Amoebiasis, or amoebic dysentery, is a gastrointestinal disorder caused by the parasite Entamoeba histolytica. The disease is endemic in parts of Africa, Asia, North and South America, leading to several deaths annually. Reported adverse effects associated with the current first-line treatment for amoebiasis, coupled with the evolution of resistance to it, call for the need to search for plant-based alternatives. This study systematically reviews medicinal plants with activity against Entamoeba histolytica.

The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines were followed to retrieve scholarly literature. The study reviewed 70 articles from 7 popular databases: Google Scholar, PubMed, ScienceDirect, Booksc.org, Emerald, Scopus, and MEDLINE, highlighting several plants with anti-amoebic properties.

The primary parts of the plant used in the treatment of Entamoeba histolytica were the leaves (61%), followed by rhizomes (13%), roots (8%), seeds (8%), stems (4%), and fruits (4%). The families Asteraceae (18%) and Zingiberaceae (18%) contain most plants that are effective against Entamoeba histolytica. These medicinal plants families are rich in phytochemicals such as terpenoids and flavonoids that have anti-entamoeba histolytica activity. Maceration is the most commonly used extraction method.

The results suggest that plants are a promising source of new agents to combat amoebiasis caused by Entamoeba histolytica. The most frequently used plant parts were leaves (61%), and the maceration method was the most common extraction technique due to its simplicity and cost-effectiveness. The majority of studies were limited to in vitro models, with only one plant (Adenophyllum aurantium) tested in vivo. Further research is needed to establish their mechanisms of action, toxicities, and clinical potential.

Guaiac fecal occult blood test (gFOBT) is often used to evaluate evidence of food protein-induced allergic proctocolitis (FPIAP) in children in primary care and gastroenterology settings; however, it has not been validated for this diagnosis, and little is known about the positivity rates in early infancy. In this study, we used samples from healthy asymptomatic infants aged two weeks to two months to evaluate the gFOBT positivity rate compared to those diagnosed with FPIAP.

This was a nested case-control study. Frozen stool samples from infants aged two days to five months enrolled in the Gastrointestinal Microbiome and Allergic Proctocolitis study were evaluated using gFOBT (n = 123). The results were interpreted by three blinded staff members, including a trained clinical research coordinator, a pediatric gastroenterologist, and an experienced medical assistant. Additionally, the samples were analyzed using a quantitative fecal immunochemical test (FIT) for hemoglobin to compare with gFOBT results.

Eight percent of samples from the 100 healthy asymptomatic infants were gFOBT positive (11% when including positive and equivocal results). Seventy-four percent of samples from infants diagnosed with FPIAP were gFOBT positive. The interrater reliability of gFOBT interpretation was 81%. Of the healthy samples that yielded a positive gFOBT result, 50% also yielded a positive FIT result. Of the 23 FPIAP samples that yielded a positive gFOBT result, 29% yielded a positive FIT result.

Healthy asymptomatic infants in early infancy were gFOBT positive up to 11% of the time. Caution should be used when interpreting gFOBT results in young infants in a diagnostic setting.

Temporal lobe epilepsy (TLE) is the most common focal epilepsy, with many patients developing drug-resistant epilepsy. Surgical interventions, including stereoelectroencephalography (SEEG)-guided temporal lobe resection (TLR) and SEEG-guided responsive neurostimulation (RNS), are key treatment options. This systematic review compares the efficacy and safety of these interventions in drug-resistant TLE.

A systematic review was conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) 2020 guidelines. A comprehensive search of multiple databases was performed (January 23–February 14, 2025). Eligible studies included adult patients with drug-resistant TLE undergoing SEEG-guided TLR or RNS (where SEEG was used pre-implant for localization). Primary outcomes assessed included seizure freedom, seizure reduction, adverse events, and quality of life (QoL) improvements. Quality assessments were performed using appropriate tools for randomized and observational studies.

Fifteen studies met the inclusion criteria, with sample sizes ranging from 10 to 440 participants. SEEG-guided TLR achieved an average seizure freedom rate of 58.5% (range: 32–85%) and a mean seizure reduction of 75% (range: 60–90%). SEEG-guided RNS resulted in an average seizure freedom rate of 12.85% and seizure reduction of 63.2%, with variability across studies. QoL improvements were reported in 80–82% of patients. Adverse events were infrequent but varied between interventions.

This review highlights the effectiveness of SEEG-guided TLR and RNS in managing drug-resistant TLE. While both interventions reduce seizure burden and improve QoL, seizure freedom rates are higher with resection. However, gaps remain in understanding long-term cognitive outcomes and demographic influences on treatment response. Future research should address these factors to refine patient selection and optimize epilepsy care.

Super-enhancers (SEs) are highly enriched clusters of transcriptional regulatory elements within the genome, occupying a central position in tumorigenesis and development. This review aims to synthesize the rapidly expanding body of knowledge on SEs as the central hub of tumor transcriptional regulation.SEs integrate specific transcription factors, dynamic epigenetic modifications (such as H3K27ac), and restructure the three-dimensional spatial architecture of the genome to aberrantly drive the expression of proto-oncogenes and cell identity-related genes. This activity sustains the malignant phenotype, stem cell properties, metabolic reprogramming, and therapy resistance of tumor cells. Their functions involve emerging physical mechanisms such as phase separation forming transcriptional condensates and long-range chromatin looping. The activity of SEs exhibits high tumor-type and tissue specificity. They are activated through unique mechanisms in different cancers, becoming key nodes of “transcriptional addiction” in tumor cells. This characteristic also makes them highly promising therapeutic targets. Inhibitors targeting core SE components (such as the BET protein BRD4 and transcriptional kinases CDK7/9), epigenetic drugs, and strategies aimed at disrupting their phase-separated condensates have shown selective efficacy in various preclinical tumor models. In conclusion, SEs serve as pivotal hubs of transcriptional addiction in cancer by integrating diverse molecular mechanisms to drive oncogenic programs, and their specific components present promising therapeutic targets; future advances in multi-omics and precision strategies will be key to translating these findings into clinical applications.

Traumatic brain injury (TBI)-associated cognitive impairment is highly prevalent, severely impacting patients’ daily life and social functioning, with its mechanisms incompletely understood. Globally, TBI affects over 69 million people annually, and post-TBI cognitive impairment may last for years, or even a lifetime, imposing heavy burdens on patients’ families. The brain-lymphatic axis (glymphatic + peripheral lymphatic systems, especially meningeal vessels) has gained attention: glymphatic dysfunction (dependent on astrocyte endfeet Aquaporin-4 polarization, key for clearing β-amyloid and other wastes) causes metabolic waste accumulation and neuroinflammation, while peripheral lymphatic stasis worsens cognitive decline. This review aims to summarize their roles, dissect mechanisms, and outline therapies. The review found that most current studies explore the glymphatic system and the peripheral lymphatic system in isolation, lacking understanding of their dynamic interplay (e.g., bidirectional inflammatory factor transmission, immune cell migration, synergistic dysfunction); longitudinal studies that track axis changes across TBI stages (acute, subacute, chronic) are scarce; diagnostic tools are insufficient (non-invasive biomarkers lack large-scale clinical validation, and imaging has limited clinical use); and existing therapeutic strategies mostly target single subsystems, with few combined interventions for the whole axis. In conclusion, this review highlights critical gaps in current knowledge and proposes integrated, axis-targeted approaches as a promising direction for future research and therapeutic development.

Digital pathology (DP) is transitioning from an adjunct technology to an enterprise diagnostic platform in the United States. Despite accelerating clinical adoption, many laboratories face persistent barriers, including high capital and operating costs, workflow disruption, interoperability challenges, and a complex regulatory and reimbursement environment. This narrative review proposes a practical lifecycle framework for implementing and sustaining DP programs, with an emphasis on defining and operationalizing institutional artificial intelligence (AI) readiness for safe and sustainable adoption.

We performed a targeted narrative review informed by searches of PubMed/MEDLINE and Google Scholar for English-language publications from January 1, 2014 through December 31, 2025. Core search concepts included DP, whole slide imaging, image management/viewing systems, laboratory information system integration, validation, reimbursement, U.S. Food and Drug Administration clearance, Clinical Laboratory Improvement Amendments oversight, College of American Pathologists accreditation, interoperability standards, cybersecurity, and AI. We supplemented database searches with reference screening and review of primary guidance and public databases from regulatory and professional organizations in the United States. We prioritized peer-reviewed literature and used web-based regulatory sources when they represented the authoritative primary reference. We also incorporated our professional experience and knowledge in DP and AI.

Key implementation domains span foundational infrastructure (scanners, storage/networking, and integrated image management platforms), workflow redesign across pre-analytic, analytic, and post-analytic phases, validation and quality management, regulatory compliance and accreditation, cost capture, interoperability strategy, cybersecurity and access control, education and change management, and long-term governance. We also describe an institution-level AI readiness model that can be assessed across data quality, integration, validation, monitoring, governance, and workforce capabilities to support safe clinical AI deployment.

Successful DP implementation requires a lifecycle approach that couples technical build-out with workflow redesign and institutional governance. Early planning for compliance, interoperability, reimbursement strategy, and AI readiness can reduce implementation risk and position laboratories for sustained clinical and computational innovation.

Full or partial trisomy of human chromosome 21 results in dysregulation of gene expression, leading to the manifestation of specific phenotypes described in individuals with Down syndrome (DS). Defects in brain development, coupled with impairment in neurogenesis, are ultimately expressed as cognitive deficiency, Alzheimer disease (AD), and dementia. Amid the triplication of all human chromosome 21 (HSA21) genes, dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A)-mediated neurogenesis and dendritic development have been attributed to the learning and memory deficits and cognitive impairment in the DS population. Upregulated DYRK1A perturbs the development and function of the brain, collectively affecting neurogenesis, synaptogenesis, synaptic transmission, and cell signaling pathways, which might disproportionately produce inhibitory neurotransmission and contribute to the cognitive phenotype. However, the lack of distinct gene-phenotype associations acts as a potential barrier to therapeutic improvement of cognitive performance and amelioration of AD-related neurodegeneration. The present review aims to summarize the neurogenetic consequences of triplicated DYRK1A in the DS population in relation to sexual dimorphism and expression of the Apolipoprotein Eε4 (APOE ε4) genotype. Notably, normalization of trisomic DYRK1A demonstrated improved synaptic plasticity, glutamatergic/GABAergic (excitatory/inhibitory) balance, and learning and memory in DS mouse models. Therapeutic approaches using inhibitors of DYRK1A, including catechins present in green tea extract and several other natural and synthetic agents, produced variable outcomes in cognitive improvement, depending on age and dose of administration. Mitigation of impairment in neurogenetic differentiation and cognitive performance might help control AD-related dementia and enhance quality of life. This review highlights the consequences of upregulated DYRK1A kinase on impairment of neurogenesis and cognitive deficits, and the therapeutic challenges associated with DYRK1A inhibitors for ameliorating dysregulated gene expression in DS models and human DS.

Nanobiotechnology has driven transformative advancements in healthcare, particularly in the development of innovative solutions for wound treatment, a persistent and costly global health concern. Among these advancements, the combination of biopolymers and metallic nanoparticles has attracted considerable interest due to their excellent biocompatibility and potent antimicrobial activity. This scoping review explores recent technological progress in wound care, with a focus on alginate-based dressings functionalized with metallic nanoparticles. Alginate, a highly versatile biopolymer, was frequently employed in diverse formats, including hydrogels, sponges, beads, films/membranes, and fibers, across the analyzed studies. Silver nanoparticles were the most extensively investigated agents, owing to their well-established efficacy and the development of strategies to mitigate associated risks. Other metallic nanoparticles were also reported, contributing to a growing body of evidence supporting their therapeutic relevance. The synergistic integration of alginate and metallic nanoparticles has shown promising potential to enhance the performance of wound dressings, representing a significant step forward in the design of next-generation materials for effective and targeted wound management.

Endometrial polyp (EMP) is one of the most common diagnoses in the evaluation of women with abnormal uterine bleeding. Understanding the malignancy risk associated with EMPs and related risk factors is essential for guiding both pathology practice and clinical management. This study aimed to explore risk factors for malignancy in EMPs.

The pathology database was searched for women diagnosed with EMP between 2021 and 2022. Patient age, polyp size, background endometrium, recurrence, and (if applicable) cancer types were recorded. Immunohistochemistry (IHC) for p53 and p16 was performed on selected cases. Risk factors for malignancy were analyzed using Chi-square and analysis of variance tests.

Among the 740 EMP cases analyzed, 94% were benign, 2% were premalignant, and 4% were malignant. The median patient age was 54 years (range: 19–92). Minimal serous carcinoma (n = 14, 2%) was the most prevalent cancer. Among the 52 cases with p53 IHC, 38 were diagnosed as benign, supported by a wild-type p53 pattern, while 14 were diagnosed as serous carcinoma, supported by a mutant p53 pattern. Malignant polyps were found to be significantly associated with advanced age and malignant background endometrium (p < 0.001). Large size and recurrence were not identified as significant risk factors.

EMPs carry a low risk of malignancy, which is not significantly influenced by the polyp’s size or its recurrence. Our findings highlight the significantly elevated risk of malignancy in elderly patients and the importance of p53 IHC in improving diagnostic accuracy.