Motivation: The study of genetic regulatory networks has received a major impetus from the recent development of experimental techniques allowing the measurement of patterns of gene expression in a massively parallel way. This experimental progress calls for the development of appropriate computer tools for the modeling and simulation of gene regulation processes.
Results: We present Genetic Network Analyzer (GNA), a computer tool for the modeling and simulation of genetic regulatory networks. The tool is based on a qualitative simulation method that employs coarse-grained models of regulatory networks. The use of GNA is illustrated by a case study of the network of genes and interactions regulating the initiation of sporulation in Bacillus subtilis.
Availability: GNA and the model of the sporulation network are available at http://www-helix.inrialpes.fr/gna.
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http://dx.doi.org/10.1093/bioinformatics/btf851 | DOI Listing |
Metab Brain Dis
January 2025
Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, 530000, China.
Alzheimer's disease (AD) is a neurodegenerative disease that primarily affects the elderly population and is the leading cause of dementia. Meanwhile, the vascular hypothesis suggests that vascular damage occurs in the early stages of the disease, leading to neurodegeneration and hindered waste clearance, which in turn triggers a series of events including the accumulation of amyloid plaques and Tau protein tangles. Non-coding RNAs (ncRNAs), including long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), have been found to be involved in the regulation of AD.
View Article and Find Full Text PDFCrit Care
January 2025
HCor Research Institute, Hospital do Coração, Rua Desembargador Eliseu Guilherme 200, 8th Floor, São Paulo, SP, 04004-030, Brazil.
Background: Limited data is available to evaluate the burden of device associated healthcare infections (HAI) [central line associated bloodstream infection (CLABSI), catheter associated urinary tract infection (CAUTI), and ventilator associated pneumonia (VAP)] in low and-middle-income countries. Our aim is to investigate the population attributable mortality fraction and the absolute mortality difference of HAI in a broad population of critically ill patients from Brazil.
Methods: Multicenter cohort study from September 2019 to December 2023 with prospective individual patient data collection.
Alzheimers Res Ther
January 2025
Department of Bioengineering, University of California, San Diego, La Jolla, CA, 92093, USA.
Background: PSEN1, PSEN2, and APP mutations cause Alzheimer's disease (AD) with an early age at onset (AAO) and progressive cognitive decline. PSEN1 mutations are more common and generally have an earlier AAO; however, certain PSEN1 mutations cause a later AAO, similar to those observed in PSEN2 and APP.
Methods: We examined whether common disease endotypes exist across these mutations with a later AAO (~ 55 years) using hiPSC-derived neurons from familial Alzheimer's disease (FAD) patients harboring mutations in PSEN1, PSEN2, and APP and mechanistically characterized by integrating RNA-seq and ATAC-seq.
BMC Med Genomics
January 2025
Yuyao People's Hospital of Zhejiang Province, Ningbo, Zhejiang, China.
Enhancer RNA (eRNA) has emerged as a key player in cancer biology, influencing various aspects of tumor development and progression. In this study, we investigated the role of eRNAs in kidney renal clear cell carcinoma (KIRC), the most common subtype of renal cell carcinoma. Leveraging high-throughput sequencing data and bioinformatics analysis, we identified differentially expressed eRNAs in KIRC and constructed eRNA-centric regulatory networks.
View Article and Find Full Text PDFEMBO Rep
January 2025
Rudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.
The protein interactome of p65/RELA, the most active subunit of the transcription factor (TF) NF-κB, has not been previously determined in living cells. Using p65-miniTurbo fusion proteins and biotin tagging, we identify >350 RELA interactors from untreated and IL-1α-stimulated cells, including many TFs (47% of all interactors) and >50 epigenetic regulators belonging to different classes of chromatin remodeling complexes. A comparison with the interactomes of two point mutants of p65 reveals that the interactions primarily require intact dimerization rather than DNA-binding properties.
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