Research Awards Nationwide

Research Awards Nationwide 2012-2013This year’s Research Awards Nationwide is searchable. Please use the dropdown boxes to search by topic, state, or grant. If no topic or state is selected, all the information for that area will be displayed.

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  • ASTHMA CLINICAL RESEARCH CENTERS
    Co-funded by GlaxoSmithKline

    Long-acting Beta Agonist Step-Down Study (LASST)

    Current asthma guidelines recommend stepping down therapy once asthma is controlled for at least three months. For patients treated with inhaled corticosteroids (ICS) alone, a dose reduction of 25–50 percent to a minimal dose that controls disease is established. However, the optimal approach to reducing treatment in patients with asthma that is well-controlled on fixed dose combination ICS/LABA (long-acting beta agonists) is not clear. The study will compare three approaches of care to patients with asthma well-controlled for three months on combination ICS/LABA therapy: reduction of ICS dose and maintenance of LABA, initial discontinu-ation of LABA with continuation of ICS and continuation of stable dose ICS/LABA. The data will allow the de-termination of the optimal treatment strategy defined as that which results in the lowest rate of treatment failure over 48 weeks of follow up. Additional exploratory analyses will include assessing risk factors for step-down failure and assessing the optimal duration of time that asthma control should be maintained before therapy is reduced.

  • ASTHMA CLINICAL RESEARCH CENTERS
    Co-Funded by the National Institutes of Health’s National Heart, Lung and Blood Institute

    Effect of Positive Airway Pressure on Reducing Airway Reactivity in Patients with Asthma (CPAP)

    The development of alternative methods to drug use in improving asthma control is necessary. This study will test whether the use of CPAP, a current treatment for sleep apnea, will improve asthma control. CPAP rhythmi-cally increases airway pressure by applying external pressure through the nose or mouth to prevent large airway collapse during sleep. The researchers propose that applying the same rhythmic pressure to the smaller airways will reduce the airway constriction that occurs during an asthma attack. The results of this study may lead to prescribing CPAP to patients with difficulties in achieving asthma control. This proof-of-principle clinical trial will randomize 192 participants, with stable documented asthma and who do not have sleep disorders, into one of three treatment groups for 12 weeks. Treatment arms include: nocturnal CPAP 10 cm H2O, nocturnal CPAP 5 cm H2O and nocturnal sham CPAP (

  • ASTHMA CLINICAL RESEARCH CENTERS
    Co-Funded by the National Institutes of Health’s National Heart, Lung and Blood Institute

    Smoking Asthmatics Pilot Study (SAPS)

    About 20% of all people with asthma smoke. Smokers are consistently excluded from therapeutic trials for asthma. As a result current asthma treatment guidelines may not be appropriate for smokers. Indeed, there is good evidence that inhaled corticosteroids, the mainstay for treating persistent asthma, are less effective in smokers. The SAPS trial is designed to test the feasibility of a large scale clinical trial looking at the four main therapeutic options for asthmatic patients who still smoke and are not well controlled on standard asthma therapy. Smoking cessation remains the primary strategy for treating these patients but this study represents an important step toward improving care for that significant population of individuals with asthma for whom smoking cessation remains a struggle.

  • ASTHMA CLINICAL RESEARCH CENTERS
    Co-Funded by the National Institutes of Health’s National Heart, Lung and Blood Institute

    Use of Mobile Devices and the Internet to Streamline An Asthma Clinical Trial (MICT)

    Finding participants for research trials is not easy, likely because of the time and effort required on the partic-ipant’s part as well as logistical barriers. The MICT trial will study whether the use of mobile devices and in-ternet technology make clinical trials more convenient and cost effective. Participants in the study will be pro-vided an iPad to take home to complete questionnaires and health information diaries. Rather than coming to the clinic for their appointments, they will utilize FaceTime, a live, video-telephone software application de-veloped by Apple that is built into the device. This will allow them to have real-time interaction with the study staff in the comfort and convenience of their home. Depending on the results of this clinical trial pilot, and, if full-scale clinical trials are conducted, this could potentially change the way that clinical trials are completed in the future, resulting in the potential for even more medical breakthroughs.

  • AUDREESH BANERJEE, MD
    University of Pennsylvania, Philadelphia, PA
    Biomedical Research Grant

    How Class of Drugs Decreases Airway Hyperresponsiveness

    Histone deacetylase inhibitors are a class of drugs which are being evaluated for use in a variety of diseases. It has been proposed that these drugs decrease airway hyperresponsiveness (over reaction to stimuli), which is a hallmark of asthma. These drugs will be given to mice, some with experimentally-induced asthma, to further improve the understanding of how histone deacetylase decreases airway hyperresponsiveness.

  • XIAOYONG BAO, PhD
    University of Texas Medical Branch, Galveston, TX
    Biomedical Research Grant

    Developing Vaccine Against Virus That Can be Deadly in Children

    Human metapneumovirus (hMPV) has been identified as a leading cause of bronchiolitis, pneumonia, lung failure, and asthma exacerbations in children under age 5. Dr. Bao and team recently discovered that the pro-tein M2-2 inhibits the human immune response to hMPV and helps sustain and grow the virus. The research-ers have identified two molecular mechanisms that M2-2 uses to combat host immunity as well as domains responsible for its inhibitory role. Agonists that trigger immune responses are currently being tested to en-hance immune responses against viruses, which could lead to safer and more effective vaccine candidates and therapeutic molecules modifying M2-2-host interaction.

  • MALLAR BHATTACHARYA, MD
    University of California, San Francisco, San Francisco, CA
    Biomedical Research Grant

    Blunting Airway Constriction in Asthma

    In an asthma attack, the airways of the lung constrict because of the contraction of a type of muscle known as smooth muscle. Using a mouse model of human asthma, Dr. Bhattacharya will study airway hyperresponsive-ness, or oversensitivity. He has identified a protein known as IQGAP1 that appears to blunt the constrictive re-sponse of smooth muscle when it is triggered by a substance called acetylcholine. He hopes to uncover the way in which IQGAP1 relaxes smooth muscle contraction. By broadening the understanding of smooth muscle con-traction, Dr. Bhattacharya hopes to identify new pathways that could lead to novel treatments for airway con-striction in asthma.

  • TREVER BIVONA, MD, PhD
    University of California, San Francisco, San Francisco, CA
    Lung Cancer Discovery Award

    How to Reduce Resistance to Tarceva

    Personalized treatments that are specifically targeted to the genetic cause of an individual patient's lung can-cer have become available and are less toxic and more effective against specific tumors. Dr. Bivona’s research is based on his team’s discovery that the protein AXL causes resistance to Tarceva in lung cancer. Tarceva is a targeted therapy that is effective but does not result in cures because lung cancers develop resistance to the drug. Dr. Bivona’s goal is to define how best to use inhibitors of AXL along with Tarceva to improve the survival of lung cancer patients.

  • THOMAS BRETT, PhD
    Washington University, St. Louis, MO
    Biomedical Research Grant

    Understanding Mucus Overproduction in Asthma

    Mucus acts as a protective barrier and filter by coating the lining of organs to trap foreign substances, pre-venting them from invading the body and causing sickness. A number of lung diseases can cause excess mucus to build up in the lungs leading to coughing and difficulty breathing. Using advanced biochemical and structural biology techniques, Dr. Brett and his team will examine how a protein called CLCA1 works to mediate the overproduction of mucus. This information will be used to develop inhibitors to CLCA1 that could be used as anti-mucus treatments for asthma.

  • TIMOTHY BURNS, MD, PhD
    University of Pittsburgh, Pittsburgh, PA
    Lung Cancer Discovery Award

    Determining How Two Genes Interact in Lung Cancer

    Recent advances in the treatment of lung cancer have confirmed that the disease is not a single disease entity but rather a collection of distinct cancers driven by cancer genes called oncogenes which cause the tumors to grow. This knowledge has led to the development of targeted therapies for a percentage of patients. One im-portant oncogene, c-MET, is required for a tumor to grow while another gene, TWIST 1, has been shown to regulate the c-MET gene. This study will determine how these two genes interact and how drugs may modu-late their activity.

  • FLORENT CARRETTE, PhD
    Sanford-Burnham Medical Research Institute, Orlando, FL
    Senior Research Training Fellowship

    Investigating How Immune Cells Respond to Influenza Virus

    A subset of cells in the immune system, called CD8 T lymphocytes, are essential for killing cells infected with the flu virus. Yet, understanding how these cells respond to the influenza virus and protect individuals from repeat infections are limited. In this project, Dr. Carrette and team will investigate the mechanisms involved in controlling the generation of memory CD8 T lymphocyte pool during an influenza infection, with the ultimate goal to discover new targets to improve vaccine strategies.

  • KAREN CAVASSANI, PhD
    University of Michigan, Ann Arbor, MI
    Dalsemer Research Grant

    Protective Role of Receptor in Pulmonary Fibrosis.

    Under certain disease conditions, myofibroblasts accumulate in the lungs causing excess tissue scarring and impaired lung function. While the lung has an innate ability to prevent scarring, little is known about how my-ofibroblasts trigger anti-fibrotic factor(s). This research will examine the regulation of processes in the lung which limit scarring in the face of agents which ordinarily promote it.

  • CHEN-HUA CHUANG, PhD
    Stanford University, Stanford, California
    Senior Research Training Fellowship

    Molecular Biography of Lung Cancer Metastasis

    It is unclear as to how lung cancer cells gain the ability to invade into surrounding tissue, spread to distant or-gans, and successfully form metastases. Dr. Chuang’s research will characterize the gene expression changes that drive lung cancer invasion and metastasis by assigning a unique barcode ID to every tumor cell to allow the easy connection of the primary lung cancer to the metastases it produced.

  • J. ROBERT COLEMAN, PhD
    State University of New York, Farmingdale, NY
    Biomedical Research Grant

    Funded in Partnership with support from the Mary Fuller Russell Research Fund

    New Streptococcus Pneumonia Vaccine Would Protect Against All Strains

    Streptococcus pneumonia (SP) is the leading cause of bacterial pneumonia in the United States and worldwide. There are two current vaccines for SP—one for adults and one for children. However, each is limited as neither vaccine protects against all 92 strains of SP that have emerged and caused disease in susceptible populations. Dr. Coleman and his team have begun to genetically re-design genes shared by all 92 serotypes to construct a ‘universal’ vaccine to produce a weakened strain that over-expresses ‘protective’ proteins. Some in the pneu-mococcal field have suggested that a whole-cell/live vaccine approach may be the most promising avenue to achieve 92-serotype protection and their project pursues this approach.

  • VINICIO DE JESUS PEREZ, MD
    Stanford University, Stanford, CA
    Biomedical Research Grant

    How Blood Vessel Cells Promote Pulmonary Arterial Hypertension

    Not much is known regarding the origin of Idiopathic pulmonary arterial hypertension (IPAH), a devastating disorder associated with the progressive increase in pulmonary pressure resulting from loss and impaired re-generation of small blood vessels. It has been postulated that failure of pericytes, a highly specialized blood vessel cell which helps to promote small vessel maturation and survival, leads to vascular dysfunction. This research will attempt to determine the role these blood vessel cells have in the origin of IPAH.

  • TAYLOR DOHERTY, MD
    University of California, San Diego, San Diego, CA
    American Lung Association/American Academy of Allergy, Asthma & Immunology Allergic Respiratory Disease Award

    How Do ‘Natural Helper Cells’ Lead to Asthma After Mold Exposure?

    Many people with asthma have lung inflammation that is worsened by triggers including allergens. Recently, a new population of white blood cells called “type-2 innate lymphoid cells or ILC2” have been discovered to produce several factors that may contribute to inflammation similar to that found in asthma. Dr. Doherty has detected ILC2 cells in the lungs of mice and has shown that the fungal allergen Alternaria rapidly activates these cells leading to airway inflammation. If ILC2 are shown to have a critical role in pathogenic immune re-sponses to Alternaria, the findings may lead to new therapeutic strategies for asthma.

  • JOYITA DUTTA, PhD
    Massachusetts General Hospital, Boston, MA
    Senior Research Training Fellowship

    Using PET/MRI Images in Late-Stage Lung Cancer Treatment

    Advanced non-small cell lung cancer (NSCLC) has only a 4% 5-year survival rate. Determining an optimal treatment plan for patients with late stage non-small cell lung cancer would help to improve the currently low probability of patient survival. Using new and emerging PET/MRI technology, the researchers hope to be able to first reconstruct a high quality 3D PET image of tumors from the motion information of the MRI and then correlate it with the actual outcome in patients. It is hoped that the motion-compensated PET/MRI image could assist in guiding treatment plans for non-small cell lung cancer.

  • MAHA FARHAT, MD
    Massachusetts General Hospital, Boston, MA
    Biomedical Research Grant

    Gene Mutations and Tuberculosis Resistance

    Anti-tuberculosis (TB) drug resistance is a major public health problem that threatens progress made in TB care and control. Drug resistance in TB is caused by genetic mutations. By investigating the genetic sequences of 28 known and 4 candidate resistant genes for a large panel of TB drugs, Dr. Farhat and team will attempt to determine which mutations predict the extent of resistance, and if specific combinations of mutations interact to affect this resistance level. The information will be used to guide the development of a much needed rapid diagnostic test for drug resistant TB.

  • YOICHI FURUYA, PhD
    Albany Medical College, Albany, NY
    Senior Research Training Fellowship

    Generating Future Protection Against Flu For Asthma Patients

    Having seasonal influenza virus should confer future protection against the same or similar virus strains. However, Dr. Furuya has found that asthmatic mice do not acquire strong immunity against a pandemic strain following natural immunization, and they have defective airway antibody responses. This may explain why pa-tients with asthma have increased susceptibility to both seasonal and pandemic influenza infections. The re-searchers are studying ways to stimulate antibody responses in asthmatic mice and why asthmatics cannot generate optimal antibody responses against secondary influenza virus infections. The findings may help de-velop better treatments or vaccinations against respiratory infections for people with asthma.

  • FABIENNE GALLY, PhD
    National Jewish Health, Denver, CO
    Biomedical Research Grant

    Protein Could Boost Immune System Against Cigarette Smoke

    Cigarette smoke is known to impair the immune system, reducing the body’s defense against bacterial infec-tions. A novel protein known as the Fatty Acid Binding Protein 5 (FABP5), has been identified as having a cen-tral role in modulating natural immunity. The concentration of this protein is reduced by cigarette smoke ex-posure. The researchers will examine the potential involvement of FABP5 in the reduction of lung immune re-sponse resulting from cigarette smoke exposure in white blood cells called monocytes. Dr. Gally and team ex-pect that the addition of FABP5 will protect monocytes against bacterial infection when exposed to cigarette smoke.

  • ARIS GARRO, MD, MPH
    Rhode Island Hospital, Providence, RI
    American Lung Association/The CHEST Foundation Asthma Clinical Patient Care Grant

    Which Children With Uncontrolled Asthma Need Inhaled Steroids?

    Many children with poorly controlled asthma use emergency departments (ED) for asthma care, but are in-frequently prescribed inhaled steroids at these visits. Dr. Garro and his team have recruited 33 families to compare whether those prescribed inhaled steroids in the ED will have better asthma control than children who receive routine asthma discharge instructions. He will also interview parents to identify what determines whether they fill the prescriptions and use the medicine appropriately. His research could determine the best way to assist emergency doctors in deciding which children should be prescribed inhaled steroids at ED dis-charge and how they can best educate families to give the appropriate medicines to their children.

  • GREGORY MARK GAUTHIER, MD
    University of Wisconsin, Madison, WI
    Biomedical Research Grant

    Funded in Partnership with the American Lung Association of the Upper Midwest

    Switching Between Mold and Yeast to Cause Infection in the Lungs

    Worldwide, dimorphic fungi (fungi that have two different forms) are the most common cause of invasive fungal infection. These fungi grow as mold in soil and produce infectious particles called spores. When the soil is dis-rupted, spores enter the air and can be inhaled into the lungs. Once inside humans’ warmer lungs, the spores convert into round, budding yeast to cause pneumonia. Dr. Gauthier and team will examine how these fungi sense temperature and convert between mold and yeast forms, allowing these organisms to cause human infec-tion. He will attempt to uncover the genes that regulate the switch between mold and yeast in the fungi. The re-sults have the potential to help identify novel antifungal drug targets and drugs which are desperately needed.

  • SERGEI GRANDO, MD, PhD, DSCI
    University of California, Irvine, CA
    Lung Cancer Discovery Award

    Funded by the American Lung Association of California

    Interfering in Tobacco’s Cancer-Causing Effect on Lung Cells

    Identifying the mechanisms by which tobacco leads to the cancerous transformation of lung cells may help in preventing lung cancer and enhancing the efficacy of drug treatment. Dr. Grando will investigate nico-tine-induced changes of binding of a hormone-like molecule called acetylcholine to its receptors on lung cells, called nicotinic acetylcholine receptors (nAChRs). He will determine if specific drugs that block the ability of can-cer-causing tobacco byproducts called nitrosamines to bind to lung nAChRs can also decrease their cancer-causing effect on lung cancer and lung tumor development in mice. The results will enhance understanding of the way in which tobacco exposure leads to cancer and help develop new treatment approaches.

  • PAMELA GUERRERIO, MD, PhD
    Johns Hopkins University, Baltimore, MD
    American Lung Association/American Academy of Allergy, Asthma & Immunology Allergic Respiratory Disease Award

    While current asthma therapies improve control of symptoms in many patients, there is little evidence that these treatments prevent or reverse the remodeling of the airways that results from repeated inflammation and injury. Airway remodeling leads to irreversible airway obstruction and worsening lung function in asthmatic children as young as 4 years old. Strong evidence suggests that airway remodeling results from overexpression of the molecule “transforming growth factor beta” (TGFbeta). Losartan, an FDA-approved drug that’s been safely used for years to treat patients with hypertension, has been found to down regulate TGFbeta signaling and is remarkably effective in treating conditions caused by excessive TGFbeta signaling. Dr. Guerrerio will test whether losartan can reduce TGFbeta signaling in the lungs of mice with asthma, and thereby improve lung function, reduce airway inflammation, and prevent and/or reverse airway remodeling. If this approach proves to be successful in mice, then human trials of losartan to treat asthma could follow quickly.

  • FINN HAWKINS, MB, BCh, BAO
    Boston University, Boston, MA
    Senior Research Training Fellowship

    Funded in Partnership with the American Lung Association of the Northeast

    Working Toward Regenerating Damaged Lung Tissue

    Patients with end-stage lung disease such as pulmonary fibrosis and cystic fibrosis, who are fortunate enough to receive a donor lung for are at risk of complications such as organ rejection and infections. An ideal alterna-tive would be to repair or regenerate damaged lungs. In 2006, scientists in Japan made a significant break-through when they discovered induced pluripotent stem cells (iPS)—adult cells that have been genetically re-programmed into a cell that has the ability to turn into any cell type in the body. Dr. Hawkins’ group has devel-oped a method to instruct iPS cells to begin the journey towards an adult lung cell. They are now testing the ability of corrected cystic fibrosis iPS to make functional ciliated cells.

  • DEBORAH WEIDE HENDRICKS, PhD * LUNG INFECTIONS SCHOLAR
    University of California, San Francisco, San Francisco, CA
    Senior Research Training Fellowship

    Learning How Immune Cells Fight Respiratory Infections

    When a cell is infected with a virus, natural killer cells (NK) respond rapidly, producing proteins that kill the cell directly or that helps other immune cells fight the virus. NK cells recognize certain viruses, and that they may “remember” their first encounter with a virus and provide better protection during the next infection. These qualities make vaccinations possible. Dr. Hendricks and team will study the function and characteristics of these NK cells during parainfluenza virus infection, a highly transmissible respiratory infection that is responsible for widespread illness especially among children, older adults and those with suppressed immune systems. The knowledge gained from this research could translate into better treatments for respiratory infections.

  • CAROLINE HERNDON, PhD
    The CBR Institute for Biomedical Research, Boston, MA
    Senior Research Training Fellowship

    Insights Into the Body’s Immune Response to Influenza

    Although vaccination against influenza usually causes a protective antibody response, the ability of the virus to mutate allows new strains to invade the immune system and cause infection. Studies in mice have shown that the ability of respiratory dendritic cells (RDCs) to bind influenza in the lungs and transport it to the lung-draining lymph node (LN) is critical for the start of the body’s immune response to influenza. Dr. Herndon will study these mechanisms, focusing on the complement system, a series of proteins that circulate in the blood and become activated in response to bacteria and viruses. This could lead to better strategies against influenza and other respiratory pathogens, such as dendritic cell-targeted vaccines.

  • KEVIN HILL, MD, MHS
    McLean Hospital, Belmont, MA
    Clinical Patient Care Research Grant

    TB Drug Could Aid Smoking Cessation

    A U.S. Food and Drug Administration (FDA) approved antibiotic for the treatment of tuberculosis may assist people attempting to quit smoking. Preliminary evidence suggests that the drug, known as D-cycloserine (DCS), when combined with nicotine replacement therapy (NRT) and cognitive behavioral therapy (CBT) may improve low rates of smoking cessation by enhancing a smoker’s ability to learn how to avoid smoking. If the drug is found effective in helping people to quit smoking, the translation into practice would be relatively quick, since this drug is already readily available.

  • LANDON INGE, PhD
    St. Joseph’s Hospital & Medical Center, Phoenix, AZ
    Biomedical Research Grant

    Compound Could Help Some Patients With Non-Small Cell Lung Cancer

    Non-small cell lung cancer (NSCLC) is a deadly disease, accounting for the majority of cancer-related deaths in the United States. Recent evidence points towards inactivation of the protein, LKB1, as playing a critical role in the progression of a large portion of NSCLC tumors. Work in Dr. Inge’s laboratory suggests that the compound 2-Ddeoxyglucose (2DG) may cause death to NSCLC tumors deficient for LKB1. Using a genetic mouse model of LKB1 deficient NSCLC, Dr. Inge and his team will attempt to validate 2DG as a therapeutic alternative and ex-plain the molecular mechanisms behind the anti-tumor activity of 2DG in LKB1 deficient NSCLC. This is signifi-cant, as patients lacking LKB1 face a poor prognosis. The findings will provide a new avenue for treatment of NSCLC.

  • FAYE JOHNSON, MD, PhD
    University of Texas M.D. Anderson Cancer Center, Houston, TX
    Lung Cancer Discovery Award

    Drug May Inactivate Pathway That Promotes Lung Cancer

    Advanced non-small cell lung cancer (NSCLC) has only a 2% 5-year survival rate. Traditional treatment is chemotherapy, but personalized therapy that targets genetic changes in tumors can be effective. However, definition of targets is lacking for about 85% of patients with NSCLC. The researchers have demonstrated that the anti-cancer drug dasatinib stopped tumor progression in a patient with a mutation in a protein called BRAF. The molecular mechanisms behind this are not yet understood. Dr. Johnson’s team has started a clinical trial in which NSCLC patients with mutant BRAF will be treated with dasatinib. It is hoped that Dr. Johnson’s work may provide major clinical benefits to thousands of patients with an otherwise incurable cancer.

  • JOHN KOOMEN, PhD
    H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL
    Lung Cancer Discovery Award

    Funded in Partnership with the American Lung Association of the Southeast

    Targeting Kinases in Lung Cancer Treatment

    Targeted therapy has become a powerful tool for treating adenocarcinoma lung cancer. For example, patients with EGFR mutations which cause tumor formation and progression can be treated with drugs, including erlo-tinib and gefitinib, which specifically shut down the signaling of the EGFR. Unfortunately, similar advances have not been found in squamous cell carcinoma. As these drugs work on molecules called kinases, the re-searchers will attempt to characterize these kinases in the hope of finding a key to aid in development of drugs which can specifically target them.

  • GEE LAU, PhD
    University of Illinois at Urbana-Champaign, Champaign, IL
    DeSouza Research Award

    Funded by the American Lung Association of the Southwest

    Toxin Could Provide Clues to Bronchiectasis Treatment

    Pseudomonas aeruginosa (PA) is an important pathogen infecting the lungs of patients with cystic fibrosis and other forms of bronchiectasis. Dr. Lau and his team have determined that PA secretes a toxin called pyocyanin, which causes oxidative stress and alters immune response in diseased lungs, causing an exaggerated inflam-matory response and worsened mucus overproduction. His team is now examining whether pyocyanin inacti-vates a protein known as FoxA2 that inhibits the excess mucus secretion in bronchiectatic and asthmatic lungs and if so, identify the determinants behind it. It is hoped that this research will lead to the development of nov-el therapeutics that maintain FoxA2 function and improve morbidity and mortality.

  • RYAN LARSON, PhD
    Seattle Biomedical Research Institute, Seattle, WA
    Senior Research Training Fellowship

    How Suppressive Immune Cells Slow Down Body’s Response to TB

    Tuberculosis (TB) is a global health problem of massive proportions with almost 9 million new cases and over one million deaths per year. Despite widespread vaccination efforts that have spanned nearly 90 years, TB has not been successfully controlled by immunization. It has been postulated that the TB bacterium slows down the immune response by activating a subset of immune cells that specialize in dampening immunity. Dr. Larson and team will attempt to determine how these suppressive immune cells impede the protective im-munity during TB.

  • IAN LEWKOWICH, PhD
    Cincinnati Children's Hospital, Cincinnati, OH
    Biomedical Research Grant

    Why Do Regulatory T Cells Not Work in People with Allergic Asthma?

    Asthma is a chronic lung disease resulting from an immune response to normally harmless allergens (i.e. dan-der or house dust mites). In mild asthma, the immune response is dominated by type 2 helper T (Th2) cells, which produce proteins that cause the airways to narrow and lung cells to fill with mucus, causing asthma symptoms - coughing, and shortness of breath. This research will examine how these Th2 proteins interact in controlling airway diameter and mucus secretion. The findings may yield important information that can be used to develop new asthma treatments.

  • HOI YAN AMANDA LIN, PhD
    Johns Hopkins University, Baltimore, MD
    Senior Research Training Fellowship

    Modifying Molecules’ Relationship to Treat Pulmonary Hypertension

    The blood vessel muscle molecule [SOCE] is important in the development of pulmonary hypertension [high blood pressure in the lungs]. Dr. Lin and team will test the relationship between SOCE and another molecule [RyR] using current techniques of physiology in animals with the goal of modifying this system with drugs used for heart disease, looking for ways to undo the pulmonary hypertension.

  • NARSA MACHIREDDY, PhD * ACUTE LUNG INJURY Scholar
    University of Illinois, Chicago, IL
    Biomedical Research Grant

    Funded in Partnership with the American Lung Association of the Upper Midwest

    Oxygen Therapy in Treating Acute Lung Injury

    Acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), are common pulmonary syndromes affecting approximately 190,000 patients per year in the United States. Oxygen sup-plementation is widely used to support critically ill patients with ALI/ARDS, however, it can cause cell death and exacerbate preexisting lung injury and inflammation. Dr. Machireddy and team will attempt to target the pathway r(bZIP) transcription factor, which is critical for the stimulation of genes involved in the protection against toxic and oxidant insults and limits oxygen-induced lung injury and inflammation in critically ill pa-tients.

  • CHRISTOPHER MAHER, PhD
    Washington University, St. Louis, MO
    Biomedical Research Grant

    Identifying Genetic Mutations in Lung Cancer Patients

    About half of lung cancer patients have been shown to have mutations that may be responsive to existing thera-pies. Recent technological advances have made it possible to comprehensively study genetic sequencing for all lung cancer patients, with an approach called high-throughput sequencing. However, this technology produces an immense amount of data, making it difficult to translate discoveries into real-world applications to benefit patient care. Dr. Maher will attempt to develop a computational approach to identify and prioritize an under-studied class of long intergenic non-coding RNAs that may serve as lung cancer biomarkers. The goal is to find new diagnostic markers and help determine which patients will respond to therapy.

  • HECTOR MARQUEZ, MD
    Boston University, Boston, MA
    Senior Research Training Fellowship

    Are Low Levels of Vitamin A Implicated in Asthma?

    Asthma is characterized by reversible airflow obstruction caused by increased inflammation, hyperrespon-siveness [over reaction to stimuli] of airway smooth muscles (SM), and increased mucus production in the airways. Accumulating data indicates that airway hyperresponsiveness in asthma is SM cell dependent and that low levels of retinoic acid (vitamin A) are associated with the development of airway hyperresponsive-ness. This proposal aims to determine how vitamin A regulates airway SM differentiation via gene regulators.

  • JOSHUA MEZRICH, MD
    University of Wisconsin, Madison, WI
    Biomedical Research Grant

    Funded in Partnership with the American Lung Association of the Upper Midwest

    APreventing Environmentally Triggered Asthma Flareups

    Research has shown that polycyclic aromatic hydrocarbons (PAH) may be responsible for aggravating asthma through the activation of the of the aryl hydrocarbon receptor (AHR). This activation leads to the generation of a pathogenic population of T cells that generates IL-17, which in turn, worsen airway inflammation in some models. Dr. Mezrich and his team believe that this represents a new, very specific mechanism for airway in-flammation in response to pollution. Their goal is to prove this mechanism is dependent on the AHR in T cells in murine models of airway inflammation, to identify whether PAHs are causing this effect, and also show that they can block or at least reduce this inflammatory response by modulating the response of the AHR on these T cells./p>

  • CHRISTOPHER MIGLIACCIO, PhD
    University of Montana, Missoula, MT
    Biomedical Research Grant

    Funded in Partnership with support from the Mary Fuller Russell Research Fund

    Investigating Wood Smoke’s Effect on the Lungs

    Macrophages are considered to be the first line of defense in the lung engulfing and clearing out inhaled partic-ulates that bombard the lungs. However, some particulates can kill or alter the function of macrophages. One such exposure may be wood smoke inhalation from wood stoves, forest fires, and cooking. Wood smoke is a major contributor to particulate matter. Dr. Migliaccio has found that in mice, there is a decrease in bacterial clearance from the lungs following inhalation of wood smoke. His research will study the health effects of in-haled wood smoke on lung macrophages to deepen the current understanding of its adverse effects on the lung’s immune response. The findings may generate powerful targets for therapeutic treatments of smoke ex-posure.

  • SHARON MORLEY, MD,PhD
    Washington University, St. Louis, MO
    Biomedical Research Grant

    Lack of Protein Leads to Pneumococcal Infection

    The most important cause of bacterial pneumonia is infection with Streptococcus pneumoniae, also called the pneumococcus. Dr. Morley and her team have developed a mouse model that is highly susceptible to pulmo-nary pneumococcal infection. These mice lack a protein that is required to control the movement and activa-tion of cells in the immune system. In the absence of this protein, pneumococcal bacteria are not cleared ef-fectively from the lungs of mice and the mice rapidly die of infection. The researchers seek to determine the requirements for this protein in multiple aspects of alveolar macrophage biology, including development, ap-pearance, movement and activation.

  • SEAN VINCENT MURPHY, PhD
    Wake Forest University Health Sciences, Winston-Salem, NC
    Senior Research Training Fellowship

    Using Fetal Stem Cells in Cystic Fibrosis Treatment

    Patients with cystic fibrosis have a defect in a gene that allows for proper regulation of salts and water in var-ious tissues. This alteration causes normal mucus in the lungs to become thick and dehydrated, ultimately blocking the airway passages, resulting in a predisposition towards chronic bacterial infections and lung dis-ease. Dr. Murphy and team have discovered that fetal stem cells in the amniotic fluid are able to form function-al cells in the laboratory. Fetal stem cells give rise to many of the specialized cell types found in the human body. They are easily obtainable, since they are found in leftover birth tissue, and can be grown in large quanti-ties—they typically double in number every 36 hours. They are using these cells to try and restore normal lung function in patients with cystic fibrosis.

  • TORU NYUNOYA, MD
    Biomedical Research Institute of New Mexico, Albuquerque, NM
    Biomedical Research Grant

    Cigarette Smoke Affects Lungs’ “Biological Clock”

    Exposure to cigarette smoke increases the risk of emphysema. One possible mechanism may be that contents of smoke shorten the length of telomeres, the ends of chromosomes that control the process by which each cell ages. Dr. Nyunoya's hypothesis is that aldehyde dehydrogenase 3A1 (ALDH3A1), an enzyme used to detox-ify reactive aldehydes contained in cigarette smoke may change the biological clock. His in vitro studies demonstrated that an increased amount of ALDH3A1 protects against DNA damage and cell death in response to cigarette smoke exposure. Based on the mechanisms identified by this research, he plans to develop a nov-el treatment for emphysema.

  • WANDA PHIPATANAKUL, MD
    Children’s Hospital Boston, Boston, MA
    American Lung Association/American Academy of Allergy, Asthma & Immunology Allergic Respiratory Disease Award

    Exposure to mouse allergen/mold/pollutants in the school environment can worsen asthma, even after con-trolling for home allergen exposures. Dr. Phipatanakul and her team are implementing a school based inter-vention in 12 inner city schools examining the use of enhanced integrated pest management, classroom air purifiers and cleaning with corresponding improvements to asthma morbidity. The researchers hope to learn the best way to design and implement more cost and time efficient school-based environmental interventions that may potentially help a community of children with asthma, allergic diseases, and their associated morbid-ity.

  • SAMMETA VAMSEE RAJU, PhD
    University of Alabama, Birmingham, AL
    Senior Research Training Fellowship

    Neutralizing Acrolein, a Cigarette Smoke Toxin

    Therapy for COPD is largely limited to oxygen and bronchodilators, providing symptomatic relief without cor-recting the underlying factors, which are still not very well understood. Recently it has been discovered that cigarette smoke reduces the function of CFTR, the gene that is defective in cystic fibrosis and causes reduced mucus clearance in the lungs, increased lung infections and bronchitis. These are all symptoms similar to those identified with COPD. Dr. Raju will test how acrolein, a respiratory toxin present in cigarette smoke, transmits systemic CFTR dysfunction and how nacetylcysteine, a drug and nutritional supplement neutralizes acrolein, and rescues CFTR function. This may be beneficial in cigarette smoking related lung disease.

  • STEPHEN REEVES, MD, PhD
    Seattle Children's Hospital, Seattle, WA
    Senior Research Training Fellowship

    How Airways of Children With Asthma Are Damaged

    Research has indicated that decreased lung function caused by childhood asthma does not improve as a child ages, despite appropriate treatment with medications. Current leading theories of mechanisms underlying the decline in lung function involve the concept of airway remodeling - this proposes that the airways of asthmatic children are altered over time as part of the disease state. Using state-of-the-art molecular techniques Dr. Reeves and his team will examine the way fibroblasts, cells known to promote airway remodeling, lead to irreversible lung damage in asthmatic children.

  • KATHERINE RIVERA-SPOLJARIC, MD
    Washington University, St. Louis, MO
    Clinical Patient Care Research Grant

    Best Time to Start Treatment for Respiratory Tract Illness

    Respiratory tract illness is a common trigger of asthma exacerbations in children. Preliminary data suggests that parents can confidently identify non-respiratory and upper respiratory signs and symptoms that occur before the development of an exacerbation, and that, with education and follow-up, they are able to institute treatment at the onset of such symptoms. This clinical study will test whether initiation of additional therapy at incidence of non-respiratory and upper respiratory symptoms will be more successful in preventing need for oral corticosteroids than later in the course when lower respiratory symptoms develop, as is typically recommended by most asthma management plans.

  • CENDRINE ROBINSON, BS
    Uniformed Services University of the Health Sciences, Bethesda, MD
    Lung Health Dissertation

    Using Smartphones to Reduce Smoking Cravings

    African Americans are more likely to live in communities that are saturated with tobacco cues such as tobacco advertisements, making it more difficult to quit. Although it is difficult to modify the number of smok-ing-related cues in the environment, it may be possible to modify the attention smokers pay to cues. Using a smartphone-based intervention, the researchers will train smokers to automatically attend away from smok-ing cues and in turn, experience fewer cravings.

  • VIKRAM SAINI, PhD
    University of Alabama, Birmingham, AL
    Senior Research Training Fellowship

    Link Between Cigarette Smoke and Multi-Drug Resistant Tuberculosis

    Multi-drug resistant tuberculosis (MDR-TB) is a particularly dangerous form of TB, as it is resistant to two of the most powerful anti-TB drugs and requires up to two years of treatment with second-line anti-TB drugs. Many countries with a high prevalence of TB also have a high prevalence of smoking. However a link between ciga-rette smoking and MDR-TB has not yet been established. Dr. Saini has shown that harmful components of ciga-rette smoke mutate the DNA of tuberculosis-causing bacterium Mycobacterium tuberculosis (Mtb). Some of these mutations are in genes that confer drug resistance to Mtb. Dr. Saini and team will use a mouse model to examine whether exposure of Mtb cells to cigarette smoke leads to the development of MDR-TB.

  • LOBELIA SAMAVATI, MD * INTERSTITIAL LUNG DISEASE SCHOLAR
    Wayne State University, Detroit, MI
    Biomedical Research Grant

    How Immune System Works Differently in Sarcoidosis

    Sarcoidosis is an inflammatory disorder that can affect multiple organs throughout the body. Its course and outcome are difficult to predict in each individual patient. Normally, immune protein cells in the body are equipped to recognize invaders, triggering an inflammatory response in an attempt to kill the invading foreign pathogens. In healthy individuals, inflammation shuts down once an infection is fought off; however, this pro-cess remains sustained in sarcoidosis patients. Dr. Samavati and team will investigate why these immune pro-teins work differently and how the inflammatory process continues to be activated in sarcoidosis patients compared to healthy individuals. The findings may lead to more effective drug therapies.

  • ANDREAS SCHWINGSHACKL, MD, PhD
    University of Tennessee Health Science Center, Memphis, TN
    Biomedical Research Grant

    Funded in Partnership with the American Lung Association of the Midland States

    Identifying New Targets to Treat Acute Lung Injury

    Mechanical ventilation and oxygen therapy are common treatment options for acute lung injury (ALI), alt-hough both therapies are known to cause further damage to the lungs. Recent studies suggest that a particu-lar type of ion channel, 2-pore domain potassium (K2P), can sense signals at the cell membrane and convert them into specific cellular functions. The central hypothesis of this proposal is that the K2P channel is regulat-ed by the treatments above and, in turn, regulates the release of inflammatory mediators. Dr. Schwingshackl and team hope to identify these channels as new potential targets for the development of novel treatment strategies against ALI.

  • JESSICA SEELIGER, PhD * Tuberculosis Scholar
    State University of New York, Stony Brook, NY
    Biomedical Research Grant

    Funded in Partnership with support from the Mary Fuller Russell Research Fund

    Targeting Latent and Multi-Drug Resistant TB

    Mycobacterium tuberculosis (Mtb), infects one-third of the world’s population. Most infected individuals have latent TB infections and have no symptoms. However, decreased immune responses can trigger latent TB to reactivate and cause infectious disease. Some TB disease can become resistant to first line medications and therefore, new therapies are needed to treat multi- and extremely drug-resistant TB strains. Dr. Seeliger and team will use a novel chemical method to evaluate a family of Mtb enzymes with diverse functions essential for bacterial survival as potential drug targets. These enzymes may be promising for developing next-generation therapies against latent infections and multi-drug resistant TB.

  • SHILADITYA SENGUPTA, PhD
    Brigham and Women's Hospital, Boston, MA
    Lung Cancer Discovery Award

    Funded by the American Lung Association of the Northeast

    Using Nanoparticles to Improve Lung Cancer Treatment

    Despite advances in molecular understanding of cancer, traditional chemotherapy still relies on highly toxic drugs as first line therapy. As such, there is an urgent need for a new approach in the management of cancer. Using tiny particles [nanoparticles] designed to hone in on specific cancers, Dr. Sengupta and team will try to attach these particles to both standard chemotherapy drugs and the new, more specific, drugs to create a novel and more effective medication.

  • ABDUL SHEIKH, PhD
    Yale University, New Haven, CT
    Senior Research Training Fellowship

    Abnormal Lung Blood Vessel Muscle Formation and Pulmonary Hypertension

    Pulmonary hypertension (PH) is a devastating disease characterized by elevated blood pressure in the blood vessels of the lung. In PH, the right heart pumps against the increased pressure in the lungs, which eventually results in its failure. In lungs with PH, the small blood vessels, which normally have no muscle in the walls, develop abnormal muscle formation. Dr. Sheikh and team will attempt to identify key steps in abnormal lung blood vessel muscle formation using a mouse model of human PH.

  • SUNNY SHIN, PhD
    University of Pennsylvania, Philadelphia, PA
    Biomedical Research Grant

    How Immune Cells Clear Legionnaire’s Disease Bacteria from Lungs

    Lung infections are a leading cause of disease and death in the United States. Designing strategies to combat lung infection requires a better understanding of how the immune system responds to such infection and controls it. Dr. Shin and her team hope to understand how immune cells detect bacterial infection in the lung and generate a successful response that clears the infection using the lung pathogen Legionella pneumophila, the causative agent of the severe bacterial pneumonia Legionnaire's disease.

  • HIDEKI SHISHIDO, PhD * PEDIATRIC LUNG DISEASE SCHOLAR
    Oregon Health and Science University, Portland, OR
    Senior Research Training Fellowship

    Developing New Method to Study Cystic Fibrosis Protein

    Cystic fibrosis (CF) is a life-threatening inherited disease that primarily affects the lungs and digestive system of affected patients. In patients with CF, a protein called the cystic fibrosis transmembrane conductance regu-lator (CFTR) is malformed, causing the lungs to be susceptible to bacterial infections. An important goal of CF therapy is to understand how CFTR acquires its structure and to identify new therapies that assist in prevent-ing this malformation. Dr. Shishido and team are determined to develop an entirely new method to study how different regions of CFTR fold as they are synthesized in the cell. Results will hopefully provide a promising new approach for CF drug discovery that corrects the underlying molecular defect in CF patients.

  • JESSICA SIEREN, PhD
    University of Iowa, Iowa City, IA
    Lung Cancer Discovery Award

    Funded in Partnership with the American Lung Association of the Upper Midwest

    Identifying Which COPD Patients are Most at Risk of Lung Cancer

    The risk of lung cancer is significantly higher in people with chronic obstructive pulmonary disease (COPD), independent of their smoking history. While chronic inflammation is thought to play a role, it is not known which people affected by COPD are most susceptible to developing lung cancer. Dr. Sieren will use computed tomography (CT) scans to generate anatomic measurements of lung tissue for each lobe of the lung, as well as each airway, down to the very small airway branches. These measurements can be used to identify computed tomography biomarkers for lung cancer risk assess-ment, to guide targeted detection and treatment strategies.

  • ANURAG SINGH, PhD
    Boston University, Boston, MA
    Lung Cancer Discovery Award

    Understanding Role of Mutated KRAS Gene in Lung Cancer

    Lung cancers frequently have altered [mutated] genes. Of these, the mutated KRAS gene is now viewed as a central linchpin in driving cancer progression; this mutation is found in 20-30% of lung cancer cases. Dr. Singh and team aims to identify molecules that are regulated by mutant KRAS, cause changes in cancer cell appear-ance and behavior in mouse tumor models, or may affect how tumors respond to anti-cancer chemothera-peutic agents.

  • ROGER TSIEN, PhD
    University of California, San Diego
    American Lung Association/American Asthma Foundation Senior Investigator Award

    Learning Proteases’ Role in Asthma Inflammation

    Dr. Tsien is a Nobel Prize winner in chemistry who is using his expertise to bring a new perspective to the study of asthma. He will be focusing on the work of proteases, ubiquitous enzymes involved in many biological pro-cesses including the inflammation that underlies asthma. The development of agents to target these enzymes for the treatment of asthma requires knowledge of exactly where, when and how they act in the lung. Eventu-ally, Dr. Tsien says the findings from the study could be applied to human patients for diagnosis and potential-ly for the evaluation of new treatments for asthma.

  • CAROLIEN WANSLEEBEN, PhD
    Duke University Medical Center, Durham, NC
    Senior Research Training Fellowship

    Shedding Light on the Stem Cells of Mucus-Producing Glands

    Airway diseases are characterized by an overproduction of mucus that causes airflow obstruction, setting the stage for respiratory infections. Mucus is produced by submucosal glands, small groups of cells that lie under the surface of the airways. In the diseased lung, the submucosal glands become enlarged and often produce more mucus. Using a mouse model, Dr. Wansleeben and her team will study the basic mechanisms of stem cell behavior in mucus-producing glands. Stem cells renew tissue over time, and these cells play a role in con-trolling the structure of that tissue. The results will provide insight into the development of overgrowth of submucosal cells and could be useful in developing new targets for disease therapy.

  • MONTE WINSLOW, PhD
    Stanford University, Stanford, CA
    Biomedical Research Grant

    Factors in the Spread of Lung Cancer

    Metastases of lung cancer is a major barrier to successful therapy and survival. Using a genetically-engineered mouse model, in which tumors are initiated by genetic mutations similar to those that occur in the human disease, Dr. Winslow and team will attempt to determine whether disseminated tumors cells are present in the pleural fluid and blood of mice with very high numbers of early lung cancer lesions. This will allow the re-searchers to further understand the factors which limit or promote metastasis of lung cancer.

  • GUTIAN XIAO, PhD * Lung Cancer Scholar
    University of Pittsburgh, Pittsburgh, PA
    Lung Cancer Discovery Award

    Funded by the American Lung Association of the Upper Midwest

    Using Protein to Help Diagnose and Treat Lung Cancer

    Lung cancer’s high death rate is largely due to late diagnosis and the fact that lung cancer easily becomes re-sistant to chemotherapy. Research has shown that PDLIM2, a widely found protein molecule in the lungs, functions as a tumor suppressor and may also play a critical role in the response of lung cancer to chemother-apy. Dr. Xiao and team will seek to establish PDLIM2 as a diagnostic, and predictive biomarker of human lung cancer as well as a therapy for lung cancer.

  • XUEXIAN YANG, PhD * Obstructive Lung Disease Scholar
    University of New Mexico, Albuquerque, NM
    Biomedical Research Grant

    How Lack of CIS Molecule Leads to Allergic Lung Disease

    Allergic asthma is a major health problem, but the causes are not well understood. Research has newly identi-fied a molecule called CIS that may be deficient in people with allergic lung disease. This research will explore the ways in which levels of this molecule are regulated in the body. Dr. Yang will study how CIS is regulated, what cellular signals are disrupted by CIS, how CIS controls the development of pro-allergic immune cells called T helper cells, and how CIS deficiency leads to allergic lung disease. The results will potentially provide novel insights into the development of allergic lung disease, and may suggest new therapeutic and preventive methods.

  • HONGWEI YAO, PhD, MD
    University of Rochester, Rochester, NY
    Biomedical Research Grant

    Link Between Cigarette Smoke and Lung Premature Aging

    Cigarette smoking is the main risk factor for developing chronic obstructive pulmonary disease (COPD), ac-counting for at least 75% of COPD deaths. Recent research suggests COPD develops as a result of accelerated premature aging of the lungs. Despite knowledge linking cigarette smoke and premature lung aging, little is known about the mechanisms that cause this process. Dr. Yao hopes to identify the factors responsible for regulating cigarette smoke-induced premature aging in lung cells. He will focus on Sirtulin 1 (SIRT1), a gene with anti-aging activity. Outcomes of this research could contribute to development of novel and more selec-tive approaches and treatments to prevent or limit premature lung aging caused by tobacco smoke.

  • JAE-KWANG YOO, PhD
    University of Virginia, Charlottesville, VA
    Senior Research Training Fellowship

    Novel Immune Cell Promotes Influenza-Fighting Response

    Dr. Yoo and his team are studying how the immune system fights the influenza virus. When a person is infect-ed with the virus, the immune system responds using B cells which produces neutralizing antibodies that are essential both to prevent reinfection and to eliminate the infection from the respiratory tract. These B cells are dependent on immune cells called T follicular helper cells (TFH) to assist with fighting influenza. In an ani-mal model of Influenza A virus (IAV) infection, the researchers demonstrated that a novel immune cell, the late activator antigen presenting cell promotes an anti-IAV TFH response. Dr. Yoo’s results can be used to im-prove the efficiencies of the vaccine for the seasonal flu, and potentially for a pandemic flu.

  • ZBIGNIEW ZASLONA, PhD
    University of Michigan, Ann Arbor, MI
    Senior Research Training Fellowship

    Deciphering Macrophages’ Role in Asthma

    Alveolar macrophages (AMs) are immune cells that play a pivotal role in the coordination of inflammatory re-sponses in the lung. AMs are elevated in asthma, but the mechanisms responsible for this are poorly under-stood. Dr. Zaslona and team have found that resident AMs are protective in asthma, since their depletion augments allergic inflammation. By contrast, macrophages accumulating in asthma by recruitment of periph-eral blood monocytes called leukotrienes, promote asthma. These findings highlight the importance of mac-rophages in asthma, and in the coming year the team will test whether interference with AM recruitment by affecting eicosanoid lipid mediator pathways can translate to improved therapies for asthma.

  • IGOR ZELKO, PhD
    University of Louisville, Louisville, KY
    Biomedical Research Grant

    Blocking Remodeling in Lung’s Blood Vessels in Pulmonary Arterial Hypertension

    Pulmonary Arterial Hypertension (PAH) is a devastating disease; only about half of patients survive five years after diagnosis. The lung’s blood vessels are remodeled and constrict, leading to heart failure due to an en-larged right ventricle. Current drug used to treat the disease enlarge the blood vessels, but do not block the eventual thickening of the artery walls, and do not improve survival. Dr. Zelko and team are studying the mechanisms that regulate remodeling of blood vessel walls in the lung. They are focusing on a substance that inhibits an enzyme called histone deacetylase, which could provide clues leading to better therapy for PAH. If it is successful, this drug could be used in human trials to stop, or even reverse progression of the disease.

  • JINMING ZHAO, PhD
    University of Pittsburgh, Pittsburgh, PA
    Biomedical Research Grant

    Suppressing Enzyme Involved in Asthma Activation

    Dr. Zhao and team are trying to identify which cellular factor(s) are responsible for asthma. Based on their clinical database, they observed a higher level of an enzyme named 15LO1 in asthmatic patients compared to non-asthmatic people. Additional research found that another protein, PEBP1, could interact with 15LO1 to enhance its enzyme activity leading to the development of asthma. Dr. Zhao will culture human primary epi-thelial cells and modulate this enzyme activation by biomedical approaches to see whether this will change biological events representative of asthmatic symptoms. He believes that control of this enzyme could im-prove asthmatic symptoms and ultimately unveil a highly novel pathway in asthma, which could lead to new treatments.

  • GUOFEI ZHOU, PhD
    University of Illinois, Chicago, IL
    Biomedical Research Grant

    Funded in Partnership with the American Lung Association of the Upper Midwest

    Role of Tumor Suppressor Protein in Pulmonary Fibrosis

    Idiopathic pulmonary fibrosis (IPF) is a devastating disease associated with progressive and irreversible de-struction of the lung architecture. The cause of IPF remains largely unknown even as the annual incidence of IPF is rising. It has been suggested that patients with IPF express increased levels of a certain tumor suppressor protein [VHL] in centers of scarring. This research will attempt to address the regulation of VHL and the causal role of VHL in pulmonary fibrosis.