Maureen R Horton

Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States

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Publications (70)395.63 Total impact

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    ABSTRACT: The mouse is now the primary animal used to model a variety of lung diseases. To study the mechanisms that underlie such pathologies, phenotypic methods are needed that can quantify the pathologic changes. Furthermore, to provide translational relevance to the mouse models, such measurements should be tests that can easily be done in both humans and mice. Unfortunately, in the present literature few phenotypic measurements of lung function have direct application to humans. One exception is the diffusing capacity for carbon monoxide, which is a measurement that is routinely done in humans. In the present report, we describe a means to quickly and simply measure this diffusing capacity in mice. The procedure involves brief lung inflation with tracer gases in an anesthetized mouse, followed by a 1 min gas analysis time. We have tested the ability of this method to detect several lung pathologies, including emphysema, fibrosis, acute lung injury, and influenza and fungal lung infections, as well as monitoring lung maturation in young pups. Results show significant decreases in all the lung pathologies, as well as an increase in the diffusing capacity with lung maturation. This measurement of lung diffusing capacity thus provides a pulmonary function test that has broad application with its ability to detect phenotypic structural changes with most of the existing pathologic lung models.
    Journal of visualized experiments : JoVE. 01/2015;
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    ABSTRACT: Lovastatin has a unique ability to bind Leukocyte Function Antigen-1 (LFA-1), an integrin necessary for the full expression of inflammatory cytokines induced by the low molecular weight form of the extracellular matrix glycosaminoglycan hyaluronan (LMW HA). We hypothesized that lovastatin could inhibit LMW HA inflammatory signals via interaction with LFA-1, and attenuate bleomycin induced pulmonary fibrosis.
    International journal of biomedical science: IJBS 09/2014; 10(3):146-57.
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    ABSTRACT: Laryngotracheal stenosis (LTS) lacks an ideal animal model to study its unique wound-healing pathophysiology and the effect of interventions.
    JAMA otolaryngology-- head & neck surgery. 08/2014; 140(10).
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    ABSTRACT: Pulmonary fibrosis is an untreatable, fatal disease characterized by excess deposition of extracellular matrix and inflammation. Although the etiology of pulmonary fibrosis is unknown, recent studies have implicated dysregulated immune responses and wound healing. Since n-3 polyunsaturated fatty acids (n-3 PUFAs) may beneficially modulate immune responses in a variety of inflammatory disorders, we investigated the therapeutic role of docosahexaenoic acid (DHA), a single n-3 PUFA, in lung fibrosis. Intratracheal DHA or PBS was administered to mouse lungs 4 days prior to intratracheal bleomycin treatment. Body weight and survival were monitored for 21 days. Bronchoalveolar fluid (BALF) and lung inflammatory cells, cytokines, eicosanoids, histology and lung function were determined on serial days (0, 3, 7, 14, 21) after bleomycin injury. Intratracheal administration of DHA mitigated bleomycin-induced lung injury. Mice pretreated with DHA had significantly less weight loss and mortality after bleomycin injury. The lungs from DHA-pretreated mice had markedly less fibrosis. DHA pretreatment also protected the mice from the functional changes associated with bleomycin injury. Bleomycin-induced cellular inflammation in BALF and lung tissue was blunted by DHA pretreatment. These advantageous effects of DHA pretreatment were associated with decreased IL-6, LTB4, PGE2 and increased IL-10. Our findings demonstrate that intratracheal administration of DHA, a single PUFA, protected mice from the development of bleomycin-induced pulmonary inflammation and fibrosis. These results suggest that further investigations regarding the role of n-3 polyunsaturated fatty acids in fibrotic lung injury and repair are needed.
    BMC Pulmonary Medicine 04/2014; 14(1):64. · 2.49 Impact Factor
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    ABSTRACT: SGK1 is an AGC kinase that regulates the expression of membrane sodium channels in renal tubular cells in a manner dependent on the metabolic checkpoint kinase complex mTORC2. We hypothesized that SGK1 might represent an additional mTORC2-dependent regulator of the differentiation and function of T cells. Here we found that after activation by mTORC2, SGK1 promoted T helper type 2 (TH2) differentiation by negatively regulating degradation of the transcription factor JunB mediated by the E3 ligase Nedd4-2. Simultaneously, SGK1 repressed the production of interferon-γ (IFN-γ) by controlling expression of the long isoform of the transcription factor TCF-1. Consistent with those findings, mice with selective deletion of SGK1 in T cells were resistant to experimentally induced asthma, generated substantial IFN-γ in response to viral infection and more readily rejected tumors.
    Nature Immunology 04/2014; · 24.97 Impact Factor
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    ABSTRACT: Overwhelming lung inflammation frequently occurs following exposure to both direct infectious and noninfectious agents and is a leading cause of mortality worldwide. In that context, immunomodulatory strategies may be used to limit severity of impending organ damage. We sought to determine whether priming the lung by activating the immune system, or immunological priming, could accelerate resolution of severe lung inflammation. We assessed the importance of alveolar macrophages, regulatory T cells, and their potential interaction during immunological priming. We demonstrate that oropharyngeal delivery of low-dose LPS can immunologically prime the lung to augment alveolar macrophage production of IL-10 and enhance resolution of lung inflammation induced by a lethal dose of LPS or by Pseudomonas bacterial pneumonia. IL-10-deficient mice did not achieve priming and were unable to accelerate lung injury resolution. Depletion of lung macrophages or regulatory T cells during the priming response completely abrogated the positive effect of immunological priming on resolution of lung inflammation and significantly reduced alveolar macrophage IL-10 production. Finally, we demonstrated that oropharyngeal delivery of synthetic CpG-oligonucleotides elicited minimal lung inflammation compared with low-dose LPS but nonetheless primed the lung to accelerate resolution of lung injury following subsequent lethal LPS exposure. Immunological priming is a viable immunomodulatory strategy used to enhance resolution in an experimental acute lung injury model with the potential for therapeutic benefit against a wide array of injurious exposures.
    The Journal of Immunology 03/2014; · 5.36 Impact Factor
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    ABSTRACT: Here we explored the impact of hydrogen sulfide (H2S) on biophysical properties of the primary human airway smooth muscle (ASM)-the end effector of acute airway narrowing in asthma. Using Magnetic Twisting Cytometry (MTC), we measured dynamic changes in the stiffness of isolated ASM, at the single-cell level, in response to varying doses of GYY4137 (1-10 mM). GYY4137 slowly released appreciable levels of H2S in the range of 10-275 μM, and H2S released was long lived. In isolated human ASM cells, GYY4137 acutely decreased stiffness (i.e. an indicator of the single-cell relaxation) in a dose-dependent fashion, and stiffness decreases were sustained in culture for 24h. Human ASM cells showed protein expressions of cystathionine-γ-lyase (CSE; a H2S synthesizing enzyme) and ATP-sensitive potassium (KATP) channels. The KATP channel opener pinacidil effectively relaxed isolated ASM cells. In addition, pinacidil-induced ASM relaxation was completely inhibited by the treatment of cells with the KATP channel blocker glibenclamide. Glibenclamide also markedly attenuated GYY4137-mediated relaxation of isolated human ASM cells. Taken together, our findings demonstrate that H2S causes the relaxation of human ASM and implicate as well the role for sarcolemmal KATP channels. Finally, given that ASM cells express intrinsic enzymatic machinery of generating H2S, we suggest thereby this class of gasotransmitter can be further exploited for potential therapy against obstructive lung disease.
    Biochemical and Biophysical Research Communications 03/2014; · 2.28 Impact Factor
  • Robert W Hallowell, Maureen R Horton
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    ABSTRACT: Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by the destruction of articular joint structures. RA is a systemic condition that often affects multiple organs, including the heart, lungs, and kidneys. Pulmonary complications of RA are relatively common and include pleural effusion, rheumatoid nodules, bronchiectasis, obliterative bronchiolitis, and opportunistic infections. Interstitial lung disease (ILD) is a common occurrence in patients with RA, and can range in severity from an asymptomatic incidental finding to a rapidly progressing life-threatening event. Usual interstitial pneumonia and non-specific interstitial pneumonia are the two most common patterns, though others have been reported. Various disease-modifying anti-rheumatic drugs-in particular, methotrexate and the tumor necrosis factor-alpha inhibitors-have been associated with RA-ILD in numerous case reports and case series, though it is often difficult to distinguish association from causality. Treatment for RA-ILD typically involves the use of high-dose corticosteroids, often in conjunction with alternative immunosuppressant agents such as azathioprine or mycophenolate mofetil, and outcomes vary widely depending on the initial pattern of lung disease. Additional research into the mechanisms driving RA-ILD is needed to guide future therapy.
    Drugs 02/2014; 74(4). · 4.13 Impact Factor
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    ABSTRACT: Proteins as well as small molecules have demonstrated success as therapeutic agents, but their pharmacologic properties sometimes fall short against particular drug targets. Although the adenosine 2a receptor (A2AR) has been identified as a promising target for immunotherapy, small molecule A2AR agonists have suffered from short pharmacokinetic half-lives and the potential for toxicity by modulating non-immune pathways. To overcome these limitations, we have tethered the A2AR agonist CGS-21680 to the immunoglobulin Fc domain using expressed protein ligation with Sf9 cell secreted protein. The protein small molecule conjugate Fc-CGS retained potent Fc receptor and A2AR interactions and showed superior properties as a therapeutic for the treatment of a mouse model of autoimmune pneumonitis. This approach may provide a general strategy for optimizing small molecule therapeutics.
    Journal of the American Chemical Society 02/2014; · 11.44 Impact Factor
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    ABSTRACT: Chronic idiopathic pulmonary fibrosis (IPF) is a progressive, fatal, and untreatable disease with unclear etiology. There are few models of this chronic pathology, and although delivery of bleomycin to induce acute lung injury is the most common animal model of pulmonary fibrosis, there is considerable uncertainty about whether this acute injury resolves in those animals that survive. In this report, we have systematically followed groups of mice for up to 6 months following a single insult of bleomycin. We assessed changes in lung function and pathology over this time course, with measurements of the diffusion capacity for carbon monoxide, lung mechanics, quantitative stereology, and collagen. Our results show that, while there is some repair over this extended time course, the injury in the lung never fully resolves. This persistent degree of fibrosis may have similarities to many features of human IPF. Thus, these chronic fibrotic changes in mouse lungs could be a useful model to evaluate potential therapeutic interventions to accelerate repair and possible treat this debilitating disease.
    Physiological reports. 02/2014; 2(2):e00249.
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    ABSTRACT: The transcription factor Early Growth Response 3 (Egr3) has been shown to play an important role in negatively regulating T cell activation and promoting T cell anergy in Th1 cells. However, its role in regulating other T helper subsets has yet to be described. We sought to determine the role of Egr3 in a Th17 response using transgenic mice that overexpress Egr3 in T cells (Egr3 TG). Splenocytes from Egr3 TG mice demonstrated more robust generation of Th17 cells even under non-Th17 skewing conditions. We found that while Egr3 TG T cells were not intrinsically more likely to become Th17 cells, the environment encountered by these cells was more conducive to Th17 development. Further analysis revealed a considerable increase in the number of γδ T cells in both the peripheral lymphoid organs and mucosal tissues of Egr3 TG mice, a cell type which normally accounts for only a small fraction of peripheral lymphocytes. Consistent with this marked increase in peripheral γδ T cells, thymocytes from Egr3 TG mice also appear biased toward γδ T cell development. Coculture of these Egr3-induced γδ T cells with wildtype CD4+ T cells increases Th17 differentiation, and Egr3 TG mice are more susceptible to bleomycin-induced lung inflammation. Overall our findings strengthen the role for Egr3 in promoting γδ T cell development and show that Egr3-induced γδ T cells are both functional and capable of altering the adaptive immune response in a Th17-biased manner. Our data also demonstrates that the role played by Egr3 in T cell activation and differentiation is more complex than previously thought.
    PLoS ONE 01/2014; 9(1):e87265. · 3.53 Impact Factor
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    ABSTRACT: Hyaluronan (HA) is the major glycosaminoglycan in the extracellular matrix. During inflammation there is an increased breakdown of HA, resulting in the accumulation of low molecular weight (LMW) HA and activation of monocytes and macrophages. Eicosanoids, derived from cytosolic phospholipase A2 group IVA (cPLA2α) activation, are potent lipid mediators also attributed to acute and chronic inflammation. The aim of this study was to determine the effect of LMW HA on cPLA2α activation, arachidonic acid (AA) release and subsequent eicosanoid production, and to examine the receptors and downstream mechanisms involved in these processes in monocytes and differently polarized macrophages. LMW HA was a potent stimulant of AA release in a time and dose-dependent manner, induced cPLA2α, ERK 1/2, p38 and JNK phosphorylation, as well as activated COX2 expression and PGE2 production in primary human monocytes, murine RAW264.7 and wild-type bone-marrow derived macrophages. Specific cPLA2α inhibitor blocked HA-induced AA release and PGE2 production in all of these cells. Using CD44, TLR4, TLR2, MyD88, Rhamm or Stabilin-2 siRNA-transfected macrophages and monocytes we found that AA release, cPLA2α, ERK 1/2, p38 and JNK phosphorylation, COX2 expression and PGE2 production were activated by LMW HA through a TLR4/MyD88 pathway. Likewise, PGE2 production and COX2 expression were blocked in Tlr4(-/-) and MyD88(-/-)mice, but not in Cd44(-/-) mice, after LMW HA stimulation. Moreover, we demonstrated that LMW HA activated M1 macrophage phenotype with the unique cPLA2α/COX2(high) and COX1/ALOX15/ALOX5/LTAH4(low) gene and PGE2/PGD2/15-HETE(high) and LXA4(low) eicosanoid profile. These findings reveal a novel link between HA-mediated inflammation and lipid metabolism.
    Journal of Biological Chemistry 12/2013; · 4.60 Impact Factor
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    ABSTRACT: Approximately 3 billion people, half the worldwide population, are exposed to extremely high concentrations of household air pollution (HAP) due to the burning of biomass fuels on inefficient cookstoves, accounting for 4 million annual deaths globally. Yet, our understanding of the pulmonary responses to HAP exposure and the underlying molecular and cellular events are limited. The two most prevalent biomass fuels in India are wood and cow dung, and typical 24-h mean particulate matter (PM) concentrations in homes that use these fuels are 300-5,000 µg/m3. We dissected the mechanisms of pulmonary responses in mice after either acute or sub-chronic exposure to wood or cow dung PM collected from rural Indian homes during biomass cooking. Acute exposures resulted in robust pro-inflammatory cytokine production, neutrophilc inflammation, airway resistance and hyper-responsiveness, all of which were significantly higher in mice exposed to PM from cow dung. On the contrary, sub-chronic exposures induced eosinophilic inflammation, PM-specific antibody responses, and alveolar destruction that was highest in wood PM-exposed mice. To understand the molecular pathways that trigger biomass PM-induced inflammation, we exposed TLR2, 3, 4, 5, and IL-1R deficient mice to PM, and found that IL-1R, TLR4 and TLR2 are the predominant receptors that elicit inflammatory responses via MyD88 in mice exposed to wood or cow dung PM. In conclusion this study demonstrates that sub-chronic exposure to PM collected from households burning biomass fuel elicits a persistent pulmonary inflammation largely through activation of TLR and IL-1R pathways, which could increase the risk for chronic respiratory diseases.
    American Journal of Respiratory Cell and Molecular Biology 10/2013; · 4.15 Impact Factor
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    ABSTRACT: BACKGROUND: The extracellular matrix plays a critical role in insuring tissue integrity and water homeostasis. However, breakdown products of the extracellular matrix have emerged as endogenous danger signals, designed to rapidly activate the immune system against a potential pathogen breach. Type I interferons play a critical role in the immune response against viral infections. In the lungs, hylauronan (HA) exists as a high molecular weight, biologically inert extracellular matrix component that is critical for maintaining lung function. When lung tissue is injured, HA is broken down into lower molecular weight fragments that alert the immune system to the breach in tissue integrity by activating innate immune responses. HA fragments are known to induce inflammatory gene expression via TLR-MyD88-dependent pathways. METHODS: Primary peritoneal macrophages from C57BL/6 wild type, TLR4 null, TLR3 null, MyD88 null, and TRIF null mice as well as alveolar and peritoneal macrophage cell lines were stimulated with HA fragments and cytokine production was assessed by rt-PCR and ELISA. Western blot analysis for IRF3 was preformed on cell lysates from macrophages stimulate with HA fragments RESULTS: We demonstrate for the first time that IFNbeta is induced in murine macrophages by HA fragments. We also show that HA fragments induce IFNbeta using a novel pathway independent of MyD88 but dependent on TLR4 via TRIF and IRF-3. CONCLUSIONS: Overall our findings reveal a novel signaling pathway by which hyaluronan can modulate inflammation and demonstrate the ability of hyaluronan fragments to induce the expression of type I interferons in response to tissue injury even in the absence of viral infection. This is independent of the pathway of the TLR2-MyD88 used by these matrix fragments to induce inflammatory chemokines. Thus, LMW HA may be modifying the inflammatory milieu simultaneously via several pathways.
    Journal of Inflammation 05/2013; 10(1):23. · 2.22 Impact Factor
  • Noah Lechtzin, Marisa E Hilliard, Maureen R Horton
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    ABSTRACT: ABSTRACT BACKGROUND: Cough is a pervasive and disabling symptom of idiopathic pulmonary fibrosis (IPF) and is an independent predictor of disease progression. The Cough Quality of Life Questionnaire (CQLQ) is a validated measure of cough specific quality of life (QoL) that could be used as an outcome measure in therapeutic trials for IPF. This study aimed to assess the reliability and validity of the CQLQ in individuals with IPF. METHODS: The CQLQ was administered as an outcome within a previously published 27 week placebo controlled, cross-over trial of thalidomide for cough in IPF. Participants were adults with IPF and chronic cough. A cough visual analog scale (VAS) and the St. George's Respiratory Questionnaire (SGRQ) were administered to establish concurrent validity of the CQLQ. RESULTS: Internal consistency was high (α>0.70) for the CQLQ total score and 4 of 6 subscales. The CQLQ total score demonstrated concurrent validity via significant correlations with scores on the cough VAS and SGRQ total and subscale scores (r range=0.63-0.81, p<0.05). The intraclass correlation for the CQLQ completed at baseline and following a therapeutic wash-out period at week 15 was 0.87, indicating very good test retest reliability. CONCLUSIONS: This study provides evidence in support of CQLQ as a valid and reliable instrument in IPF and should be used to assess cough specific QOL in therapeutic trials.
    Chest 03/2013; · 7.13 Impact Factor
  • Noah Lechtzin, Maureen R Horton
    Annals of internal medicine 03/2013; 158(6):498-9. · 16.10 Impact Factor
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    ABSTRACT: Rationale: Acute respiratory distress syndrome (ARDS) causes significant morbidity and mortality. Exacerbating factors increasing the risk of ARDS remain unknown. Supplemental oxygen is often necessary in both mild and severe lung disease. Among its potential effects may include augmentation of lung inflammation by inhibiting anti-inflammatory pathways in alveolar macrophages. Objectives: To determine oxygen-derived effects on the anti-inflammatory A2A adenosinergic (ADORA2A) receptor in macrophages and its role in lung injury. Methods: WT and ADORA2A-/- mice were given intratracheal lipopolysaccharide (IT LPS) followed 12 hours later by continuous exposure to 21% oxygen (control) or 60% oxygen for 1-3 days. We measured phenotypic endpoints of lung injury and the alveolar macrophage inflammatory state. We tested an ADORA2A specific agonist, CGS-21680, in LPS plus oxygen-exposed WT and ADORA2A-/- mice. We determined specific effects of myeloid ADORA2A using chimera experiments. Results: Compared to WT, ADORA2A-/- mice exposed to IT LPS and 60% oxygen had significantly more histologic lung injury, alveolar neutrophils and protein. Macrophages from ADORA2A-/- mice exposed to LPS plus oxygen expressed higher levels of pro-inflammatory cytokines and co-signaling molecules, CGS-21680 prevented oxygen-induced augmentation of lung injury after LPS only in WT mice. Chimera experiments demonstrated that transfer of WT but not ADORA2A-/- bone marrow cells into irradiated ADORA2A-/- mice reduced lung injury following LPS plus oxygen, demonstrating myeloid ADORA2A protection. Conclusions: ADORA2A is protective against lung injury after LPS and oxygen. Oxygen after LPS increases macrophage activation to augment lung injury by inhibiting the ADORA2A pathway.
    American Journal of Respiratory Cell and Molecular Biology 01/2013; · 4.15 Impact Factor
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    ABSTRACT: The mammalian target of rapamycin (mTOR) signaling pathway is a master regulator of T cell differentiation. mTOR integrates various signals in the immune microenvironment, including costimulatory ligands, cytokines, and the availability of nutrients to determine the outcome of T cell differentiation. Recently, we identified the serum- and glucocorticoid-regulated kinase 1 (SGK1) as a downstream target of mTORC2 that is a critical regulator of CD4 effector differentiation into Th1 and Th2 subsets. Specifically, SGK1 promotes Th2 differentiation by negatively regulating the NEDD4-2 E3 ligase mediated destruction of JunB. Simultaneously, SGK1 represses the production of IFN- by controlling the expression of the long isoform of TCF-1. Consistent with these functions, mice lacking SGK1 specifically in T cells fail to generate a Th2 response and are resistant to experimentally induced asthma. Likewise, such mice generate robust levels of IFN- in response to vaccines and more readily reject tumors. In addition, loss of SGK1 in CD8 T cells promotes memory differentiation by regulating the expression of CD127, CD62L, and eomesodermin. In summary, our findings reveal a novel role for SGK1 as an essential component of the mTOR pathway that guides differentiation of both CD4 and CD8 T cells. Targeting SGK1, therefore, may be a useful strategy for fine-tuning immune responses by manipulating T cell differentiation.
    The Journal of Immunology; 01/2013
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    ABSTRACT: TCR-induced NF-AT activation leads to the expression of both activating and inhibitory proteins. Previously, we had identified Egr-2 and Egr-3 as NF-AT-induced transcription factors which promote the inhibition of T cell activation. In this report we identify Sprouty1 as a downstream target of Egr-3. CD4(+) T cells lacking Spry1 demonstrate enhanced proliferation and cytokine production. Likewise, Spry1(Flox/Flox) Lck Cre CD8(+) T cells display increased cytolytic activity. Mechanistically, Spry1 acts at the level of PLC-γ promoting the inhibition of both Ca(++) induced NF-AT activation and MAP-kinase induced AP-1 activation while sparing NF-κB signaling. In vivo, mice in which Spry1 is selectively deleted in T cells demonstrate enhanced responses to a tumor vaccine and subsequently reject tumors more robustly than Wt mice. These findings suggest that targeting Spry1 might prove to be a novel means of enhancing tumor immunotherapy.
    PLoS ONE 11/2012; 7(11):e49801. · 3.53 Impact Factor
  • M R Horton, R W Hallowell
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    ABSTRACT: Thalidomide is an infamous drug whose use by pregnant women in the middle of last century tragically resulted in serious birth defects. However, as a result of its potent immunomodulatory, anti-inflammatory and antiangiogenic properties, thalidomide may be a potential therapy in many diseases. In recent years, thalidomide has been used effectively to treat various malignancies, including multiple myeloma, myelodysplastic syndromes, renal cell cancer, glioblastoma multiforme and prostate cancer. In addition, thalidomide has also proven effective against other immune-related diseases, including erythema nodosum leprosum and sarcoidosis. Idiopathic pulmonary fibrosis (IPF) is a deadly fibrotic disease with no effective treatment options. However, there is data to suggest that thalidomide may be useful in treating the chronic, disabling cough that accompanies IPF. It remains to be seen whether the immunomodulatory and antiangiogenic properties of thalidomide will also make it a potential therapy against the clinical progression of IPF.
    Drugs of today (Barcelona, Spain: 1998) 10/2012; 48(10):661-71. · 1.00 Impact Factor

Publication Stats

2k Citations
395.63 Total Impact Points

Institutions

  • 2011–2014
    • Johns Hopkins Bloomberg School of Public Health
      • Department of Environmental Health Sciences
      Baltimore, Maryland, United States
  • 1997–2014
    • Johns Hopkins University
      • • Department of Medicine
      • • Division of Pulmonary and Critical Care Medicine
      • • Department of Pharmacology and Molecular Sciences
      • • Department of Pathology
      Baltimore, Maryland, United States
    • University of Pennsylvania
      Philadelphia, Pennsylvania, United States
  • 1999
    • Johns Hopkins Medicine
      • Division of Pulmonary and Critical Care Medicine
      Baltimore, MD, United States