Int J Med Sci
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Background: Breast cancer (BC) is the most common cancer among women globally and poses the leading health threat to women worldwide, with persistently high incidence rates. Mitophagy is a selective autophagy process that specifically targets mitochondria within the cell, maintaining cellular energy balance and metabolic health by identifying and degrading damaged mitochondria. Although there is an understanding of the relationship between mitophagy and cancer, the specific mechanisms remain unclear due to the complexity and diversity of mitophagy, suggesting that it could be an effective and more targeted therapeutic approach for BC. ⋯ To enhance clinical applicability, age and staging were incorporated into the risk score, and a more comprehensive nomogram was constructed to predict OS. This nomogram was validated and showed good predictive performance, with area under the curve (AUC) values for 1-year, 3-year, and 5-year OS of 0.895, 0.765, and 0.728, respectively. Conclusion: Our findings underscore the profound impact of prognostic genes on the immune response and prognostic outcomes in BC, indicating that they can provide new avenues for personalized BC treatment and potentially improve clinical outcomes.
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Objectives: To create a nomogram using single photon emission computed tomography (SPECT) myocardial perfusion imaging and 18F-FDG positron emissions tomography (PET) gated myocardial metabolism imaging to forecast major adverse cardiovascular events (MACE) in chronic total occlusion (CTO) patients treated with optimal medical therapy (OMT). Methods: A total of 257 patients who received OMT between January 2016 and December 2021 were included in this retrospective study. Patients were randomly divided into development (n=179) and validation (n=78) cohorts. ⋯ The nomogram demonstrated excellent discrimination with C-indexes of 0.931 and 0.911 in the development and validation cohorts. DCA determined that the model exhibited a considerably superior net advantage in predicting MACE. Conclusion: A new nomogram integrating clinical factors and imaging features was created to predict the risk of MACE in patients with CTO.
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In the early stages of pregnancy, the maternal-fetal interface is enriched with natural killer (NK) cells that release growth factors to support fetal development and promote the remodeling of uterine spiral arteries. Previous studies have shown that the aberrant frequency and activity of decidual natural killer (dNK) cells are associated with recurrent pregnancy loss (RPL). Various factors regulate the roles of dNK cells and their interactions with trophoblasts to facilitate the colonization and maturation of semiallogeneic embryos. ⋯ Although there are few studies on the intervention of malfunctioning dNK cells, this strategy shows promise in regulating abnormal miRNA production in NK cells. This study confirmed miR-122-5p downregulation in dNK cells from patients experiencing unexplained RPL. miR-122-5p regulates apoptosis, inflammatory factor secretion, and cytotoxicity of NK cells. miR-122-5p may contribute to immune tolerance at the maternal-fetal interface by targeting transcription factor T-bet. This study provides a deeper understanding of the mechanisms by which miR-122-5p regulates the function of dNK cells and trophoblasts at the maternal-fetal interface to ensure successful pregnancy.
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Background: Both observational studies and clinical trials have demonstrated a link between the gut microbiota and the geriatric syndrome. Nevertheless, the exact nature of this relationship, particularly concerning causality, remains elusive. Mendelian randomization (MR) is a method of inference based on genetic variation to assess the causal relationship between an exposure and an outcome. ⋯ Similarly, insomnia demonstrated nine positive and two negative causal connections, while depression presented nine positive and two negative causal relationships. Conclusions: Using the TSMR method and data from the public GWAS database and, we observed associations between specific microbiota groups and geriatric syndromes. These findings suggest a potential role of gut microbiota in the development of geriatric syndromes, providing valuable insights for further research into the causal relationship between gut microbiota and these syndromes.
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Purpose: The high tumor mutational burden (TMB) of transformed follicular lymphoma (tFL) leads to tumor heterogeneity and poor prognosis in follicular lymphoma, in which endogenous DNA damage and epigenetic modification are the key factors. This study aims to evaluate the efficacy of anlotinib in tFL and to investigate its potential therapeutic mechanism. Methods: Cell viability and apoptosis were tested with CCK-8 and annexin V/PI staining kits, respectively. ⋯ Anlotinib administration resulted in a significant dose-dependent increase in the level of p-p53. Furthermore, anlotinib greatly downregulated the antiapoptotic proteins Mcl-1 and in parallel upregulated the proapoptotic element BAX and Bak, accompanied by caspase-3 activation and PARP degradation. Conclusion: Anlotinib has a good proapoptotic effect on tumor cells in vitro and in vivo, and its possible mechanism is related to the inhibition of the DNA damage response by disrupting SETD1A.