In the post-genomic era, long non-coding RNAs (lncRNAs) have emerged as critical regulators in various cancers and hold potential as minimally invasive diagnostic biomarkers. This study aimed to perform microarray analysis of the peripheral blood mononuclear cell (PBMC) transcriptome to evaluate differential lncRNA expression in women with luminal A breast cancer.

A one-color microarray analysis was conducted using SurePrint G3 Human Unrestricted 8×60K arrays and a SureScan Microarray Scanner (Agilent Technologies, USA). The study cohort comprised 16 participants: eight patients diagnosed with luminal A breast cancer and eight healthy controls. Bioinformatic analysis was performed using the “limma” and “tidyverse” packages in the R statistical environment. Functional enrichment analysis was conducted to identify significantly differentially expressed gene clusters. The false discovery rate-adjusted p-value (padj) was applied to ensure methodological rigor. Associations between lncRNAs and disease progression were explored using the LncRNADisease 2.0 database.

Differential expression was observed for long intergenic non-coding (LINC), LOC, and antisense RNA genes. Notably, LINC RNA 974 (LINC00974) exhibited significant differential expression (log fold change > |1.5|, padj < 0.05) after multiple comparison correction. Analysis using the LncRNADisease 2.0 database revealed associations between LINC and antisense RNAs and other oncological disorders.

This study is the first to demonstrate differential lncRNA expression in PBMCs of patients with luminal A breast cancer. Despite the limited sample size, the study demonstrates statistically significant differences between groups, highlighting the potential of PBMC-derived lncRNAs as minimally invasive biomarkers. These findings enhance our understanding of the utility of PBMC-derived lncRNAs as biomarkers for breast cancer.

Regular exercise is fundamental for people with metabolic dysfunction-associated steatotic liver disease (MASLD), yet exercise maintenance is generally poor. This generative co-design process aimed to embed the voices and opinions of people with lived experience of MASLD and their care stakeholders to (i) frame barriers and enablers to exercise maintenance and (ii) highlight priorities for exercise-focused research agendas in MASLD.

A generative co-design framework was applied. Two virtual co-design sessions were undertaken: Session 1 – Framing the issue, where initial discovery was conducted with people with lived experience of MASLD; and Session 2 – Generative design and sharing ideas with lived experience partners and healthcare stakeholders. Sessions were audio-recorded and transcribed, and key determinants and considerations were discerned by two independent researchers.

Lived experience partners (n = 5, 53 ± 16 years, 40% male) ranked five equally important barriers to exercise maintenance: musculoskeletal and pain issues, lack of access to exercise equipment/facilities, cost, competing priorities, and low energy levels, which influenced core positive and negative determinants. Alongside lived experience partners, healthcare stakeholders (hepatologists [n = 3], exercise professionals [n = 3], 67% male) identified three core needs with eight considerations. Some disconnects in priorities were observed. Lived experience partners emphasized affordability, accessibility, and considerations for comorbidities, while healthcare partners advocated for research on natural history, prevention, behavior change, cost-effectiveness, and health system change.

This co-design methodology highlights unique consumer-informed research questions. Exercise interventions and their associated implementation trials will benefit from being co-designed with both people with MASLD and care stakeholders.

Gastric cancer remains a significant global health burden, with limited therapeutic options and poor clinical outcomes. Although conventional treatments such as surgery and chemotherapy are widely used, their effectiveness is often hindered by adverse effects and high recurrence rates, highlighting the urgent need for safer and more effective alternatives. Scleromitrion diffusum (Willd.) (S. diffusum), a well-established anticancer herb in traditional Chinese medicine, has demonstrated promising clinical potential against gastric cancer. This review systematically examines the bioactive components of S. diffusum and their multi-target mechanisms of action against gastric cancer. Key active compounds, including flavonoids, anthraquinones, and terpenoids, have been identified as exerting synergistic anti-gastric cancer effects. These compounds collectively target critical pathways in gastric cancer pathogenesis, including apoptosis induction, suppression of proliferation and angiogenesis, and immune modulation. The mechanistic elucidation presented in this review not only validates the traditional use of S. diffusum in cancer management but also provides a molecular basis for its potential application in precision medicine strategies for gastric cancer. Beyond summarizing existing evidence, this work highlights critical gaps in current knowledge and proposes essential directions for future research, providing important references for integrating traditional medicine with modern oncology approaches.

Type 1 diabetes (T1D) develops when the immune system targets and destroys pancreatic β-cells responsible for insulin production, ultimately resulting in reduced insulin levels. Islet transplantation has garnered significant attention as a potential treatment, but it presents numerous challenges that hinder its effectiveness for T1D patients. A primary issue is the immune system’s tendency to reject transplanted islets, leading to a gradual decline in their functionality. Furthermore, many individuals remain reliant on additional insulin therapy. These challenges are exacerbated by the global shortage of organ donors, which limits the availability of pancreata for transplantation. This review outlines several innovative strategies to regenerate insulin-producing β-cells for the treatment of T1D, with a primary focus on pancreatic progenitor and stem cells. The strategy of converting non-β cells, particularly pancreatic α-cells, into functional β-cells continues to show promise. Moreover, α-cells, which are less vulnerable to autoimmune attacks, present a distinct opportunity for β-cell regeneration in individuals with T1D. While the use of progenitor or stem cells for β-cell regeneration appears encouraging, various hurdles, such as immune rejection, suboptimal differentiation, and other challenges, still impede the implementation of this strategy. Nonetheless, this approach may ultimately pave the way for long-lasting treatment and potential cures for T1D.

Metabolic dysfunction-associated fatty liver disease (MAFLD) poses a significant challenge in modern medicine due to its high prevalence. The pathogenesis of MAFLD involves a complex dysmetabolic process consistent with the “multiple-hit” hypothesis. This process includes excessive triglyceride (TC) accumulation within hepatocytes, lipotoxicity, insulin resistance (IR), chronic low-grade inflammation, and increased oxidative stress. The role of leptin in the liver has been extensively studied, demonstrating both direct effects on hepatic cells and indirect actions mediated through the central nervous system (CNS). In MAFLD, leptin modulates several physiological processes: it improves glucose metabolism by enhancing insulin sensitivity and lowering glucose levels; regulates lipid metabolism by promoting β-oxidation and TC export while inhibiting lipogenesis; and contributes to fibrogenesis by upregulating transforming growth factor-β (TGF-β) expression and activating hepatic stellate cells (HSCs) and the immune response. This review explores the structure of leptin, its primary physiological functions, its potential role in MAFLD pathogenesis, and its promise as a novel therapeutic target.

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.

Further decompensation in cirrhosis is associated with increased mortality. However, reliable tools to predict further decompensation after transjugular intrahepatic portosystemic shunt (TIPS) are currently limited. This study aimed to investigate the incidence and risk factors of further decompensation within one year post-TIPS in patients with cirrhosis and to develop a predictive model for identifying high-risk individuals.

This retrospective cohort study enrolled 152 patients with cirrhosis undergoing TIPS for variceal bleeding and/or refractory ascites (January 2018–January 2024). Patients were stratified according to one-year decompensation outcomes. LASSO regression and multivariable logistic analysis were used to identify predictors, and a nomogram was constructed and internally validated using bootstrapping (1,000 replicates).

Among the 152 patients (median age 57.5 years [IQR 50.0–66.0]; 58.6% male; 58.6% viral/alcohol-associated etiology), 65.8% (100/152) achieved clinical stability at one year post-TIPS, while 34.2% (52/152) developed further decompensation. LASSO regression identified right hepatic lobe volume, spleen volume, and portal pressure gradient (PPG) reduction as key predictors, all independently associated with further decompensation risk in multivariable analysis (OR [95% CI]: 0.683 [0.535–0.873], 1.435 [1.240–1.661], and 0.961 [0.927–0.996], respectively). The nomogram demonstrated superior discrimination compared with PPG reduction alone and benchmark prognostic scores (AUC 0.854 [0.792–0.915] vs. 0.619–0.652; ΔAUC +0.201–+0.235, p < 0.001) with 92.3% sensitivity. High-risk patients (score > 86) had a 10.7-fold higher risk of further decompensation than low-risk patients (60.0% vs. 5.6%; p < 0.0001).

This validated model, combining hepatosplenic volumetry and PPG reduction, accurately stratifies further decompensation risk post-TIPS and may guide targeted surveillance and preventive interventions.