Biosketch / Results /
Linda Rogers, M.D.
Assistant Professor; Med Dir BV Chest Clin Ast Dir BV Asthma ClinicDepartments of Hospital for Joint Diseases and Medicine (Pulmy&CCM Div)
Clinical Addresses
Bellevue Hospital462 FIRST AVENUE
NEW YORK, NY 10016
Handicap Access: yes
Phone: 212-562-4141
Board Certification
1998 — Critical Care Medicine (Internal Med)2005 — Internal Medicine
2007 — Pulmonary Disease (Internal Med)
Education
1992 — NYU Medical Center, Medical Education1992-1995 — Columbia-Presbyterian Medical Center (Internal Medicine), Residency Training
1992-1995 — Columbia-Presbyterian Medical Center (Internal Medicine), Internship
1995-1998 — NYU Medical Center (Pulmonary & Critical), Clinical Fellowships
All data from NYU Health Sciences Library Faculty Bibliography — -
Contact:
http://hsl.med.nyu.edu/faculty-bibliography-search#about
Stepping down asthma treatment: how and when
Rogers, Linda; Reibman, Joan
2012 Jan;18(1):70-75, Current opinion in pulmonary medicine
PURPOSE OF REVIEW: Guidelines suggest that asthma medication should be reduced once asthma control is sustained. Moderate-dose inhaled corticosteroids (ICS) can typically be reduced, but questions remain about the lowest effective ICS dose and the role of non-ICS controllers in treatment reduction. Long-acting beta agonist (LABA) safety concerns have created controversy about how to step down patients on ICS/LABA therapy. This review will focus on the current status of these issues. RECENT FINDINGS: Intermittent ICS treatment, often in fixed combination with short-acting beta agonist, is an emerging strategy for control of mild asthma. Addition of leukotriene modifiers, LABAs, and omalizumab to ICS can allow for reduced ICS dosing. Doses of ICS that control symptoms may be inadequate to control exacerbations. Reducing ICS dose before discontinuing LABAs may be the more effective approach for patients on combination therapy. SUMMARY: Use of non-ICS controllers allows for ICS dose reduction with superior outcomes. Tapering of ICS prior to LABA discontinuation may be the favored approach for patients on ICS/LABA therapy, but an understanding of long-term outcomes and further safety data are required. The lowest ICS dose that adequately controls both asthma impairment and risk remains to be determined
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id: 145767,
year: 2012,
vol: 18,
page: 70,
stat: Journal Article,
Lung pathologic findings in a local residential and working community exposed to world trade center dust, gas, and fumes
Caplan-Shaw, Caralee E; Yee, Herman; Rogers, Linda; Abraham, Jerrold L; Parsia, Sam S; Naidich, David P; Borczuk, Alain; Moreira, Andre; Shiau, Maria C; Ko, Jane P; Brusca-Augello, Geraldine; Berger, Kenneth I; Goldring, Roberta M; Reibman, Joan
2011 Sep;53(9):981-991, Journal of occupational & environmental medicine
OBJECTIVE: : To describe pathologic findings in symptomatic World Trade Center-exposed local workers, residents, and cleanup workers enrolled in a treatment program. METHODS: : Twelve patients underwent surgical lung biopsy for suspected interstitial lung disease (group 1, n = 6) or abnormal pulmonary function tests (group 2, n = 6). High-resolution computed axial tomography and pathologic findings were coded. Scanning electron microscopy with energy-dispersive x-ray spectroscopy was performed. RESULTS: : High-resolution computed axial tomography showed reticular findings (group 1) or normal or airway-related findings (group 2). Pulmonary function tests were predominantly restrictive. Interstitial fibrosis, emphysematous change, and small airway abnormalities were seen. All cases had opaque and birefringent particles within macrophages, and examined particles contained silica, aluminum silicates, titanium dioxide, talc, and metals. CONCLUSIONS: : In symptomatic World Trade Center-exposed individuals, pathologic findings suggest a common exposure resulting in alveolar loss and a diverse response to injury
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id: 137445,
year: 2011,
vol: 53,
page: 981,
stat: Journal Article,
Asthma in the elderly: Current understanding and future research needs-a report of a National Institute on Aging (NIA) workshop
Hanania, Nicola A.; King, Monroe J.; Braman, Sidney S.; Saltoun, Carol; Wise, Robert A.; Enright, Paul; Falsey, Ann R.; Mathur, Sameer K.; Ramsdell, Joe W.; Rogers, Linda; Stempel, David A.; Lima, John J.; Fish, James E.; Wilson, Sandra R.; Boyd, Cynthia; Patel, Kushang V.; Irvin, Charles G.; Yawn, Barbara P.; Halm, Ethan A.; Wasserman, Stephen I.; Sands, Mark F.; Ershler, William B.; Ledford, Dennis K.;
2011 SEP ;128(3 S S):S4-S24, Journal of allergy & clinical immunology
Asthma in the elderly is underdiagnosed and undertreated, and there is a paucity of knowledge on the subject. The National Institute on Aging convened this workshop to identify what is known and what gaps in knowledge remain and suggest research directions needed to improve the understanding and care of asthma in the elderly. Asthma presenting at an advanced age often has similar clinical and physiologic consequences as seen with younger patients, but comorbid illnesses and the psychosocial effects of aging might affect the diagnosis, clinical presentation, and care of asthma in this population. At least 2 phenotypes exist among elderly patients with asthma; those with longstanding asthma have more severe airflow limitation and less complete reversibility than those with late-onset asthma. Many challenges exist in the recognition and treatment of asthma in the elderly. Furthermore, the pathophysiologic mechanisms of asthma in the elderly are likely to be different from those seen in young asthmatic patients, and these differences might influence the clinical course and outcomes of asthma in this population. (J Allergy Clin Immunol 2011;128:S4-24.)
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id: 139068,
year: 2011,
vol: 128,
page: S4,
stat: Journal Article,
Genetic Variants of TSLP and Asthma in an Admixed Urban Population
Liu, Mengling; Rogers, Linda; Cheng, Qinyi; Shao, Yongzhao; Fernandez-Beros, Maria Elena; Hirschhorn, Joel N; Lyon, Helen N; Gajdos, Zofia K Z; Vedantam, Sailaja; Gregersen, Peter; Seldin, Michael F; Bleck, Bertram; Ramasamy, Adaikalavan; Hartikainen, Anna-Liisa; Jarvelin, Marjo-Riitta; Kuokkanen, Mikko; Laitinen, Tarja; Eriksson, Johan; Lehtimaki, Terho; Raitakari, Olli T; Reibman, Joan
2011 ;6(9):e25099-e25099, PLoS ONE
BACKGROUND: Thymic stromal lymphopoietin (TSLP), an IL7-like cytokine produced by bronchial epithelial cells is upregulated in asthma and induces dendritic cell maturation supporting a Th2 response. Environmental pollutants, including tobacco smoke and diesel exhaust particles upregulate TSLP suggesting that TSLP may be an interface between environmental pollution and immune responses in asthma. Since asthma is prevalent in urban communities, variants in the TSLP gene may be important in asthma susceptibility in these populations. OBJECTIVES: To determine whether genetic variants in TSLP are associated with asthma in an urban admixed population. METHODOLOGY AND MAIN RESULTS: Ten tag-SNPs in the TSLP gene were analyzed for association with asthma using 387 clinically diagnosed asthmatic cases and 212 healthy controls from an urban admixed population. One SNP (rs1898671) showed nominally significant association with asthma (odds ratio (OR) = 1.50; 95% confidence interval (95% CI): 1.09-2.05, p = 0.01) after adjusting for age, BMI, income, education and population stratification. Association results were consistent using two different approaches to adjust for population stratification. When stratified by smoking status, the same SNP showed a significantly increased risk associated with asthma in ex-smokers (OR = 2.00, 95% CI: 1.04-3.83, p = 0.04) but not significant in never-smokers (OR = 1.34; 95% CI: 0.93-1.94, p = 0.11). Haplotype-specific score test indicated that an elevated risk for asthma was associated with a specific haplotype of TSLP involving SNP rs1898671 (OR = 1.58, 95% CI: 1.10-2.27, p = 0.01). Association of this SNP with asthma was confirmed in an independent large population-based cohort consortium study (OR = 1.15, 95% CI: 1.07-1.23, p = 0.0003) and the results stratified by smoking status were also validated (ex-smokers: OR = 1.21, 95% CI: 1.08-1.34, p = 0.003; never-smokers: OR = 1.06, 95% CI: 0.94-1.17, p = 0.33). CONCLUSIONS: Genetic variants in TSLP may contribute to asthma susceptibility in admixed urban populations with a gene and environment interaction
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id: 138030,
year: 2011,
vol: 6,
page: e25099,
stat: Journal Article,
Pharmacologic approaches to life-threatening asthma
Rogers, Linda; Reibman, Joan
2011 Dec;5(6):397-408, Therapeutic advances in respiratory disease
Following a peak in asthma mortality in the late 1980s and early 1990s, we have been fortunate to see a substantial decrease in asthma deaths in recent years. Although most asthma deaths occur outside the hospital, near-fatal events are commonplace, with anywhere from 2-20% of patients with acute asthma admitted to intensive care, and 2-4% intubated for respiratory failure. Standard therapies for acute severe and near-fatal asthma include administration of systemic corticosteroids, and frequent or continuous inhaled beta agonists. Controversy remains regarding the optimal therapy of those who fail to respond to these initial treatments, those who remain at risk of acute respiratory failure, and patients requiring mechanical ventilation. There remain significant gaps in our knowledge regarding relative benefits of intravenous versus oral corticosteroids, intermittent versus continuous beta agonists, and the role of various adjunctive treatments including intravenous magnesium, systemic beta agonists, aminophylline, and helium-oxygen mixtures. Using models and radiolabeled aerosols, there is a greater understanding regarding effective administration of inhaled beta-agonists in ventilated patients. There is limited available evidence for treatment of near-fatal asthma, a fact reflected by the significant variability in asthma critical care practice. Much of the data guiding treatment in this setting has been generalized from studies of acute asthma in the ED and from general populations of hospitalized patients with acute asthma. This review will focus on pharmacologic approaches to life-threatening asthma by reviewing current guideline recommendations, reviewing the scientific basis of the guidelines, and highlighting gaps in our knowledge in treatment of refractory acute or near-fatal asthma
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id: 150555,
year: 2011,
vol: 5,
page: 397,
stat: Journal Article,
Emerging exposures and respiratory health: world trade center dust
Rom, William N; Reibman, Joan; Rogers, Linda; Weiden, Michael D; Oppenheimer, Beno; Berger, Kenneth; Goldring, Roberta; Harrison, Denise; Prezant, David
2010 May;7(2):142-145, Proceedings of the American Thoracic Society
The attack on the World Trade Center (WTC) on 9/11/2001 produced a massive dust cloud with acute exposure, and the rubble pile burning over 3 months exposed more than 300,000 residents, rescue workers, and clean-up workers. Firefighters in the New York City Fire Department had significant respiratory symptoms characterized by cough, dyspnea, gastroesophageal reflux, and nasal stuffiness with a significant 1-year decline in FVC and FEV(1). Bronchial hyperreactivity measured by methacholine challenge correlated with bronchial wall thickening on CT scans. Compared with the NHANES III data for FVC and FEV(1), 32% of 2,000 WTC dust-exposed residents and clean-up workers were below the lower 5th percentile. The most common abnormality was a low FVC pattern, a finding similar to that also described for individuals in rescue and recovery activities. Among those complaining of respiratory symptoms and normal spirometry, almost half had abnormalities detected with impedance oscillometry consistent with distal airways' disease. Follow-up with the WTC Health Registry and the WTC Environmental Health Center will help discern whether treatment with anti-inflammatory medications or bronchodilators in those with respiratory symptoms may prevent the development of chronic obstructive pulmonary disease
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id: 109531,
year: 2010,
vol: 7,
page: 142,
stat: Journal Article,
A case of immune reconstitution syndrome secondary to discontinuation of anti-TNF agents in a patient with pulmonary tuberculosis
Abounasr K.K.; Rogers L.
2009 ;136(4):?-?, Chest
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id: 111413,
year: 2009,
vol: 136,
page: ?,
stat: Journal Article,
Characteristics of a residential and working community with diverse exposure to World Trade Center dust, gas, and fumes
Reibman, Joan; Liu, Mengling; Cheng, Qinyi; Liautaud, Sybille; Rogers, Linda; Lau, Stephanie; Berger, Kenneth I; Goldring, Roberta M; Marmor, Michael; Fernandez-Beros, Maria Elena; Tonorezos, Emily S; Caplan-Shaw, Caralee E; Gonzalez, Jaime; Filner, Joshua; Walter, Dawn; Kyng, Kymara; Rom, William N
2009 May;51(5):534-541, Journal of occupational & environmental medicine
OBJECTIVE: To describe physical symptoms in those local residents, local workers, and cleanup workers who were enrolled in a treatment program and had reported symptoms and exposure to the dust, gas, and fumes released with the destruction of the World Trade Center (WTC) on September 11, 2001. METHODS: Symptomatic individuals underwent standardized evaluation and subsequent treatment. RESULTS: One thousand eight hundred ninety-eight individuals participated in the WTC Environmental Health Center between September 2005 and May 2008. Upper and lower respiratory symptoms that began after September 11, 2001 and persisted at the time of examination were common in each exposure population. Many (31%) had spirometry measurements below the lower limit of normal. CONCLUSIONS: Residents and local workers as well as those with work-associated exposure to WTC dust have new and persistent respiratory symptoms with lung function abnormalities 5 or more years after the WTC destruction
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id: 98897,
year: 2009,
vol: 51,
page: 534,
stat: Journal Article,
Asthma is inversely associated with Helicobacter pylori status in an urban population
Reibman, Joan; Marmor, Michael; Filner, Joshua; Fernandez-Beros, Maria-Elena; Rogers, Linda; Perez-Perez, Guillermo I; Blaser, Martin J
2008 ;3(12):e4060-e4060, PLoS ONE
BACKGROUND: Microbial exposures have been suggested to confer protection from allergic disorders and reduced exposures to gastrointestinal microbiota have been proposed as an explanation for the increase in asthma prevalence. Since the general prevalence of Helicobacter pylori has been decreasing, we hypothesized that H. pylori serostatus would be inversely related to the presence of asthma. METHODS: Adults were recruited to participate in the New York University (NYU)/Bellevue Asthma Registry in New York City. Adult asthma cases (N = 318) and controls (N = 208) were identified and serum IgG antibodies to H. pylori whole cell antigens or the immunodominant CagA antigen were measured. RESULTS: As expected, the asthma cases and controls differed with respect to atopy and lung function. Seropositivity to H. pylori or CagA antigen was present in 47.1% of the total case and control study population. Asthma was inversely associated with CagA seropositivity (OR = 0.57, 95% CI = 0.36-0.89). Median age of onset of asthma (doctor's diagnosis) was older (21 years) among individuals with CagA+ strains than among H. pylori- individuals (11 years) (p = 0.006). CONCLUSION: These data are consistent with the hypothesis that colonization with CagA+ H. pylori strains is inversely associated with asthma and is associated with an older age of asthma onset in an urban population. The data suggest H. pylori as a marker for protection
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id: 91964,
year: 2008,
vol: 3,
page: e4060,
stat: Journal Article,
Cardioprotective effects of cerium oxide nanoparticles in a transgenic murine model of cardiomyopathy
Niu, Jianli; Azfer, Asim; Rogers, Linda M; Wang, Xihai; Kolattukudy, Pappachan E
2007 Feb 1;73(3):549-559, Cardiovascular research
OBJECTIVE: Cerium oxide (CeO2) nanoparticles have been shown to protect cells in culture from lethal stress, but no protection in vivo has been reported. Cardiac-specific expression of monocyte chemoattractant protein (MCP)-1 in mice causes ischemic cardiomyopathy associated with activation of endoplasmic reticulum (ER) stress. The aim of this study was to assess the effects of CeO2 nanoparticles on cardiac function and remodeling as well as ER stress response in this murine model of cardiomyopathy. METHODS: MCP-1 transgenic mice (MCP mice) and wild-type controls were administered intravenously 15 nmol of CeO2 nanoparticles or vehicle only twice a week for 2 weeks. Cardiac function, myocardial histology, nitrotyrosine formation, expression of cytokines, and ER stress-associated genes were evaluated. RESULTS: Treatment with CeO2 nanoparticles markedly inhibited progressive left ventricular dysfunction and dilatation in MCP mice and caused a significant decrease in serum levels of MCP-1, C-reactive protein, and total nitrated proteins. The infiltration of monocytes/macrophages, accumulation of 3-nitrotyrosine, apoptotic cell death, and expression of proinflammatory cytokines, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 in the myocardium were markedly inhibited by CeO2 nanoparticles. Expression of the key ER stress-associated genes, including glucose-regulated protein 78 (Grp78), protein disulfide isomerase (PDI), and heat shock proteins (HSP25, HSP40, HSP70), were also suppressed by CeO2 nanoparticles. CONCLUSIONS: CeO2 nanoparticles protect against the progression of cardiac dysfunction and remodeling by attenuation of myocardial oxidative stress, ER stress, and inflammatory processes probably through their autoregenerative antioxidant properties
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id: 94480,
year: 2007,
vol: 73,
page: 549,
stat: Journal Article,
Allergic bronchopulmonary aspergillosis in association with Mounier-Kuhn syndrome
Patel, AV; Herscovici, P; Rogers, L
2007 OCT ;132(4):713S-713S, Chest
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id: 87208,
year: 2007,
vol: 132,
page: 713S,
stat: Journal Article,
Environment, genes, and immune mechanisms in asthma
Reibman, Joan; Rogers, Linda; Fernandez-Beros, Maria Elena
Environmental and occupational medicine Philadelphia : Wolters Kluwer/Lippincott Williams & Wilkins, 2007,
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id: 5362,
year: 2007,
vol: ,
page: ?,
stat: Chapter,
Activation of endoplasmic reticulum stress response during the development of ischemic heart disease
Azfer, Asim; Niu, Jianli; Rogers, Linda M; Adamski, Frances M; Kolattukudy, Pappachan E
2006 Sep;291(3):H1411-H1420, American journal of physiology. Heart & circulatory physiology
Endoplasmic reticulum (ER) stress has been found to be associated with neurodegenerative diseases and diabetes mellitus. Whether ER stress is involved in the development of heart disease is not known. Cardiac-specific expression of monocyte chemoattractant protein-1 (MCP-1) in mice causes the development of ischemic heart disease. Here we report that microarray analysis of gene expression changes in the heart of these transgenic mice revealed that a cluster of ER stress-related genes was transcriptionally activated in the heart during the development of ischemic heart disease. The gene array results were verified by quantitative real-time PCR that showed highly elevated transcript levels of genes involved in unfolded protein response such as ER and cytoplasmic chaperones, oxidoreductases, protein disulfide isomerase (PDI) family, and ER-associated degradation system such as ubiquitin. Immunoblot analysis confirmed the expression of chaperones, PDI, and ubiquitin. Immunohistochemical analyses showed that ER stress proteins were associated mainly with the degenerating cardiomyocytes. A novel ubiquitin fold modifier (Ufm1) that has not been previously associated with ER stress and not found to be induced under any condition was also found to be upregulated in the hearts of MCP mice (transgenic mice that express MCP-1 specifically in the heart). The present results strongly suggest that activation of ER stress response is involved in the development of ischemic heart disease in this murine model
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id: 94481,
year: 2006,
vol: 291,
page: H1411,
stat: Journal Article,
The World Trade Center residents' respiratory health study: new-onset respiratory symptoms and pulmonary function
Reibman, Joan; Lin, Shao; Hwang, Syni-An A; Gulati, Mridu; Bowers, James A; Rogers, Linda; Berger, Kenneth I; Hoerning, Anne; Gomez, Marta; Fitzgerald, Edward F
2005 Apr;113(4):406-411, Environmental health perspectives
The destruction of the World Trade Center (WTC) on 11 September 2001 in New York City resulted in the massive release of pulverized dust and combustion products. The dust and smoke settled in the surrounding area, which encompassed a large residential community. We hypothesized that previously normal residents in the community surrounding the former WTC would have an increased incidence of persistent respiratory symptoms and abnormalities in screening spirometry. A hybrid cross-sectional and retrospective cohort study using a symptom-based questionnaire and onsite screening spirometry in residents in an exposed area and in a control area was performed 12 +/- 4 months after the collapse. Surveys were analyzed from 2,812 residents. New-onset respiratory symptoms were described by 55.8% of residents in the exposed area, compared with 20.1% in the control area after the event. Persistent new-onset symptoms were identified in 26.4 versus 7.5% of residents in the exposed area versus control area, respectively. No differences in screening spirometry between the groups were detected. A small pilot study suggested the possibility of an increase in bronchial hyperresponsiveness in exposed participants with persistent symptoms. The data demonstrate an increased rate of new-onset and persistent respiratory health effects in residents near the former WTC compared with a control population
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id: 55975,
year: 2005,
vol: 113,
page: 406,
stat: Journal Article,
Homoserine and asparagine are host signals that trigger in planta expression of a pathogenesis gene in Nectria haematococca
Yang, Zhennai; Rogers, Linda M; Song, Yuanda; Guo, Wenjin; Kolattukudy, P E
2005 Mar 15;102(11):4197-4202, Proceedings of the National Academy of Sciences of the United States of America
Some pathogenesis-related genes are expressed in fungi only when the pathogen is in the host, but the host signals that trigger these gene expressions have not been identified. Virulent Nectria haematococca infects pea plants and requires either pelA, which is induced by pectin, or pelD, which is induced only in planta. However, the host signal(s) that trigger pelD expression was unknown. Here we report the isolation of the host signals and identify homoserine and asparagine, two free amino acids found in uniquely high levels in pea seedlings, as the pelD-inducing signals. N. haematococca has evolved a mechanism to sense the host tissue environment by using the high levels of two free amino acids in this plant, thereby triggering the expression of pelD to assist the pathogenic process
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id: 94483,
year: 2005,
vol: 102,
page: 4197,
stat: Journal Article,
Regulation of constitutively expressed and induced cutinase genes by different zinc finger transcription factors in Fusarium solani f. sp. pisi (Nectria haematococca)
Li, Daoxin; Sirakova, Tatiana; Rogers, Linda; Ettinger, William F; Kolattukudy, P E
2002 Mar 8;277(10):7905-7912, Journal of biological chemistry
Cutin monomers, generated by the low levels of constitutively expressed cutinase, induce high levels of cutinase that can help pathogenic fungi to penetrate into the host through the cuticle whose major structural polymer is cutin. We cloned three highly homologous cutinase genes, cut1, cut2, and cut3, from Fusarium solani f. pisi (Nectria haematococca). Amino acid sequence deduced from the nucleotide sequence of cut1 and cut2/3 matched with that of the peptides from cutinase 1 and cutinase 2, respectively, isolated from F. solani pisi grown on cutin as the sole carbon source. Induction of beta-glucuronidase gene fused to the promoters of the cutinases integrated into F. solani pisi genome indicates that cut2 is constitutively expressed and induced under starvation, whereas cut1 is highly induced by cutin monomers. A palindrome binding protein (PBP) previously cloned binds only to palindrome 1 of cut1 promoter but not palindrome 1 of cut2/3 which contains two base substitutions. PBP is thought to interfere with the binding of CTF1 alpha, the transcription factor involved in induction, to cut1 promoter and thus keep cut1 gene repressed until induced by cutin monomers. Because PBP cannot bind palindrome 1 of cut2, this gene is not repressed. CTF1 alpha does not transactivate cut2 promoter. A new Cys(6)Zn(2) motif-containing transcription factor, CTF1 beta, that binds palindrome 2 was cloned and sequenced. In yeast, CTF1 beta transactivates cut2 promoter but not cut1 promoter unless its palindrome 1 is mutated, unlike CTF1 alpha which transactivates cut1. Thus, CTF1 beta is involved in the constitutive expression of cut2 that causes production of low levels of cutin monomers that strongly induce cut1 using CTF1 alpha as the transcription factor
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id: 94484,
year: 2002,
vol: 277,
page: 7905,
stat: Journal Article,
Asthma in the elderly: cockroach sensitization and severity of airway obstruction in elderly nonsmokers
Rogers, Linda; Cassino, Cara; Berger, Kenneth I; Goldring, Roberta M; Norman, Robert G; Klugh, Thomas; Reibman, Joan
2002 Nov;122(5):1580-1586, Chest
STUDY OBJECTIVES: To test the hypothesis that the presence of sensitization to indoor allergens is associated with increased severity of airway obstruction in elderly subjects with asthma. DESIGN: Cohort study of subjects enrolled in a public hospital asthma clinic. SETTING: Asthma clinic in a municipal public hospital serving an indigent population in New York City. PATIENTS: Subjects aged > or = 60 years with asthma who were enrolled in the Bellevue Hospital Asthma Clinic. Total serum IgE and allergen-specific IgE measurements were performed in a cohort of elderly never-smokers who had asthma (45 patients) who had undergone spirometry before and after bronchodilator (BD) therapy. MEASUREMENTS AND RESULTS: The results of radioallergosorbent tests demonstrated that most subjects (ie, 60%) were sensitized to at least one allergen, with many sensitized to at least one indoor allergen. Cockroach (CR) was the most common allergen to which subjects were sensitized, with 47% displaying an elevated serum-specific IgE level. Fewer subjects were sensitized to dust mite, cat, dog, or ragweed. Subjects sensitized to CR (CR+) had greater reductions in airflow compared to subjects not sensitized to CR (CR-) [64 +/- 4.4% predicted vs 77.1 +/- 4.1% predicted FEV(1), respectively; p < 0.05]. Following BD administration, only 29% of CR+ subjects achieved a normal post-BD FEV(1) compared to 58% of CR- subjects. Lung volume measurements differed between CR+ and CR- subjects, with a greater elevation of functional residual capacity in CR+ subjects. CONCLUSION: In a population of elderly urban patients with asthma, the presence of CR-specific serum IgE is associated with more severe asthma, as reflected by an increase in airway obstruction and hyperinflation
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id: 39563,
year: 2002,
vol: 122,
page: 1580,
stat: Journal Article,
Emergence of un-correlated common-mode oscillations in the sensory cortex
Kozma, R; Alvarado, M; Rogers, L; Lau, B; Freeman, WJ
2001 JUN ;38(25):747-755, Neurocomputing
Simultaneous EEG recordings from various cortical areas indicate the presence of common-mode, spatially coherent oscillations. These oscillations are characterized by a common wave form with a spatially distributed pattern of amplitude modulation (AM). We observe highly reproducible AM patterns across spatially separated channels within various areas, yet the temporal correlations between the channels are low. In the framework of the present research, a nonlinear, spatially distributed dynamical model of neuronal populations (KIII) is used for the interpretation of the observed spatial coherence. The theoretical findings are in good agreement with experiments performed with chronically implanted rabbits. (C) 2001 Elsevier Science B,V. All rights reserved
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id: 98283,
year: 2001,
vol: 38,
page: 747,
stat: Journal Article,
Elevated total end specific IgE in elderly inner city asthmatics
Rogers, L; Cassino, C; Ciotoll, C; Kramer, B; Reibman, J
1999 MAR ;159(3):A856-A856, American journal of respiratory & critical care medicine
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id: 53896,
year: 1999,
vol: 159,
page: A856,
stat: Journal Article,
Inhibitory C/EBP beta suppress viral and cytokine promoters alter an inflammatory stimulus
Tanaka, N; Nakata, K; Honda, Y; Rogers, L; Rom, WN; Weiden, M
1999 MAR ;159(3):A660-A660, American journal of respiratory & critical care medicine
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id: 53887,
year: 1999,
vol: 159,
page: A660,
stat: Journal Article,
Type I interferon induces inhibitory 16-kD CCAAT/ enhancer binding protein (C/EBP)beta, repressing the HIV-1 long terminal repeat in macrophages: pulmonary tuberculosis alters C/EBP expression, enhancing HIV-1 replication
Honda Y; Rogers L; Nakata K; Zhao BY; Pine R; Nakai Y; Kurosu K; Rom WN; Weiden M
1998 Oct 5;188(7):1255-1265, Journal of experimental medicine
We have previously observed that HIV-1 replication is suppressed in uninflamed lung and increased during tuberculosis. In vitro THP-1 cell-derived macrophages inhibited HIV-1 replication after infection with Mycobacterium tuberculosis. Suppression of HIV-1 replication was associated with inhibition of the HIV-1 long terminal repeat (LTR) and induction of ISGF-3, a type I interferon (IFN)-specific transcription factor. Repression of the HIV-1 LTR required intact CCAAT/enhancer binding protein (C/EBP) sites. THP-1 cell-derived macrophages infected with M. tuberculosis, lipopolysaccharide, or IFN-beta induced the 16-kD inhibitory C/EBPbeta isoform and coincidentally repressed HIV-1 LTR transcription. C/EBPbeta was the predominant C/EBP family member produced in THP-1 macrophages during HIV-1 LTR repression. In vivo, alveolar macrophages from uninflamed lung strongly expressed inhibitory 16-kD C/EBPbeta, but pulmonary tuberculosis abolished inhibitory C/EBPbeta expression and induced a novel C/EBP DNA binding protein. Therefore, in vitro, proinflammatory stimulation produces an IFN response inhibiting viral replication by induction of a C/EBPbeta transcriptional repressor. THP-1 cell-derived macrophages stimulated with type I IFN are similar to alveolar macrophages in the uninflamed lung in vivo. In contrast, the cellular immune response in active pulmonary tuberculosis disrupts this innate immunity, switching C/EBP expression and allowing high level viral replication
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id: 8036,
year: 1998,
vol: 188,
page: 1255,
stat: Journal Article,


