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.
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|
|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||Preceptor In-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|
|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|
|Han, Seunghye||MD||Asst. Prof.||Medicine- Pulmonary and Critical Care||The role of epithelial mitochondrial dysfunction in chronic lung inflammation and fibrosis||Preceptor In-Training|
|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|
|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|
|Morales-Nebreda, Luisa||MD||Asst. Prof.||Medicine- Pulmonary and Critical Care||The impact of epigenetic changes with aging on the reparative role of Tregs after pneumonia||Preceptor In-Training|
|Morimoto, Richard I.||PhD||Prof.||Molecular Biosciences||Stress responses and chaperone networks and mechanisms of protein conformational disease||Preceptor|
|Pickens, Chiagozie||MD||Asst. Prof.||Medicine- Pulmonary and Critical Care||Identification and characterization of clinical and molecular phenotypes in severe pneumonia||Preceptor In-Training|
|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|
|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||Preceptor In-Training|
|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|
|Vaughan, Douglas E||MD||Prof.||Medicine-Cardiology||Mammalian plasminogen activator system and the role this system plays in cardiovascular disease and aging.||Preceptor, Mentor|
|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|
Meet current trainees and learn more about their research projects; view a list of trainee publications on PubMed.
Joseph Bailey, MD
Mentor: Ravi Kalhan, MD
As the COVID-19 pandemic has progressed, thousands of Americans have found themselves suffering from a prolonged course of illness with a wide range of symptoms, such as brain fog, breathlessness, fatigue, chest pain, and others. These symptoms are collectively referred to as Post-Acute Sequelae of SARS-CoV-2 (PASC). The risk factors for developing PASC are unknown, as are its duration and long-term health effects. PASC symptoms may significantly affect people's ability to work, care for themselves and their families, and participate in their communities for years to come. I have worked to establish myself within this burgeoning area of research.
To investigate this developing clinical syndrome, Dr. Bailey has worked with leadership at Northwestern Medicine to develop the Northwestern Comprehensive COVID-19 Center (CCC). This center was established based on a multidisciplinary commitment to provide comprehensive care, aligned with embedded research, to every patient experiencing any sustained impact of SARS-CoV-2 infection. To date, the center has evaluated over 1100 patients. Working with Dr. Sznajder, he is preparing a manuscript describing the clinical phenotypes of patients within this center, to characterize long COVID. He has developed a research program consenting patients within the CCC for biospecimen collection and have spearheaded collection of bronchoalveolar lavage (BAL) fluid from over 30 patients. He is preparing a manuscript correlating imaging improvement in these patients with monocyte-derived alveolar macrophages within BAL fluid.
However, referral bias limits the validity of the CCC as an exclusive source of data to understand the true incidence of PASC, its risk factors, and how it has impacted the lives of individuals previously infected with SARS-CoV-2. To address this, Dr. Bailey has worked with Dr. Kalhan to develop COVID-19 Clinical Recovery Cohort. This is a low-touch electronic survey study of all survivors of COVID-19 within the NM system. This project received a pilot grant from the Northwestern University Clinical and Translation Sciences Institute. This study seeks to better understand the prevalence, characteristics, and risk factors of PASC as well as the long-term financial, psychosocial, and physical recovery of SARS-CoV-2 patients throughout the Chicago metropolitan area. By providing this new and critical knowledge, this study will help providers at NM and around the nation understand and treat the long-term effects of SARS-CoV-2 infection.
Catherine A. Gao, MD
Mentors: Richard Wunderink, MD; Luís A. Nunes Amaral, PhD
The COVID-19 pandemic has presented challenges but also opportunities to address fundamental questions in the care of critically ill patients with respiratory failure from pneumonia. There is much still we do not understand about this population of patients with either COVID pneumonia, non-COVID viral pneumonia, and bacterial pneumonias. As the amount of electronic medical record data grows, it provides endless opportunities for analysis. Dr. Gao hopes to serve as a physician bridge between the electronic data warehouse team and clinicians. Data science will only grow to be more important in the analysis of clinical data, and she hopes the skills she develops will lead to further collaboration and scientific discoveries. She is working with an expert in the field of pneumonia and critical care, Dr. Richard Wunderink, to dissect bronchoalveolar lavage characteristics, bacterial and fungal super-infections, and outcomes for the COVID-19 patients. To further her technical analytical skills of data science and to learn advanced modeling and machine learning techniques, she’s learning from the lab of Dr. Luis Amaral, a multi-disciplinary data science expert, who directs a university center to foster quantitative data scientific research across all academic disciplines. Clinical questions she hopes to answer include the effects of steroids on bronchoalveolar lavage characteristics and superinfection among COVID-19 patients, and modeling predictors of outcomes after critical illness. Dr. Gao recently received a fundable score on an NIH F32 proposal.
Gabrielle Liu, MD
Mentor: Ravi Kalhan, MD
Dr. Liu’s current research interest is in examining the significance of interstitial lung abnormalities (ILA) seen on chest CT scans of healthy participants in the CARDIA Lung study, an ongoing, multi-center, longitudinal cohort study spanning 35 years which is led at Northwestern (Kahlan, PI). Under the leadership of her research mentor, Ravi Kalhan, and in collaboration with George Washko and Rachel Putman at Brigham and Women’s Hospital/Harvard Medical School, she will be reviewing the CT scans obtained at year 25 and year 35 after enrollment to evaluate for ILA and other evidence of lung fibrosis. She will then be able to use this data to identify early predictors of ILA and better understand the natural progression of ILA and their clinical significance. Her longer-term research goals also involve working with data from the Lung Health Cohort, another study led at Northwestern (Kalhan, PI) and the first longitudinal cohort of healthy 25-35 year olds in the US specifically designed to study ideal respiratory health and the transitions to impaired health and chronic lung disease. With identification of the risk factors and biomarkers associated with these transitions, she hope to find ways to intervene to halt the development of lung disease. In February 2022, Dr. Liu received an NIH F32 award which aims to provide a target for the interception of impaired respiratory health which may progress to ILD.
Taylor Poor, MD
Mentor: Navdeep Chandel, PhD
Dr. Poor joined the laboratory of Dr. Chandel in July 2019 and since that time has been rapidly learning multiple new techniques used in the study of mitochondrial function and immunometabolism. Dr. Chandel’s laboratory has shown that mitochondrial function is critical for the proper function of immune cells and plays an important role in cancer biology. Since joining the laboratory, Dr. Poor has been learning mouse genetics and has established breeding programs to develop multiple new lines of mice containing tamoxifen-inducible knockouts of various metabolic proteins. He has also been learning how to isolate primary cells directly from mouse tissue, as well as the mRNA, protein, and functional assays (such as measuring the oxygen consumption rate) that are used to study the effects of these novel constructs on the function of mitochondria. Over the next several months, Dr. Poor will be using these mice and techniques to begin studying how mitochondrial function in myeloid cells is required for clearance and repair of lung tissues in influenza infection.
Andrew D. Prigge, MD
Mentor: Karen M. Ridge, PhD
Viral pneumonia disproportionately affects young children and can progress to life threatening disease. Children with severe viral pneumonia typically present to the pediatric intensive care unit with an established infection and lung injury. Current therapies are supportive and do not alter the pathology of severe viral pneumonia or accelerate recovery. In murine models of viral pneumonia, juveniles exhibit a persistent, excessive inflammatory response relative to adults despite adequate viral clearance. The resulting injury suggest juveniles fail to resolve inflammation and repair the alveolar epithelium. Observations in children and murine models suggest an inadequate T cell response contributes to impaired recovery. Regulatory T cells (Tregs) are a subset of CD4+ T cells that play an essential role in mediating the resolution of inflammation and repair of tissue. Adult murine models define an essential role for Tregs in recovery from viral pneumonia, however studies in age-appropriate murine models are lacking. The focus of this project is to determine the role of Tregs during recovery from viral pneumonia in children using an age-appropriate juvenile mouse model that recapitulates clinical disease.
Since joining the NULSTP in July 2021, Dr. Prigge has been learning new research techniques, training in computer programming and data analysis, applying to extramural grants, and has published a first authored manuscript. One of his career development goals is to develop expertise in pediatric lung biology and T cell immunology. To achieve this goal, he is training in the methodologies and techniques required to investigate recovery and repair mechanisms through hands-on experience in the Ridge laboratory. He has utilized these skills to generate preliminary data suggesting juveniles Tregs fail to mitigate excessive inflammation and promote lung repair following influenza infection. These preliminary data have formed the foundation of extra mural grant applications submitted in the previous 6 months. In parallel, he published a co‑1st author manuscript demonstrating age-related differences in the expression of genes involved in T cell receptor signaling in children and adults with asymptomatic to mild SARS-CoV-2. The study additionally reported that SARS-CoV-2 infected children and adults mount an interferon response in the nasal mucosa similar in magnitude to children infected with respiratory syncytial virus. Notably, they found that expression of ACE2 and TMPRSS2, key entry factors for SARS-CoV-2, did not correlate with age. He has submitted another co-1st author manuscript that describes an association between nasal gene expression and clinical outcomes in children with critical respiratory syncytial bronchiolitis. They obtained nasal mucosal samples early in hospitalization when participants were clinically indistinguishable. Retrospectively, they divided participants by the duration of non-invasive respiratory support required and found an association with the nasal gene expression.
Mentor: Karen Ridge, PhD
Mr. Anakella's research focuses on understanding how viral pneumonia affects the cardiopulmonary system and cause cardiovascular complications such as heart failure, cardiac arrhythmias, and stroke in the elderly. Patients with pneumonia have high circulating levels of cytokines and chemokines that are necessary to control the infection by increasing chemotaxis and generating leukocyte extravasation into the lungs; however, persistent or uncontrolled inflammation increases tissue damage and impairs cardiac function (i.e. heart inotropism is diminished in hearts exposed to high concentrations of cytokines). Importantly, there is growing evidence of prolonged systemic inflammation long after the virus has been cleared. Thus, systemic inflammation in the elderly due to viral pneumonia is an important and modifiable risk factor for CVD. Monocyte-derived alveolar macrophages (MoAMs) are the major effector cells in host defense against respiratory infections and play a critical role in the pathobiology of viral pneumonia. He, and others, have previously shown that MoAMs with a proinflammatory phenotype are recruited in mouse models of lung injury, such as bleomycin and LPS treatment. Preliminary data shows that morbidity during influenza A virus (IAV) infection is much higher in aged mice than in young mice. Based on this, Mr. Anakella hypothesizes that the aging lung microenvironment triggers an increased pro-inflammatory response in MoAMs, leading to exacerbated systemic inflammation and impaired cardiac function during pneumonia. To address this hypothesis, he will perform time course RNA sequencing (RNA-seq) on the flow-sorted population of MoAMs from young and aged mice following influenza A virus infection. He will develop novel approaches to analyze time-course RNA-seq data. Under the joint mentorship of Dr. Karen Ridge and Dr. Deborah Winter, he will receive the training necessary to develop expertise in functional genomics and bioinformatic approaches to study cardiopulmonary diseases.
Mentor: Cara Gottardi, PhD
Ms. Quinn wants to explore the maintenance of epithelial barriers and how adhesion is regulated during morphogenetically challenging states. The Gottardi laboratory previously established that phosphorylation of a-catenin, a member of the primary cell-cell adhesion complex, promotes adhesive strength and is required in fly development. The dynamic control of a-catenin phosphorylation(i.e., where and when it occurs), however, remains completely unknown. Nor is it understood how this elaborate, multi-site modification alters epithelial adhesive barrier functions. They hypothesize that phosphorylation of a-catenin is crucial for controlling cell-cell adhesion during tensile events such as mitosis, so as to maintain barrier function during this morphogenetically challenging process. Preliminary data confirms that a-catenin is differentially phosphorylated throughout the cell cycle. Ms. Quinn’s thesis project aims to understand the upstream signals/pathways that drive these phosphorylations as well as downstream consequences for F-actin binding/epithelial barrier function. She will utilize phospho-mutant and phospho-mimic forms of a-catenin in epithelial cell lines and mouse models. With a spectrum of a-catenin responsiveness to biochemical and mechanical signals, she plans to employ flow cytometry, live cell imaging, fluorescence resonance energy transfer, and other collaboration-established methods. Over the course of her PhD, she will study a-catenin phospho-form localization, coupling to the cytoskeleton, and related conformational changes. These investigations demonstrate how cells integrate chemical and physical signals, which is crucial for pulmonary homeostasis and aberrant in cases of lung injury.
Manuel A. Torres Acosta
Mentor: Benjamin Singer, MD
Mr. Torres Acosta’s general research interests are centered around understanding the multifactorial nature of carcinogenesis, and his academic and professional careers have allowed him to explore many of these factors while developing skills that are essential to the arts of conducting science and communicating it. As an undergraduate at The Ohio State University(OSU), he had the opportunity to train in Dr. Gustavo Leone’s basic science lab for two years, where he researched the role of dysregulated cell cycle proteins in cancer. From this experience stemmed multiple funding opportunities, a successful thesis defense, and an unwavering commitment to pursuing a career in basic science research. During his undergraduate senior year, he worked in Dr. David Carbone’s translational research lab, where he was tasked to elucidate mechanisms through which cancer stem cells become chemo-resistant, and to conduct the sample preparation of a Brazilian population-based lung adenocarcinoma cancer study, for which he received the prestigious Pelotonia Undergraduate Research Fellowship. It was in this lab that he was exposed to advanced tasks independent investigators undertake such as grant writing and the nuanced publication process. Here, he also developed a desire to frame his future scientific goals and interests around facilitating advanced care to underrepresented communities in medicine such as the Latino community; as an underrepresented minority himself, he has become very passionate about this long-term career goal and has been proactive with pursuing leadership opportunities that allow him to grow as a present and future advocate for diversity and inclusion in science and medicine. Since graduating from OSU, he has been privileged with the opportunity to pursue a career as a physician scientist in Northwestern’s MSTP, where he is transitioning to the graduate phase after finishing his 2nd year of medical school. He has consistently maintained good academic standing, has become involved in the MSTP’s recruitment efforts as a Student Interview Captain, and has facilitated the spearheading of the MSTP’s first diversity and inclusion committee as committee chairman. He has also committed to pursue a PhD in Dr. Benjamin Singer’s lab, where the physiology and metabolism of regulatory immune cells and their role in lung injury resolution is being studied. By dedicating his PhD to the study of the immune system and the role of metabolism in maintaining homeostasis, he hopes to grow his understanding of how these same processes relate to carcinogenesis. Furthermore, he hopes to further develop his repertoire of lab techniques, begin to master the publication and grant writing processes, and continue to refine his scientific communication skills; under the wing of a seasoned physician-scientist like Dr. Singer, he is confident that this experience will enrich himself with the tools he needs to pursue the career in medical oncology he so desires.
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 encouraged to join the Department of Medicine New Investigator Career Enhancement (NICE) group and visit the NIH T32 Kiosk.
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. Khalilah Gates, MD, serves as the Diversity and Inclusion Committee Chair for the Training Program in Lung Science.
For more information on Northwestern’s commitment to diversity please see the following resources: