Genetic epidemiology focuses on the familial and, in particular, genetic, determinants of disease and the joint effects of genes and environmental factors. Thus, genetic epidemiology aims at quantifying the risk of disease, cancer included, associated with genetic variation within a given population. In spite of the fact that most cases of cancer are initiated based on environmental exposures accumulated during a life-time, the carcinogenetic process itself is governed by a set of specified and unspecified genetic malfunctions, making genetic epidemiology a valuable methodological platform in cancer research. Details are given on known and suspected causes of cancer, including presumable gene-gene and gene-environment interactions.
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PLoS One
January 2025
Veterinary School, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Salmonella Dublin is a serovar that causes severe infections and cattle. Despite the importance of this agent, research on achieving its elimination from dairy farms is limited, which complicates risk mitigation and control efforts. This study thus aimed to assess the prevalence of S.
View Article and Find Full Text PDFPLoS Negl Trop Dis
January 2025
Center for Infection and Molecular Medicine, Amsterdam UMC location University of Amsterdam, Amsterdam, the Netherlands.
The global priorities in the field of infectious diseases are constantly changing. While emerging viral infections have regularly dominated public health attention, which has only intensified after the COVID-19 pandemic, numerous bacterial diseases have previously caused, and continue to cause, significant morbidity and mortality-deserving equal attention. Three potentially life-threatening endemic bacterial diseases (leptospirosis, melioidosis, and rickettsioses) are a huge public health concern especially in low- and middle-income countries.
View Article and Find Full Text PDFAnnu Rev Pharmacol Toxicol
January 2025
Center for Cardiovascular Research, Division of Cardiology, Department of Medicine, Washington University School of Medicine, Saint Louis, Missouri, USA; email:
Although human genetics has substantial potential to illuminate novel disease pathways and facilitate drug development, identifying causal variants and deciphering their mechanisms remain challenging. We believe these challenges can be addressed, in part, by creatively repurposing the results of molecular trait genome-wide association studies (GWASs). In this review, we introduce techniques related to molecular GWASs and unconventionally apply them to understanding , a human coronary artery disease risk locus.
View Article and Find Full Text PDFBull Math Biol
January 2025
Section of Epidemiology, University of Copenhagen, Copenhagen, Denmark.
Using genetic data to infer evolutionary distances between molecular sequence pairs based on a Markov substitution model is a common procedure in phylogenetics, in particular for selecting a good starting tree to improve upon. Many evolutionary patterns can be accurately modelled using substitution models that are available in closed form, including the popular general time reversible model (GTR) for DNA data. For more complex biological phenomena, such as variations in lineage-specific evolutionary rates over time (heterotachy), other approaches such as the GTR with rate variation (GTR ) are required, but do not admit analytical solutions and do not automatically allow for likelihood calculations crucial for Bayesian analysis.
View Article and Find Full Text PDFFunct Integr Genomics
January 2025
Department of Hepatobiliary Surgery, Jintan Affiliated Hospital of Jiangsu University, 213200, Changzhou, Jiangsu, China.
One of the outstanding features of chronic hepatitis B infection (CHB) is its strong association with liver fibrosis. CHB induced inflammation and injury trigger multiple biochemical and physical changes that include the promotion of a wide range of cytokines, chemokines and growth factors that activate hepatic stellate cells (HSCs) CHB induced activation of hepatic stellate cells (HSCs) is regarded as a central event in fibrogenesis to directly promote the synthesis of myofibroblasts and the expression of a range of materials to repair injured liver tissue. Fibrogenesis is modulated by the mainstream epigenetic machinery, as well as by non-coding RNA (ncRNA) that are often referred to as an ancillary epigenetic response to fine tune gene expression.
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