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The role of NOTCH2NLC in Parkinson's disease: A clinical, neuroimaging, and pathological study.
Eur J Neurol
June 2022
Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Background And Purpose: Recently, the pathogenic and intermediate GGC repeat expansion in NOTCH2NLC was detected in Parkinson's disease (PD). However, detailed clinical, neuroimaging, and pathological information of clinically diagnosed PD patients with pathogenic GGC repeat expansion in NOTCH2NLC remains scarce. Thus, we aimed to elucidate the clinical, neuroimaging, and pathological characteristics of PD patients carrying the pathogenic GGC repeat expansion in NOTCH2NLC.
View Article and Find Full Text PDFProgressive multifocal leukoencephalopathy in idiopathic CD4 lymphocytopenia: A case report and review of literature.
Neuropathology
December 2019
Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease due to a lytic infection of oligodendrocytes caused by polyoma virus (JC virus) infection. PML usually occurs in a setting of severe immunosuppression and is most commonly associated with human immunodeficiency virus (HIV) infection. Idiopathic CD4 lymphocytopenia is a very rare cause of PML and only a few cases have been reported in the literature.
View Article and Find Full Text PDFNuclear actin aggregation is a hallmark of anti-synthetase syndrome-induced dysimmune myopathy.
Neurology
March 2015
From the Departments of Neuropathology (W.S., C.P., D.P., F.L.H., H.H.G.) and Rheumatology (U.S.), Charité-Universitätsmedizin Berlin, Germany; the Département de Médecine Interne et Immunologie Clinique (Y.A., O.B.), Centre de Référence Maladies Neuro-Musculaires Paris Est, Assistance Public-Hôpitaux de Paris Université Pierre et Marie Curie, Hôpital Pitié-Salpêtrière, Paris, France; the Section of Neuropathology, Department of Anatomical Pathology (R.J.), Path West Laboratory Medicine, Royal Perth Hospital, Perth; School of Pathology and Laboratory Medicine (R.J.), University of Western Australia, Nedlands, Australia; the Institute of Neuropathology (K.N., K.G.C., J.W.) and the Department of Neurology (K.G.C.), RWTH Aachen, Germany; the Department of Pathology and Neuropathology (E.A.), AMC University, Amsterdam, the Netherlands; the Department of Neuropathology (V.K., E.R.), University of Zürich, Switzerland; and the Department of Neuropathology (H.H.G.), University Medicine, Johannes Gutenberg University, Mainz, Germany.
Objective: To analyze antisynthetase syndrome-associated myositis by modern myopathologic methods and to define its place in the spectrum of idiopathic inflammatory myopathies (IIMs).
Methods: Skeletal muscle biopsies from antisynthetase syndrome-associated myositis and other IIMs from different institutions worldwide were analyzed by histopathology, quantitative PCR, and electron microscopy.
Results: Myonuclear actin filament inclusions were identified as a unique morphologic hallmark of antisynthetase syndrome-associated myositis.
Interleukin-33 potentiates bleomycin-induced lung injury.
Am J Respir Cell Mol Biol
December 2013
1 Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Maryland School of Medicine, Baltimore; and.
The mechanisms of interstitial lung disease (ILD) remain incompletely understood, although recent observations have suggested an important contribution by IL-33. Substantial elevations in IL-33 expression were found in the lungs of patients with idiopathic pulmonary fibrosis and scleroderma lung disease, as well as in the bleomycin injury mouse model. Most of the observed IL-33 expression was intracellular and intranuclear, suggesting involvement of the full-length (fl) protein, but not of the proteolytically processed mature IL-33 cytokine.
View Article and Find Full Text PDFTubular nuclear accumulation of Snail and epithelial phenotypic changes in human myeloma cast nephropathy.
Hum Pathol
August 2011
AP-HP, Hôpital Tenon, Urgences Néphrologiques & Transplantation Rénale, F-75020 Paris, France.
The transcription factor Snail is an important repressor of E-cadherin gene expression. It plays a key role in the induction of epithelial-mesenchymal transition, an essential process important not only in embryonic development and tumor progression but also in organ fibrogenesis. We studied the expression of Snail by immunohistochemistry, along with several epithelial phenotypic changes suggestive of epithelial-mesenchymal transition, in 14 patients with multiple myeloma cast nephropathy.
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