T32: Training Program in Lung Science
The long-term goal of the Northwestern University Lung Sciences Training Program (NULSTP) is to encourage bright, enthusiastic, well-trained, academically-oriented MDs and PhDs to pursue a career in Pulmonary Biology investigation. The trainees supported by our training grant focus their research efforts on the cellular and molecular pathophysiology of lung disease and the translation of these findings to the bedside. The trainees are provided with the scientific environment, didactic training and career development mentorship required to initiate a successful career in research. The training is fostering an environment for the acquisition of scientific skills, collaborative interactions and critical thinking required to pursue careers in pulmonary and critical care investigation.
The “Training Program in Lung Sciences” is now in its 10th year of supporting and training a new generation of pre- and post-doctoral fellows who will focus their efforts on lung science. This program has been very successful, reaching the goals described in our previous application. Of the 14 pre-doctoral candidates supported by the award, 12 remain in academic medicine. Similarly, of the 26 post-doctoral fellows supported by the award, 23 remain in academic medicine--11 with the rank of Assistant or Associate Professor and 7 at the rank of Instructor. This success is attributable to the talented trainees we are fortunate to recruit to our program and the diverse, accomplished and highly collaborative group of mentors with whom they are training.
Jacob I Sznajder, MD
Senior Research Administrator
Program Eligibility and Application Process
We are currently accepting applications to the Training Program in Lung Science for pre-doctoral and postdoctoral positions. To apply, please send a recommendation letter from your mentor, your CV, and a short cover letter describing your research activities and interest to email@example.com with the subject line: Training Program Applicant. The deadline to apply is six months prior to when you would like funding to begin.
All candidates to the Northwestern University Lung Sciences Training Program must meet NRSA citizenship and support requirements:
- Citizenship: Any individual to be trained must be a citizen or noncitizen national of the United States or have been lawfully admitted for permanent residence at the time of appointment.
- NRSA Support: No individual trainee may receive more than 5 years of aggregate Kirschstein-NRSA support at the predoctoral level and 3 years of aggregate Kirschstein-NRSA support at the postdoctoral level, including any combination of support from Kirschstein-NRSA institutional research training grants and individual fellowships.
For more information on NRSA eligibility requirements, see the NIH Grants Policy Statement on Kirschstein NRSAs.
Predoctoral Applicant Eligibility
The Northwestern University Lung Sciences Training Program has funding to support three predoctoral trainees. Predoctoral trainees from the following programs are eligible to apply for this training program:
- Driskoll Graduate Program (DGP)
- Interdepartmental Biological Sciences Program (IBiS)
- Medical Scientist Training Program (MSTP)
- Biomedical Engineering Program (BME)
- Material Science and Engineering Program (MSE)
All predoctoral applicants should have completed their rotations and required coursework and passed their qualifying examinations.
Postdoctoral Applicant Eligibility
The Northwestern University Lung Sciences Training Program has funding to support five postdoctoral trainees. Applicants should be recent PhD postdoctoral fellows with at least one year of training or MD physicians in our fellowship program with at least two years of training in clinical pulmonary and critical care medicine, who aspire to pursue an academic career and have conducted research with one of the mentors of the NULSTP.
Application Process and Deadlines
We are currently accepting applications to the Training Program in Lung Science for pre-doctoral and postdoctoral positions. To apply, please send a recommendation letter from your mentor, your CV, and a short cover letter describing your research activities and interest to firstname.lastname@example.org with the subject line: Training Program Applicant. The deadline to apply is 6 months prior to when you would like funding to begin.
|Name||Degree(s)||Rank||Primary Department or Program||Research Interest||Training Role|
|Amaral, Luis A.||PhD||Prof.||Chemical and Biological Engineering||Development of methods for extracting scale-relevant information from metabolic, proteomic and genomic networks||Preceptor|
|Bagheri, Neda||PhD||Asst. Prof.||Chemical and Biological Engineering||Computational systems biology and complex regulatory networks, dynamical systems and control theory, applications to immunology, cancer, aging, and circadian rhythms||Preceptor|
|Bharat, Ankit||MBBS||Assoc. Prof.||Surgery- Thoracic Surgery||Lung preservation, transplant immunology and airway biology||Preceptor|
|Budinger, G.R. Scott||MD||Prof.||Medicine- Pulmonary and Critical Care||Inhaled particulates, acute respiratory failure, hyperoxic lung injury, lung cell apoptosis||Co-Director,Exec. Comm., Preceptor|
|Carnethon, Mercedes R.||PhD||Assoc. Prof.||Preventive Medicine||Cardiovascular disease epidemiology||Preceptor|
|Chandel, Navdeep S.||PhD||Prof.||Medicine- Pulmonary and Critical Care||Mitochondria as signaling organelles, metabolism||Preceptor|
|Coates, Bria M.||MD||Asst. Prof.||Pediatrics||Differences in the inflammatory response to viral respiratory infections in children and adults||PreceptorIn-Training|
|Dada, Laura A.||PhD||Res. Assoc. Prof.||Medicine- Pulmonary and Critical Care||Acute lung injury, alveolar epithelial cell biology, effect of hypoxia and hypercapnia on lung function; ubiquitination in lung disease||Preceptor|
|Gates-Hill, Khalilah L.||MD||Asst. Prof.||Medicine- Pulmonary and Critical Care||Effects of hypercapnia on pulmonary host defense and immune mechanisms that contribute to pulmonary disease||PreceptorIn-Training|
|Gottardi, Cara J.||PhD||Assoc. Prof.||Medicine- Pulmonary and Critical Care||Molecular mechanisms of cell-cell adhesion regulation required for normal tissue morphogenesis; how alterations in cell adhesion complexes drive disease states such as cancer, fibrosis and asthma||Preceptor|
|Hauser, Alan R.||MD, PhD||Prof.||Microbiology -Immunology||Pathogenesis of healthcare-associated bacterial pathogens||Preceptor|
|Hersam, Mark C.||PhD||Prof.||Materials Science and Engineering||Scanning probe microscopy; semiconductor surfaces; nanoelectronics; nanophotonics; sensors; carbon nanotubes; graphene||Preceptor|
|Jain, Manu||MD||Prof.||Medicine- Pulmonary and Critical Care||Respiratory diseases, cytokines, lungs and breathing problems -- ARDS, sepsis, cystic fibrosis- bacterial genotypic and phenotypic diversity, mechanisms of fibrosis in lung disease||Preceptor|
|Kalhan, Ravi||MD||Associate Prof.||Medicine- Pulmonary and Critical Care||Asthma, COPD, respiratory epidemiology||Preceptor|
|Kamp, David W.||MD||Prof.||Medicine- Pulmonary and Critical Care||Asbestos, air-borne particulate matter, idiopathic interstitial lung disease||Preceptor|
|Lam, Ai (Anna) P.||MD||Asst. Prof.||Medicine- Pulmonary and Critical Care||Understanding the fundamentals of how the lung responds to injury and how this resultant abnormal wound healing leads to fibrotic diseases of the lung, in order to translate these findings into the development of novel therapeutic strategies for pulmonary fibrosis||Preceptor|
|Liu, Jing||PhD||Associate Prof.||Medicine- Pulmonary and Critical Care||Signaling by JNK and NF-kB in cell death, inflammation and tumorigenesis, COPD||Preceptor|
|Misharin, Alexander V.||MD/PhD||Asst. Prof.||Medicine- Pulmonary and Critical Care||Macrophage biology in the context of lung diseases, aging, transcriptomics||Preceptor In-Training|
|Morimoto, Richard I.||PhD||Prof.||Molecular Biosciences||Stress responses and chaperone networks and mechanisms of protein conformational disease||Preceptor|
|Ridge, Karen M.||PhD||Prof.||Medicine- Pulmonary and Critical Care||Acute lung injury, alveolar epithelial cell biology, macrophage cell biology, inflammasome, mechanotransduction in the lung||PD/PI, Exec. Comm, Preceptor|
|Schleimer, Robert P.||PhD||Prof.||Medicine- Allergy-Immunology||Mechanisms of pathogenesis in allergic disease; role of cytokines and chemokines, mechanism of action of glucocorticoids; role of innate and adaptive immune responses in airways; translational investigations in humans to molecular biological assessment||Preceptor|
|Schumacker, Paul T.||PhD||Prof.||Pediatrics||Cellular mechanisms underlying oxygen sensing, and the role of mitochondrial redox signaling in promoting survival, proliferation and metastatic behavior of tumor cells||Preceptor|
|Seed, Patrick C.||MD/PhD||Prof.||Pediatrics||Host mucosal-microbial interactions and the early-life microbiome||Preceptor|
|Shilatifard, Ali||PhD||Prof.||Biochemistry and Molecular Genetics||Molecular mechanisms underlying leukemogenesis and potential targets for therapy through detailed studies of proteins and protein complexes that regulate chromatin modifications, transcription initiation, and transcription elongation||Preceptor|
|Singer, Benjamin D.||MD||Asst. Prof.||Medicine- Pulmonary and Critical Care||DNA methylation as a determinant of T-cell function in the injured lung||PreceptorIn-Training|
|Smith, Lewis J.||MD||Prof.||Medicine- Pulmonary and Critical Care||The role of diet and obesity in asthma, including the effect of dietary antioxidants, soy isoflavones and other interventions||Preceptor|
|Sporn, Peter H.||MD||Prof.||Medicine- Pulmonary and Critical Care||Airway inflammation and remodeling; mechanical stress and airway remodeling; hypercapnia and innate immunity in the lung||Preceptor|
|Starren, Justin B.||MD, PhD||Prof.||Preventive Medicine- Health and Biomedical Informatics||Biomedical informatics; health informatics; data science, precision medicine; computational biology; information systems; internet intervention; medical informatics; post-graduate medical education||Preceptor|
|Sznajder, Jacob I.||MD||Prof.||Medicine- Pulmonary and Critical Care||Acute respiratory failure, alveolar epithelial cell biology, effect of hypoxia and hypercapnia on lung and muscle function; proteostasis and ubiquitination in lung disease||PD/PI, Exec. Comm, Preceptor|
|Winter, Deborah R.||PhD||Asst. Prof.||Medicine- Rheumatology||Mapping the gene regulatory networks of immune cells in health and disease, particularly macrophages in rheumatic disease, biomedical informatics||Preceptor In-Training|
|Wunderink, Richard G.||MD||Prof.||Medicine- Pulmonary and Critical Care||Diagnosis, pathogenesis, epidemiology, treatment, and prevention of infections in the critically ill, especially community-acquired pneumonia and hospital-acquired pneumonia; quality improvement in the ICU; septic shock; acute respiratory distress syndrome (ARDS)||Co-Director,Exec. Comm., Preceptor|
T32 Executive Committee
Meet current trainees and learn more about their research projects; view a list of trainee publications on PubMed.
Paul Reyfman, MD
Mentor: G.R. Scott Budinger, MD
Dr. Reyfman is performing research with his mentors Drs. Budinger and Amaral. His primary project is using systems biology approaches to study aging in the lung and the mechanisms of aging-related susceptibility to lung diseases. He is constructing a transcriptional map of aging in the murine lung using RNA-seq applied to two key lung cellular constituent populations: alveolar macrophages (AMs) and alveolar type II epithelial (AT2) cells. Messenger RNA from AMs and AT2 cells has been collected and sequenced from mice at six ages over the lifespan: 2 weeks, and 3, 6, 12, 18, and 24 months both at rest and after infection with the influenza A virus. Dr. Reyfman is also involved in projects to use in droplet based single cell RNA-Seq (10X genomics) for the analysis of human lung tissue and in murine models of lung disease. He has developed novel computational tools to combine single cell RNA-Seq data from more than 60,000 single cells obtained from lung explants from patients with pulmonary fibrosis and the corresponding donor lung. Dr. Reyfman is also completing a degree in Master of Science in Health and Bioinformatics.
James Walter, MD
Mentor: Scott Budinger, MD
Pseudomonas aeruginosa pneumonia is one of the most common hospital-acquired infections, and treatment failure even with appropriate antibiotic therapy is common. Innovation is needed to improve our ability to rapidly identify patients with P. aeruginosa pneumonia who are at high risk of treatment failure to guide the use of targeted therapies and refine enrollment in clinical trials. At Northwestern Medicine, non-bronchoscopic bronchoalveolar lavage (NBBAL) is routinely used to sample alveolar fluid from mechanically ventilated patients with pneumonia. Dr. Walter, Dr. Shah and his colleagues have taken advantage of this unique resource to develop and validate techniques to measure the transcriptome of flow-sorted alveolar macrophages and to assess the DNA alveolar microbiome. Dr. Walter will perform these measures serially in patients with P. aeruginosa pneumonia to test the hypothesis that treatment failure in patients with P. aeruginosa pneumonia can be identified by a unique host transcriptomic response to the pathogen and treatment-related alterations of the microbiome. First, serial NBBAL samples will be collected from 50 mechanically ventilated patients with P. aeruginosa pneumonia and 50 uninfected controls. Both resident and recruited alveolar macrophages will be isolated using fluorescence-activated cell sorting. Standard bioinformatics tools will be applied to compare gene expression profiles between treatment responders and non-responders, and machine learning approaches that incorporate clinical data will be used to predict the response to treatment. From these analyses, Dr. Walter will identify clinical and transcriptomic signatures that predict treatment failure. Then he will perform shotgun metagenomic sequencing of alveolar fluid from these NBBAL samples to identify patterns in the alveolar microbiome that predict outcome in severe P. aeruginosa pneumonia.
Chiagozie Pickens, MD
Mentor: Richard Wunderink, MD
Dr. Pickens’s first research project has focused on validating a rapid diagnostic test that detects bacteria directly from whole blood. This test, the T2 Bacteria panel, was developed by T2 Biosystems and can detect Eschericia coli, Staphylococcus aureus, Acinetobacter baumannii, Pseudomonas Aeroginosa, Klebsiella pneumonia, and Enterococcus faecium within five hours. To first determine the operating characteristics of this test, Dr. Pickens retrospectively screened 895 samples and ran 62 of the samples on the T2Dx instrument. Running each sample involved thawing the samples, pipetting the sample into the T2 cartridge, and assembling the assay to load into the instrument. Dr. Pickens performed basic analysis comparing the result from the T2Bacteria panel to the result from traditional bacteria culture. These data were presented at the Associate for Molecular Pathology Conference. Dr. Pickens has submitted a protocol to the Institutional Review Board to prospectively study this diagnostic test in 300 patients with sepsis or septic shock. The protocol is close to approval and the study is anticipated to begin in January 2018.
Jacqueline Kruser, MD, MS
Mentor: Richard Wunderink, MD
Dr. Kruser is a health services researcher focused on improving patient-centered care for patients with critical illness. During her internal medicine residency, she joined an interprofessional health services research team and developed a novel communication tool to improve high-risk surgical decision-making for patients and their families called “Best Case/Worst Case.” Dr. Kruser gained experience using qualitative methods to investigate latent phenomena in complex decision-making, developing a patient-centered communication intervention, and pilot testing the intervention in a clinical trial.
SeungHye Han, MD, MPH
Mentors: Navdeep Chandel, PhD,
Co-Mentor: Scott Budinger, MD
Dr. Han’s long-term research goal is to find a new therapeutic target to promote lung repair in patients with acute respiratory distress syndrome (ARDS). The main objective of Dr. Han’s current project is to determine the role of mitochondrial complex I on postnatal lung development and lung repair after influenza viral infection, and to identify metabolites and candidate pathways that link complex I driven respiration to lung stem/progenitor cells.
Cong Chen, PhD
Mentor: Jing Liu, PhD
Signaling through the transcription factor NF-kB plays a critical role in the development of acute and chronic lung diseases including pneumonia and COPD. While working in Dr. Liu’s laboratory, Dr. Chen made important contributions to her discovery that the transcription factor Miz1 is induced by TNF signaling and subsequently interacts with C/EBPd to act as a transcriptional repressor that dampens NF-kB signaling. They used a murine model of P. aeruginosa pneumonia to show this pathway plays a key role in the production of cytokines necessary for bacterial clearance. Dr. Chen went on to generate mice with tissue specific deletions of Miz1 in the lung. He found that mice lacking Miz1 in the lung epithelium (but not in inflammatory cells) demonstrated spontaneous age-related emphysema. He has gone on to show the importance of Miz1 in murine models of cigarette smoke induced emphysema and in patients with end stage emphysema undergoing lung transplantation. He is currently working with a genetic deletion system to determine whether inflammation induced senescence of the epithelium is responsible for these phenotypes.
Elizabeth Malsin, MD
Mentor: David Kamp, MD
Co-Mentor: Anna Lam, MD
Reactive oxygen species generated in multiple stress-related and pro-inflammatory pathways lead to oxidative mitochondrial DNA (mtDNA) damage, which has been demonstrated in multiple pulmonary disease states: asbestosis, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and the aging lung. Repair of mtDNA damage via 8-oxo-guanine DNA glycosolase (OGG-1) has been demonstrated to ameliorate the fibrosis seen in asbestosis. Outside the lung, there is evidence that mtDNA repair also regulates activation of the NLRP3 inflammasome; in a murine model of atherosclerosis OGG knockout mice had increased inflammatory markers and larger atherosclerotic plaques, but selectively eliminating the NLRP3 response reversed this phenotype. The intermediate filament vimentin has also been shown to be necessary to activate the NLRP3 inflammasome; vimentin knockout mice have attenuation of the markers of acute lung injury when challenged with known pulmonary toxins. Dr. Malsin’s current research investigates the link between mtDNA damage and the NLRP3 inflammasome in acute lung injury and whether vimentin is a necessary upstream, downstream, or bidirectional component in this pathway.
Leah Billingham, BA
Mentor: Navdeep Chandel, PhD
Two main ways that mitochondria signal are through the generation of reactive oxygen species (ROS) and metabolic intermediates. The mitochondrial electron transport chain (ETC) generates ROS at complexes I (CI) and III (CIII) as it passes electrons from NADH and FADH2 to ubiquinone and then oxygen. The relative levels of metabolites in the cell can dictate cellular outcome. A primary example of such regulation by metabolites is in epigenetics, with TCA cycle intermediates acting as substrates or competitive inhibitors for histone demethylases. Immune cell fate and function are driven by changes in metabolism. Macrophages exist on a spectrum from inflammatory to anti-inflammatory, acting as the first line of defense against infection and as the cleanup crew involved in tissue and wound repair, respectively. Polarization of macrophages requires specific metabolic profiles. Ms. Billingham plans to utilize unique genetic approaches and pharmaceutical interventions to elucidate the mechanisms by which ETC function and metabolic signaling is required for polarization of macrophages and response to inflammatory stimuli.
Alexandra Berr, BS
Mentor: Karen Ridge, PhD
Cellular migration plays a key role in the development of lung disease, particularly lung cancer, where cellular migration is necessary for both local and metastatic tumor progression and in pulmonary fibrosis where motile myofibroblasts play a key role in disease pathogenesis. The Ridge lab has used mice genetically deficient in vimentin to show that this intermediate filament protein is necessary for cellular migration and also serves as a cellular scaffold required for activation of the inflammasome in response to injury. Ms. Berr has been involved in two projects in Dr. Ridge’s laboratory focused on the importance of vimentin for cellular migration during lung cancer and fibrosis. In her first project, Ms. Berr seeks to understand the molecular underpinnings of an observation by the Ridge laboratory that vimentin-null cells were unable to metastasize in a mouse model of lung adenocarcinoma by studying signaling by TGF-b and Akt in a cellular model of tumor migration through Matrigel-coated transwells, and in murine models of lung adenocarcinoma.
Ziyou Ren, BS
Mentors: Luis Amaral, PhD, and G.R. Scott Budinger, MD
Pulmonary fibrosis is a devastating disease characterized by the excessive deposition of extracellular matrix. The increased matrix results in a progressive decline in lung function, which manifests clinically as worsening shortness of breath, respiratory failure and death. While newer therapeutics can slow disease progression through mechanisms that remain obscure, virtually all patients continue to suffer from progressive disease that eventually results in death or lung transplantation. Single cell transcriptomic analysis (scRNA-seq) offers promise for the identification of pathways that can be targeted for therapeutic development, the development of molecular biomarkers that can predict the response to therapy, and understanding the complex relationships between the more then 40 cell populations present in the lung during disease.
Program Expectations and FAQ
Each trainee is expected to have their research results accepted for publication. Each trainee is expected to attend all Pulmonary Research In Progress conferences and present their research at our Lung Symposium. All trainees are expected to complete the Responsible Conduct of Research course. All trainees are expected to submit and abstract and attend a national or international conference related to their research. Each trainee is expected to create an Individual Development Plan with their mentor which will be reviewed annually.
The training grant provides:
- Stipend support for the development of physician, pre-doctoral, and post-doctoral research scientists.
- Mentorship by senior investigators.
- The laboratory environment, training and supervision required for the development of independent investigators.
- The educational resources in the form of didactic courses, invited speakers and collaborative interactions that will foster the skills required for an independent research career.
- Administrative structure that will facilitate the trainee’s acquisition of protected time from activities not directly related to research.
What is a Payback Obligation and how do I know if I incur one?
Any NRSA postdoctoral trainees or fellow incurs a payback obligation during their first year of support. Pre-doctoral NRSA trainees do not incur a payback obligation. Payback means that you will perform qualified research or teaching activities for a length of time equal to the period of NRSA support you received. Receiving 12 months of postdoctoral training support obligates you to perform 12 months of qualified research or teaching activities as payback. Only the first year of training incurs a payback obligation; the second year of training pays back the first year, with each month of qualifying payback activity paying back one month of NRSA support. If you receive two full years of NRSA training, you will have completed your payback obligation. In general, payback activity must involve at least 20 hours per week and be conducted over 12 consecutive months. Special exceptions to these requirements may be considered on a case-by-case basis.
See a list of resources dedicated to T32 trainees. All trainees are encouranged to join the Department of Medicine New Investigator Career Enhancement (NICE) group and vist the NIK T32 Kiosk.
Diversity and Inclusion
The Department of Medicine at Northwestern University seeks to attract inquisitive, motivated residents and fellows and is committed to providing them with every opportunity for success. The greatest challenges facing the medical field are complex, and addressing them will require a diverse body of physicians and researchers who can work collaboratively. Northwestern offers unparalleled training and research opportunities and encourages fellowship applications from those who seek to become future leaders in the subspecialties of medicine. We are committed to and inspired by a diverse and inclusive work environment that allows each trainee to achieve their personal goals.
For more information on Northwestern’s commitment to diversity please see the following resources: