Background: Zeste White 10 (ZW10) is a key component of the spindle assembly checkpoint (SAC) that maintains chromosomal stability during mitosis. Dysregulation of ZW10 can cause chromosomal instability and aneuploidy-hallmarks of many cancers, including breast cancer, particularly triple-negative breast cancer (TNBC). However, its prognostic and therapeutic relevance in breast cancer remains unclear. Objectives: This study aimed to systematically investigate the expression pattern, prognostic significance, mutational profile, and immune associations of ZW10 in breast cancer using integrated omics data. Design: A computational, cross-cohort bioinformatics analysis combining transcriptomic, proteomic, mutational, and clinical data from publicly available databases. Methods: The ZW10 expression levels were assessed across normal and cancerous tissues using The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and the Human Protein Atlas data sets. Immune infiltration correlations were analyzed using TIMER2.0, Gene Set Cancer Analysis (GSCA), and TNMplot. Survival analyses were performed using Kaplan-Meier Plotter and TCGA clinical data sets. Protein-protein interaction (PPI) and functional enrichment analyses were conducted using STRING and EnrichR, and mutation data were retrieved from COSMIC and cBioPortal. Results: The ZW10 expression was markedly upregulated across multiple cancers, with the highest expression in TNBC. Elevated ZW10 levels correlated with immune cell infiltration and adverse overall survival, while lower ZW10 expression predicted improved relapse-free survival. Protein-protein interaction and enrichment analyses revealed ZW10's close interaction with key mitotic regulators and its involvement in spindle checkpoint and vesicular trafficking pathways. Mutation analysis identified predominant A > G and A > T substitutions and frequent gene amplifications across malignancies. Conclusion: The ZW10 acts as a potential prognostic biomarker and therapeutic target in breast cancer, particularly TNBC, through its dual roles in mitotic regulation and immune modulation. Further experimental validation is warranted to confirm its mechanistic role and therapeutic potential.
The coronavirus disease 2019 (COVID-19) pandemic has been associated with a wide range of neurological complications, among which persistent cognitive impairment and memory deficits are increasingly recognized as key symptoms of the post-acute sequelae of SARS-CoV-2 infection (PASC or long COVID). Although clinical and epidemiological studies have documented these symptoms across diverse patient populations, the underlying neurobiological mechanisms remain incompletely understood. Growing evidence from human studies, neuropathological analyses, and experimental models indicates that neuroimmune and inflammatory processes plays a central role in COVID-19-associated cognitive dysfunction. As the brain’s resident immune cells, microglia are vital for synaptic health, neuroplasticity, and memory, yet these processes may be compromised after SARS-CoV-2 infection. Systemic inflammation, blood–brain barrier (BBB) disruption, endothelial injury, and cytokine signaling can induce sustained microglial activation and priming, leading to inflammasome activation, complement-mediated synaptic remodeling, oxidative stress, and impaired hippocampal neurogenesis. These processes collectively disrupt neural circuits involved in learning and memory and may underlie the persistent “brain fog” reported by COVID-19 survivors. This review synthesizes clinical, biomarker, neuroimaging, and mechanistic evidence linking SARS-CoV-2 infection to microglia-mediated neuroinflammation and memory impairment. In contrast to prior reviews that broadly describe neuroinflammation in COVID-19, we integrate multidimensional evidence into a microglia-centric immunovascular framework that highlights converging pathogenic pathways underlying cognitive symptoms. We further discuss emerging biomarkers of glial activation and evaluate current and prospective therapeutic strategies targeting microglial and neuroimmune pathways. Understanding the role of microglial dysregulation in post-COVID cognitive impairment may facilitate the development of targeted interventions to mitigate long-term neurological consequences of COVID-19.
Abstract Fine particulate matter (PM₂.₅) poses significant public and environmental health risks in urban areas. Chicago’s dense industry and traffic create variable air quality, yet monitoring is unevenly distributed, resulting in undersampling of air quality data in some city areas. This study applied a hybrid approach using GIS-based kernel density mapping, interpolation modeling (IDW, Spline, Kriging) of USEPA monitoring data, multi-scale temporal trend analyses (hourly to annual), and ESDA. Accordingly, the density surface showed that monitors are concentrated in the affluent north, northwest, and southwest sides of Chicago (up to ~ 0.07 stations per sq mile), while the south and southeast regions, with predominantly minority communities, have virtually no coverage. Overall, citywide coverage is minimal (~ 4–5 monitors total; ~0.02 per sq mile; ≈1 per 600,000 residents). Temporal analyses showed that the city’s mean annual PM₂.₅ (~ 10.8 µg/m³) exceeds USEPA/WHO standards (9 µg/m³), with summer means (~ 17.1 µg/m³) significantly higher than other seasons. Diurnally, a clear pattern was observed, with PM₂.₅ concentrations peaking overnight (00:00–03:00) and during the morning rush hours, and dipping during midday to late afternoon. Spatial distribution of PM₂.₅ identified hotspots near O’Hare Airport, the downtown Loop area, and south-side neighborhoods, contrasting with lower concentrations on the north side, revealing Chicago’s socioeconomic divides and resulting environmental inequities. The findings underscore the need for expanded monitoring and targeted interventions in under-monitored, high-pollution communities to advance equitable community health.
Pistacia vera L. (P. vera) is a dioecious tree species of high agronomic and ecological importance and serves as a suitable model for investigating sex-specific responses to abiotic stress. In this study, we evaluated the physiological and molecular responses of female and male P. vera seedlings exposed to salinity stress (250mM NaCl) at five time points (0, 1, 3, 7, and 14 days). Under salinity, both sexes exhibited significant Na⁺ accumulation in leaves; however, males accumulated higher Na⁺ levels while displaying a comparatively more tolerant phenotype, characterized by a higher root-to-shoot length ratio and reduced leaf abscission compared with females. Distinct temporal patterns were observed in oxidative and metabolic responses. Male seedlings maintained a more sustained activation of antioxidant and phenolic defenses, accompanied by chlorophyll recovery (20% higher than that of females) at later stages of stress exposure. In contrast, females exhibited an earlier but more transient response and showed higher lipid peroxidation (MDA) in roots (1.8-fold) and leaves (1.2-fold) compared with males. These contrasting physiological responses were associated with early differential expression of key salt-responsive genes, including SOS1 (ion efflux), CDPK (Ca²⁺ signaling), and PAL (phenylpropanoid pathway), as well as sex-dependent patterns of ABA (stress signaling) accumulation. These patterns suggest a coordinated, sex-dependent temporal regulation of stress signaling, gene expression, ion homeostasis, osmotic adjustment, antioxidant defense, and secondary metabolism. Collectively, our findings indicate that sexual dimorphism in pistachio salinity responses arises from distinct temporal coordination of physiological, biochemical, and molecular processes under salt stress.
Abstract Introduction The goal of this study, conducted at the Medical Education Department of Azerbaijan Medical University, was to improve the quality and effectiveness of teaching in medical and health sciences through faculty development, curriculum innovation, competency-based education, and educational research. This was aligned with current changes and challenges in the world of educational technology and methodologies. The long-term goal is to prepare future healthcare professionals who are competent, compassionate, and socially responsible. Methods In this study, we applied competency-based education principles, developed new curricula aligned with WFME standards, trained faculty through WHO-supported programs, and introduced innovative assessment methods, including OSCE and OSPE. We also promoted educational research and interdisciplinary collaboration to improve the quality of teaching and learning. Results Assessing educational goals involved using structured frameworks, accreditation standards, and key performance indicators (KPIs). Frameworks guide competency evaluation, while standards like WFME and LCME ensure curriculum quality and institutional alignment. KPIs measure academic outcomes (e.g., exam scores, graduation rates), operational effectiveness (e.g., satisfaction, curriculum alignment), and strategic impact (e.g., community engagement). Evaluation models such as Kirkpatrick’s help track progress and support continuous improvement. The reports indicated a significant improvement and enhancement of our educational goals. Conclusion We conclude that the university should focus on advancing competency-based learning, integrating innovative technologies, and promoting interdisciplinary collaboration. Emphasis should be placed on equity, community health, and preparing students as leaders and change agents. Faculty development and learner well-being must also be prioritized. These goals align education with evolving healthcare needs and societal expectations. Funding Source n/a Topic Categories Immunology Education and Communication (EDU)
