Targeted drug delivery remains a major challenge in cancer therapy, often limiting both efficacy and safety. Although microRNA sponges and short-hairpin RNAs show potential for gene-based cancer treatment, their clinical use is restricted by delivery inefficiency, off-target effects, cytotoxicity, and instability. Viral vectors offer high efficiency but are associated with issues such as immune responses, insertional mutagenesis, and limited cargo capacity. Non-viral carriers are safer and more affordable but suffer from poor transfection efficiency, instability, and inadequate endosomal escape. These limitations hinder the clinical application of RNA therapeutics. The Vir-inspired Biotechnical Vector (VIBV) is a novel hybrid platform that combines viral and non-viral elements with nanotechnology to enable personalized, tumor-specific gene therapy. Engineered with a spindle-shaped nanocore and a polyethylene glycolylated liposomal shell, VIBV ensures immune evasion, prolonged circulation, and controlled therapeutic release triggered by tumor microenvironmental cues such as acidity, hypoxia, and elevated glutathione levels. It delivers oncogenic microRNA sponges, short-hairpin RNAs, tumor-specific antigens, and cyclin-targeting RNAs to enhance gene silencing, immune activation, and tumor suppression. This review examines the limitations of current delivery systems and presents VIBV as a promising next-generation strategy with improved biocompatibility, targeting precision, and potential for cost-effective, personalized cancer therapy, while also addressing its remaining challenges and prospects.

The advent of nanoparticle technology has transformed oncology therapeutics through its capacity for accurate drug delivery and regulated pharmaceutical release, boosting treatment effectiveness while minimizing adverse reactions. Various nanostructures, including polymeric carriers, liposomal formulations, and metal-based nanoparticles, can be engineered with tumor-specific targeting molecules to facilitate cellular uptake in malignant cells. Despite these advancements, issues such as production scalability, potential chronic toxicity, and regulatory approval processes still need to be addressed. Viral nanoparticles and virus-like particles (VLPs) represent innovative tools in nanotechnology and biomedicine, offering exceptional potential for targeted therapies, immune modulation, and diagnostic applications. Their natural biocompatibility, precise structural organization, and capacity for surface modification make them highly suitable for developing strategies to treat malignant tumors. Alongside VLP development, other approaches have also been investigated, such as magnetic hyperthermia, where magnetic nanoparticles are used to generate localized heat under an external magnetic field, selectively destroying cancer cells while sparing healthy tissue. This paper presents a brief review of nanocarriers in drug delivery systems and discusses the integration of nanoparticles, viral nanoparticles, and VLPs. Additionally, we explore the challenges and propose cutting-edge solutions, offering a forward-looking perspective on how the combination of these advanced technologies could transform oncology.

Autoimmune hepatitis (AIH) is an inflammatory liver disease influenced by genetic, environmental, and immunologic factors. Individuals diagnosed with AIH may exhibit concurrent autoimmune manifestations affecting multiple organ systems. The prevalence of AIH associated with other autoimmune diseases has been reported to range from 20% to 40%. This review indicates that the associations between AIH and autoimmune thyroiditis, type 1 diabetes mellitus, ulcerative colitis, Crohn disease, and celiac disease appear to be significant. However, the associations between AIH and primary sclerosing cholangitis, primary biliary cholangitis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren syndrome, and vitiligo are not well-supported. The aim of this review is to evaluate the strength of the reported associations between AIH and other autoimmune diseases, and to update and present the available evidence on their prevalence, proposed underlying pathogenic mechanisms, diagnostic considerations, and treatment approaches.

Portal vein thrombosis (PVT) frequently occurs in patients with porto-sinusoidal vascular disease (PSVD), but its clinical characteristics and outcomes remain poorly understood. This study aimed to investigate the clinical features and outcomes of PVT in PSVD.

A total of 169 patients with PSVD confirmed by hepatic histology were included. PVT was diagnosed using contrast-enhanced magnetic resonance imaging or computed tomography. Demographic, clinical, and laboratory data, portal hypertension-related complications, comorbidities, and mortality were collected and compared between patients with and without PVT. The primary outcomes were baseline clinical characteristics and liver-transplantation-free mortality; the secondary outcome was the dynamic changes of PVT during follow-up.

At baseline, 45 (26.6%) PSVD patients had PVT. Compared to those without PVT, patients with PVT had significantly higher rates of esophageal variceal bleeding (62.2% vs. 29.0%), ascites (73.3% vs. 35.5%), antithrombin III deficiency (78.1% vs. 38.4%) (all p < 0.001), and a history of hematological disorders (11.1% vs. 0.8%, p = 0.005). After a median follow-up of 40.1 (23.4–62.3) months, liver-transplantation-free mortality rates were 7.9% (3/38) and 1.8% (2/112) in patients with and without PVT, respectively (log-rank p = 0.110). Among 41 patients followed for a median of 17.1 (7.4–39.3) months, PVT resolved in 9.1% (1/11) of those with baseline PVT and developed in 13.3% (4/30) of those without PVT at baseline. The one- and two-year cumulative incidence rates of PVT were 3.3% and 6.7%, respectively.

PSVD patients with PVT experience more portal hypertension-related complications, complex coagulation profiles, hematological disorders, and a higher risk of death compared to those without PVT.

Mechanical valve replacement is a primary treatment for rheumatic heart disease, yet prosthesis-related adverse outcomes remain underreported in India. This study aimed to examine the in-hospital mortality rate among patients who underwent prosthetic heart valve replacement surgeries in the past five years.

A retrospective analysis of 221 rheumatic heart disease patients (2019–2023) who underwent aortic valve replacement (AVR), mitral valve replacement (MVR), or double valve replacement (DVR) was conducted. Comorbidities (hypertension, type-2 diabetes mellitus) and valve origin (Indian vs. foreign-made) were also evaluated. Data were analyzed using SPSS (v25.0), with p < 0.05 considered statistically significant.

Among 221 patients, 262 valves were implanted (54 AVR, 126 MVR, 41 DVR). Overall in-hospital mortality was 7.24% (16/221), with rates of 5.55% (AVR), 7.14% (MVR), and 9.75% (DVR). No sex-based differences were observed (p > 0.05). The five-year actuarial survival rate was 92.8±4.8%, with no intergroup disparities (p > 0.05). Mortality was higher in patients >50 years (13/16 deaths) and in females (10/16 deaths), though these differences were not statistically significant. Hypertension was more prevalent in females and type-2 diabetes mellitus in males, but neither condition showed a significant association with outcomes (p > 0.05). Most fatalities were associated with thromboembolism, acute kidney injury, and congestive heart failure, and valve origin did not significantly impact mortality.

Over the past five years, we observed a 7.24% mortality rate at our tertiary care facility following prosthetic heart valve implantation across all age groups. The data suggest that mortality may be more common among females and older individuals; however, these differences did not reach statistical significance.

Metabolic dysfunction-associated steatohepatitis (MASH) represents a critical step in the progression from simple fatty liver disease to more severe conditions such as cirrhosis and hepatocellular carcinoma, and it remains difficult to treat. Arctigenin (ATG), a monomer of Fructus Arctii, exhibits anti-inflammatory activity. Therefore, we aimed to examine its potential protective role against MASH and explore the underlying mechanisms.

Male C57BL/6 mice were divided into four groups: control, MASH, low-dose ATG (30 mg/kg/day), and high-dose ATG (120 mg/kg/day). MASH was induced through a choline-deficient, L-amino acid-defined high-fat diet for eight weeks, with concurrent preventive ATG administration. Liver injury, lipid metabolism, inflammation, oxidative stress, and fibrosis were assessed. Network pharmacology was employed to identify the potential protective mechanisms of ATG. Key factors were evaluated in vitro to verify the ATG targets.

ATG administration prevented the progression of MASH in a dose-dependent manner. High-dose ATG significantly reduced hepatic macrophage and neutrophil infiltration, serum enzyme levels, and lipid peroxidation, while enhancing antioxidant enzyme activity. Mechanistic network pharmacology identified modulation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome as the central pathway underlying ATG’s bioactivity. Functional analyses in lipopolysaccharide-stimulated RAW264.7 cells confirmed that ATG inhibited NLRP3 expression, pyroptosis-related protein cleavage (hereinafter referred to as GSDMD-N), and pro-inflammatory chemokine production in a concentration-dependent manner. Notably, ATG disrupted NLRP3/GSDMD-N axis activity in macrophages without causing cellular toxicity.

ATG may inhibit the inflammatory cascade primarily by targeting macrophage NLRP3 inflammasomes, thereby preventing the progression of MASH.

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.