Gotowe bibliografie tematyczne / Lymphangioleiomyomatosis

Gotowa bibliografia na temat „Lymphangioleiomyomatosis”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 11 marca 2023

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Artykuły w czasopismach na temat "Lymphangioleiomyomatosis"

Yamashita, Cory M., David Lynch i Gregory P. Downey. "Lymphangioleiomyomatosis". Clinical Pulmonary Medicine 15, nr 6 (listopad 2008): 325–31. http://dx.doi.org/10.1097/cpm.0b013e31818cbafb.

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Krymskaya, Vera P., i J. Michael Shipley. "Lymphangioleiomyomatosis". American Journal of Respiratory Cell and Molecular Biology 28, nr 5 (maj 2003): 546–50. http://dx.doi.org/10.1165/rcmb.f267.

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Johnson, S. R. "Lymphangioleiomyomatosis". European Respiratory Journal 27, nr 5 (maj 2006): 1056–65. http://dx.doi.org/10.1183/09031936.06.00113303.

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McCormack, Francis X., William D. Travis, Thomas V. Colby, Elizabeth P. Henske i Joel Moss. "Lymphangioleiomyomatosis". American Journal of Respiratory and Critical Care Medicine 186, nr 12 (15.12.2012): 1210–12. http://dx.doi.org/10.1164/rccm.201205-0848oe.

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Taveira-Dasilva, Angelo M., Wendy K. Steagall i Joel Moss. "Lymphangioleiomyomatosis". Cancer Control 13, nr 4 (październik 2006): 276–85. http://dx.doi.org/10.1177/107327480601300405.

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Zarogiannis, S., C. Hatzoglou, P. A. Molyvdas i K. Gourgoulianis. "Lymphangioleiomyomatosis". European Respiratory Journal 28, nr 6 (1.12.2006): 1284. http://dx.doi.org/10.1183/09031936.00099606.

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Sietsema, Kathy E., i Francis X. McCormack. "Lymphangioleiomyomatosis". American Journal of Respiratory and Critical Care Medicine 168, nr 12 (15.12.2003): 1405–6. http://dx.doi.org/10.1164/rccm.2310006.

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Tattersfield, Anne E., i Marilyn K. Glassberg. "Lymphangioleiomyomatosis". American Journal of Respiratory and Critical Care Medicine 173, nr 1 (styczeń 2006): 2–4. http://dx.doi.org/10.1164/rccm.2509010.

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Ansótegui Barrera, Emilio, Nuria Mancheño Franch, Francisco Vera-Sempere i José Padilla Alarcón. "Lymphangioleiomyomatosis". Archivos de Bronconeumología ((English Edition)) 47, nr 2 (styczeń 2011): 85–93. http://dx.doi.org/10.1016/s1579-2129(11)70019-2.

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Sclafani, Alyssa, i Paul VanderLaan. "Lymphangioleiomyomatosis". New England Journal of Medicine 378, nr 23 (7.06.2018): 2224. http://dx.doi.org/10.1056/nejmicm1712581.

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Rozprawy doktorskie na temat "Lymphangioleiomyomatosis"

Chang, William Y. C. "Metalloproteinases in lymphangioleiomyomatosis". Thesis, University of Nottingham, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664270.

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Matrix metalloproteinases (MMPs) have been implicated in the lung destruction seen in lymphangioleiomyomatosis (LAM) as elevated MMP levels have been detected in tissue, serum and urine from LAM patients but a causal link has not been established. It has also been hypothesised that inhibition of MMPs with the tetracycline antibiotic doxycycline may provide a potential treatment for LAM. Previously proposed mechanisms of actions of doxycycline were examined. In Eker rat derived ELT3 cells doxycycline at doses ~25 micrograms/ml inhibited cell proliferation and adhesion, possibly by a toxic effect. This was also seen in human angiomyolipoma-derived cells. There was no effect of doxycycline on MMP-2 expression or activity in vitro. In a xenograft model, doxycycline had no effect on tumour growth, final tumour weight, or tumour lysate MMP levels. The role of MMPs as potential biomarkers was also compared with vascular endothelial growth factor D (VEGF-D). Serum VEGF-D, Angiotensin coverting enzyme (ACE) and total matrix metalloproteinase 2 (MMP-2) levels were elevated in patients. VEGF-D was the strongest discriminator between patients and controls and the addition VEGF-D measurement to ERS criteria reduced the need for biopsy to confirm diagnosis. Finally, we performed a 2 year, randomised, double blind placebo controlled study of doxycycline in 23 patients with LAM and found no evidence that it prevented decline in lung function, or improved exercise tolerance of quality of life.

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NG, Ho Yin. "Cellular Characteristics of Lymphangioleiomyomatosis". Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/9510.

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Lymphangioleiomyomatosis (LAM) is a rare lung disease in young women. Dysfunction of the tuberous sclerosis gene complex (TSC)-1 and TSC2 contributes to the manifestations of enhanced proliferation and migration of smooth muscle-like cells (LAM cells), elevated matrix metalloproteinase (MMP) activity and increased lymphangiogenesis. Currently there is no effective treatment for this fatal disease. This study aimed to assess the effectiveness of potential pharmacotherapies (doxycycline, statins and lamstatin) in targeting the different pathological aspects of LAM. Studies in this thesis examined the effects of doxycycline in human LAM cells and in a cellular model for LAM. Doxycycline had no effect on cell proliferation, but reduced elevated MMP2 activity, migratory capability and wound closure. In addition, doxycycline reduced cell migration through the inhibition of RhoA-GTPase and focal adhesion kinase (FAK), proteins that are involved in the regulation of cell motility. These findings were extended to show that the combination of doxycycline and rapamycin (inhibitor of the mammalian target of rapamycin compelx 1 [mTORC1] which is a potent inhibitor of cell proliferation) exhibited an additive effect on the inhibition of wound closure compared to the individual drugs alone. MMP profiles in people with LAM were also examined and confirmed previous findings of elevated serum MMP2 and MMP9. In addition elevated serum levels of MMP1 and MMP3 were identified. The effectiveness of statins as a treatment for LAM was examined in studies which investigated their effects on the enhanced proliferation, migration, wound closure and MMP2 activity in TSC2-deficient cells. All parameters were reduced by simvastatin and fluvastatin. The anti-lymphangiogenic protein lamstatin (NC1 domain of collagen IV α5) is absent in the lungs of people with LAM. Results showed that lamstatin and its consensus peptide, CP17 inhibited the proliferation, migration and wound closure in a cellular model of LAM. These studies have enhanced our understanding of the disease mechanisms underlying LAM and have revealed potential molecular targets for future therapy in this disease.

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Kinder, Brent W. M. D. "Clinical Predictors of Survival in Lymphangioleiomyomatosis". University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1298041138.

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Herranz, Ors Carmen 1992. "Towards improving lymphangioleiomyomatosis care : a study of biomarkers and therapies". Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668273.

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LAM is a rare metastasizing and destructive disorder of the lung. The disease is caused by cells carrying mutations in the TSC1/2 genes, but the tissue of origin of diseased cells remains unknown. The standard of care for LAM is the inhibition of mTOR with sirolimus. The standard of care for LAM is the inhibition of mTOR with sirolimus. However, the therapy has variable tolerability. LAM diagnosis and monitoring can be challenging due to the heterogeneity of symptoms. In this thesis, we aimed to provide evidence for improving LAM care through the identification of useful biomarkers and exploration of novel therapeutic approaches. In parallel, we also studied disease origin. At the level of biomarkers, the major histamine-derived metabolite MIAA has been found to be more abundant in LAM plasmas. Combined studies of LAM lung tissues and cell models showed enhanced monoamine metabolism and histamine-mediated signaling. In addition, the inhibition of these two pathways decreased LAM tumorigenesis in mouse models. The results of this thesis may help improve the diagnostic process, clinical monitoring and therapeutic management of LAM patients.
LAM es un trastorno pulmonar raro, destructivo y metastásico. Esta enfermedad está causada por células que tienen mutaciones en los genes TSC1/2 cuyo origen sigue siendo desconocido. El tratamiento de LAM consiste en la inhibición de mTOR con sirolimus. Sin embargo, esta terapia presenta una tolerabilidad variable. El diagnóstico de LAM y su monitorización puede ser un desafío ya que los síntomas son muy heterogéneos. En esta tesis, nuestro objetivo era mejorar la atención de LAM a través de la identificación de biomarcadores y la exploración de nuevos enfoques terapéuticos. Paralelamente, también estudiamos el origen de la enfermedad. En cuanto a los biomarcadores, el principal metabolito derivado de la histamina MIAA estaba aumentado en el plasma de pacientes de LAM. Estudios combinados de tejidos pulmonares y modelos celulares mostraron un aumento en el metabolismo de las monoaminas y en la vía de señalización de la histamina. Además, la inhibición de estas dos rutas redujo la tumorogénesis de modelos LAM de ratón. Los resultados de esta tesis podrían ayudar a mejorar el diagnóstico, la monitorización y el tratamiento de las pacientes de LAM.

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Contini, Paola <1975&gt. "Effect of estrogen suppression on lung function in pulmonary Lymphangioleiomyomatosis". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4497/1/contini_paola_tesi.pdf.

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Background: Lymphangioleiomyomatosis (LAM), a rare progressive disease, is characterized by the proliferation of abnormal smooth muscle cells (LAM cells) in the lung, which leads to cystic parenchymal destruction and progressive respiratory failure. Estrogen receptors are present in LAM cells. LAM affects almost exclusively women of childbearing age. These findings, along with reports of disease progression during pregnancy or treatment with exogenous estrogens, have led to the assumption that hormonal factors play an important role in the pathogenesis of LAM. So, various therapies aim at preventing estrogen receptors (ER) by lowering circulating estrogen levels, by trying to block ER activity, or by attempting to lower ER expression in LAM. Prior experience have yielded conflicting results. Objective: The goal of this study was to evaluate, retrospectively, the effect of estrogen suppression in 21 patients with LAM. Design: We evaluated hormonal assays, pulmonary function tests and gas-exchange at baseline and after 12, 24 and 36 months after initiating hormonal manipulation. Results: The mean yearly rates of decline in FEV1 and DLCO are lower than those observed in prior studies and just DLCO decline was statistically significant. We also found an improvement of mean value of FVC and PaO2. Conclusions: Estrogen suppression appears to prevent decline in lung function in LAM.

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Delaney, Sean Phillip. "Modeling and Therapeutic Development for the Tuberous Sclerosis Related Neoplasm Lymphangioleiomyomatosis". Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39810.

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The multisystemic tumors characteristic of the monogenic neoplastic diseases, tuberous sclerosis complex (TSC) and lymphangioleiomyomatosis (LAM), share common signaling aberrations upon the loss of heterozygosity in either the TSC1 or TSC2 genes. However, their physical manifestations are vastly different and can generally be classified as being either neurological (TSC) or mesenchymal (TSC & LAM; referred to herein as LAM for simplicity) in origin. In this study, I present a comprehensive stem cell model of LAM utilizing multiple TSC2 knockout (TSC2-/-) pluripotent stem cell lines differentiated to the putative cell of origin for mesenchymal tumors, neural crest cells (NCCs). TSC2-/- NCCs faithfully recapitulate LAM phenotypes and temporal RNA-seq analysis of neural and neural crest differentiation was performed to model disease pathogenesis. Analysis revealed immediate activation of stress response signaling resulting in protein aggregation and lysosome and autophagosome accumulation upon neuralization in TSC2-/- cells. This resulted in acute and lasting effects specific to neural progenitor cells (NPCs), that are transient and ameliorated in NCCs. These lineage-specific effects resulted in selective sensitization of NPCs to cell death via proteasome inhibition, suggesting a potential therapeutic avenue for neurological TSC, but not LAM. Thus, a genome-wide CRISPR knockout screen was performed in TSC2-/- NCCs. Analysis of synthetic lethal genes reveals pathways previously targeted for LAM, but provides gene-level resolution to the vulnerable nodes within these pathways. Importantly, 18 novel gene targets were identified that display synthetic lethality to TSC2-/- cells with high specificity. 3 genes within this list were targetable using commercially available small molecule inhibitors, one of which, FGFR1, shows highly selective lethal targeting of TSC2-/- NCCs. Importantly, this model system, paired with the expansive resource of transcriptomic and synthetic lethal data, serves as a foundation for the development of next generation treatment strategies for LAM, and potentially the entire spectrum of TSC manifestations.

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Vafamand, Shahpar. "Knowledge, Attitude, Lifestyle Practices, and Quality of Life in Sporadic Lymphangioleiomyomatosis Patients". ScholarWorks, 2014. http://scholarworks.waldenu.edu/dissertations/208.

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Lymphangioleiomyomatosis (LAM) is a rare lung disease recognized by abnormal growth of smooth muscle cells proliferating in lungs parenchyma, developing benign tumors, migrating to the other organs, and ultimately leading to respiratory failure and death. Despite existing literature mainly on clinical aspects of LAM, there is a gap of literature in regards to the knowledge, attitude, and lifestyle practices (KAPs) of LAM patients and their effects on their quality of life. The purpose of this quantitative study was to investigate the KAPs of the sporadic LAM patients as measured by the Bristol Chronic Obstructive Pulmonary Disease Knowledge Questionnaire, Beliefs and Behavior Questionnaire, Determinants of Lifestyle Behavior Questionnaire; these KAPs were then analyzed for their relationship to quality of life reports as measured by the St George’s Quality of Life Questionnaire. Transtheoretical model (TTM) was used to describe the relationship among the variables. The data were collected through online survey questionnaires from 143 sporadic LAM patients registered at the LAM Foundation. Pearson’s correlations and linear regression were used to analyze the data. The results of the analysis showed that there was a significant positive relationship between attitude, lifestyle practices, and quality of life and a negative relationship between knowledge and quality of life. The outcome achieved by this study and its implication on social change identifies the need to initiate more study-specific KAPs within LAM populations, including individuals with tuberous sclerosis complex LAM. The results could also encourage the LAM community as well as other stakeholders to implement programs, workshops, and interventions that could promote and enhance quality of life.

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Davies, David Mark. "mTOR inhibition as a therapeutic strategy in tuberous sclerosis or sporadic lymphangioleiomyomatosis". Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/54431/.

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Tuberous sclerosis is an autosomal dominant multisystem disorder characterised by the development of benign tumours in many organs, including the brain, skin, kidneys and heart, seizures and intellectual disability. The condition results from mutations in either of two genes, TSC1 (encoding TSC1) or TSC2 (encoding TSC2). Loss of functional TSC1 or TSC2 leads to activation of mTORCl (mammalian target of rapamycin complex 1), a key regulator of multiple cellular processes including cell growth and division. Lymphangioleiomyomatosis (LAM) is a lung disorder which can lead to respiratory failure and is characterised by the proliferation of abnormal 'LAM' cells LAM occurs in patients with tuberous sclerosis and can also occur as a sporadic disorder due to acquired mutations in TSC2. Renal angiomyolipomas are benign tumours which affects80% of patients with tuberous sclerosis and 40% of patients with sporadic LAM. Sirolimus is an inhibitor of mTORCl and is used in clinical practice as an immunosuppressant. Preclinical studies suggest that TSC1 or TSC2 deficiency renders cells sensitive to mTOR inhibition. This thesis describes a phase 2 trial to assess the safety and efficacy of 2 years of treatment with sirolimus for renal angiomyolipomas in patients with tuberous sclerosis or LAM. Response of angiomyolipoma was the primary efficacy end point. Effects of sirolimus on lung function and neurocognitive function are also reported. Our data show an angiomyolipoma response rate, by RECIST criteria, of 50% in the intention to treat population. There was little change in lung function. Recall but not recognition memory tended to improve. Adverse events were common and consistent with the known toxicities of sirolimus. Our findings suggest that mTOR inhibition is a potential therapeutic strategy in the treatment of tuberous sclerosis and lymphangioleiomyomatosis.

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Boustany, Sarah. "Mechanisms of Airway Remodelling". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3577.

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Asthma is an inflammatory disease characterised by tissue remodelling. A prominent feature of this remodelling is an increase in the number and size of the blood vessels- formed from pre-existing capillaries – angiogenesis (Siddiqui et al., 2007; Wilson, 2003). This is triggered by many different endogenous angiogenic stimulators such as vascular endothelial growth factor (VEGF), and inhibited by endogenous angiogenic inhibitors such as tumstatin. Tumstatin is the non-collagenous domain (NC1) of the collagen IV α3 chain which, when cleaved, inhibits endothelial cell proliferation and induces apoptosis. Experiments described in this thesis have for the first time demonstrated the absence of tumstatin in the airways of individuals with asthma and lymphangioleiomyomatosis (LAM) as well as the functional responses to tumstatin as an angiogenic inhibitor, both in vitro and in vivo, in the airway. Although tumstatin was absent from the airways of asthmatic and LAM individuals it was present in the airways of individuals with no airways disease, chronic obstructive pulmonary disease, bronchiectasis and cystic fibrosis. No significant difference was seen in the levels of the Goodpasture Binding Protein (GPBP), a phosphorylating protein responsible for the alternate folding of tumstatin, between asthmatic, LAM and individuals with no airways disease. The αvβ3 integrin, reported to be necessary for the activity of tumstatin, as well as the individual αv and β3 sub-units were shown to be equally expressed in the airways of all patient groups. Co-localisation of tumstatin, VEGF and the αvβ3 integrin was seen in the disease free airways, however, a different pattern of VEGF and the αvβ3 integrin expression was observed in asthmatic and LAM airways with minimal co-localisation. Tumstatin was detected in serum and bronchoalveolar lavage fluid (BAL-f) samples from asthmatics and individuals with no airway disease, however there was no significant difference in the level of expression between the two groups. It was demonstrated that the tumstatin detected in the serum and BAL-f samples from asthmatics and individuals with no airway disease was part of the whole collagen IV α3 chain and not in its free and potentially active form. The ability of recombinant tumstatin to inhibit tube formation and proliferation of primary pulmonary endothelial cells was demonstrated for the first time. Further, the functional response of tumstatin was demonstrated in vivo in a mouse model of allergic airway disease. Tumstatin inhibited angiogenesis in the airway and decreased airway hyperresponsiveness. Whether there is potential for tumstatin, or a derivative thereof, to be of therapeutic value in airways diseases in which angiogenesis is a component should be the subject of future studies.

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Książki na temat "Lymphangioleiomyomatosis"

Joel, Moss, red. LAM and other diseases characterized by smooth muscle proliferation. New York: Marcel Dekker, 1999.

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Bar-Ziv, Stacey Pollock. The lung transplant experiences of women with pulmonary lymphangioleiomyomatosis. 2005.

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Publications, ICON Health. The Official Patient's Sourcebook on Lymphangioleiomyomatosis: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002.

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Dixon, Bradley P., J. Christopher Kingswood i John J. Bissler. Tuberous sclerosis complex renal disease. Redaktor Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0330.

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Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder affecting almost all organs. It has wider phenotypic variation than often appreciated, with less than half showing the combination of characteristic facial angiofibromas, epilepsy, and mental retardation. Renal angiomyolipomata or cysts are found in 90% and renal failure was historically a common mode of adult death from the disease. Pulmonary lymphangioleiomyomatosis is restricted to females. Angiomyolipomata or cystic disease, or both, may cause renal failure. Angiomyolipomata may also haemorrhage, especially from larger lesions. Manifestations of brain involvement substantially complicate management of many patients with TSC. The causative genes TSC1 and TSC2 encode tuberin and hamartin which are involved in control of the mammalian target of rapamycin pathway. Inhibitors of that pathway, such as sirolimus and everolimus, are therefore logical approaches to therapy and have been shown to be effective in reducing angiomyolipomata volume. It remains to be seen whether they can protect renal function.

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Części książek na temat "Lymphangioleiomyomatosis"

Henske, Elizabeth P., i Francis X. McCormack. "Lymphangioleiomyomatosis". W Molecular Basis of Pulmonary Disease, 85–110. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-59745-384-4_4.

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Seyama, Kuniaki. "Lymphangioleiomyomatosis". W Treatment of Cystic Fibrosis and Other Rare Lung Diseases, 87–98. Basel: Springer Basel, 2017. http://dx.doi.org/10.1007/978-3-0348-0977-1_5.

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Mocellin, Simone. "Lymphangioleiomyomatosis". W Soft Tissue Tumors, 523–25. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-58710-9_163.

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Wright, Angela M., i Philip T. Cagle. "Lymphangioleiomyomatosis". W Encyclopedia of Pathology, 260–64. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-69263-0_235.

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Rossi, Giulio, Mirca Valli, Alessandra Dubini i Paolo Spagnolo. "Lymphangioleiomyomatosis". W Transbronchial cryobiopsy in diffuse parenchymal lung disease, 133–40. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14891-1_14.

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Johnson, Simon R. "Lymphangioleiomyomatosis". W Orphan Lung Diseases, 271–83. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2401-6_17.

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Seyama, Kuniaki, Toshio Kumasaka, Teruhiko Sato i Keiko Mitani. "Lymphangioleiomyomatosis". W Lymphangiogenesis in Cancer Metastasis, 185–209. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2247-9_8.

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Popper, Helmut H., Nader Morad, Issam A. Al-Bozom, Imaad Bin Mujeeb i Armando E. Fraire. "Lymphangioleiomyomatosis". W Atlas of Neoplastic Pulmonary Disease, 69–72. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-89839-1_17.

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Johnson, Simon R. "Lymphangioleiomyomatosis". W Diffuse Parenchymal Lung Disease, 275–84. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000102697.

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Berg, Jeannette Zinggeler, i Lisa Young. "Lymphangioleiomyomatosis". W Gender, Sex Hormones and Respiratory Disease, 173–87. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-23998-9_8.

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Streszczenia konferencji na temat "Lymphangioleiomyomatosis"

Garcia Moyano, M., L. Ceberio Hualde, B. González Quero, I. González Muñoz, F. J. Martínez Núñez, M. Lázaro Serrano, A. Gandiaga Mandiola i B. Gener Querol. "Lymphangioleiomyomatosis and Genetics". W ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.129.

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Alsharif, M., i T. Vo. "A Rare Case of Lymphangioleiomyomatosis". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5021.

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Taveira-DaSilva, AM, WK Steagall, A. Rabel, OM Hathaway, S. Harari, R. Cassandro, M. Stylianou i J. Moss. "Reversible Airflow Obstruction in Lymphangioleiomyomatosis." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4345.

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Radzikowska, Elżbieta, Joanna Nowacka-Ejsmont, Joanna Miłkowska-Dymanowska, Elzbieta Wiatr, Katarzyna Błasinska, Adriana Rozy i Miquel Angel Pujana. "Allergy in patients with lymphangioleiomyomatosis". W ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.241.

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Riley, L., H. Venigandla, H. D. Tazelaar, P. Tunsupon i A. Ataya. "Lymphangioleiomyomatosis Presenting as Diffuse Alveolar Hemorrhage". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1467.

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Clements, D., LM Markwick i SR Johnson. "The CXCR4/CXCL12 Axis in Lymphangioleiomyomatosis." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4350.

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Hirose, M., Y. Inoue, A. Matsumuro, T. Arai, C. Sugimoto, S. Minamoto, K. Tachibana i in. "Impact of Th2 Cytokines in Lymphangioleiomyomatosis." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4340.

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Revilla Lopez, Eva, Cristina Berastegui, Berta Saez, Alejandra Mendez, Manuel Lopez Meseguer, Irene Sansano, Susana Gomez Olles i Antonio Roman. "Long-term sirolimus treatment in lymphangioleiomyomatosis". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3687.

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Oprescu, Nicolae C., Frank X. McCormack, Sue Byrnes i Brent W. Kinder. "Clinical Predictors Of Survival In Lymphangioleiomyomatosis". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2099.

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Baptista, Mafalda Martins, Natália Melo, Patrícia Mota, Helder Novais E. Bastos, Susana Guimarães, Conceição Souto-Moura, André Carvalho, José Miguel Jesus, Rui Cunha i António Morais. "Lymphangioleiomyomatosis – experience of a university hospital". W ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2371.

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Raporty organizacyjne na temat "Lymphangioleiomyomatosis"

Faber, V., G. M. Wing, L. Winter i J. D. Zahrt. Analysis of Lymphangioleiomyomatosis (LAM) patent tomograms: Stereology and modeling. Office of Scientific and Technical Information (OSTI), luty 1995. http://dx.doi.org/10.2172/10114236.

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Hammes, Stephen R., i Betty Diamond. Uterine-Specific Knockout of Tsc-2: A Mouse Model for Lymphangioleiomyomatosis. Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada597787.

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