Michał Fornalik

Artificial intelligence (AI) technology is advancing significantly, with many applications already in medicine, healthcare, and biomedical research. Among these fields, the area that AI is remarkably reshaping is biomedical scientific writing. Thousands of AI-based tools can be applied at every step of the writing process, improving time effectiveness, and streamlining authors’ workflow. Out of this variety, choosing the best software for a particular task may pose a challenge. While ChatGPT receives the necessary attention, other AI software should be addressed. In this review, we draw attention to a broad spectrum of AI tools to provide users with a perspective on which steps of their work can be improved. Several medical journals developed policies toward the usage of AI in writing. Even though they refer to the same technology, they differ, leaving a substantially gray area prone to abuse. To address this issue, we comprehensively discuss common ambiguities regarding AI in biomedical scientific writing, such as plagiarism, copyrights, and the obligation of reporting its implementation. In addition, this article aims to raise awareness about misconduct due to insufficient detection, lack of reporting, and unethical practices revolving around AI that might threaten unaware authors and medical society. We provide advice for authors who wish to implement AI in their daily work, emphasizing the need for transparency and the obligation together with the responsibility to maintain biomedical research credibility in the age of artificially enhanced science.

Senescent cells have been linked to the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the effectiveness of senolytic drugs in reducing liver damage in mice with MASLD is not clear. Additionally, MASLD has been reported to adversely affect male reproductive function. Therefore, this study aimed to evaluate the protective effect of senolytic drugs on liver damage and fertility in male mice with MASLD. Three-month-old male mice were fed a standard diet (SD) or a choline-deficient western diet (WD) until 9 months of age. At 6 months of age mice were randomized within dietary treatment groups into senolytic (dasatinib + quercetin [D + Q]; fisetin [FIS]) or vehicle control treatment groups. We found that mice fed choline-deficient WD had liver damage characteristic of MASLD, with increased liver size, triglycerides accumulation, fibrosis, along increased liver cellular senescence and liver and systemic inflammation. Senolytics were not able to reduce liver damage, senescence and systemic inflammation, suggesting limited efficacy in controlling WD-induced liver damage. Sperm quality and fertility remained unchanged in mice developing MASLD or receiving senolytics. Our data suggest that liver damage and senescence in mice developing MASLD is not reversible by the use of senolytics. Additionally, neither MASLD nor senolytics affected fertility in male mice.

Cancer-related cognitive impairment (CRCI) affects a significant proportion of cancer patients and survivors, impacting their memory, focus, mood, and quality of life. While non-pharmacological interventions have shown effectiveness in managing this condition, some studies have also explored various pharmacological agents, including donepezil, a reversible acetylcholinesterase inhibitor. This compound demonstrated beneficial effects on cognition in Alzheimer's disease; however, its effectiveness in CRCI remains unknown. This systematic review and meta-analysis aims to evaluate the efficacy of donepezil in improving cognitive outcomes in cancer patients. We conducted a search of PubMed/Medline, Embase, Cochrane Library, ClinicalTrials.gov, and the International Clinical Trials Registry Platform. Both randomized controlled trials and observational studies were included. We extracted data on cognitive outcomes of donepezil treatment, including the Hopkins Verbal Learning Test-Revised (HVLT-R), Trail Making Test (TMT), and Controlled Oral Word Association Test (COWA), as well as reported adverse events (AEs). Out of 896 identified records, nine studies involving 837 patients met the inclusion criteria, including five RCTs and four observational studies. Donepezil failed to demonstrate significant improvements in cognitive outcomes in HVLT-R, TMT, and COWA. Fatigue, measured as a secondary outcome, also showed no significant improvement. AEs, such as insomnia and headache, were more prevalent in adults than children. Donepezil did not increase the risk of AEs compared to placebo. This meta-analysis found that donepezil does not provide cognitive improvements for CRCI patients. Given the complex and multifactorial nature of CRCI, the lack of efficacy suggests that donepezil may not address the underlying mechanisms of the condition.

Adenosine deaminase acting on RNA 1 (ADAR1) plays an essential role in the development of malignancies by modifying the expression of different oncogenes. ADAR1 presents three distinct activities: adenosine-to-inosine RNA editing, modulating IFN pathways, and response to cellular stress factors. Following stressors such as heat shock, ADAR1p110 isoform relocates from the nucleus to the cytoplasm, where it suppresses RNA degradation which leads to the arrest of apoptosis and cell survival. In this study, we assessed the expression of ADAR1 across different cancer cell lines. We revealed that the presence of ADAR1 varies between cells of different origins and that a high transcript level does not reflect protein abundance. Additionally, we subjected cells to a heat shock in order to evaluate how cellular stress factors affect the expression of ADAR1. Our results indicate that ADAR1 transcript and protein levels are relatively stable and do not change under heat shock in examined cell lines. This research lays a groundwork for future directions on ADAR1-related studies suggesting in which types of cancer ADAR1 may be a promising target for novel therapeutic approaches.