Collegium Medicum in Bydgoszcz

Thromboembolic cardiovascular diseases (CVD), including acute coronary syndromes, ischemic stroke, and venous thromboembolism, remain a leading cause of morbidity and mortality worldwide. Despite significant improvements in prevention and diagnosis, thromboembolic CVD remains a major global health challenge, reflecting the incomplete control of multifactorial vascular risk. Growing evidence indicates that air, noise, and light pollution are important yet underrecognized contributors to cardiovascular morbidity. Exposure to particulate matter (PM2.5, PM10), gaseous pollutants (NO2, SO2, CO, O3), chronic noise, and artificial light at night promotes endothelial dysfunction, oxidative stress, inflammation, and platelet activation-key mechanisms fostering a prothrombotic setting. Although regulatory progress has been achieved, air pollution remains the most significant environmental determinant of cardiovascular health globally, and the combined effects of coexisting pollutants are not fully understood. The convergence of urbanization, industrialization, and increasing light exposure further amplifies environmental impacts on vascular health. This scientific statement aims to synthesize current epidemiological and mechanistic evidence, highlight the complex interactions among air, noise, and light pollution, identify critical research gaps, and provide a comprehensive conceptual framework for understanding how environmental stress contributes to thromboembolic cardiovascular complications. Strengthening multidisciplinary research, integrating exposome-based data, and implementing effective prevention policies are essential steps toward mitigating the cardiovascular burden of environmental pollution.

Wstp: Neuroborelioza jest jedn z najczstszych pozamzgowych manifestacji zakaenia Borrelia burgdorferi i moe prowadzi do uszkodzenia nerwu twarzowego.Poraenie nerwu VII skutkuje asymetri twarzy, ograniczeniem funkcji mini mimicznych, trudnociami w artykulacji, poykaniu i mimice emocjonalnej.Rehabilitacja w przebiegu neuroboreliozy obejmuje zarwno kinezyterapi, jak i metody fizykalne, w tym elektrostymulacj mini twarzy, ktrej celem jest pobudzenie osabionych wkien miniowych,

Wstp: Neuroborelioza jest jedn z najczstszych pozamzgowych manifestacji zakaenia Borrelia burgdorferi i moe prowadzi do uszkodzenia nerwu twarzowego.Poraenie nerwu VII skutkuje asymetri twarzy, ograniczeniem funkcji mini mimicznych, trudnociami w artykulacji, poykaniu i mimice emocjonalnej.Rehabilitacja w przebiegu neuroboreliozy obejmuje zarwno kinezyterapi, jak i metody fizykalne, w tym elektrostymulacj mini twarzy, ktrej celem jest pobudzenie osabionych wkien miniowych,

Wstp: Neuroborelioza jest jedn z najczstszych pozamzgowych manifestacji zakaenia Borrelia burgdorferi i moe prowadzi do uszkodzenia nerwu twarzowego.Poraenie nerwu VII skutkuje asymetri twarzy, ograniczeniem funkcji mini mimicznych, trudnociami w artykulacji, poykaniu i mimice emocjonalnej.Rehabilitacja w przebiegu neuroboreliozy obejmuje zarwno kinezyterapi, jak i metody fizykalne, w tym elektrostymulacj mini twarzy, ktrej celem jest pobudzenie osabionych wkien miniowych,

The present Reply addresses the commentary by Pagnoni et al. on our recent study exploring explainable artificial intelligence (AI) for mortality risk prediction in pulmonary arterial hypertension (PAH). We acknowledge the importance of several key issues raised by the authors, including endpoint selection, calibration, decision thresholds, and external validation, all of which are central to translating AI-based prognostic models into clinical practice. Our original endpoint, defined as death by the next follow-up visit, was driven by the structure of nationwide registry data and reflects real-world clinical workflows, although we recognize the advantages of predefined time horizons and time-to-event approaches for future analyses. We discuss the trade-off between sensitivity and precision, emphasizing our deliberate prioritization of minimizing false-negative classifications in high-risk patients, while acknowledging the need for structured clinical pathways to manage false-positive results. We further address calibration and threshold selection, underscoring the necessity of additional clinical studies to support intervention-oriented recommendations. The role of phenotypic determinants and modifiable risk factors in enhancing personalization is highlighted as a key direction for future model development. We reaffirm the value of SHAP-based explainability for improving model transparency, while recognizing the need for continued refinement and clinical validation. Finally, we emphasize the strengths and challenges inherent to registry-based analyses, the importance of external validation, and the need for methodologically sound comparisons with established risk calculators. Overall, this exchange underscores the critical role of interdisciplinary collaboration in advancing clinically actionable and interpretable AI solutions for PAH.

Background: Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, is characterized by chronic relapsing intestinal inflammation driven by dysregulated immune responses and impaired epithelial barrier function. Increasing evidence highlights short-chain fatty acids (SCFAs)—particularly acetate, propionate, and butyrate—produced by gut microbiota as key mediators linking microbial composition to immune regulation and maintenance of intestinal homeostasis. Methodology: This review was conducted through an extensive analysis of clinical, experimental, and translational studies indexed in PubMed, Google Scholar, and the Cochrane Library, focusing on gut microbiota composition, SCFA metabolism, epithelial barrier integrity, immune mechanisms, and SCFA-targeted therapeutic strategies in IBD. Results: Patients with IBD consistently show reduced abundance of SCFA-producing bacteria, especially butyrate-generating taxa such as Faecalibacterium and Roseburia, accompanied by decreased fecal SCFA levels and impaired epithelial SCFA utilization. SCFAs exert potent anti-inflammatory effects via histone deacetylase inhibition and activation of SCFA-responsive G protein-coupled receptors, promoting regulatory immune phenotypes and suppressing pro-inflammatory signaling. Concurrently, they enhance intestinal barrier function by stimulating mucus production, reinforcing tight junctions, and supporting epithelial metabolic activity. Dietary fiber enrichment, prebiotics, probiotics, and microbiota-directed therapies demonstrate potential to restore SCFA availability and improve inflammatory and clinical outcomes, although responses remain heterogeneous. Conclusions: SCFAs represent a crucial interface between gut microbiota, immune regulation, and epithelial barrier integrity, positioning SCFA-related mechanisms as promising therapeutic targets in IBD. Despite encouraging evidence, further well-designed, mechanistic, and personalized studies are needed to clarify causality, optimize SCFA-based interventions, and translate findings into effective clinical strategies.

Ischemic stroke accounts for approximately 80-85% of all stroke cases and triggers a complex cascade of metabolic, immunological, and neurodegenerative processes. Among the key mediators involved, TNF-α occupies a central position due to its distinctly dual and phase-dependent actions. Importantly, the biological effects of TNF-α are not static but evolve dynamically over time following ischemic insult. During the acute phase of ischemia, a rapid increase in TNF-α levels, primarily originating from activated microglia, leads to the predominant activation of the TNFR1 receptor. This results in enhanced apoptosis and necroptosis, disruption of the blood-brain barrier, increased leukocyte recruitment, and the progression of secondary neuronal injury. In later phases, the role of TNF-α shifts, with signaling through TNFR2 becoming more prominent, thereby supporting reparative mechanisms, including neurogenesis, angiogenesis, and synaptic remodeling. The dual nature of TNF-α means that both its excessive activation and complete inhibition may produce detrimental effects. Notably, the therapeutic relevance of TNF-α critically depends on the timing of intervention relative to stroke onset. A comprehensive analysis of current evidence underscores the central, temporally and contextually dependent role of TNF-α in the pathophysiology of ischemic stroke. It also indicates that future therapeutic strategies should aim to selectively suppress the harmful TNFR1-mediated signaling while preserving or enhancing TNFR2-dependent neuroprotective pathways. Such time-sensitive and receptor-selective modulation holds promise for limiting acute ischemic injury and promoting endogenous repair processes, representing a compelling direction for the development of next-generation neuroprotective therapies.