Atrial septal defects (ASDs) present a significant healthcare challenge, demanding accurate and timely diagnosis and precise management to ensure optimal patient outcomes. Artificial intelligence (AI) applications in healthcare are rapidly evolving, offering promise for enhanced medical decision-making and patient care. In the context of cardiology, the integration of AI promises to provide more efficient and accurate diagnosis and personalized treatment strategies for ASD patients. In interventional cardiology, sometimes the lack of precise measurement of the cardiac rims evaluated by transthoracic echocardiography combined with the floppy aspect of the rims can mislead and result in complications. AI software can be created to generate responses for difficult tasks, like which device is the most suitable for different shapes and dimensions to prevent embolization or erosion. This paper reviews the current state of AI in healthcare and its applications in cardiology, emphasizing the specific opportunities and challenges in applying AI to ASD diagnosis and management. By exploring the capabilities and limitations of AI in ASD diagnosis and management. This paper highlights the evolution of medical practice towards a more AI-augmented future, demonstrating the capacity of AI to unlock new possibilities for healthcare professionals and patients alike.

Worldwide, prostate cancer (PC) has a rising incidence and is the sixth leading cause of death globally, especially with increasing cases in developing countries. Risk factors for PC include genetic predisposition, family history, race/ethnicity, and various occupational factors like diet, obesity, smoking, and transmitted diseases. The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway can be activated by hormones, cytokines, and growth factors, and it plays a role in many vital biological processes such as cell growth, differentiation, immune regulation, and apoptosis. Dysregulation of JAK/STAT3 can lead to cancer, inflammation, diabetes, and neurodegenerative disorders. In cancers, including PC, STAT3 promotes cell survival, progression, angiogenesis, and metastasis. Inhibitors targeting JAK and STAT3 tested in vivo have shown potential to inhibit malignant cell growth. Additionally, flavonoids are bioactive plant compounds that are important in preventing inflammation, oxidative stress, and cancer. Research indicates that natural flavonoids can be developed into cancer-preventive and therapeutic agents. Experimental studies have demonstrated that some flavonoids can inhibit PC development. The main goal of this review is to present the incidence and risk factors of PC, the JAK/STAT3 pathway and its inhibitors, and how flavonoids may influence this pathology.

Background: Psychological distress is increasingly recognized as an important determinant of health-related quality of life (HRQoL) in adults with diabetes mellitus (DM). However, data quantifying this burden in Eastern European populations remains limited. Objectives: This study aimed to assess psychological distress—defined as anxiety, depressive symptoms, or perceived stress—and HRQoL among Romanian adults with DM compared with healthy controls, and to explore potential differences between diabetes subtypes. Methods: A cross-sectional study was conducted, including 400 adults (201 with DM and 199 healthy controls). Psychological distress was evaluated using the State–Trait Anxiety Inventory (STAI-Y1, STAI-Y2), Beck Depression Inventory (BDI), and Holmes–Rahe Stress Scale, while HRQoL was assessed using the EQ-5D Visual Analogue Scale. Group comparisons were performed using appropriate parametric or non-parametric tests, with additional multivariable analyses adjusting for age, sex, and body mass index. Results: Adults with diabetes exhibited significantly higher levels of anxiety, depressive symptoms, and perceived stress, and lower HRQoL, compared with controls (all p < 0.001). These differences remained statistically significant after adjustment for age, sex, and body mass index. Exploratory analyses revealed no statistically significant differences between diabetes subtypes, although subgroup comparisons were limited by sample size. Conclusions: Psychological distress is highly prevalent among Romanian adults with DM and is associated with poorer self-perceived health-related quality of life. The results support the relevance of incorporating systematic psychosocial assessment into routine diabetes care.

Microbiome dysbiosis has become recognized as an important interface connecting environmental exposures to chronic inflammatory and degenerative diseases. Although prior research has largely considered heavy metals as biomarkers of exposure and toxicity, their function as ecological modulators of host-associated microbial communities remains underexplored. The oral cavity is a distinct exposome–microbiome interface where environmental, behavioral, and intraoral metal sources converge and interact with structured biofilms and mucosal immunity. This review adopts an ecological systems perspective, interpreting chronic low-dose exposure to metals such as cadmium, lead, mercury, nickel, chromium, arsenic, and aluminum as a sustained selective force on oral microbial networks. A resilience–threshold model is proposed in which cumulative metal pressure progressively diminishes microbial community stability, alters network topology, and drives transitions toward persistent dysbiosis. These modifications are further reinforced by oxidative–inflammatory feedback loops at the host–microbiome interface, facilitating a self-sustaining ecological imbalance. Sketching on insights from microbial ecology, environmental toxicology, and host response biology, this review presents a framework that links metallomic patterns to microbial restructuring, redox imbalance, immune activation, and regulatory adaptation. The analysis emphasizes ecological perturbations from stable dysbiotic states and identifies key methodological limitations that currently restrict causal inference. By conceptualizing heavy metals as active ecological drivers rather than passive exposure indicators, this work establishes a foundation for understanding microbiome-mediated disease susceptibility within an exposome-informed systems biology framework.

Cytokines are key regulators of immune responses and tissue remodeling, playing a central role in physiological homeostasis and pathological inflammation. Dysregulation of cytokine signaling networks has been implicated in a wide range of diseases, where persistent inflammatory activation leads to progressive tissue destruction and impaired repair mechanisms. In the oral environment, cytokines critically influence the balance between tissue resorption and regeneration, particularly in processes involving dentin and alveolar bone remodeling. Pathological root resorption (PRR) represents a clinically significant model of cytokine-driven tissue destruction, characterized by the loss of dental hard tissues mediated by osteoclast-like cells within a dysregulated inflammatory microenvironment. Although mechanical, infectious, and iatrogenic factors are well-established triggers, they alone do not fully explain the variability in clinical outcomes, suggesting an important role for host-related factors. New research highlights the relationship between inflammatory signaling pathways, genetic susceptibility, and molecular biomarkers in shaping the onset and progression of PRR. In particular, the RANK/RANKL/OPG axis, cytokine networks, and gene polymorphisms have been identified as key determinants of osteoclast activation and resorptive activity. At the same time, advances in salivary and gingival crevicular fluid biomarker research provide new opportunities for early detection and real-time monitoring. Despite these advances, current knowledge remains fragmented, with heterogeneous study designs, inconsistent genetic associations, and a lack of standardized diagnostic protocols, all of which limit clinical translation. Therefore, a comprehensive and integrative synthesis of cytokine-mediated mechanisms in PRR is needed. This review aims to provide an updated and critical overview of cytokine and chemokine involvement in PRR, integrating molecular pathways, genetic determinants, and emerging biomarkers within a unified framework while highlighting translational implications for precision dentistry.

Background and Clinical Significance: Penile carcinoma is a rare malignancy in developed countries, yet it remains associated with significant morbidity due to its aggressive local behavior and potential for lymphatic dissemination. Human Papillomavirus (HPV) infection plays a central role in its pathogenesis, while lymph node involvement represents the most important prognostic factor. Case Presentation: In this retrospective case series (n = 3), we evaluated three representative patients treated at a tertiary referral center in Romania between August 2020 and December 2024. Clinical, pathological, and therapeutic data were analyzed, with emphasis on tumor stage, nodal involvement, surgical management, and follow-up outcomes. Immunohistochemical analysis, including p16 expression, was performed to assess HPV-related tumor profiles. Conclusions: Three representative cases illustrating distinct clinical scenarios were included. Patients with localized disease and negative lymph nodes achieved favorable long-term outcomes, including 3-year disease-free survival (documented follow-up through December 2023; follow-up data beyond 2023 were unavailable, capping documented disease-free follow-up at 36 months). In contrast, advanced disease with nodal metastasis was associated with poor prognosis despite aggressive multimodal treatment. Immunohistochemical profiling revealed both HPV-associated and HPV-independent tumor patterns, which appeared to correlate with clinical outcomes. A case of locally advanced disease demonstrated that radical surgical intervention combined with adjuvant therapy may achieve prolonged recurrence-free survival. Penile carcinoma requires prompt diagnosis and individualized management.