Mild traumatic brain injury (mTBI) represents the majority of head injury presentations in emergency departments (EDs), yet only a minority of patients have acute intracranial lesions on computed tomography (CT). This leads to widespread use of unnecessary CT scans. Point-of-care (POC) biosensing, defined as analytical testing performed at or near the site of patient care, offers a promising solution to this dilemma by enabling rapid biomarker quantification to inform CT decision-making. This review aims to evaluate POC-compatible biosensing strategies for ultra-early mTBI triage, with emphasis on platforms, matrix effects, and benchmarking aligned with CT-based decision-making. Two key precedents support this approach: (1) the integration of S100B into Scandinavian Neurotrauma Committee guidelines, which has demonstrated the potential for safe reduction of CT scans, and (2) the regulatory clearance of glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1) testing to rule out the need for head CT in adults with suspected mTBI (Glasgow Coma Scale 13–15) when serum is collected within 12 hours of injury. Accordingly, this review focuses on the most implementable use case for mTBI, namely CT triage/rule-out. It synthesizes the current biomarker landscape (S100B, GFAP, UCH-L1), analyzes POC-suitable sensing modalities, and proposes a practical validation and benchmarking framework aligned with this intended use. A critical component is interference testing and real-world sample robustness, including vulnerabilities such as hemolysis-related elevation of UCH-L1. In conclusion, the most reliable path for biosensor translation in mTBI is to anchor development and validation to the ED CT-triage use case, emphasizing decision-point robustness and resilience to real-world sample variability over pure analytical sensitivity.

The optimal surgical management for spontaneous supratentorial intracerebral hemorrhage (SSICH) remains controversial because conventional approaches often fail to balance rapid decompression with effective hematoma evacuation. This study aimed to evaluate the efficacy and safety of new combined surgical strategies (“two-in-one” and “three-in-one”) versus conventional methods for SSICH.

This retrospective cohort study included 451 SSICH patients treated between January 2019 and December 2023. Based on clinical severity, patients were stratified into Group I (non-herniation, n = 374) and Group II (herniation, n = 77). Within each subgroup, patients were further categorized by treatment period: a historical control cohort (2019–2020) receiving conventional surgery, and an intervention cohort (2021–2023) receiving combined strategies (“two-in-one” for Group I; “three-in-one” for Group II). Outcomes included decompression time, hematoma evacuation rate, complications, and six-month functional recovery (Glasgow Outcome Scale/modified Rankin Scale), were compared.

In Group I, the “two-in-one” strategy achieved faster decompression (4.65 min) and a high evacuation rate (92.15%), which was comparable to neuroendoscopy alone (90.58%) and significantly higher than stereotactic aspiration alone (44.55%). This was associated with improved six-month outcomes (poor outcome rates were 39.39%, 54.35%, and 42.86% in Groups I-A, I-B, and I-C, respectively, overall P = 0.034). In Group II, the “three-in-one” strategy demonstrated shorter decompression time (4.73 vs. 37.85 min, P < 0.001) and higher evacuation rates (80.51% vs. 63.50%, P < 0.001) than decompressive craniectomy alone. Logistic regression further supported the prognostic advantage of the “two-in-one” strategy in Group I.

These combined strategies may integrate the advantages of multiple techniques to enable rapid decompression and effective hematoma clearance in SSICH. Prospective studies are warranted.

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.

Cortisol, the body’s primary glucocorticoid, is central to maintaining homeostasis through its regulation of metabolism, immunity, cardiovascular tone, and neurobehavioral functions. However, chronic dysregulation of the hypothalamic–pituitary–adrenal axis, whether from persistent psychological stress, lifestyle imbalance, or circadian disruption, contributes to diverse metabolic, psychiatric, and inflammatory disorders. This comprehensive review aims to explore cortisol physiology, mechanisms of dysregulation, and emerging strategies for restoring hormonal balance through integrative management. Conventional approaches such as pharmacotherapy and surgical interventions remain essential for severe endocrine disorders like Cushing’s syndrome and Addison’s disease; however, they inadequately address chronic, stress-related dysfunction. Nutritional modulation, sleep optimization, moderate physical activity, and mind-body therapies, including yoga, meditation, and mindfulness-based stress reduction, demonstrate measurable reductions in cortisol and inflammatory cytokines. Adaptogenic botanicals such as Withania somnifera, Ocimum tenuiflorum, Rhodiola rosea, and Panax ginseng exhibit robust evidence for normalizing cortisol and enhancing resilience through hypothalamic–pituitary–adrenal axis modulation. Complementary modalities such as acupuncture, naturopathy, and homeopathy show potential in improving autonomic and neuroendocrine balance. By synthesizing biomedical, nutritional, psychological, and traditional perspectives, this review proposes an integrated model of cortisol management that harmonizes physiology and behavior. Such multidimensional frameworks offer promising, evidence-based pathways for mitigating stress-related diseases and promoting holistic well-being.

Glioblastoma remains a highly challenging malignancy with a pronounced tendency for recurrence. The hypoxic microenvironment is a key contributor to its therapy resistance. Hyperbaric oxygen therapy (HBOT), which elevates tissue oxygen pressure and reverses hypoxia, exhibits a “dual effect” in glioblastoma management. This review aims to evaluate the therapeutic potential of HBOT in glioblastoma by examining its multifaceted effects on tumor biology and treatment response. On one hand, it enhances radiosensitivity through reactive oxygen species generation, increases chemotherapy efficacy by augmenting cytotoxicity and improving vascular perfusion, and remodels the tumor microenvironment via vessel normalization, edema reduction, and immune cell modulation. Furthermore, HBOT attenuates cancer stem cell properties by downregulating stemness markers and inhibiting self-renewal capacity. On the other hand, HBOT may also promote tumor progression: oxidative stress can induce genomic instability, while concomitant activation of HIF-, NF-κB-, and VEGF-mediated pro-survival pathways may facilitate malignant cell adaptation and proliferation. Given these opposing considerations, the clinical application of HBOT in glioblastoma management remains exploratory. In conclusion, future research should focus on optimizing HBOT protocols. In addition, exploring combination with other therapeutic approaches is equally important. These efforts are essential for the safe and effective integration of HBOT into comprehensive treatment strategies for glioblastoma.

This review aims to advocate for a paradigm shift in herbal safety by proposing a cohesive molecular framework that integrates advanced “omics” technologies with artificial intelligence (AI) to address the clinical challenges of herb-induced liver injury (HILI). Traditional herbal medicine constitutes a substantial, yet often unregulated, component of global healthcare, driving high patient exposure alongside a significant and escalating clinical burden of HILI. Current pharmacovigilance systems are critically undermined by fundamental deficits, including severe underreporting, unknown population denominators, and pervasive product quality failures. Furthermore, the complexity of multi-ingredient formulations and the frequency of herb-drug interactions complicate causality assessment, particularly for high-risk drugs. To bridge the gap between empirical practice and contemporary safety standards, this integrated “omics”-AI paradigm transforms herbal safety from a reactive, population-level assessment into an evidence-based, personalized system. By enabling precise risk mitigation, this approach establishes a scientifically rigorous foundation for the future of integrative liver health. In conclusion, the synergy of molecular profiling and computational intelligence provides the necessary tools to modernize herbal pharmacovigilance, ensuring that traditional wisdom is effectively harmonized with modern technological standards for enhanced patient safety.

The intestinal barrier, a critical interface between the body and the external environment, is essential for maintaining internal homeostasis. Comprising mechanical, chemical, immune, and biological components, its dysfunction underpins multiple gastrointestinal pathologies. Circular RNAs (circRNAs), covalently closed non-coding RNAs, have emerged as central regulators of gut barrier homeostasis. This review synthesizes advances in circRNA roles in intestinal stem cell renewal, apoptosis-proliferation balance, microbiome interactions, and immune regulation. Key findings highlight circRNA networks operating via competitive endogenous RNA mechanisms, protein interactions, and translational potential to influence barrier function. We further discuss circRNAs as diagnostic biomarkers in inflammatory bowel disease and their therapeutic potential in barrier-related pathologies. Advances in RNA nanotechnology (e.g., lipid nanoparticles) and synthetic biology position engineered circRNAs as next-generation therapies for precision intervention in gastrointestinal disorders. Importantly, this review also critically examines the current limitations of these translational approaches, including delivery challenges, safety considerations, and the preliminary nature of many preclinical findings, providing a balanced perspective on the path from bench to bedside.

Steatotic donor livers are highly susceptible to post-transplant dysfunction; however, the underlying mechanisms remain incompletely understood. This study aimed to investigate the role of galectin-3 (LGALS3)-mediated pyroptosis in steatotic liver graft injury and explore its therapeutic potential.

A mouse model of steatotic liver transplantation was established. Graft tissues were subjected to RNA sequencing to identify key regulators. In vitro, LGALS3 was modulated in steatotic hepatocytes under ischemia/reperfusion stress to assess its impact on the NLRP3 inflammasome and pyroptosis. The regulatory mechanism by which LGALS3 modulates NLRP3 ubiquitination was further examined. Finally, the therapeutic efficacy of LGALS3 inhibition was evaluated in an orthotopic liver transplantation model.

Transcriptomic analysis identified LGALS3 as a key upregulated molecule in steatotic grafts, associated with pyroptosis pathways. In vitro, LGALS3 overexpression enhanced NLRP3 inflammasome activation and pyroptotic cell death, whereas LGALS3 knockdown exerted protective effects. Mechanistically, LGALS3 modulated NLRP3 inflammasome activity by regulating its ubiquitination. In vivo, pharmacological inhibition of LGALS3 significantly improved graft function, reduced histological injury, suppressed pyroptosis, and prolonged recipient survival.

This study demonstrates that LGALS3 drives steatotic graft injury by promoting NLRP3-mediated pyroptosis through the regulation of ubiquitination. These findings identify LGALS3 as a promising therapeutic target for improving the outcomes of liver transplantation using steatotic donor organs.

Development of mixed histiocytosis (Langerhans cell histiocytosis (LCH))/Erdheim–Chester disease (ECD)) after treatment in patients with an initial skull LCH lesion has not been well recognized. An elderly woman initially developed LCH at the left temporal bone, preceded by polyuria and polydipsia five years earlier; the lesion was surgically removed. Two years thereafter, she experienced her first LCH relapse with a right parietal skull lesion, in which a BRAF V600E mutation was confirmed, and chemotherapy was initiated. After a second LCH relapse involving the left parietal bone, the patient presented with a third relapse at the L2 vertebra. This lesion was pathologically diagnosed as mixed histiocytosis (LCH/ECD), resulting in refractoriness to conventional chemotherapy, and was successfully treated with targeted therapy using BRAF and MEK inhibitors. Spinal mixed histiocytosis (LCH/ECD) may develop following relapses of skull LCH after chemotherapy, for which targeted therapy could be effective.