Background: Sjögren's syndrome is a tissue-specific autoimmune disease that affects exocrine tissues, especially salivary glands and lacrimal glands. Despite a large body of evidence gathered over the past 60 years, significant gaps still exist in our understanding of Sjögren's syndrome. The goal of this study was to develop a database that collects and organizes gene and protein expression data from the existing literature for comparative analysis with future gene expression and proteomic studies of Sjögren's syndrome.
Description: To catalog the existing knowledge in the field, we used text mining to generate the Sjögren's Syndrome Knowledge Base (SSKB) of published gene/protein data, which were extracted from PubMed using text mining of over 7,700 abstracts and listing approximately 500 potential genes/proteins. The raw data were manually evaluated to remove duplicates and false-positives and assign gene names. The data base was manually curated to 477 entries, including 377 potential functional genes, which were used for enrichment and pathway analysis using gene ontology and KEGG pathway analysis.
Conclusions: The Sjögren's syndrome knowledge base ( http://sskb.umn.edu) can form the foundation for an informed search of existing knowledge in the field as new potential therapeutic targets are identified by conventional or high throughput experimental techniques.
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http://dx.doi.org/10.1186/1471-2474-13-119 | DOI Listing |
JAMA Psychiatry
January 2025
Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania.
Importance: Mania/hypomania is the pathognomonic feature of bipolar disorder (BD). As BD is often misdiagnosed as major depressive disorder (MDD), replicable neural markers of mania/hypomania risk are needed for earlier BD diagnosis and pathophysiological treatment development.
Objective: To replicate the previously reported positive association between left ventrolateral prefrontal cortex (vlPFC) activity during reward expectancy (RE) and mania/hypomania risk, to explore the effect of MDD history on this association, and to compare RE-related left vlPFC activity in individuals with and at risk of BD.
Int J Cardiovasc Imaging
January 2025
Department of Cardiovascular Surgery, JCHO Kyushu Hospital, Kitakyushu City, Japan.
World J Pediatr
January 2025
The First Hospital of Peking University, Beijing, China.
Background: Glucose transporter 1 deficiency syndrome (Glut1DS) was initially reported by De Vivo and colleagues in 1991. This disease arises from mutations in the SLC2A1 and presents with a broad clinical spectrum. It is a treatable neuro-metabolic condition, where prompt diagnosis and initiation of ketogenic dietary therapy can markedly enhance the prognosis.
View Article and Find Full Text PDFIndian J Pediatr
January 2025
Pediatric Neurology Unit, Department of Pediatrics, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Neurol Sci
January 2025
Division of Pediatric Neurology, Ankara University Faculty of Medicine, Ankara, Turkey.
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