Colorectal polyp detection from endoscopic images is critical for the early diagnosis of colorectal cancer. However, traditional deep learning methods often suffer from limited generalization when deployed across datasets containing different polyp morphologies. This work aimed to investigate whether vision-language foundation models can facilitate zero-shot generalization across multiple polyp datasets without target-domain fine-tuning.

We introduced a zero-shot colorectal polyp detection framework based on Contrastive Language-Image Pretraining (CLIP) to improve cross-dataset detection performance. Key innovations include: (1) a background patch contrastive loss using pseudo-normal tissue patches to teach the model to distinguish normal mucosa from polyps; (2) attribute-enhanced text prompts that incorporate domain-specific descriptors of polyp appearance, improving the model’s semantic generalization to novel polyp morphologies; and (3) an enhanced CLIP visual adapter with per-layer adaptive feature fusion and generalized mean pooling to capture multi-scale features for better polyp localization. During training, we use one annotated colorectal polyp dataset (e.g., CVC-ColonDB) to learn patch-level image-text correspondence. The model is then evaluated in a zero-shot manner on different polyp datasets (CVC-ClinicDB, Kvasir-SEG, and CVC-300), where we evaluate pixel-level anomaly detection performance.

The framework demonstrated robust zero-shot generalization on unseen test cohorts. Without any dataset-specific fine-tuning, the model achieved a mean pixel-level AUROC of 0.94 and a mean average precision of 0.81 across the 12 leave-one-dataset-out zero-shot transfer settings. In the CVC-ColonDB-source benchmark, the model achieved a mean Dice coefficient of 0.84 across CVC-ClinicDB, Kvasir-SEG, and CVC-300. This high level of performance was consistent across datasets with distinct visual characteristics, underscoring the ability of the model to detect diverse polyp morphologies that it had not been explicitly trained to recognize.

Our findings demonstrate that an anomaly-aware vision-language model significantly improves cross-dataset polyp detection generalization without requiring normal images for training. This multimodal strategy may facilitate the robust deployment of artificial intelligence-based colorectal screening systems by enabling reliable detection of diverse polyp morphologies across different clinical settings. Extension to non-polyp colorectal pathologies (e.g., ulcerative colitis and colorectal tumors) remains an important direction for future work, pending the availability of pixel-level annotated datasets for these lesion categories.

Reporting quality in clinical research is critical for evidence-based medicine and reproducibility of clinical studies. Previous work has mostly focused on the reporting quality of clinical trials and observational longitudinal studies. However, few studies have examined the reporting quality of trend analyses. Moreover, the reporting of recommended statistical metrics in trend analyses remains largely unclear. Therefore, we assessed the reporting quality of trend analyses based on reporting of recommended statistical metrics. We systematically searched the PubMed for the trend-analysis articles published in 10 leading medicine and oncology journals over an 11-year period (2008–2018). Studies published after 2019 were excluded due to a sudden, significant increase in publication numbers during and immediately after the COVID-19 pandemic. Only original articles, research letters, and meta-analyses/systematic reviews were included. We scored the reporting quality of these articles based on whether they reported p-values, effect sizes, beta/coefficient/slope/annual-percentage-change (APC). 297 articles met the inclusion criteria. Among these, 193 (66.0%) reported p-values and 216 (72.7%) reported effect sizes. Only 13 (5.8%) analyses reported neither p-values/effect sizes nor beta/coefficient/slope/APC. In multivariable regression models, authors affiliated with epidemiology departments were less likely to report effect sizes, whereas those from statistics departments were more likely to do so. Interestingly, U.S.-based senior authors (versus non-U.S.) more likely reported p-values. No factors were independently associated with reporting APC. Overall, the reporting quality of trend analyses in leading medicine and oncology journals appears moderate and warrants improvement. We thus call for increased awareness and further research on reporting quality in trend analyses in oncology research and beyond.

The optimal management strategy for adults with immune-tolerant (IT) chronic hepatitis B infection remains undefined. This study aimed to investigate the efficacy and predictive factors of a pegylated interferon (Peg-IFN)-based treatment strategy in IT patients with chronic HBV infection.

In this pilot, open-label, prospective study, 286 patients aged 18 to 60 years with IT characteristics were enrolled and allocated to one of three groups. The combination group received Peg-IFN for 48–96 weeks, with tenofovir disoproxil fumarate (TDF) initiated at week 12 and continued through week 96 (n = 103). The monotherapy group received TDF monotherapy alone (n = 125), and the control group was monitored without therapeutic intervention (n = 58).

No patients in the control group met any predefined efficacy endpoints. Intention-to-treat analysis showed that patients in the combination group achieved significantly higher virological response rates (71.8% vs. 53.6%, p = 0.005), hepatitis B e antigen seroconversion rates (15.5% vs. 1.6%, p < 0.001), and hepatitis B surface antigen (HBsAg) loss rates (10.7% vs. 0%, p < 0.001) compared with those in the monotherapy group at week 96. In the combination group, the cumulative rate of HBsAg loss was 5.4% at week 48 and increased to 11.8% by week 96. Independent predictors of achieving either hepatitis B e antigen seroconversion or HBsAg loss were baseline age under 30 years (odds ratio = 0.217, 95% confidence interval: 0.048–0.976, p = 0.046) and a decline in HBsAg level greater than 1 log10 IU/mL by week 24 (odds ratio = 13.976, 95% confidence interval: 2.506–77.932, p = 0.003).

A Peg-IFN-based treatment strategy significantly increases response rates compared with TDF monotherapy or observation in patients with IT characteristics.

Liver transplant rejection significantly affects patient prognosis. Myeloid-derived suppressor cells (MDSCs), known for their potent immunoregulatory functions, represent a promising target for managing liver transplant rejection. This study aimed to systematically characterize the diversity of MDSC subsets and their context-dependent functions, particularly within the context of transplant tolerance.

We analyzed clinical and murine liver transplants using single-cell RNA sequencing, bulk RNA sequencing, flow cytometry, multiplex immunohistochemistry, and co-culture assays to phenotype MDSC subsets.

Single-cell RNA sequencing analysis of human and murine samples revealed MDSC involvement in transplant rejection. In mice, MDSC scores followed a normal distribution during the first week post-transplant and correlated with clinical flow cytometry data at one month. A distinct LDLR+ monocytic MDSC (M-MDSC) subset was identified and confirmed through spatial mapping by multiplex immunohistochemistry. Flow cytometry demonstrated dynamic changes in LDLR+ M-MDSCs across tissues (liver, spleen, peripheral blood, bone marrow, and lymph nodes), with a peak during acute rejection. Co-culture experiments showed that LDLR−/− M-MDSCs exhibited reduced Arg-1/iNOS expression and an impaired capacity to induce inhibitory receptors (TIGIT, PD1, CTLA-4) or suppress effector molecules (GZMB, IFN-γ, IL-2) in CD8+ T cells.

These findings highlight the critical role of MDSCs in liver transplant rejection. LDLR+ M-MDSCs exhibited enhanced immunosuppressive properties, underscoring their potential clinical relevance in mitigating rejection and promoting immune tolerance.

Acute liver failure (ALF) is a severe hepatic injury associated with high short-term mortality. Our previous study found that 1,5-anhydroglucitol (1,5AG) levels correlate with clinical outcomes in patients with liver failure. This study aimed to explore the potential effects and mechanisms of 1,5AG in ALF.

An experimental model of ALF was established using LPS and D-GalN. 1,5AG was administered to mice by gavage before modeling. Empagliflozin was then administered to reduce 1,5AG levels in mice. Peroxisome proliferator-activated receptor alpha (PPARα) agonists were also used to explore the role of 1,5AG in mice with liver failure.

1,5AG pretreatment significantly increased ALT and AST levels, aggravated histological damage and hepatocyte apoptosis, and increased mortality in ALF mice. Transcriptomic analysis and western blot validation revealed that 1,5AG significantly inhibited the PPARα signaling pathway and its downstream target, fibroblast growth factor 21. Empagliflozin treatment reduced 1,5AG levels, alleviated liver injury and hepatocyte apoptosis, and promoted the PPARα signaling pathway in ALF. PPARα agonists effectively reversed the effects of 1,5AG on ALF, thereby alleviating liver damage, pathological injury, and hepatocyte apoptosis.

1,5AG exacerbated liver injury in ALF mice by inhibiting the hepatic PPARα pathway, thereby promoting hepatocyte apoptosis.

Cirrhotic cardiomyopathy (CCM) is a significant complication of cirrhosis, but its progression and underlying mechanisms remain incompletely understood. This study aimed to investigate dynamic changes in cardiac function, pathology, inflammation, and mitochondrial damage in a mouse model of CCM, and to compare echocardiographic characteristics in patients with cirrhosis.

Bile duct ligation was performed in male C57BL/6J mice to induce cirrhosis. Longitudinal analyses were conducted over eight weeks. Cardiac function was assessed using serum biomarkers, echocardiography, and electrocardiography. Pathology was examined with hematoxylin and eosin, Masson’s trichrome, Sirius Red, and wheat germ agglutinin staining. Western blotting and immunohistochemistry were used to detect markers of inflammation, fibrosis, apoptosis, and mitochondrial function. Cardiac and liver function markers were also evaluated in patients with cirrhosis.

Mice subjected to bile duct ligation developed progressive cardiac dysfunction, including reduced cardiac output and diastolic dysfunction (end-diastolic interventricular septal thickness, left ventricular internal diameters, stroke volume, and left ventricular end-diastolic volume decreased, whereas ejection fraction and fractional shortening increased), as well as cardiac atrophy. Myocardial apoptosis, inflammation (elevated tumor necrosis factor, interleukin-6, and p65), and fibrosis worsened over time. Mitochondrial injury was characterized by reduced carnitine palmitoyltransferase 1A and peroxisome proliferator-activated receptor alpha, with increased hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase A. In patients with cirrhosis, impaired cardiac function and elevated brain natriuretic peptide levels correlated with total bilirubin.

The progression of CCM is closely associated with cirrhosis severity and appears to be driven by myocardial atrophy, apoptosis, inflammation, fibrosis, and mitochondrial dysfunction.

Unlike the traditional staging treatment of tumors, the core of “Green Tumor Treatment” is to divide the treatment of tumors into three stages: Hegemony (directly targeting the cancer focus), Kingship (supporting the body’s vital energy and eliminating pathogenic factors), and Imperialism (improving the internal environment), based on the urgency of the tumor and the patient’s physical condition. This approach guides the clinical treatment of tumors. Its treatment system incorporates all minimally invasive and low-damage treatment methods, combining internal and external treatments, traditional Chinese medicine and Western medicine, as well as local and systemic treatments. It aims to maximize treatment outcomes while ensuring the patient’s quality of life, which is highly consistent with the treatment goals for primary liver cancer. This review aims to explore the integrated Traditional Chinese and Western medicine treatment model for primary liver cancer under the guidance of the Green Tumor Treatment concept.

This narrative review provides a detailed and comprehensive examination of hemoadsorption therapy and its role in treating severe poisoning. First, the global problem of suicidal and nonsuicidal self-injury is described, with regional differences in the types of poisons used noted. Lower- and middle-income countries are disproportionately affected by pesticides compared to high-income countries. Organophosphates often constitute the majority of pesticide poisoning in many of these countries. Next, we review the history of hemoadsorption therapy from its early origins to its current evolution. The key physical and chemical principles underlying extracorporeal therapy and its effectiveness are described. A review of the literature examining the evidence for the efficacy of hemoadsorption therapy in poisoning is presented. Current evidence-based guidelines are summarized, including toxin types, clinical indications, and the extracorporeal therapies recommended. Emerging evidence regarding the use of hemoadsorption therapy for severe organophosphate and calcium channel blocker poisoning is also considered. A care pathway for considering hemoadsorption in poisonings where formal guidelines are lacking is proposed. Both the hemoadsorption strategies used and the potential adverse effects of this therapy are discussed. For this narrative review, the PubMed/Medline was searched from inception to April 30, 2025, using the terms (“hemoperfusion” OR “hemadsorption”) AND (“poisoning”). Clinical trials, randomized controlled trials, and meta-analyses were included, along with additional relevant studies identified through a manual review of references. The role of modern resin bead hemoadsorption therapy for severe poisoning is expanding to include removal of commonly encountered poisons that are protein-bound and have a large volume of distribution. Using a multicycle approach, hemoadsorption therapy has shown improved outcomes for both calcium channel blockers and organophosphate poisoning.

Cardiorenal syndrome is associated with high morbidity and mortality and is characterized by bidirectional interactions between cardiac and renal dysfunction. The advent of sodium-glucose cotransporter 2 inhibitors (SGLT2i) and the nonsteroidal mineralocorticoid receptor antagonist finerenone has substantially changed the therapeutic landscape. Combination therapy with SGLT2i and finerenone may provide additional benefits through complementary mechanisms, representing a potential paradigm shift in the management of cardiorenal syndrome. In this review, we examine the pathophysiological pathways that characterize cardiorenal syndrome, clinical data from major randomized controlled trials, and the rationale for the concomitant use of these two drug classes. SGLT2 inhibitors significantly reduce hospitalization for heart failure, slow renal function decline, and provide benefits in both heart failure with reduced ejection fraction and heart failure with preserved ejection fraction, irrespective of diabetes status. Finerenone has been shown to reduce the risk of cardiovascular events and chronic kidney disease progression in patients with type 2 diabetes and chronic kidney disease, with a more favorable safety profile than steroidal mineralocorticoid receptor antagonists. Emerging evidence suggests that combination therapy may reduce hospitalizations for heart failure and slow renal disease progression beyond the effects of either monotherapy. However, implementation of these therapeutic options requires careful patient selection, ongoing monitoring of renal function and electrolytes, and close collaboration between cardiologists and nephrologists.