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Artykuły w czasopismach na temat "Immune-mediated necrotizing myopathies"
Mohammed, Abdel Gaffar A., Ayanda Gcelu, Farzana Moosajee, Stella Botha i Asgar Ali Kalla. "Immune Mediated Necrotizing Myopathy: Where do we Stand?" Current Rheumatology Reviews 15, nr 1 (12.12.2018): 23–26. http://dx.doi.org/10.2174/1573397114666180406101850.
Pełny tekst źródłaAllenbach, Yves, i Olivier Benveniste. "Peculiar clinicopathological features of immune-mediated necrotizing myopathies". Current Opinion in Rheumatology 30, nr 6 (listopad 2018): 655–63. http://dx.doi.org/10.1097/bor.0000000000000547.
Pełny tekst źródłaPinal-Fernandez, Iago, i Andrew L. Mammen. "Spectrum of immune-mediated necrotizing myopathies and their treatments". Current Opinion in Rheumatology 28, nr 6 (listopad 2016): 619–24. http://dx.doi.org/10.1097/bor.0000000000000335.
Pełny tekst źródłaKnauss, Samuel, Corinna Preusse, Yves Allenbach, Sarah Leonard-Louis, Mehdi Touat, Norina Fischer, Helena Radbruch i in. "PD1 pathway in immune-mediated myopathies". Neurology - Neuroimmunology Neuroinflammation 6, nr 3 (10.04.2019): e558. http://dx.doi.org/10.1212/nxi.0000000000000558.
Pełny tekst źródłaLee, Jong-Mok. "Immune-Mediated Necrotizing Myopathy: A Review for Clinicians". Journal of Electrodiagnosis and Neuromuscular Diseases 24, nr 3 (31.12.2022): 57–61. http://dx.doi.org/10.18214/jend.2022.00087.
Pełny tekst źródłaAkbar, Shalla, Sandhya Dasaraju i Osama Elkadi. "A Case of Immune-Mediated Necrotizing Myopathy With Associated Skeletal Muscle Involvement by Sarcoid Granulomata: A Rare Association". American Journal of Clinical Pathology 152, Supplement_1 (11.09.2019): S69. http://dx.doi.org/10.1093/ajcp/aqz113.078.
Pełny tekst źródłaSwafford, Collin, i E. Steve Roach. "Juvenile Dermatomyositis and the Inflammatory Myopathies". Seminars in Neurology 40, nr 03 (6.04.2020): 342–48. http://dx.doi.org/10.1055/s-0040-1705120.
Pełny tekst źródłaMecoli, Christopher A., Arash H. Lahouti, Robert A. Brodsky, Andrew L. Mammen i Lisa Christopher-Stine. "High-dose cyclophosphamide without stem cell rescue in immune-mediated necrotizing myopathies". Neurology - Neuroimmunology Neuroinflammation 4, nr 5 (11.07.2017): e381. http://dx.doi.org/10.1212/nxi.0000000000000381.
Pełny tekst źródłaPark, Sunha, Dae-Hyun Jang, Jae-Min Kim i Nara Yoon. "Prominent Asymmetric Muscle Weakness and Atrophy in Seronegative Immune-Mediated Necrotizing Myopathy". Diagnostics 11, nr 11 (8.11.2021): 2064. http://dx.doi.org/10.3390/diagnostics11112064.
Pełny tekst źródłaChiapparoli, Ilaria, Claudio Galluzzo, Carlo Salvarani i Nicolò Pipitone. "A glance into the future of myositis therapy". Therapeutic Advances in Musculoskeletal Disease 14 (styczeń 2022): 1759720X2211002. http://dx.doi.org/10.1177/1759720x221100299.
Pełny tekst źródłaRozprawy doktorskie na temat "Immune-mediated necrotizing myopathies"
Mahoudeau, Alexandrine. "Physiopathologie des myopathies inflammatoires idiopathiques : étude de la myostatine et spécificité des myopathies nécrosantes auto-immunes". Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS563.pdf.
Pełny tekst źródłaIdiopathic inflammatory myopathies (IIM) are a group of rare autoimmune diseases which can be divided into four subgroups: antisynthetase syndrome (ASyS), dermatomyositis (DM), immune-mediated necrotizing myopathy (IMNM), and inclusion body myositis (IBM). These subgroups differ in terms of physiopathogenesis, phenotype and prognosis. The main characteristic of IIM is muscle weakness with different degrees of severity being observed between subgroups. ASyS and DM patients have mild to moderate muscle involvement whereas IMNM and IBM patients display a more severe muscle weakness with poor recovery of muscle strength after remission. While most DM, IMNM, and ASyS patients present an acute onset of the symptoms, IBM is characterised by slowly progressing muscle weakness. Disease activity in IIM is difficult to assess. Some markers exist but are not applicable to all subgroups. In this thesis, I first wanted to see if myostatin, an inhibitor of muscle growth could be a marker of disease activity in IIM subgroups. For that, myostatin was dosed at the protein level in the serum and at the transcriptomic level in the muscle of IIM patients and healthy donors. Myostatin is decreased in patients in the blood and in the muscle. Lowered circulating myostatin levels in active ASyS and DM patients are increased when the disease is controlled. Myostatin could therefore be used as a disease activity biomarker in these subgroups. However, in IMNM patients, myostatin levels do not change with the disease activity, suggesting underlying specific pathomechanisms explaining the poor outcome of these patients. I was then particularly interested in IMNM pathogenesis. IMNM is characterised by proximal muscle weakness and a particular fibro-fatty infiltration in muscle over the course of the disease sustaining muscle weakness as well as necrotic fibers, macrophages infiltrates and auto-antibodies. I first tried to establish 2D and 3D in vitro cellular models but they were not conclusive. I then performed an analysis of patients’ muscle biopsies using spatial transciptomics and compared them to healthy donors biopsies. This method allows us to have transcripts of 55µm tissue domains across the entire muscle biopsy. Three major clusters emerge from this analysis: 2 macrophages clusters with an interferon signature, one being pro-inflammatory and the other one anti-inflammatory, and one fibro-adipogenic progenitors’ (FAP) cluster. These progenitors being able to differentiate either into fibroblasts or adipocytes, they could be the origin of the fibro-fatty infiltrate in IMNM patients. This FAPs increase was confirmed by a CD90 staining on muscle biopsies
Książki na temat "Immune-mediated necrotizing myopathies"
Limaye, Vidya Sadanand. Overview and epidemiology. Redaktorzy Hector Chinoy i Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0001.
Pełny tekst źródłaCzęści książek na temat "Immune-mediated necrotizing myopathies"
Stenzel, Werner, Hans-Hilmar Goebel, Olivier Benveniste i Yves Allenbach. "Immune-mediated necrotizing myopathies". W International Neurology, 508–10. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118777329.ch123.
Pełny tekst źródłaGaspar, Balan Louis. "Specific Forms of Immune-Mediated Necrotizing Myopathies". W Immune-Mediated Myopathies and Neuropathies, 73–100. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-8421-1_5.
Pełny tekst źródłaLundberg, Ingrid E., Hector Chinoy i Robert Cooper. "Inflammatory myopathies". W Oxford Textbook of Medicine, redaktor Richard A. Watts, 4537–46. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0457.
Pełny tekst źródłaMilone, Margherita, i Teerin Liewluck. "Progressive Weakness and Rash". W Mayo Clinic Cases in Neuroimmunology, redaktorzy Andrew McKeon, B. Mark Keegan i W. Oliver Tobin, 154–56. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197583425.003.0050.
Pełny tekst źródłaStreszczenia konferencji na temat "Immune-mediated necrotizing myopathies"
Fischer, N., C. Preusse, Y. Allenbach, T. Ruck, HH Goebel, D. Pehl, S. Meuth, O. Benveniste i W. Stenzel. "Sequestosome-1 staining pattern and chaperone-mediated autophagy in immune mediated necrotizing myopathies". W 24. Kongress des Medizinisch-Wissenschaftlichen Beirates der Deutschen Gesellschaft für Muskelkranke (DGM) e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685026.
Pełny tekst źródłaCarvalho, Ana Cláudia Pires, Fernanda Rezende Dias, Luisa Crevelin Costa i Natália de Castro Fim Nakao. "Myopathy following statin use". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.512.
Pełny tekst źródłaPires Borges, Isabela Bruna, Diego Sales de Oliveira, Suely Kazue Nagahashi Marie, Antonio Marcondes Lenario, Sueli Mieko Oba-Shinjo i Samuel Katsuyuki Shinjo. "Exercise training attenuates ubiquitin-proteasome pathway and increases genes related to autophagy on skeletal muscle of patients with dermatomyositis and immune-mediated necrotizing myopathies". W Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.16830.
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