Propolis is a candidate for cancer treatment with its activity against different tumor cells and, has a wide spectrum of biological and pharmacological activities due to the diversity of its components. In this study, antitumorigenic activities of ethanol extract of propolis (EEP) and ethanol extract of propolis loaded niosome (PLN) were compared using 2D and 3D cell culture. Niosome formulations were prepared by thin film hydration technique. Cell viability of EEP and PLN was analyzed on MCF7, A549, MDA-MB-231, SK-MEL, SK-BR-3, DU145 and L-929 cell lines using MTT assay. L929, MCF7 and A549 cells were cultured using the 3D petri dish technique and their spherical forms were obtained after 142 h. After 24 h, PLN and EEP application, cell viability analysis was performed on 3D cultures with WST assay. As a result, niosome formulations containing EEP showed higher activity than ethanol extract of propolis in cancer cells. While a slow decrease was observed in cell viability in EEP treated cancer cells, it was observed that the percentage viability rates decreased in a shorter time in PLN treated cancer cells. Also, PLN can be used as an anticancer activity drug such as Doxorubicin, but this is not the case for EEP.

Overproduction of reactive oxygen species occurs when inflammation induces oxidative stress in macrophages and microglia, leading to a self-sustaining cycle of cellular damage and neuroinflammation. Oxidative stress and neuroinflammation are well-established contributors to the pathophysiology of autism spectrum disorders, which are associated with impaired neuronal function, neuronal loss, and behavioral deficits. Damaged cells, through microglial activation, release additional inflammatory mediators under conditions of oxidative stress, exacerbating neuronal damage. Quercetin, a powerful dietary antioxidant, has been shown to scavenge free radicals, reduce oxidative stress, and inhibit inflammatory pathways. Given these properties, we hypothesize that quercetin may improve learning and social skills in individuals with autism spectrum disorders by alleviating oxidative stress and reducing brain levels of inflammatory cytokines. In this study, an autism model was established in 30 rats by intraperitoneal injection of 250 mg/kg/day propionic acid (PPA) for five days. The study groups were as follows: Group 1: Normal ontrol (n = 10); Group 2: PPA + saline (PPAS, n = 10); Group 3: PPA + Quercetin (PPAQ, n = 10). All treatments were administered for 15 days. At the end of the treatment, histological and biochemical analyses of brain tissue and behavioral tests related to autistic-like behaviors were performed. Malondialdehyde, tumor necrosis factor-alpha, and interleukin-13 levels in brain homogenates were significantly higher in the PPAS group compared to the control group, indicating elevated oxidative stress and inflammation following PPA exposure. The PPAQ group significantly reduced oxidative stress parameters and inflammatory biomarkers, demonstrating its antioxidant and anti-inflammatory effects. This biochemical improvement was accompanied by preserving Purkinje cells and neuronal populations, significantly reduced in the PPAS group. Moreover, quercetin-treated rats exhibited improved social behavior and learning, which were severely impaired in the PPAS group. These findings, when interpreted together, suggest that quercetin exerts its neuroprotective effects by targeting oxidative stress and neuroinflammation, thereby preventing neuronal cell loss and alleviating behavioral deficits associated with autism spectrum disorders. Graphical Abstract

Idiopathic pulmonary fibrosis is an aging-related, chronic lung disease, with unclear pathogenesis and no effective treatment. One of the triggering factors in cell aging is oxidative stress and it is known to have a role in idiopathic pulmonary fibrosis. In this paper, the protective effect of the E-CG-01 (3,4-lacto-cycloastragenol) molecule in terms of its antioxidant properties was evaluated in the bleomycin induced mice lung fibrosis model. Bleomycin sulfate was administered as a single dose (2.5 U/kg body weight) intratracheally to induce lung fibrosis. E-CG-01 was administered intraperitoneally in three different doses (2 mg/kg/day, 6 mg/kg/day, and 10 mg/kg/day) for 14 days, starting three days before the bleomycin administration. Fibrosis was examined by Hematoxylin-Eosin, Masson Trichrome, and immunohistochemical staining for TGF-beta1, Type I collagen Ki-67, and gama-H2AX markers. Activity analysis of catalase and Superoxide dismutase enzymes, measurement of total oxidant, total glutathione, and Malondialdehyde levels. In histological analysis, it was determined that all three different doses of the molecule provided a prophylactic effect against the progression of fibrosis compared to the bleomycin control group. However, it was observed that only the molecule applied in the high dose decreased the total oxidant stress level. Lung weight ratio increased in the BLM group but significantly reduced with high-dose E-CG-01. E-CG-01 at all doses reduced collagen deposition, TGF-β expression, and Ki-67 expression compared to the BLM group. Intermediate and high doses of E-CG-01 also significantly reduced alveolar wall thickness and edema formation. These findings suggest that E-CG-01 has potential therapeutic effects in mitigating lung fibrosis through its antioxidant properties.

This chapter explores the transformative role of digital twin technology in modern medicine, focusing on its integration with artificial intelligence (AI), big data, and predictive analytics to enhance personalized healthcare. Digital twins, virtual representations of patients based on biomedical data, enable advanced disease modeling, risk assessment, and individualized treatment simulations. By leveraging diverse data sources, including pathology, radiology, and biomarker analysis, AI-driven models provide clinicians with precise decision-support tools for early diagnosis, treatment optimization, and proactive patient management. The chapter examines recent examples and highlighting how digital twins enhance predictive healthcare and clinical outcomes. Ethical considerations, data privacy, and regulatory challenges are also discussed, ensuring responsible implementation of this emerging technology in patient care.

Aim: Determining oocyte quality is crucial for successful fertilization and embryonic development, and there is a serious correlation between live birth rates and oocyte quality. Parameters such as the regular/irregular formation of the cumulus cell layer around the oocyte, the number of cumulus cell layers and the homogeneity of the appearance of the ooplasm are used to determine the quality of the oocytes to be used in in vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) methods. Material and Methods: In this study, classification processes have been carried out using convolutional neural networks (CNN), a deep learning method, on the images of the cumulus-oocyte complex selected based on the theoretical knowledge and professional experience of embryologists. A convolutional neural network with a depth of 4 is used. In each depth level, one convolution, one ReLU and one max-pooling layer are included. The designed network architecture is trained using the Adam optimization algorithm. The cumulus-oocyte complexes (n=400) used in the study were obtained by using the oocyte aspiration method from the ovaries of the bovine slaughtered at the slaughterhouse. Results: The CNN-based classification model developed in this study showed promising results in classifying three-class image data in terms of cumulus-oocyte complex classification. The classification model achieved high accuracy, precision, and sensitivity values on the test dataset. Conclusion: Continuous research and optimization of the model can further improve its performance and benefit the field of cumulus-oocyte complexes classification and oocyte quality assessment.

Inflammation-induced oxidative stress in macrophages and microglia is associated with excessive production of reactive oxygen species, initiating a damaging cycle of neuroinflammation and cellular injury. These processes are significant contributors to the pathophysiology of autism spectrum disorders, which involve neuronal dysfunction, cell loss, and behavioral impairments. Under conditions of oxidative stress, activated microglia release pro-inflammatory mediators, further intensifying neuronal damage. Bismuth subsalicylate (BSS), a compound with well-documented anti-inflammatory and antioxidant properties, has shown potential in mitigating such neurodegenerative processes. This study aimed to evaluate the effects of BSS in reducing neuroinflammation and oxidative stress in a propionic acid (PPA)-induced autism model, alongside its impact on behavioral outcomes. The study utilized 30 male Wistar albino rats, with PPA administered intraperitoneally at 250 mg/kg/day for 5 days to induce an autism-like phenotype. Rats were divided into three groups: Group 1 (Normal control, n = 10); Group 2 (PPA + saline, PPAS, n = 10); and Group 3 (PPA + BSS, PPAB, n = 10). Treatments were administered for 15 days. Behavioral performance was assessed through three-chamber sociability, open field, and passive avoidance learning tests, followed by biochemical and histological evaluations of brain tissues. Biochemical analysis revealed a significant increase in malondialdehyde, tumor necrosis factor-alpha, and interleukin-17 levels in the PPAS group, indicating heightened oxidative stress and inflammation. Treatment notably reduced these markers, suggesting its efficacy in mitigating oxidative damage and inflammatory responses. Immunohistochemical results demonstrated reduced glial activation and enhanced neuronal preservation in the hippocampal and cerebellar regions of treated rats. Additionally, behavioral impairments in social interaction, exploration, and memory were significantly improved with BSS therapy. These results suggest that BSS may confer neuroprotective effects through attenuation of oxidative stress and neuroinflammation, potentially contributing to improved neuronal function and behavioral performance in a PPA-induced autism model.