@book{brody_brody_2013, title={The science class you wish you had: The seven greatest scientific discoveries in history and the people who made them}, publisher={New York: Perigee/Penguin Group}, author={Brody, D. E. and Brody, A. R.}, year={2013} }
 @article{lin_degan_theriot_fischer_strachan_liang_pierce_sunday_noble_kraft_et al._2012, title={Chronic treatment in vivo with beta-adrenoceptor agonists induces dysfunction of airway beta(2)-adrenoceptors and exacerbates lung inflammation in mice}, volume={165}, ISSN={["1476-5381"]}, DOI={10.1111/j.1476-5381.2011.01725.x}, abstractNote={BACKGROUND AND PURPOSE Inhalation of a β‐adrenoceptor agonist (β‐agonist) is first‐line asthma therapy, used for both prophylaxis against, and acute relief of, bronchoconstriction. However, repeated clinical use of β‐agonists leads to impaired bronchoprotection and, in some cases, adverse patient outcomes. Mechanisms underlying this β2‐adrenoceptor dysfunction are not well understood, due largely to the lack of a comprehensive animal model and the uncertainty as to whether or not bronchorelaxation in mice is mediated by β2‐adrenoceptors. Thus, we aimed to develop a mouse model that demonstrated functional β‐agonist‐induced β2‐adrenoceptor desensitization in the context of allergic inflammatory airway disease.}, number={7}, journal={BRITISH JOURNAL OF PHARMACOLOGY}, author={Lin, Rui and Degan, Simone and Theriot, Barbara S. and Fischer, Bernard M. and Strachan, Ryan T. and Liang, Jiurong and Pierce, Richard A. and Sunday, Mary E. and Noble, Paul W. and Kraft, Monica and et al.}, year={2012}, month={Apr}, pages={2365–2377} }
 @article{brody_2010, title={Asbestos and Lung Disease}, volume={42}, ISSN={["1535-4989"]}, DOI={10.1165/rcmb.2010-2002ed}, number={2}, journal={AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY}, author={Brody, Arnold R.}, year={2010}, month={Feb}, pages={131–132} }
 @article{kai_d'costa_yoon_brody_sills_kim_2010, title={Characterization of side population cells in human malignant mesothelioma cell lines}, volume={70}, ISSN={["1872-8332"]}, DOI={10.1016/j.lungcan.2010.04.020}, abstractNote={Side population (SP) assay composed of Hoechst 33342 staining and subsequent flow cytometric analysis has been widely utilized for characterizing putative cancer stem cells (CSCs) in various human malignancies. The present study was designed to evaluate the SP assay as a research tool for mesothelial CSCs. A distinct fraction of SP cells was identified in various human malignant mesothelioma (HMM) cell lines, ranging from 0.05 to 1.32%. The sorted mesothelial SP cells exhibited enhanced proliferation potentials and higher expression of stem-cell genes, compared to non-SP (NSP) cells. Cisplatin treatment increased percentage of SP cells in the HMM cell lines. However, tumorigenic potential of SP cells in immunodeficient mice was similar to that of the NSP cells. These data indicated that SP assay may not be appropriate for enriching putative CSCs in HMM cell lines, and thus warrants the development of a novel tool for mesothelial CSC study.}, number={2}, journal={LUNG CANCER}, author={Kai, Kiyonori and D'Costa, Susan and Yoon, Byung-Il and Brody, Arnold R. and Sills, Robert C. and Kim, Yongbaek}, year={2010}, month={Nov}, pages={146–151} }
 @article{miller_lankford_adler_brody_2010, title={Mesenchymal Stem Cells Require MARCKS Protein for Directed ChemotaxisIn Vitro}, volume={43}, ISSN={1044-1549 1535-4989}, url={http://dx.doi.org/10.1165/rcmb.2010-0015RC}, DOI={10.1165/rcmb.2010-0015rc}, abstractNote={Mesenchymal stem cells (MSCs) reside within tissues such as bone marrow, cord blood, and dental pulp and can differentiate into other mesenchymal cell types. Differentiated MSCs, called circulating fibrocytes, have been demonstrated in human lungs and migrate to injured lung tissue in experimental models. It is likely that MSCs migrate from the bone marrow to sites of injury by following increasing chemokine concentrations. In the present study, we show that primary mouse bone marrow mesenchymal stem cells (BM-MSCs) exhibit directed chemotaxis through transwell inserts toward increasing concentrations of the chemokines complement component 5a, stromal cell-derived factor-1alpha, and monocyte chemotactic protein-1. Prior research has indicated that myristoylated alanine-rich C kinase substrate (MARCKS) protein is critically important for motility in macrophages, neutrophils, and fibroblasts, and here we investigated a possible role for MARCKS in BM-MSC directed chemotaxis. The presence of MARCKS in these cells as well as in human cord blood MSC was verified by Western blotting, and MARCKS was rapidly phosphorylated in these cells after exposure to chemokines. A synthetic peptide that inhibits MARCKS function attenuated, in a concentration-dependent manner, directed chemotaxis of BM-MSCs, while a missense control peptide had no effect. Our results illustrate, for the first time, that MARCKS protein plays an integral role in BM-MSC-directed chemotaxis in vitro.}, number={3}, journal={American Journal of Respiratory Cell and Molecular Biology}, publisher={American Thoracic Society}, author={Miller, Jeffrey D. and Lankford, Susan M. and Adler, Kenneth B. and Brody, Arnold R.}, year={2010}, month={Sep}, pages={253–258} }
 @article{ryman-rasmussen_cesta_brody_shipley-phillips_everitt_tewksbury_moss_wong_dodd_andersen_et al._2009, title={Inhaled carbon nanotubes reach the subpleural tissue in mice}, volume={4}, ISSN={["1748-3395"]}, DOI={10.1038/NNANO.2009.305}, abstractNote={Carbon nanotubes are shaped like fibres and can stimulate inflammation at the surface of the peritoneum when injected into the abdominal cavity of mice, raising concerns that inhaled nanotubes may cause pleural fibrosis and/or mesothelioma. Here, we show that multiwalled carbon nanotubes reach the subpleura in mice after a single inhalation exposure of 30 mg m(-3) for 6 h. Nanotubes were embedded in the subpleural wall and within subpleural macrophages. Mononuclear cell aggregates on the pleural surface increased in number and size after 1 day and nanotube-containing macrophages were observed within these foci. Subpleural fibrosis unique to this form of nanotubes increased after 2 and 6 weeks following inhalation. None of these effects was seen in mice that inhaled carbon black nanoparticles or a lower dose of nanotubes (1 mg m(-3)). This work suggests that minimizing inhalation of nanotubes during handling is prudent until further long-term assessments are conducted.}, number={11}, journal={NATURE NANOTECHNOLOGY}, author={Ryman-Rasmussen, Jessica P. and Cesta, Mark F. and Brody, Arnold R. and Shipley-Phillips, Jeanette K. and Everitt, Jeffrey I. and Tewksbury, Earl W. and Moss, Owen R. and Wong, Brian A. and Dodd, Darol E. and Andersen, Melvin E. and et al.}, year={2009}, month={Nov}, pages={747–751} }
 @article{salazar_lankford_brody_2009, title={Mesenchymal stem cells produce Wnt isoforms and TGF-beta(1) that mediate proliferation and procollagen expression by lung fibroblasts}, volume={297}, ISSN={["1522-1504"]}, DOI={10.1152/ajplung.90347.2008}, abstractNote={ Studies have been carried out previously to determine whether mesenchymal stem cells (MSC) influence the progression of pulmonary fibrosis. Here, we asked whether MSC (derived from mouse bone marrow and human umbilical cord blood) produce factors that mediate lung fibroblast (LF) growth and matrix production. MSC-conditioned media (CM) were found by ELISA to contain significant amounts of PDGF-AA and transforming growth factor-β1 (TGF-β1). Proliferation was increased in a concentration-dependent manner in LF cell lines and primary cells cultured in MSC-CM, but neither anti-PDGF antibodies nor PDGF receptor-specific antibodies affected proliferation, nor did a number of other antibodies to well-known mitogenic factors. However, proliferation was significantly inhibited by the Wnt signaling antagonist, secreted frizzled related protein-1 (sFRP-1). In addition, anti-Wnt1 and anti-Wnt2 antibodies attenuated MSC-CM-induced proliferation, and increased expression of Wnt7b was identified. As would be expected in cells activated by Wnt, nuclear β-catenin was increased. The amount of TGF-β1 in MSC-CM and its biological activity were revealed by activation at acidic pH. The stem cells synthesized and released TGF-β1 that increased α1-procollagen gene expression by LF target cells. Addition of anti-TGF-β to the MSC-CM blocked upregulation of collagen gene expression. These data demonstrate that MSC from mice and humans produce Wnt proteins and TGF-β1 that respectively stimulate LF proliferation and matrix production, two hallmarks of fibroproliferative lung disease. It will be essential to determine whether these factors can play a role in attempts to use MSC for therapeutic approaches. }, number={5}, journal={AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY}, author={Salazar, Keith D. and Lankford, Susan M. and Brody, Arnold R.}, year={2009}, month={Nov}, pages={L1002–L1011} }
 @misc{welch_anderson_balmes_braun_brody_castleman_davis_dement_frank_gochfeld_et al._2009, title={Research on mesothelioma from brake exposure: Corporate influence remains relevant concern}, volume={15}, number={2}, journal={International Journal of Occupational and Environmental Health}, author={Welch, L. S. and Anderson, H. A. and Balmes, J. and Braun, L. and Brody, A. and Castleman, B. and Davis, D. and Dement, J. M. and Frank, A. and Gochfeld, M. and et al.}, year={2009}, pages={234–238} }
 @article{lai_pociask_ferris_nguyen_miller_brody_sullivan_2009, title={Small Interfering RNAs (siRNAs) Targeting TGF-beta(1) mRNA Suppress Asbestos-Induced Expression of TGF-beta(1) and CTGF in Fibroblasts}, volume={28}, ISSN={["2162-6537"]}, DOI={10.1615/JEnvironPatholToxicolOncol.v28.i2.30}, abstractNote={Interstitial lung disease (ILD) afflicts millions of people worldwide. ILD can be caused by a number of agents, including inhaled asbestos, and may ultimately result in respiratory failure and death. Currently, there are no effective treatments for ILD. Transforming growth factor-beta1 (TGF-beta1) is thought to play an important role in the development of pulmonary fibrosis, and asbestos has been shown to induce TGF-beta1 expression in a murine model of ILD. To better define the role of TGF-beta1 in ILD, we developed several small interfering RNAs (siRNAs) that target TGF-beta1 mRNA for degradation. To assess the efficacy of each siRNA in reducing asbestos-induced TGF-beta1 expression, Swiss 3T3 fibroblasts were transfected with TGF-beta1 siRNAs and then treated with chrysotile asbestos for 48 h. Two independent siRNAs targeting TGF-beta1 mRNA knocked-down asbestos-induced expression of TGF-beta1 mRNA by 72-89% and protein by 70-84%. Interestingly, siRNA knockdown of TGF-beta1 also reduced asbestos-induced expression of connective tissue growth factor (CTGF). CTGF can be upregulated by TGF-beta1 and appears to play an important role in the development of pulmonary fibrosis. These results suggest that siRNAs could be effective in preventing or possibly arresting the progression of pulmonary fibrosis. Studies are underway in vivo to test this postulate.}, number={2}, journal={JOURNAL OF ENVIRONMENTAL PATHOLOGY TOXICOLOGY AND ONCOLOGY}, author={Lai, Tai-Cheng and Pociask, Derek A. and Ferris, MaryBeth and Nguyen, Hong T. and Miller, Charles A., III and Brody, Arnold R. and Sullivan, Deborah E.}, year={2009}, pages={109–119} }
 @article{sullivan_ferris_nguyen_abboud_brody_2009, title={TNF-alpha induces TGF-beta(1) expression in lung fibroblasts at the transcriptional level via AP-1 activation}, volume={13}, ISSN={["1582-4934"]}, DOI={10.1111/j.1582-4934.2009.00647.x}, abstractNote={Abstract Tumour necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) are peptides with multiple biological activities that influence neoplastic, immunologic and fibroproliferative diseases. There are clear interrelationships and overlap between the actions of TNF-α and TGF-β1 in lung fibrosis; therefore, we postulated that TNF-α may play a significant role in regulating TGF-β1 expression in lungs. We recently reported that TNF-α activates the extracellular regulated kinase (ERK)-specific pathway in fibroblasts resulting in stabilization of TGF-β1 mRNA and increased expression of TGF-β1. In the current study, we further investigated the molecular mechanisms involved in TNF-α regulation of TGF-β1 expression. Nuclear run-on assays showed that treatment of Swiss 3T3 fibroblasts with TNF-α increased transcription of the TGF-β1 gene in an ERK independent manner. Pre-treatment with the activator protein-1 (AP-1) inhibitor curcumin attenuated TNF-α induced transcription of the TGF-β1 gene. TNF-α induced increased levels of c-Jun and C-Fos in the nucleus accompanied by phosphorylation of c-Jun. In electrophoretic mobility shift assays, AP-1 binding to an AP-1 binding site found within the TGF-β1 promoter was increased in nuclear extracts from Swiss 3T3 fibroblasts treated with TNF-α. Together, these results suggest that TNF-α induces expression and DNA binding of AP-1 resulting in increased transcription of the TGF-β1 gene. It is essential to know which transcription pathways are activated because of the wide distribution of TNF-α and TGF-β1, the general lack of effective treatments for fibroproliferative disease and the possibility that targeting the correct transcription factors could be palliative.}, number={8B}, journal={JOURNAL OF CELLULAR AND MOLECULAR MEDICINE}, author={Sullivan, Deborah E. and Ferris, MaryBeth and Nguyen, Hong and Abboud, Elizabeth and Brody, Arnold R.}, year={2009}, month={Aug}, pages={1866–1876} }
 @article{sullivan_ferris_pociask_brody_2008, title={The latent form of TGF beta(1) is induced by TNF alpha through an ERK specific pathway and is activated by asbestos-derived reactive oxygen species in vitro and in vivo}, volume={5}, ISSN={["1547-6901"]}, DOI={10.1080/15476910802085822}, abstractNote={Tumor necrosis factor-α (TNFα) and transforming growth factor-β1 (TGFβ1) are potent peptide growth factors that are likely to play important roles in the development of interstitial pulmonary fibrosis (IPF). Previously we showed that TNFα and TGFβ1 are up-regulated in macrophages, epithelial and mesenchymal cells early after exposure to chrysotile asbestos, particularly at sites of fiber deposition in vivo. We also showed that TNFα receptor knockout mice are resistant to asbestos-induced fibrosis. Importantly, vectors that over-express TNFα cause inflammation and fibrogenesis along with increased TGFβ1 production in C57Bl/6 mice. Recently we reported that TNFα activates the extracellular regulated kinase pathway in fibroblasts leading to a 200–400% increase in TGFβ1 mRNA and protein. The mechanism of TNFα induction of TGFβ1 expression appears to be complex, involving both transcriptional and post-transcriptional mechanisms. In asbestos-exposed animals, this TGFβ1 is produced on alveolar surfaces in a latent form (controlled by binding of a latent associated peptide [LAP]) that must be activated for the TGFβ1 to bind to its receptors and induce its multiple biological effects. Thus, we recently reported that, in vitro, reactive oxygen species (ROS) derived from chrysotile and crocidolite asbestos activate TGFβ1 by oxidation of the LAP. Now, in preliminary findings, we have shown that over-expression of latent TGFβ1 prior to asbestos exposure of fibrogenic-resistant TNFα receptor knockout mice produces asbestos lesions with the same severity as seen in normal C57/Bl6 mice. This finding plus the demonstration of increased amounts of TGFβ1, increased Smad activation and amelioration of the developing disease by treating the mice with an anti-oxidant all support the concept that, in vivo, latent TGFβ1 is activated by asbestos-generated oxygen radicals and consequently mediates at least a component of the consequent fibrogenesis. Taken together, these findings support the postulate that TNFα controls fibrogenesis by regulating TGFβ1 expression and that one mechanism through which ROS induce lung fibrosis is by activating latent TGFβ 1.}, number={2}, journal={JOURNAL OF IMMUNOTOXICOLOGY}, author={Sullivan, Deborah E. and Ferris, MaryBeth and Pociask, Derek and Brody, Arnold R.}, year={2008}, pages={145–149} }
 @article{spees_pociask_sullivan_whitney_lasky_prockop_brody_2007, title={Engraftment of bone marrow progenitor cells in a rat model of asbestos-induced pulmonary fibrosis}, volume={176}, ISSN={["1073-449X"]}, DOI={10.1164/rccm.200607-1004OC}, abstractNote={RATIONALE
Bone marrow-derived cells have been shown to engraft during lung fibrosis. However, it is not known if similar cells engraft consequent to inhalation of asbestos fibers that cause pulmonary fibrosis, or if the cells proliferate and differentiate at sites of injury.


OBJECTIVES
We examined whether bone marrow-derived cells participate in the pulmonary fibrosis that is produced by exposure to chrysotile asbestos fibers.


METHODS
Adult female rats were lethally irradiated and rescued by bone marrow transplant from male transgenic rats ubiquitously expressing green fluorescent protein (GFP). Three weeks later, the rats were exposed to an asbestos aerosol for 5 hours on three consecutive days. Controls were bone marrow-transplanted but not exposed to asbestos.


MEASUREMENTS AND MAIN RESULTS
One day and 2.5 weeks after exposure, significant numbers of GFP-labeled male cells had preferentially migrated to the bronchiolar-alveolar duct bifurcations, the specific anatomic site at which asbestos produces the initial fibrogenic lesions. GFP-positive cells were present at the lesions as monocytes and macrophages, fibroblasts, and myofibroblasts or smooth muscle cells. Staining with antibodies to PCNA demonstrated that some of the engrafted cells were proliferating in the lesions and along the bronchioles. Negative results for TUNEL at the lesions confirmed that both PCNA-positive endogenous pulmonary cells and bone marrow-derived cells were proliferating rather than undergoing apoptosis, necrosis, or DNA repair.


CONCLUSIONS
Bone marrow-derived cells migrated into developing fibrogenic lesions, differentiated into multiple cell types, and persisted for at least 2.5 weeks after the animals were exposed to aerosolized chrysotile asbestos fibers.}, number={4}, journal={AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE}, author={Spees, Jeffrey L. and Pociask, Derek A. and Sullivan, Deborah E. and Whitney, Mandolin J. and Lasky, Joseph A. and Prockop, Darwin J. and Brody, Arnold R.}, year={2007}, month={Aug}, pages={385–394} }
 @article{yin_brody_sullivan_2007, title={Laser capture microdissection reveals dose-response of gene expression in situ consequent to asbestos exposure}, volume={88}, ISSN={["1365-2613"]}, DOI={10.1111/j.1365-2613.2007.00545.x}, abstractNote={Summary}, number={6}, journal={INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY}, author={Yin, Qi and Brody, Arnold R. and Sullivan, Deborah E.}, year={2007}, month={Dec}, pages={415–425} }
 @article{brody_bitterman_adler_rannels_thet l. a._i._1988, title={The lung matrix and inflammation: Part II. Biochemical and molecular mechanisms of fibrogenesis: implications for environmental lung disease}, volume={138}, journal={American Review of Respiratory Disease}, author={Brody, A. R. and Bitterman, P. B. and Adler, K. B. and Rannels, D. E. and Thet L. A., Rom W. N. and I., Rennard S.}, year={1988}, pages={1056–1057} }
 @inbook{brody_hill_hesterberg_barrett_adler_1986, title={Intracellular translocation of inorganic particles.}, DOI={10.1007/978-1-4613-2161-3_17}, booktitle={The cytoskeleton.}, author={Brody, A. R. and Hill, L. H. and Hesterberg, T. W. and Barrett, J. C. and Adler, K. B.}, year={1986}, pages={221–227} }
 @article{brody_hill_stirewalt_adler_1983, title={Actin containing microfilaments of pulmonary epithelial cells provide a mechanism for translocating inhaled asbestos to the interstitium.}, volume={83}, journal={Chest}, author={Brody, A. R. and Hill, L. and Stirewalt, W. and Adler, K. B.}, year={1983}, pages={11S–13} }
 @article{adler_brody_craighead_1981, title={Studies on the mechanism of mucin secretion by cells of the porcine tracheal epithelium.}, volume={166}, DOI={10.3181/00379727-166-41030}, abstractNote={Abstract The effects of selected pharmacological agents on mucin secretion by the tracheal epithelium of piglets were studied using organ culture. Mucin release into the culture medium was reduced, and mucin retention by secretory cells of the mucosa and submucosal glands was increased, by colchicine, vinblastine sulfate, and cytochalasin B. Dibutyryl cyclic AMP had no significant effect. Although these agents have diverse and poorly understood influences on cell functions, the results suggest a possible role for mi-crotubules and microfilaments in the intracellular movement and release of mucin.}, journal={Proceedings of the Society for Experimental Biology and Medicine}, author={Adler, K. B. and Brody, A. R. and Craighead, J. E.}, year={1981}, pages={96–106} }
 @article{davis_brody_adler_1980, title={Changes in the surface morphology of human alveolar macrophages induced by tobacco and marijuana smoking.}, volume={1}, journal={Chest}, author={Davis, G. S. and Brody, A. R. and Adler, K. B.}, year={1980}, pages={281–293} }
 @article{davis_adler_brody_1980, title={The morphology of alveolar macrophage immunologic activation: a scanning electron microscopic study.}, volume={121}, journal={American Review of Respiratory Disease}, author={Davis, G. S. and Adler, K. B. and Brody, A. R.}, year={1980}, pages={269} }
 @article{davis_brody_adler_1979, title={Functional and physiological correlates of human alveolar macrophage cell shape and surface morphology.}, volume={75S}, DOI={10.1016/s0012-3692(15)30441-4}, abstractNote={The pulmonary alveolar macrophage (PAM) participates in the immunologic responses of the lung, and is the resident phagocyte of the alveolar membrane. 1 Green GM Jakab GJ Low RB et al. Defense mechanisms of the respiratory membrane: State of the art. Am Rev Respir Dis. 1977; 115: 479-514 PubMed Google Scholar The PAM has been described as variable in size and shape, and the cell population as heterogeneous, 2 Brain JD Proctor DF Reid LM Respiratory Defense Mechanisms (part II). Marcel Dekker, New York1977: 849-892 Google Scholar but few attempts have been made to define macrophage shape quantitatively, or to relate cell shape to cell physiology and function.}, journal={Chest}, author={Davis, G. S. and Brody, A. R. and Adler, K. B.}, year={1979}, pages={280–282} }
 @article{adler_davis_woodworth_brody_1979, title={The human pulmonary alveolar macrophage: two distinct morphological populations.}, volume={3}, journal={Scanning Electron Microscopy}, author={Adler, K. B. and Davis, G. S. and Woodworth, C. W. and Brody, A. R.}, year={1979}, pages={921–928} }
 @inproceedings{adler_brody_craighead_1978, title={Association of microtubules and microfilaments with mucin granules in tracheal goblet cells their possible role in exocytosis.}, volume={2}, booktitle={Proceedings of the 9th International Congress on Electron Microscopy}, author={Adler, K. B. and Brody, A. R. and Craighead, J. E.}, year={1978}, pages={500–501} }
 @article{adler_brody_davis_1978, title={Localization of actin in surface ruffles of pulmonary alveolar macrophages: Effects of cytochalasin B, colchicine and cyclic AMP.}, volume={79}, journal={Journal of Cell Biology}, author={Adler, K. B. and Brody, A. R. and Davis, G. S.}, year={1978}, pages={276a} }
 @article{adler_brody_craighead_1978, title={Ultrastructural association of microtubules and microfilaments with mucin granules in porcine tracheobronchial tissue in organ culture.}, volume={37}, journal={404nOtfound}, author={Adler, K. B. and Brody, A. R. and Craighead, J. E.}, year={1978}, pages={266} }