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The assessment of testicular artery blood flow by colour and pulsed-Doppler ultrasonography is an important diagnostic technique to assess vascular perfusion. Recently, it has been suggested as a good predictor of sperm quality. On the other hand, through the alkaline Comet Assay, it is possible to quantify sperm oxidative DNA damage. The aim of this study was to evaluate the relationship between routine sperm parameters, testicular artery blood flow and oxidative DNA damage in canine sperm. Testicular ultrasonography and sperm collection were performed on 12 male dogs, with the animals being allocated into 2 groups, according to the classification of the ejaculates' quality, as normozoospermic (N; n = 7) or non-normozoospermic (OAT; n = 5). Seven dogs aged between 1.5 and 8.0 years old were included in group N and 5 dogs, aged between 2.0 and 11.0 years old, were included in group OAT. The sperm-rich fraction of the ejaculates was evaluated for sperm routine parameters and DNA damage by comet assay. Colour and pulsed-Doppler ultrasonography were used to evaluate the blood flow of the supratesticular and marginal arteries of right and left testis. Group OAT presented higher levels of sperm oxidative DNA damage (A.U.) in comparison to group N (N:11.7 ± 9.9; OAT:34.2 ± 6.1; P< .001). The peak of systolic velocity was positively correlated with sperm concentration (r = 0.685; P= .005). The resistive and pulsatility indexes (RI and PI) of the supratesticular artery were negatively correlated with sperm membrane integrity (HOST) (r = -0.594; P = .042; r = -0.612; P = .035, respectively). The end diastolic velocity (EDV) of the supratesticular artery was positively correlated with sperm concentration (r = 0.748; P = .005) and negatively correlated with sperm oxidative DNA damage (r = -0.766; P = .004). Our results suggest that the assessment of the testicular artery blood flow by colour and pulsed-Doppler ultrasonography could be a good predictor of sperm quality in dogs in terms of sperm concentration, membrane integrity and sperm oxidative DNA damage.
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http://dx.doi.org/10.1016/j.tcam.2020.100452 | DOI Listing |
Mutat Res Rev Mutat Res
September 2025
Institute of Environmental Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China. Electronic address:
To maintain genomic stability, cells have evolved complex mechanisms collectively known as the DNA damage response (DDR), which includes DNA repair, cell cycle checkpoints, apoptosis, and gene expression regulation. Recent studies have revealed that long non-coding RNAs (lncRNAs) are pivotal regulators of the DDR. Beyond their established roles in recruiting repair proteins and modulating gene expression, emerging evidence highlights two particularly intriguing functions.
View Article and Find Full Text PDFAnnu Rev Pathol
September 2025
3Department of Pathology, Stanford University, Stanford, California, USA;
Clonal hematopoiesis, originally identified as a precursor to hematologic malignancies, has emerged as a significant factor in various nonmalignant diseases. Recent research highlights how somatic mutations in hematopoietic stem cells lead to the expansion of circulating mutated immune cells that exert profound effects on organ function and disease progression. These mutated clones display altered inflammatory profiles and tissue-specific functional consequences, contributing to various diseases including atherosclerotic cardiovascular disease, osteoporosis, heart failure, and neurodegenerative conditions.
View Article and Find Full Text PDFPLoS Comput Biol
September 2025
Department of Genome Sciences, University of Washington, Seattle, Washington, United States of America.
Fanconi Anemia (FA) is a heritable syndrome characterized by DNA damage repair deficits, frequent malformations and a significantly elevated risk of bone marrow failure, leukemia, and mucosal head and neck squamous cell carcinomas (HNSCC). Hematopoietic stem cell gene therapy can prevent marrow failure and lower leukemia risk, but mucosal gene therapy to lower HNSCC risk remains untested. Major knowledge gaps include an incomplete understanding of how rapidly gene-corrected cellular lineages could spread through the oral epithelium, and which delivery parameters are critical for ensuring efficient gene correction.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Cancer Research Center of Marseille: Team DNA Damage and Genome Instability|CNRS, Inserm, Institut Paoli-Calmettes, Aix Marseille Université, Marseille 13009, France.
Following encounter with an unrepaired DNA lesion, replication is halted and can restart downstream of the lesion leading to the formation of a single-stranded DNA (ssDNA) gap. To complete replication, this ssDNA gap is filled in by one of the two lesion tolerance pathways: the error-prone Translesion Synthesis (TLS) or the error-free Homology Directed Gap Repair (HDGR). In the present work, we evidence a role for the RecBC complex distinct from its canonical function in homologous recombination at DNA double strand breaks.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139.
The mutagenic translesion synthesis (TLS) pathway, which is critically dependent on REV1's ability to recruit inserter TLS polymerases and the POLζ extender polymerase, enables cancer cells to bypass DNA lesions while introducing mutations that likely contribute to the development of chemotherapy resistance and secondary malignancies. Targeting this pathway represents a promising therapeutic strategy. Here, we demonstrate that the expression of the C-terminal domain (CTD) of human REV1, a ca.
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