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Your search keyword '"Taveira-Dasilva, Angelo"' showing total 290 results
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290 results on '"Taveira-Dasilva, Angelo"'

1. Pathophysiology of Lymphangioleiomyomatosis

Author

Henske, Elizabeth P., El-Chemaly, Souheil, Darling, Thomas N., Taveira-DaSilva, Angelo M., Moss, Joel, Rounds, Sharon I.S., Series Editor, Dixon, Anne, Series Editor, Schnapp, Lynn M., Series Editor, Gupta, Nishant, editor, Wikenheiser-Brokamp, Kathryn A., editor, and McCormack, Francis X., editor

Published
2021
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16. Serum VEGF-D concentration as a biomarker of lymphangioleiomyomatosis severity and treatment response: a prospective analysis of the Multicenter International Lymphangioleiomyomatosis Efficacy of Sirolimus (MILES) trial

Author

Young, Lisa R, Lee, Hye-Seung, Inoue, Yoshikazu, Moss, Joel, Singer, Lianne G, Strange, Charlie, Nakata, Koh, Barker, Alan F, Chapman, Jeffrey T, Brantly, Mark L, Stocks, James M, Brown, Kevin K, Lynch, Joseph P, 3rd, Goldberg, Hilary J, Downey, Gregory P, Swigris, Jeffrey J, Taveira-DaSilva, Angelo M, Krischer, Jeffrey P, Trapnell, Bruce C, and McCormack, Francis X

Published
2013
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18. Lymphangioleiomyomatosis Diagnosis and Management: High-Resolution Chest Computed Tomography, Transbronchial Lung Biopsy, and Pleural Disease Management. An Official American Thoracic Society/Japanese Respiratory Society Clinical Practice Guideline

Author

Gupta, Nishant, Finlay, Geraldine A., Kotloff, Robert M., Strange, Charlie, Wilson, Kevin C., Young, Lisa R., Taveira-DaSilva, Angelo M., Johnson, Simon R., Cottin, Vincent, Sahn, Steven A., Ryu, Jay H., Seyama, Kuniaki, Inoue, Yoshikazu, Downey, Gregory P., Han, MeiLan K., Colby, Thomas V., Wikenheiser-Brokamp, Kathryn A., Meyer, Cristopher A., Smith, Karen, Moss, Joel, and McCormack, Francis X.

Published
2017
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28. Genetic and morphologic determinants of pneumothorax in lymphangioleiomyomatosis

Author

Steagall, Wendy K., Glasgow, Connie G., Hathaway, Olanda M., Avila, Nilo A., Taveira-DaSilva, Angelo M., Rabel, Antoinette, Stylianou, Mario P., Lin, Jing-Ping, Chen, Xiaoling, and Moss, Joel

Subjects
Lung diseases -- Research, Cystic fibrosis -- Research, Epithelial cells -- Research, Pneumothorax -- Research, Biological sciences
Abstract

Lymphangioleiomyomatosis, a multisystem disease affecting women, is characterized by proliferation of abnormal smooth muscle-like cells in the lungs, leading to cystic destruction of the parenchyma and recurrent pneumothoraces. Clinical characteristics of lymphangio-leiomyomatosis patients were analyzed to determine the relationship of pneumothoraces to disease progression. Patients were genotyped for polymorphisms in genes of extracellular matrix proteins collagen, elastin, and matrix metalloproteinase-1 to assess their association with pneumothoraces. Clinical data and polymorphisms in the genes for types I and III collagen, elastin, and matrix metalloproteinase-1 were compared with the prevalence of pneumothorax. Of 227 patients, 57% reported having had at least one pneumothorax. Cyst size on high-resolution computed tomography scans was associated with pneumothorax; patients with a history of pneumothorax were more likely to have larger cysts than patients who had no pneumothoraces. In patients with mild disease, those with a history of pneumothorax had a faster rate of decline in forced expiratory volume in 1 s ([FEV.sub.1]; P = 0.001, adjusted for age) than those without. Genotype frequencies differed between patients with and without pneumothorax for polymorphisms in the types I and III collagen and matrix metalloproteinase-1 genes. Larger cysts may predispose lymphangioleiomyomatosis patients to pneumothorax, which, in early stages of disease, correlates with a more rapid rate of decline in [FEV.sub.1]. Polymorphisms in types I and III collagen and matrix metalloproteinase-1 genes may cause differences in lung extracellular matrix that result in greater susceptibility to pneumothorax. cystic lung disease; collagen; matrix metalloproteinases; elastin

Published
2007

29. N-Terminal pro-brain natriuretic peptide levels and risk of death in sickle cell disease

Author

Machado, Roberto F., Anthi, Anastasia, Steinberg, Martin H., Bonds, Duane, Sachdev, Vandana, Kato, Gregory J., Taveira-DaSilva, Angelo M., Ballas, Samir K., Blackwelder, William, Xiuli Xu, Barton, Bruce, Waclawiw, Myron, Gladwin, Mark T., and Castro, Oswaldo

Subjects
Sickle cell anemia -- Risk factors, Natriuretic peptides -- Research, Mortality -- Risk factors, Pulmonary hypertension -- Risk factors
Abstract

Study is presented to determine the relationship between N-Terminal pro-brain natriuretic peptide (NT-proBNP) levels and severity of pulmonary hypertension and prospective mortality in patients with sickle cell disease (SCD). Results suggest that a high NT-proBNP level is associated with pulmonary hypertension and is a major risk factor for patients dying of SCD.

Published
2006

32. Efficacy and Safety of Sirolimus in Lymphangioleiomyomatosis

Author

McCormack, Francis X., Inoue, Yoshikazu, Moss, Joel, Singer, Lianne G., Strange, Charlie, Nakata, Koh, Barker, Alan F., Chapman, Jeffrey T., Brantly, Mark L., Stocks, James M., Brown, Kevin K., Lynch, Joseph P., III, Goldberg, Hilary J., Young, Lisa R., Kinder, Brent W., Downey, Gregory P., Sullivan, Eugene J., Colby, Thomas V., McKay, Roy T., Cohen, Marsha M., Korbee, Leslie, Taveira-DaSilva, Angelo M., Lee, Hye-Seung, Krischer, Jeffrey P., and Trapnell, Bruce C.

Published
2011

36. The NHLBI Lymphangioleiomyomatosis Registry: Characteristics of 230 Patients at Enrollment

Author

Ryu, Jay H., Moss, Joel, Beck, Gerald J., Lee, Jar-Chi, Brown, Kevin K., Chapman, Jeffrey T., Finlay, Geraldine A., Olson, Eric J., Ruoss, Stephen J., Maurer, Janet R., Raffin, Thomas A., Peavy, Hannah H., McCarthy, Kevin, Taveira-DaSilva, Angelo, McCormack, Francis X., Avila, Nilo A., DeCastro, Rosamma M., Jacobs, Susan S., Stylianou, Mario, and Fanburg, Barry L.

Published
2006
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43. Celecoxib in lymphangioleiomyomatosis: results of a phase I clinical trial

Author

El-Chemaly, Souheil, primary, Taveira-DaSilva, Angelo, additional, Bagwe, Shefali, additional, Klonowska, Katarzyna, additional, Machado, Tania, additional, Lamattina, Anthony M., additional, Goldberg, Hilary J., additional, Jones, Amanda M., additional, Julien-Williams, Patricia, additional, Maurer, Rie, additional, Rosas, Ivan O., additional, Henske, Elizabeth P., additional, Moss, Joel, additional, and Kwiatkowski, David J., additional

Published
2020
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44. The NHLBI LAM Registry: Prognostic Physiologic and Radiologic Biomarkers Emerge From a 15-Year Prospective Longitudinal Analysis

Author

Gupta, Nishant, Lee, Hye-Seung, Ryu, Jay H., Taveira-DaSilva, Angelo M., Beck, Gerald J., Lee, Jar-Chi, McCarthy, Kevin, Finlay, Geraldine A., Brown, Kevin K., Ruoss, Stephen J., Avila, Nilo A., Moss, Joel, and McCormack, Francis X.

Subjects
Lipopolysaccharides, Humans, Lymphangioleiomyomatosis, Prospective Studies, Registries, Diffuse Lung Disease, National Heart, Lung, and Blood Institute (U.S.), Prognosis, Lung, Biomarkers
Abstract

BACKGROUND: The natural history of lymphangioleiomyomatosis (LAM) is mainly derived from retrospective cohort analyses, and it remains incompletely understood. A National Institutes of Health LAM Registry was established to define the natural history and identify prognostic biomarkers that can help guide management and decision-making in patients with LAM. METHODS: A linear mixed effects model was used to compute the rate of decline of FEV(1) and to identify variables affecting FEV(1) decline among 217 registry patients who enrolled from 1998 to 2001. Prognostic variables associated with progression to death/lung transplantation were identified by using a Cox proportional hazards model. RESULTS: Mean annual decline of FEV(1) was 89 ± 53 mL/year and remained remarkably constant regardless of baseline lung function. FEV(1) decline was more rapid in those with greater cyst profusion on CT scanning (P = .02) and in premenopausal subjects (118 mL/year) compared with postmenopausal subjects (74 mL/year) (P = .003). There were 26 deaths and 43 lung transplantations during the evaluation period. The estimated 5-, 10-, 15-, and 20-year transplant-free survival rates were 94%, 85%, 75%, and 64%, respectively. Postmenopausal status (hazard ratio, 0.30; P = .0002) and higher baseline FEV(1) (hazard ratio, 0.97; P = .008) or diffusion capacity of lung for carbon monoxide (hazard ratio, 0.97; P = .001) were independently associated with a lower risk of progression to death or lung transplantation. CONCLUSIONS: The median transplant-free survival in patients with LAM is > 20 years. Menopausal status, as well as structural and physiologic markers of disease severity, significantly affect the rate of decline of FEV(1) and progression to death or lung transplantation in LAM.

Published
2018

45. Analysis of the MILES cohort reveals determinants of disease progression and treatment response in lymphangioleiomyomatosis

Author

Gupta, Nishant, primary, Lee, Hye-Seung, additional, Young, Lisa R., additional, Strange, Charlie, additional, Moss, Joel, additional, Singer, Lianne G., additional, Nakata, Koh, additional, Barker, Alan F., additional, Chapman, Jeffrey T., additional, Brantly, Mark L., additional, Stocks, James M., additional, Brown, Kevin K., additional, Lynch, Joseph P., additional, Goldberg, Hilary J., additional, Downey, Gregory P., additional, Taveira-DaSilva, Angelo M., additional, Krischer, Jeffrey P., additional, Setchell, Kenneth, additional, Trapnell, Bruce C., additional, Inoue, Yoshikazu, additional, and McCormack, Francis X., additional

Published
2019
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50. Clinical features, epidemiology, and therapy of lymphangioleiomyomatosis

Author

Taveira-DaSilva, Angelo M. and Moss,Joel

Subjects
Clinical Epidemiology
Abstract

Angelo M Taveira-DaSilva, Joel Moss Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA Abstract: Lymphangioleiomyomatosis (LAM) is a multisystem disease of women, characterized by proliferation of abnormal smooth muscle-like LAM cells, leading to the formation of lung cysts, fluid-filled cystic structures in the axial lymphatics (eg, lymphangioleiomyomas), and renal angiomyolipomas. LAM is caused by mutations of the TSC1 or TSC2 genes, which encode, respectively, hamartin and tuberin, two proteins with a major role in control of the mammalian target of rapamycin (mTOR) signaling pathway. LAM occurs sporadically or in association with tuberous sclerosis complex, an autosomal-dominant syndrome characterized by widespread hamartomatous lesions. LAM may present with progressive dyspnea, recurrent pneumothorax, or chylothorax. Pulmonary function tests show reduced flow rates (forced expiratory volume in the first second) and diffusion capacity. Exercise testing may reveal gas exchange abnormalities, ventilatory limitation, and hypoxemia. The severity and progression of disease may be assessed by lung histology scores, quantification of computed tomography, pulmonary function testing, 6-minute walk tests, cardiopulmonary exercise testing, and measurement of serum vascular endothelial growth factor D levels. Sirolimus and everolimus, two mTOR inhibitors, are effective in stabilizing lung function and reducing the size of chylous effusions, lymphangioleiomyomas, and angiomyolipomas. However, inhibition of mTOR complex 1 increases autophagy, possibly enhancing LAM cell survival. Inhibition of autophagy with hydroxychloroquine, in combination with sirolimus, has been proposed as a possible treatment for LAM. Deficiency of tuberin results in increased RhoA GTPase activity and cell survival, an effect that is mediated through mTOR complex 2 signaling. Because sirolimus and everolimus only affect the activity of mTOR complex 1, therapies targeting RhoA GTPases with simvastatin, which inhibits Rho GTPases and promotes apoptosis, are being investigated. As in the case of cancer, LAM may be best treated with multiple drugs targeting signaling pathways considered important in the pathogenesis of disease. Keywords: lymphangioleiomyomatosis, tuberous sclerosis, TSC1 and TSC2 mutations, mammalian target of rapamycin signaling pathway

Published
2015

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