SimpleXMLElement Object ( [PubmedArticle] => Array ( [0] => SimpleXMLElement Object ( [MedlineCitation] => SimpleXMLElement Object ( [@attributes] => Array ( [Status] => MEDLINE [Owner] => NLM ) [PMID] => 33441124 [DateCompleted] => SimpleXMLElement Object ( [Year] => 2021 [Month] => 01 [Day] => 21 ) [DateRevised] => SimpleXMLElement Object ( [Year] => 2021 [Month] => 01 [Day] => 21 ) [Article] => SimpleXMLElement Object ( [@attributes] => Array ( [PubModel] => Electronic ) [Journal] => SimpleXMLElement Object ( [ISSN] => 1756-994X [JournalIssue] => SimpleXMLElement Object ( [@attributes] => Array ( [CitedMedium] => Internet ) [Volume] => 13 [Issue] => 1 [PubDate] => SimpleXMLElement Object ( [Year] => 2021 [Month] => 01 [Day] => 13 ) ) [Title] => Genome medicine [ISOAbbreviation] => Genome Med ) [ArticleTitle] => Disease severity-specific neutrophil signatures in blood transcriptomes stratify COVID-19 patients. [Pagination] => SimpleXMLElement Object ( [MedlinePgn] => 7 ) [ELocationID] => 10.1186/s13073-020-00823-5 [Abstract] => SimpleXMLElement Object ( [AbstractText] => Array ( [0] => The SARS-CoV-2 pandemic is currently leading to increasing numbers of COVID-19 patients all over the world. Clinical presentations range from asymptomatic, mild respiratory tract infection, to severe cases with acute respiratory distress syndrome, respiratory failure, and death. Reports on a dysregulated immune system in the severe cases call for a better characterization and understanding of the changes in the immune system. [1] => In order to dissect COVID-19-driven immune host responses, we performed RNA-seq of whole blood cell transcriptomes and granulocyte preparations from mild and severe COVID-19 patients and analyzed the data using a combination of conventional and data-driven co-expression analysis. Additionally, publicly available data was used to show the distinction from COVID-19 to other diseases. Reverse drug target prediction was used to identify known or novel drug candidates based on finding from data-driven findings. [2] => Here, we profiled whole blood transcriptomes of 39 COVID-19 patients and 10 control donors enabling a data-driven stratification based on molecular phenotype. Neutrophil activation-associated signatures were prominently enriched in severe patient groups, which was corroborated in whole blood transcriptomes from an independent second cohort of 30 as well as in granulocyte samples from a third cohort of 16 COVID-19 patients (44 samples). Comparison of COVID-19 blood transcriptomes with those of a collection of over 3100 samples derived from 12 different viral infections, inflammatory diseases, and independent control samples revealed highly specific transcriptome signatures for COVID-19. Further, stratified transcriptomes predicted patient subgroup-specific drug candidates targeting the dysregulated systemic immune response of the host. [3] => Our study provides novel insights in the distinct molecular subgroups or phenotypes that are not simply explained by clinical parameters. 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Department of Internal Medicine and Radboud Center for Infectious Diseases (RCI), Radboud University Medical Center, Nijmegen, The Netherlands. ) ) ) [1] => SimpleXMLElement Object ( [@attributes] => Array ( [ValidYN] => Y ) [LastName] => Mouktaroudi [ForeName] => Maria [Initials] => M [AffiliationInfo] => SimpleXMLElement Object ( [Affiliation] => 4th Department of Internal Medicine, National and Kapodistrian University of Athens, Medical School, Athens, Greece. ) ) [2] => SimpleXMLElement Object ( [@attributes] => Array ( [ValidYN] => Y ) [LastName] => Krämer [ForeName] => Benjamin [Initials] => B [AffiliationInfo] => SimpleXMLElement Object ( [Affiliation] => Department I of Internal Medicine, University Hospital of Bonn (UKB), Bonn, Germany. ) ) [3] => SimpleXMLElement Object ( [@attributes] => Array ( [ValidYN] => Y ) [LastName] => Oestreich [ForeName] => Marie [Initials] => M [AffiliationInfo] => SimpleXMLElement Object ( [Affiliation] => Genomics and Immunoregulation, Life & 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[Pagination] => SimpleXMLElement Object ( [MedlinePgn] => 73-84 ) [ELocationID] => 10.1007/s10875-015-0214-9 [Abstract] => SimpleXMLElement Object ( [AbstractText] => Array ( [0] => Gain-of-function (GOF) mutations in the signal transducer and activator of transcription 1 (STAT1) result in unbalanced STAT signaling and cause immune dysregulation and immunodeficiency. The latter is often characterized by the susceptibility to recurrent Candida infections, resulting in the clinical picture of chronic mucocutaneous candidiasis (CMC). This study aims to assess the frequency of GOF STAT1 mutations in a large international cohort of CMC patients. [1] => STAT1 was sequenced in genomic DNA from 57 CMC patients and 35 healthy family members. The functional relevance of nine different STAT1 variants was shown by flow cytometric analysis of STAT1 phosphorylation in patients' peripheral blood cells (PBMC) after stimulation with interferon (IFN)-α, IFN-γ or interleukin-27 respectively. Extended clinical data sets were collected and summarized for 26 patients. [2] => Heterozygous mutations within STAT1 were identified in 35 of 57 CMC patients (61%). Out of 39 familial cases from 11 families, 26 patients (67%) from 9 families and out of 18 sporadic cases, 9 patients (50%) were shown to have heterozygous mutations within STAT1. Thirteen distinct STAT1 mutations are reported in this paper. Eight of these mutations are known to cause CMC (p.M202V, p.A267V, p.R274W, p.R274Q, p.T385M, p.K388E, p.N397D, and p.F404Y). However, five STAT1 variants (p.F172L, p.Y287D, p.P293S, p.T385K and p.S466R) have not been reported before in CMC patients. [3] => STAT1 mutations are frequently observed in patients suffering from CMC. Thus, sequence analysis of STAT1 in CMC patients is advised. 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[ArticleIdList] => SimpleXMLElement Object ( [ArticleId] => 23541088 ) ) [43] => SimpleXMLElement Object ( [Citation] => J Med Genet. 2013 Sep;50(9):567-78 [ArticleIdList] => SimpleXMLElement Object ( [ArticleId] => 23709754 ) ) ) ) ) ) ) ) Jan Raabe | PubFacts

Publications by authors named "Jan Raabe"

3Publications