Central Neurogenic Respiratory Failure: A Challenging Diagnosis

Background: Central nervous system lesions are rare causes of respiratory failure. Simple observation of the breathing pattern can help localize the lesion, but the examiner needs to be aware of potential pitfalls such as metabolic or pulmonary alterations. Methods: We describe 3 cases in which central neurogenic respiratory failure occurred simultaneously with other alterations or in an unusual presentation. Results: All patients were diagnosed with central neurogenic respiratory failure and treated for it with good recovery. Conclusion: Central neurogenic respiratory failure is a challenging diagnosis and needs to be reminded in difficult-to-wean patients carrying inconclusive evidences of metabolic or pulmonary alterations

Proteomic landscape of extracellular vesicles for diffuse large b‐cell lymphoma subtyping

Funding Information: R.M. is supported by Funda??o para a Ci?ncia e a Tecnologia (CEEC position, 2019?2025 investigator). This article is a result of the projects (iNOVA4Health?UID/Multi/04462/2013), supported by Lisboa Portugal Regional Operational Programme (Lisboa2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF). This work is also funded by FEDER funds through the COMPETE 2020 Programme and National Funds through FCT?Portuguese Foundation for Science and Technology under the projects number PTDC/BTM?TEC/30087/2017 and PTDC/BTM?TEC/30088/2017. B.C.S. is supported by the Cham-palimaud Foundation and the EMBO Installation Grant 3921. Funding Information: Funding: R.M. is supported by Fundação para a Ciência e a Tecnologia (CEEC position, 2019–2025 investigator). This article is a result of the projects (iNOVA4Health—UID/Multi/04462/2013), sup‐ ported by Lisboa Portugal Regional Operational Programme (Lisboa2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF). This work is also funded by FEDER funds through the COMPETE 2020 Programme and National Funds through FCT—Portuguese Foundation for Science and Technology under the projects number PTDC/BTM‐TEC/30087/2017 and PTDC/BTM‐TEC/30088/2017. B.C.S. is supported by the Cham‐ palimaud Foundation and the EMBO Installation Grant 3921. Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.The role of extracellular vesicles (EVs) proteome in diffuse large B‐cell lymphoma (DLBCL) pathology, subclassification, and patient screening is unexplored. We analyzed by state‐of‐the‐art mass spectrometry the whole cell and secreted extracellular vesicles (EVs) proteomes of different molecular subtypes of DLBCL, germinal center B cell (GCB subtype), and activated B cell (ABC subtype). After quality control assessment, we compared whole‐cell and secreted EVs proteomes of the two cell‐of‐origin (COO) categories, GCB and ABC subtypes, resulting in 288/1115 significantly differential expressed proteins from the whole‐cell proteome and 228/608 proteins from EVs (adjust p‐value < 0.05/p‐value < 0.05). In our preclinical model system, we demonstrated that the EV prote-ome and the whole‐cell proteome possess the capacity to separate cell lines into ABC and GCB sub-types. KEGG functional analysis and GO enrichment analysis for cellular component, molecular function, and biological process of differential expressed proteins (DEP) between ABC and GCB EVs showed a significant enrichment of pathways involved in immune response function. Other enriched functional categories for DEPs constitute cellular signaling and intracellular trafficking such as B‐cell receptor (BCR), Fc_gamma R‐mediated phagocytosis, ErbB signaling, and endocyto-sis. Our results suggest EVs can be explored as a tool for patient diagnosis, follow‐up, and disease monitoring. Finally, this study proposes novel drug targets based on highly expressed proteins, for which antitumor drugs are available suggesting potential combinatorial therapies for aggressive forms of DLBCL. Data are available via ProteomeXchange with identifier PXD028267.publishersversionpublishe