Breast cancer remains a leading cause of morbidity and mortality among women worldwide, with emerging evidence underscoring the microbiota’s pivotal role in its etiology, progression, and therapeutic response. This narrative review synthesizes the intricate interplay between the breast tissue, skin, and lung microbiomes in breast cancer pathogenesis, with particular emphasis on inflammatory breast cancer (IBC) and metastatic dissemination. The healthy breast microbiome, dominated by Firmicutes, Proteobacteria, Actinobacteria, and Bacteroidetes, maintains tissue homeostasis through pH regulation, metabolite production, and immune modulation. Dysbiosis disrupts this equilibrium, fostering carcinogenesis via chronic inflammation, estrogen deconjugation, and DNA damage-induced genomic instability, with subtype-specific microbial signatures influencing tumor growth and therapy resistance. In IBC, skin microbiome alterations characterized by overgrowth of pathogens like Pseudomonas aeruginosa and Staphylococcus aureus exacerbate inflammation, epithelial-mesenchymal transition (EMT), and lymphatic invasion, while promoting a pro-tumorigenic microenvironment enriched in regulatory T cells and M2 macrophages. Concurrently, lung microbiota dysbiosis impairs immune surveillance, remodels the extracellular matrix, and facilitates metastatic seeding through neutrophil extracellular traps and cytokine storms. Cross-talk among these microbiomes amplifies systemic effects, highlighting their synergistic contributions to disease aggressiveness. Advanced analytical techniques, including 16S rRNA sequencing, metagenomics, and metabolomics, offer promising microbial biomarkers for early detection and risk stratification. By elucidating these host-microbe dynamics, this review advocates for microbiome-centric interventionssuch as probiotics, fecal microbiota transplantation, and targeted antimicrobials to enhance precision diagnostics and therapies, ultimately improving outcomes in breast cancer management.

Background: Autism spectrum disorder (ASD) affects millions of children globally, significantly impacting their quality of life. Understanding factors that contribute to symptoms, is essential for improving outcomes. This review aims to explore the relationship between screen time and ASD and provide insights for targeted interventions. Methods: PubMed, Web of Science, and Google Scholar were searched for studies on the link between screen time and ASD symptoms. Results: The findings suggest a possible link between excessive screen time and increased ASD symptoms, including social withdrawal and communication challenges. Some studies propose a bidirectional relationship, where children with this disorder may prefer more screen time due to social isolation. Conclusion: Although there is evidence suggesting a link between screen time and ASD, the relationship remains unclear; further research is needed to better understand these connections and develop effective interventions for children with this disorder.

Tethered cord syndrome (TCS) is estimated to affect approximately 25 per 100 000 live births. Despite advancements in medical knowledge and technology, the persistence of this issue is attributed to challenges in early detection and limited awareness, often resulting in undiagnosed cases until adulthood. Constipation serves as a noteworthy symptom in children with TCS, yet it frequently goes unnoticed or is ascribed to other causes, leading to delayed diagnosis and negatively impacting a child’s quality of life. The aim of this manuscript is to explore the relationship between TCS and constipation in children, focusing on the prevalence, clinical manifestations, diagnostic challenges, and existing treatment methods by synthesizing information from relevant literature. Ultimately, the goal is to shed light on the multifaceted aspects of TCS and its connection to constipation, emphasizing the need for a comprehensive, multidisciplinary approach to effectively manage this condition in children. Notably, nerve dysfunction that affects bowel motions is often the cause of constipation in children with TCS. A multimodal strategy that includes pharmaceutical treatments, dietary changes, and novel techniques, like neuromodulation and biofeedback therapy, is required for effective management. Given its safety and tolerance in children, key findings emphasize the effectiveness of osmotic laxatives, especially polyethylene glycol (PEG), as a first-line treatment for chronic constipation. Physical therapies, such as pelvic floor physiotherapy and biofeedback, show promise in enhancing rectal sensation and bowel coordination. Bowel function is typically improved with neurosurgical intervention to reduce spinal cord tethering, although there are risks, including re-tethering. Minimally invasive surgical techniques are promising, but more research is needed. Social and intellectual developments are negatively impacted by psychological effects, which are common and include anxiety and depression associated with chronic gastrointestinal problems. In conclusion, addressing constipation in children with TCS necessitates a multimodal strategy and collaborative efforts across different disciplines for optimal management.

Background: Hypertrophic cardiomyopathy (HCM) is a genetic cardiovascular disorder characterized by unexplained left ventricular hypertrophy, affecting approximately 0.2% of the global population. Around 40% of HCM cases are linked to mutations in sarcomeric protein genes such as β-myosin heavy chain and myosin-binding protein C, which impair calcium signaling and myocardial contractility. Objective: This review aims to explore the therapeutic potential of cardiac myosin inhibitors (CMIs) by assessing their effects on the underlying pathophysiology of HCM, specifically targeting sarcomere function and hypercontractility. Methods: A literature search from 2013 to 2024 using PubMed and Google Scholar identified studies on CMIs in HCM. Relevant trials and reviews were selected based on strict criteria. Two reviewers screened studies, and findings on mechanisms, efficacy, safety, and outcomes were narratively synthesized for analysis. Results: Recent studies have highlighted the role of cardiac fibroblasts and transforming growth factor-β signaling in the development of myocardial fibrosis in HCM. CMIs have shown effectiveness in reducing left ventricular outflow tract gradients, improving exercise tolerance, and lowering biomarkers such as N-terminal pro-b-type natriuretic peptide, without significantly affecting left ventricular ejection fraction (LVEF). Compared to beta-blockers and calcium channel blockers, CMIs offer a targeted approach by modulating sarcomere activity. Conclusion: CMIs represent a promising and mechanism-based treatment for HCM. Their potential to reduce the need for invasive procedures and improve patient outcomes highlights the importance of their integration into clinical practice. Further large-scale trials are needed to establish long-term safety, cost-effectiveness, and broader clinical applicability.