The development of a bacterial mutation assay using forward mutation to ampicillin-resistance is described. It is a technically simple assay using Escherichia coli D494uvrB transformed with a multi-copy mutator plasmid pGW1700. Mutation is detected by an increase in the frequency of ampicillin-resistant colonies following treatment of bacteria with the test material during logarithmic growth. The determination of viable counts allows a correction factor to be applied to compensate for the effects of sample-induced growth enhancement or toxicity on the bacterial population. The assay has been tested with a range of reference mutagens. It is particularly sensitive to base-pair substitution mutagens, detecting these at doses equal to or less than those detected in the Salmonella/microsome assay or the SOS Chromotest. The assay also detects frameshift mutagens but with lower sensitivity than the Salmonella/microsome assay.
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http://dx.doi.org/10.1093/mutage/2.6.455 | DOI Listing |
G3 (Bethesda)
January 2025
Department of Neurobiology, School of Biological Sciences, University of California San Diego, La Jolla, CA 92093.
The conserved MAP3K DLKs are widely known for their functions in synapse formation, axonal regeneration and degeneration, and neuronal survival, notably under traumatic injury and chronic disease conditions. In contrast, their roles in other neuronal compartments are much less explored. Through an unbiased forward genetic screening in C.
View Article and Find Full Text PDFClin Chem Lab Med
January 2025
Department of Medicine, University of Padova, Padova, Italy.
Objectives: Mutations in the gene encoded glycoprotein progranulin (PGRN), cause 5-10 % of all cases of frontotemporal lobar degeneration (FTLD). The aim of our study was to verify the analytical and clinical performance of an automated chemiluminescent immunoassay method for PGRN measurement recently developed (Chorus Evo, Diesse Diagnostica, Italy).
Methods: Five plasma pools and residual plasma samples (KEDTA) from 25 control subjects (11 males, 62-79 years; 14 females, 54-76 years) and 151 patients (70 males, 53-81 years; 81 females, 44-82 years) with different neurodegenerative disorders (NDs), were assayed.
Neurol Genet
February 2025
Department of Neurology and Neurosurgery, McGill University, Montreal, Canada.
In the late 1800s, Nikolaus Friedreich first described "degenerative atrophy of the posterior columns of the spinal cord," noting its connection to progressive ataxia, sensory loss, and muscle weakness, now recognized as Friedreich ataxia (FRDA). Renewed interest in the disease in the 1970s and 80s by the Quebec Cooperative Group and by Anita Harding led to the development of clinical diagnostic criteria and insights into associated biochemical abnormalities, although the primary defect remained unknown. In 1988, Susan Chamberlain mapped FRDA's location on chromosome 9.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Biology of Bacteria, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, 90-237 Lodz, Poland.
The widespread and inappropriate use of antibiotics, for therapeutic and prophylactic purposes, has contributed to a global crisis of rapidly increasing antimicrobial resistance of microorganisms. This resistance is often associated with elevated mutagenesis induced by the presence of antibiotics. Additionally, subinhibitory concentrations of antibiotics can trigger stress responses in bacteria, further exacerbating this problem.
View Article and Find Full Text PDFDiagnostics (Basel)
December 2024
Department of Medicine I (Hematology, Oncology and Stem Cell Transplantation), Freiburg University Medical Center, 79106 Freiburg, Germany.
Given the poor prognosis of metastatic pancreatic adenocarcinoma (mPDAC), closer disease monitoring through liquid biopsy, most frequently based on serial measurements of cell-free mutated ( cfDNA), has become a highly active research focus, aimed at improving patients' long-term outcomes. However, most of the available data show only a limited predictive and prognostic value of single-parameter-based methods. We hypothesized that a combined longitudinal analysis of cfDNA and novel protein biomarkers could improve risk stratification and molecular monitoring of patients with mPDAC.
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