Cardiovascular diseases (CVDs) remain the leading cause of global morbidity and mortality, highlighting the urgent need for innovative diagnostic and prognostic approaches to address their complex pathophysiology. Recent advances in molecular cardiology have unveiled immune-derived microRNAs (miRNAs), or immuno-miRs, as pivotal regulators in the interplay between immune responses and cardiovascular pathology. Secreted by immune cells such as T lymphocytes, macrophages, and neutrophils, these small non-coding RNAs modulate critical signaling pathways by regulating gene expression. Immuno-miRs influence essential processes, including inflammation, endothelial dysfunction, and fibrotic remodeling—core mechanisms underlying conditions such as atherosclerosis, myocardial infarction, and heart failure. Moreover, their presence in systemic circulation within extracellular vesicles underscores their role in intercellular communication, impacting both immune and non-immune cardiovascular cells, such as cardiomyocytes and endothelial cells. This dual functionality renders immuno-miRs promising candidates as diagnostic biomarkers for early disease detection and as prognostic tools for assessing disease progression and therapeutic efficacy. Furthermore, emerging miRNA-based interventions—such as miRNA mimics and inhibitors—show considerable promise in modulating immune dysregulation in CVDs, although clinical translation remains a significant challenge. In this review, we comprehensively examine the regulatory roles of immuno-miRs in both innate and adaptive immune responses and explore recent advancements in miRNA-based therapies. By consolidating current knowledge and identifying existing gaps, we provide a comprehensive overview of the transformative potential of immuno-miRs in CVD management. Integrating these molecules into personalized medicine may pave the way for more effective, targeted, and minimally invasive strategies to combat one of the world’s most pressing health challenges.

Autoimmune hepatitis (AIH) is a chronic, progressive inflammatory liver disease characterized by autoimmune-mediated hepatic injury. Currently, glucocorticoid drugs, primarily prednisone, with or without azathioprine, are commonly recommended as first-line therapeutic agents in treatment guidelines by many scientific associations. However, the primary objective of treatment is to achieve a complete biochemical response, which is defined as the normalization of both transaminases and immunoglobulin G levels within six to twelve months. Ideally, this should also be accompanied by histological remission. Nevertheless, corticosteroid therapy is associated with significant adverse effects, potentially resulting in treatment discontinuation. In this context, it has become evident that standard treatment is inadequate for a proportion of patients, leading to the emergence of other treatment options and lines. Novel immunomodulatory agents, a class of drugs that regulate the body’s immune functions, have been confirmed to possess properties that modulate immune balance and induce immune tolerance. In recent years, these agents have played an increasingly significant role in the clinical management of AIH. This article provided an in-depth review of recent advancements in the development of novel immunomodulators, including immune cell nucleic acid inhibitors, calmodulin phosphate inhibitors, mammalian target of rapamycin inhibitors, tumor necrosis factor-α inhibitors, interleukin-2, anti-CD20 monoclonal antibodies, and B cell-activating factor inhibitors, for the treatment of AIH.

Blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) is essential for non-invasively investigating brain function. However, conventional fMRI methods are limited by low spatial and temporal resolution. This narrative review evaluates recent advancements in deep learning techniques for high-resolution BOLD-fMRI reconstruction, focusing on super-resolution, segmentation, and image registration. A comprehensive literature search was conducted across PubMed, IEEE, Scopus, and Web of Science databases for the period 2000–2023. Studies employing deep learning methods, including convolutional neural networks, transformer-based models, and generative adversarial networks for super-resolution, segmentation, and registration of BOLD-fMRI, were included. Deep learning approaches demonstrated significant improvements in spatial resolution, segmentation accuracy, and registration robustness. Convolutional neural network-based models, particularly generative adversarial networks, notably improved image reconstruction quality and detail preservation. Preliminary studies targeting specific brain regions such as the cerebellum and hippocampus showed promise; however, systematic evaluations across broader brain areas and large-scale clinical validations remain limited. While deep learning techniques have led to substantial advancements in high-resolution BOLD-fMRI reconstruction, future research should focus on standardized protocols, multi-center validation, and improving computational efficiency and model generalization to enhance clinical utility.

Soft tissue cytopathology plays a vital role in the diagnosis and management of soft tissue neoplasms, necessitating a standardized classification system to improve diagnostic accuracy and guide clinical decision-making. This article provides a concise review of the World Health Organization (WHO) Reporting System for Soft Tissue Cytopathology and presents a practical diagnostic approach to soft tissue cytopathology.

The WHO Reporting System is reviewed in conjunction with relevant literature. The reporting system employs a six-category framework: non-diagnostic, benign, atypical, soft tissue neoplasm of uncertain malignant potential, suspicious for malignancy, and malignant.

Each category is associated with a corresponding risk of malignancy and recommended clinical management guidelines. This classification aligns with the WHO Classification of Soft Tissue and Bone Tumours (5th edition) and incorporates cytomorphologic features, ancillary studies, and clinical correlation to enhance diagnostic reproducibility and communication among pathologists and clinicians. The system supports a probabilistic approach to risk stratification, enabling more consistent diagnostic and therapeutic strategies.

This framework provides a robust foundation for the interpretation of soft tissue fine-needle aspiration biopsies and optimized patient care.

Portal hypertension can cause serious complications such as upper gastrointestinal bleeding, primarily due to esophageal and gastric varices. The risk of mortality from variceal hemorrhage is significant, particularly when the hepatic venous pressure gradient exceeds 12 mmHg. Established treatments generally include endoscopic variceal band ligation and cyanoacrylate glue for gastric varices; however, challenges such as limited availability and a lack of technical expertise can hinder the use of glue, leading to preventable complications. This study investigates the efficacy of using a 50% glucose solution for injection sclerotherapy in cases of gastric varices. We present three unique patient cases. The first case involves a 21-year-old with persistent upper gastrointestinal bleeding and a portal vein thrombus, who experienced temporary relief after receiving injection sclerotherapy but tragically succumbed to significant bleeding later. The second case describes a 24-year-old who successfully managed his bleeding with the same treatment but was subsequently lost to follow-up. Lastly, a 72-year-old patient with recurrent painless hematemesis remained free of symptoms following injection sclerotherapy. Overall, while cyanoacrylate glue remains the preferred treatment, injection sclerotherapy with 50% dextrose shows promise as an effective alternative, particularly in settings where conventional treatments are not readily available, potentially reducing the risks associated with untreated variceal bleeding.

Chronic liver cirrhosis (LC) and acute-on-chronic liver failure (ACLF) are interconnected hepatic disorders associated with substantial morbidity and mortality. Despite their distinct clinical characteristics, both conditions share common pathogenic pathways that remain inadequately understood. This study aimed to identify shared gene signatures and elucidate underlying molecular mechanisms.

In this study, we employed Weighted Gene Co-Expression Network Analysis to explore transcriptomic data from the Gene Expression Omnibus for LC and ACLF.

Key co-expression modules enriched with genes involved in glycolysis and gluconeogenesis pathways were identified, implicating metabolic dysfunction as a central feature in both conditions. Furthermore, microRNA analysis revealed that hsa-miR-122 and hsa-miR-194 play pivotal roles in regulating these metabolic pathways, potentially contributing to immune dysregulation.

Our findings indicate that these shared molecular mechanisms are critical in the progression from LC to ACLF, providing novel insights into potential therapeutic targets for mitigating disease severity and improving clinical outcomes.

Glioblastoma (GBM) is the most prevalent and aggressive form of primary brain malignancy in adults. Despite continuous advancements in standard treatment modalities, the prognosis for patients remains extremely poor, with a median survival of less than two years. In recent years, chimeric antigen receptor T-cell (CAR-T) therapy has achieved revolutionary success in hematologic malignancies, marking a significant breakthrough in the field of immunotherapy. However, the successful application of CAR-T therapy to GBM still faces dual challenges: antigen heterogeneity and the immunosuppressive tumor microenvironment. This review systematically summarizes these challenges encountered in CAR-T therapy for GBM and the innovative strategies currently under development to address these challenges, providing insights for the future clinical translation of CAR-T therapy in GBM.

Primary biliary cholangitis (PBC) is a chronic progressive autoimmune disorder characterized by small non-purulent intrahepatic bile duct destruction (ductopenia) and cholestasis. While the etiology of PBC remains unclear, it is believed to involve genetic-environmental interactions. Emerging evidence highlights gut microbiota dysbiosis in PBC patients, with increased symbiotic bacteria and decreased pathogenic bacteria. Microbial alterations potentially influence disease pathogenesis through multiple mechanisms, including immune dysregulation, intestinal barrier damage, BA metabolic dysregulation, and cholestasis. These findings suggest that the gut microbiota can serve not only as a non-invasive biomarker for diagnosis and prognosis evaluation but also as a therapeutic target for the disease. In this review, we summarize changes in PBC patients’ gut microbiota, explain how these changes affect disease occurrence and development, and discuss treatment methods with potential clinical value that intervene in gut microbiota.

Insulinoma is a neuroendocrine tumor originating in the pancreas that secretes excess amounts of insulin, leading to severe hypoglycemia. The clinical presentation of hypoglycemia is classically described by Whipple’s Triad. Due to the rarity of this diagnosis, it can often be mistaken for other etiologies with similar presentations. In this paper, we present the case of a woman in her 70s with metastatic insulinoma involving the liver, who was initially diagnosed with an insulin-like growth factor 2-secreting hepatocellular carcinoma. Biochemical and immunohistochemical analyses were instrumental in distinguishing between these two etiologies.