expression and TGF-β activation, indicating the potential mechanisms of length-dependent SWCNT-induced fibrosis. Together, our study provides new evidence for the role of fiber length in SWCNT-induced lung fibrosis and offers a rapid cell-based assay for fibrogenicity testing of nanomaterials with the ability to predict pulmonary fibrogenic response in vivo.
    International Journal of Molecular Sciences 01/2014; 15(5):7444-7461. · 2.46 Impact Factor
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    ABSTRACT: Rapid development and deployment of engineered nanomaterials such as carbon nanotubes (CNTs) in various commercial and biomedical applications have raised concerns about their potential adverse health effects, especially their long-term effects which have not been well addressed. We demonstrated here that prolonged exposure of human mesothelial cells to single-walled CNT (SWCNT) induced neoplastic-like transformation as indicated by anchorage-independent cell growth and increased cell invasiveness. Such transformation was associated with an up-regulation of H-Ras and activation of ERK1/2. Downregulation of H-Ras by siRNA or inactivation of ERK by chemical inhibitor effectively inhibited the aggressive phenotype of SWCNT-exposed cells. Integrin alpha V and cortactin, but not epithelial-mesenchymal transition (EMT) transcriptional regulators, were up-regulated in the SWCNT-exposed cells, suggesting their role in the aggressive phenotype. Cortactin expression was shown to be controlled by the H-Ras/ERK signaling. Thus, our results indicate a novel role of H-Ras/ERK signaling and cortactin in the aggressive transformation of human mesothelial cells by SWCNT.
    Frontiers in physiology. 01/2014; 5:222.

Publication Stats

3k Citations
606.81 Total Impact Points

Institutions

  • 1992–2014
    • West Virginia University
      • • Department of Basic Pharmaceutical Sciences
      • • Department of Chemical Engineering
      • • School of Pharmacy
      Morgantown, West Virginia, United States
  • 2012
    • Julphar School of Pharmacy
      Morgantown, West Virginia, United States
  • 2011–2012
    • Thomas Jefferson University
      • Department of Pathology, Anatomy & Cell Biology
      Philadelphia, PA, United States
    • Northeastern University
      • Department of Chemistry and Chemical Biology
      Boston, MA, United States
  • 2010–2012
    • Chulalongkorn University
      • • Faculty of Pharmaceutical Sciences
      • • Department of Pharmacology and Physiology
      Bangkok, Bangkok, Thailand
  • 2009–2012
    • Northwestern University
      • • Department of Medicine
      • • Division of Rheumatology
      Evanston, IL, United States
    • Hampton University
      • School of Pharmacy
      Hampton, Virginia, United States
  • 2001–2006
    • Centers for Disease Control and Prevention
      • Health Effects Laboratory Division
      Druid Hills, GA, United States
    • St. John's University
      • College of Pharmacy and Allied Health Professions
      New York City, NY, United States
  • 2002–2004
    • Prince of Songkla University
      • Faculty of Pharmaceutical Sciences
      Songkhla, Changwat Songkhla, Thailand
  • 2003
    • Pennington Biomedical Research Center
      Baton Rouge, Louisiana, United States
  • 1999
    • National Institute of Occupational Safety and Health JAPAN
      Edo, Tōkyō, Japan
  • 1997
    • Pennsylvania State University
      • Department of Pathology
      University Park, MD, United States