Background: Gynecological cancers, including ovarian, cervical, and endometrial cancers, significantly affect both survival and reproductive health in women. Cancer treatments such as chemotherapy and radiotherapy can impair ovarian function, reducing oocyte quality and fertility potential. Objective: This review aims to evaluate how vitamins and antioxidants can enhance fertility and fertility preservation outcomes for women diagnosed with gynecological cancers, particularly in the context of assisted reproductive technologies (ART). Standard treatments for these cancers, including hysterectomy, bilateral salpingo-oophorectomy, radiation, and chemotherapy, often compromise ovarian function and oocyte quality. This review focuses on the potential role of these interventions in improving oocyte quality, thereby supporting successful fertility preservation and ART outcomes. Methods: A comprehensive narrative review of the current literature was conducted, examining the effects of vitamins A, C, D3, E, and Coenzyme Q10 on oocyte quality, particularly in the context of oxidative stress and inflammation induced by cancer and its treatments. Results: The evidence suggests that certain vitamins and antioxidants may mitigate oxidative damage and enhance oocyte quality. Vitamin A supports cumulus–oocyte complex integrity, while vitamins C and E act as potent antioxidants, reducing oxidative stress in ovarian tissues. Vitamin D3 enhances ovarian reserve markers and modulates inflammatory cytokines. Coenzyme Q10 improves mitochondrial function and reduces DNA damage, increasing oocyte viability and fertilization potential. Conclusions: The incorporation of specific vitamins and antioxidants into fertility preservation strategies may enhance oocyte quality in women with gynecological cancers. Although the preliminary findings are promising, further research is needed to determine optimal dosages and establish standardized protocols for clinical use.

Custom-made dynamometry was shown to objectively analyze human muscle strength around the ankle joint with accuracy, easy portability and low costs. This paper describes the full method of calibration and measurement setup and the measurement procedure when capturing ankle torque for establishing reliability of a portable custom-built electronic dynamometer. After considering the load cell offset voltage, the pivotal position was determined, and calibration with loads followed. Linear regression was used for calculating the proportionality constant between torque and measured voltage. Digital means were used for data collection and processing. Four healthy consenting participants were enrolled in the study. Three consecutive maximum voluntary isometric contractions of five seconds each were registered for both feet during plantar flexion/dorsiflexion, and ankle torque was then calculated for three ankle inclinations. A calibration procedure resulted, comprising determination of the pivotal axis and pedal constant. Using the obtained data, a measurement procedure was proposed. Obtained contraction time graphs led to easier filtering of the results. When calculating the interclass correlation, the portable apparatus demonstrated to be reliable when measuring ankle torque. When a custom-made dynamometer was used for capturing ankle torque, accuracy of the method was assured by a rigorous calibration and measurement protocol elaboration.

Background: Asthma and atherosclerosis frequently coexist in clinical populations and share convergent immunometabolic pathways amplified by gut microbial dysbiosis. We propose the gut–lung–vascular axis as a unifying mechanistic framework connecting epithelial and endothelial inflammation providing a foundation for understanding shared inflammatory mechanisms beyond tissue-specific disease boundaries. Methods: A targeted narrative review systematically appraised clinical, experimental and multi-omics studies published over the last five years to delineate microbiota-driven pathways relevant to asthma and atherosclerosis. Particular emphasis was placed on specific microbial taxa, metabolite profiles and immunometabolic networks that connect gut dysbiosis with respiratory and cardiovascular dysfunction. Results: Across human and experimental cohorts, dysbiosis marked by depletion of short-chain fatty acids (SCFAs) producing taxa (Faecalibacterium, Roseburia, Bacteroides) and enrichment of pathobionts (Proteobacteria, Haemophilus, Moraxella, Streptococcus) promotes epithelial and endothelial barrier dysfunction, amplifying Th2/Th17-skewed inflammation and endothelial injury. Key metabolites, including SCFAs, trimethylamine N-oxide (TMAO), secondary bile acids (BA), indole/tryptophan derivatives and lipopolysaccharides (LPS), serve as molecular connectors linking gut, airway and vascular inflammation. Microbial signatures and metabolomic patterns hold emerging diagnostic and therapeutic potential, and several drug classes (e.g., statins, corticosteroids, proton-pump inhibitors (PPIs)) further modulate host–microbiota interactions. Conclusions: Shared microbial taxa and metabolite signatures in asthma and atherosclerosis support microbiota-mediated immune dysregulation along the gut–lung–vascular axis as a common pathogenic framework. Microbial and metabolite profiling may enable improved risk stratification and precise, microbiota-targeted therapies. Integrating microbiome-informed diagnostics and personalized interventions could help reduce systemic inflammation and the burden of these overlapping inflammatory diseases.

Asthma and atherosclerosis are chronic conditions with distinct pathophysiologies, but overlapping inflammatory mechanisms that suggest a potential common regulatory framework. MicroRNAs (miRNAs), small non-coding RNA molecules that modulate gene expression post-transcriptionally, could be key players in linking these disorders. This review outlines how miRNAs contribute to the complex interplay between asthma and atherosclerosis, focusing on key miRNAs involved in inflammatory pathways, immune cell regulation and vascular remodeling. We discuss specific miRNAs, such as miR-155, miR-21 and miR-146a, which have been shown to modulate inflammatory cytokine production and T cell differentiation, impacting respiratory and cardiovascular health. The common miRNAs found in both asthma and atherosclerosis emphasize their role as potential biomarkers, but also as therapeutic targets. Understanding these molecular connections may unlock novel approaches for innovative, integrated treatment strategies that address both conditions and may significantly improve patient outcomes. Further research is needed to explore mechanistic pathways and validate the translational potential of miRNA-based interventions in preclinical and clinical settings.

The negative effects of SARS-CoV-2 infection on the musculoskeletal system include symptoms of fatigue and sarcopenia. The aim of this study is to assess the impact of COVID-19 on foot muscle strength and evaluate the reproducibility of peak ankle torque measurements in time by using a custom-made electronic dynamometer. In this observational cohort study, we compare two groups of four participants, one exposed to COVID-19 throughout measurements and one unexposed. Peak ankle torque was measured using a portable custom-made electronic dynamometer. Ankle plantar flexor and dorsiflexor muscle strength was captured for both feet at different ankle angles prior and post COVID-19. Average peak torque demonstrated no significant statistical differences between initial and final moment for both groups (p = 0.945). An increase of 4.8%, p = 0.746 was obtained in the group with COVID-19 and a decrease of 1.3%, p = 0.953 was obtained in the group without COVID-19. Multivariate analysis demonstrated no significant differences between the two groups (p = 0.797). There was a very good test–retest reproducibility between the measurements in initial and final moments (ICC = 0.78, p < 0.001). In conclusion, peak torque variability is similar in both COVID-19 and non-COVID-19 groups and the custom-made electronic dynamometer is a reproducible method for repetitive ankle peak torque measurements.

Background and objectives: Regenerative medicine, with its massive development over the years, has the potential to solve some of the most problematic medical issues, such as functional organ transplantation. The aim of this study was to create a human meniscal shape 3D-printed enriched with human adipose-derived mesenchymal cells. Materials and Methods: Human infrapatellar fat pad was harvested, and mesenchymal cells were isolated. The mesenchymal stem cells were differentiated to the chondrocite lineage and a hydrogel (a nanofibrillar cellulose, sodium alginate, D-mannitol, and Hepes buffer solution combination) cell mixture was bioprinted to create three human-size meniscus structures. The obtained structures were evaluated regarding the cell viability, appropriate size in relation to a native meniscus, and some mechanical characteristics. Results: The human meniscal shape created respected the anatomic characteristic of a native structure. Cell viability of approximately 97% and extracellular matrix formation after the printing process were observed. The mean maximum force for the meniscus with mesenchymal cells was 6.5 N (+/−0.5 N) compared to the mean maximum force for the native meniscus of 10.32 N (+/−0.7 N), which is statistically relevant (p < 0.01). Conclusion: This paper presents the potential of bioprinting viable cell structures that could in the future present enough mechanical strength to replace a human organ, such as a meniscus. There are still limitations regarding the ink and the printing process, but we are confident that these problems will soon be solvable.