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The impact of a secondary, rare, non-pathogenic PKD1 variant on disease progression in autosomal dominant polycystic kidney disease.
J Nephrol
January 2025
Department of Nephrology, Beaumont Hospital, Dublin, Ireland.
Background: Autosomal dominant polycystic kidney disease (ADPKD) is caused primarily by pathogenic variants in the PKD1 and PKD2 genes. Although the type of ADPKD variant can influence disease severity, rare, hypomorphic PKD1 variants have also been reported to modify disease severity or cause biallelic ADPKD. This study examines whether rare, additional, potentially protein-altering, non-pathogenic PKD1 variants contribute to ADPKD phenotypic outcomes.
View Article and Find Full Text PDFComparison of the 2023 ISCVID and ESC Duke clinical criteria for the diagnosis of infective endocarditis among patients with positive blood cultures for new typical microorganisms.
Infection
January 2025
Infectious Diseases Service, Lausanne University Hospital, Lausanne, Switzerland.
Purpose: To evaluate the performance of the Duke clinical criteria of the European Society of Cardiology (ESC; 2015 and 2023 versions) and the 2023 International Society for Cardiovascular Infectious Diseases (ISCVID) in diagnosing infective endocarditis (IE) among patients with bacteraemia/candidaemia by pathogens introduced for the first time as typical microorganisms by ISCVID.
Methods: Retrospective study.
Setting: This study included adult patients with bacteraemia/candidaemia by such pathogens (coagulase negative staphylococci, Abiotrophia spp.
Risk factors for survival after lung transplantation in cystic fibrosis: impact of colonization with multidrug-resistant strains of Pseudomonas aeruginosa.
Infection
January 2025
Department of Thoracic Surgery, Saarland University, 66421, Homburg/Saar, Germany.
Background: Lung transplantation is the ultimate treatment option for patients with advanced cystic fibrosis. Chronic colonization of these recipients with multidrug-resistant (MDR) pathogens may constitute a risk factor for an adverse outcome. We sought to analyze whether colonization with MDR pathogens, as outlined in the German classification of multiresistant Gram-negative bacteria (MRGN), was associated with the success of lung transplantation.
View Article and Find Full Text PDFDSCI: a database of synthetic biology components for innate immunity and cell engineering decision-making processes.
Adv Biotechnol (Singap)
September 2024
MOE Key Laboratory of Gene Function and Regulation, Guangdong Province Key Laboratory of Pharmaceutical Functional Genes, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, Guangdong, 510275, China.
Although significant progress of clinical strategy has been made in gene editing and cell engineering in immunotherapy, it is now apparent that design and modification in terms of complex signaling pathways and motifs on medical synthetic biology are still full of challenges. Innate immunity, the first line of host defense against pathogens, is critical for anti-pathogens immune response as well as regulating durable and protective T cell-mediated anti-tumor responses. Here, we introduce DSCI (Database of Synthetic Biology Components for Innate Immunity, https://dsci.
View Article and Find Full Text PDFControl of virulence and physiology by the flagellin homeostasis checkpoint FliC-FliW-CsrA in the absence of motility.
mBio
January 2025
Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
Unlabelled: Mutations affecting flagellin (FliC) have been shown to be hypervirulent in animal models and display increased toxin production and alterations in central metabolism. The regulation of flagellin levels in bacteria is governed by a tripartite regulatory network involving , , and , which creates a feedback system to regulate flagella production. Through genomic analysis of clade 5 strains (non-motile), we identified they have jettisoned many of the genes required for flagellum biosynthesis yet retain the major flagellin gene and regulatory gene .
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