26 Due to the rarity of NMOSD, adequate disease-specific studies on temporal ON dynamics are scant. It can be assessed by OCT as peripapillary retinal nerve fibre layer thickness (pRNFL) or ganglion and inner plexiform layer thickness (GCIP). Retinal post-inflammatory neuroaxonal degeneration typically progresses for about 6 months after the onset of acute idiopathic ON. 23 24 After transection of optic nerve axons following acute ON, retrograde neurodegeneration leads to neuroaxonal damage in the retina. Optical coherence tomography (OCT) acquires high-resolution retinal images and plays an important role in assessing ON-associated damage in NMOSD 22 and other neuroinflammatory disorders associated with ON. These functional limitations result in impaired vision-related quality of life and a high incidence of legal blindness. 3 17 18 Patients often develop a visual disability as a result of decreased high-contrast visual acuity (HCVA) and low-contrast visual acuity, as well as colour and visual field defects. It frequently results in severe structural optic nerve damage and visual impairment, often occurs bilaterally, with common relapses. ON is one of the most common clinical manifestation of NMOSD. 13–15 The term myelin oligodendrocyte glycoprotein antibody disease has recently been proposed for this disorder. 9–12 As a different cellular target is involved, most experts consider MOG-IgG autoimmunity, or MOG-IgG-associated encephalomyelitis, as a separate disease entity, pathogenetically distinct from classic AQP4-IgG-associated NMOSD. 5 8 In some AQP4-IgG seronegative patients within the NMO disease spectrum, for example with isolated recurrent ON or myelitis, serum antibodies against myelin oligodendrocyte glycoprotein (MOG) can be detected. In the latter case, strict rules apply to the clinical presentation and paraclinical findings, in particular those from MRI for diagnosing NMOSD. 6 7 The diagnostic criteria differentiate patients with positive or negative/unknown AQP4-IgG status. 5 Pathogenic serum autoantibodies against aquaporin-4 (AQP4-IgG), an astrocytic water channel protein, can be detected in 60%–80% of patients with NMOSD. An international panel of experts published the latest NMOSD diagnostic criteria in 2015. 1–4 The current concepts of NMOSD are rapidly changing. They are clinically characterised by recurrent attacks of optic neuritis (ON), myelitis and less frequently by the brainstem and cerebral attacks, and profoundly impact patients’ quality of life. Neuromyelitis optical spectrum disorders (NMOSD) are rare autoimmune neuroinflammatory diseases spanning a broad age range. Paste web URL at the bottom of the dialog window you got in steps 4 and 5.Svenja Specovius, 1, 2 Hanna G Zimmermann, 1, 2 Frederike Cosima Oertel, 1, 2 Claudia Chien, 1, 2 Charlotte Bereuter, 1, 2 Lawrence J Cook, 3 Marco Aurélio Lana Peixoto, 4 Mariana Andrade Fontenelle, 4 Ho Jin Kim, 5 Jae-Won Hyun, 5 Su-Kyung Jung, 6 Jacqueline Palace, 7 Adriana Roca-Fernandez, 8 Alejandro Rubio Diaz, 7 Maria Isabel Leite, 7 Srilakshmi M Sharma, 9 Fereshte Ashtari, 10 Rahele Kafieh, 11 Alireza Dehghani, 12 Mohsen Pourazizi, 12 Lekha Pandit, 13 Anitha Dcunha, 13 Orhan Aktas, 14 Marius Ringelstein, 14, 15 Philipp Albrecht, 14 Eugene May, 16 Caryl Tongco, 16 Letizia Leocani, 17 Marco Pisa, 17 Marta Radaelli, 17 Elena H Martinez-Lapiscina, 18 Hadas Stiebel-Kalish, 19, 20 Mark Hellmann, 19 Itay Lotan, 19 Sasitorn Siritho, 21 Jérôme de Seze, 22 Thomas Senger, 22 Joachim Havla, 23 Romain Marignier, 24 Caroline Tilikete, 25 Alvaro Cobo Calvo, 24 Denis Bernardi Bichuetti, 26 Ivan Maynart Tavares, 27 Nasrin Asgari, 28, 29 Kerstin Soelberg, 28, 29 Ayse Altintas, 30 Rengin Yildirim, 31 Uygur Tanriverdi, 32 Anu Jacob, 33 Saif Huda, 33 Zoe Rimler, 34 Allyson Reid, 34 Yang Mao-Draayer, 35 Ibis Soto de Castillo, 36 Michael R Yeaman, 37, 38 Terry J Smith, 39, 40 Alexander U Brandt, # 1, 2, 41 Friedemann Paul, # 1, 2, 42 and GJCF International Clinical Consortium for NMOSD.
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If you do not see pencil go to bottom of page and click "Sign In" (almost hidden in small and light font). Edit this page by clicking on pencil icon in upper right.Upload your Robot Video, and CAD Animation to this folder (drag them to "Drop files here"). Click on file to get its URL.
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Click NEW to create your Google Slides file here (or upload here if you created it somewhere else).Click on "Shared With Me" => MAE3 Robots => Find your folder based upon quarter and team number.
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