Irinotecan is a camptothecin derivative that exerts its antitumor effects after conversion into the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), and it is widely used for the treatment of various advanced solid tumors. However, irinotecan-induced neutropenia (IIN) remains one of its most common and clinically significant hematological toxicities, increasing the risk of infection, treatment interruption, dose reduction, and poor therapeutic outcomes. This review aims to summarize the pathogenesis, risk factors, and management strategies of IIN to provide practical guidance for its clinical prevention and standardized management. Current evidence suggests that IIN is mainly associated with SN-38-mediated topoisomerase I inhibition and mitochondrial injury in hematopoietic stem cells, leading to impaired neutrophil production. The risk of IIN is influenced by irinotecan dosage, UGT1A and transporter gene polymorphisms, baseline patient characteristics, organ function, and concomitant chemotherapy. Preventive and therapeutic strategies include genotype-guided dose adjustment, careful dose optimization, oral alkalinizing agents, granulocyte colony-stimulating factor support, and modulation of intestinal microbiota. In conclusion, IIN is a multifactorial and potentially manageable adverse reaction. Integrating pharmacogenetic testing, individualized dosing, supportive care, and emerging approaches such as microbiota-based interventions may improve the safety and continuity of irinotecan-based chemotherapy.

The incidence and mortality of stroke are gradually increasing. In this context, post-stroke neuronal loss and the related long-term complications, along with costly treatment strategies, are significant concerns for healthcare professionals, and effective, convenient, and inexpensive therapeutic modalities are required. Natural and easily accessible herbal remedies may be the optimal option in post-stroke recovery. This narrative review aims to summarize the neuroprotective properties of Withania somnifera (Ashwagandha) and its therapeutic efficacy in neuronal plasticity and recovery after stroke. Original research articles, reviews, and case studies were sourced from databases such as PubMed, Web of Science, Scopus, Google Scholar, Medline, and Embase. Only full articles published in English up to July 2025 were considered. Keywords including W. somnifera, Ashwagandha, stroke, cerebral ischemia, neurodegeneration, neuronal loss, and post-stroke recovery were utilized for the literature search. It has been found that various plant parts of W. somnifera are abundant in bioactive compounds. The neuroprotective effects of W. somnifera are documented in numerous diseases. Nevertheless, W. somnifera is reported to be involved in modulating various biological pathways to mitigate neuroinflammation, apoptosis, and oxidative stress in stroke. W. somnifera promotes cell proliferation and enhances neurogenesis. Preclinical experiments on murine models show the effectiveness of W. somnifera in post-stroke recovery by enhancing neural plasticity and reducing neuronal loss in the infarct area. Furthermore, W. somnifera boosts neurotransmitter levels, improves motor functions, and enhances memory. It also decreases neutrophil infiltration in the infarct region and lessens neuronal loss. Therefore, the application of W. somnifera may prove advantageous in facilitating post-stroke recovery by enhancing neural function. However, well-designed clinical trials are needed to confirm the efficacy of W. somnifera in post-stroke recovery in humans.

Hepatic metastasis (HM) and lymph node metastasis in pancreatic ductal adenocarcinoma (PDAC) are associated with worse overall survival, largely due to the immunosuppressive microenvironment. However, the key immunosuppressive cells within this microenvironment remain inadequately defined. This study aimed to identify the cells contributing to HM and lymph node metastasis in PDAC and to investigate their regulatory mechanisms.

Single-cell RNA sequencing was used to profile the tumor microenvironment in HM, lymph node-negative, and lymph node-positive (LNP) PDAC tissues. Bioinformatic analyses revealed subtypes of immunosuppressive myeloid-derived suppressor cells (MDSCs). Immunofluorescence and flow cytometry were performed to detect the distribution and proportion of interleukin-1 receptor antagonist (IL1RA+) MDSCs. The immunosuppressive and pro-tumorigenic functions of IL1RA+ MDSCs were analyzed using enzyme-linked immunosorbent assay, quantitative reverse transcription polymerase chain reaction, Western blotting, and Transwell assays. Patient-derived xenograft mouse models were employed to validate the role of IL1RA+ MDSCs in vivo.

Polymorphonuclear-MDSCs were found to be recruited to metastatic PDAC tissues. Among these, IL1RA+ MDSCs were enriched in HM/LNP tissues and correlated with poorer prognosis. IL1RA+ MDSCs promoted M2 macrophage polarization and suppressed the activity of natural killer cells and cytotoxic T cells. Furthermore, IL1RA+ MDSCs accelerated PDAC migration and progression by upregulating epithelial–mesenchymal transition-related proteins in both in vitro and in vivo models.

IL1RA+ MDSCs represent a key immunosuppressive and pro-tumorigenic subtype in HM/LNP PDAC, providing a solid theoretical basis for prognostic prediction and the development of immunotherapeutic strategies targeting these cells in HM/LNP PDAC.

Dysphagia, a severe comorbidity of many neurological diseases, often lacks targeted therapies. Electrical stimulation of cranial nerves represents a novel therapeutic class. This critical review assessed the clinical effectiveness and safety of various approaches for electrical stimulation of the cranial nerves for treating dysphagia, categorized as implantable (directly targeting the nerve), minimally invasive (pharyngeal electrical stimulation), and non-invasive (transcutaneous). A critical literature review was conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. The PubMed database was comprehensively searched, and studies were rigorously assessed for inclusion and exclusion criteria. The Newcastle–Ottawa Scale was used to assess the risk of bias. The analysis included 15 clinical studies: four assessing vagus nerve stimulation (including implantable and transcutaneous approaches) and eleven assessing pharyngeal electrical stimulation. Most evaluated studies, particularly for pharyngeal electrical stimulation and transcutaneous vagus nerve stimulation, demonstrated significant beneficial effects on validated dysphagia outcome measures. Importantly, no long-term severe adverse effects were reported across the evaluated stimulation approaches. Cumulative evidence indicates that vagus nerve stimulation and pharyngeal electrical stimulation approaches can effectively alleviate dysphagia symptoms. The different stimulation approaches appear to be complementary, with distinct profiles rendering them suitable for different therapeutic contexts (e.g., short-term hospital-based vs. long-term at-home treatment). Consequently, they represent distinct and valuable options for individualized dysphagia therapy.

Artificial intelligence (AI) is increasingly reshaping diagnostic pathology, with breast pathology representing one of the most advanced and clinically impactful areas of adoption. Despite rapid progress, many practicing pathologists remain unfamiliar with core AI concepts and their practical implications. This review provides a concise and accessible overview of AI in breast pathology, focusing on foundational principles, current clinical applications, and future directions.

Pertinent literature was reviewed. Personal experiences were also summarized and incorporated.

Key AI concepts, including algorithms, models, architectures, machine learning, deep learning, neural networks, and multimodal and foundational models, are introduced to establish a common framework. Important distinctions among generative, black-box, and explainable AI are highlighted, emphasizing the need for transparency and interpretability in clinical settings. The evolution of AI in breast pathology is reviewed, from early rule-based computer-assisted diagnostic systems to modern deep learning approaches leveraging large-scale whole-slide imaging datasets. Current applications span multiple domains, including detection of lymph node metastases, Nottingham grading, classification of benign and malignant lesions, and automated quantification of critical biomarkers. AI-based approaches to prognosis, risk stratification, prediction of treatment response, and analysis of the tumor microenvironment are also discussed. Finally, the review addresses challenges associated with real-world implementation, including data quality, bias, regulatory considerations, cost, infrastructure, and workflow integration.

As AI continues to evolve toward large-scale, multimodal, and explainable models, it is expected to function as an augmentative tool rather than a replacement for pathologists, supporting diagnostic accuracy, standardization, and personalized management in breast cancer care.

Medulloblastoma (MB) is a malignant neoplasm that is relatively common in children but rare in young adults, accounting for less than 1% of all intracranial tumors. This study reports a rare case of MB metastasis to the right temporoparietal region in a 42-year-old woman, presenting with focal neurological symptoms such as weakness in the left arm and leg, speech disturbances, and impaired coordination. The patient had a history of cerebellar MB and underwent surgical resection, radiation therapy, and chemotherapy. Despite treatment, metastasis occurred, highlighting the diagnostic and therapeutic challenges in adult MB cases. The article also reviews the literature on MB in young adults, emphasizing the importance of dynamic neuroclinical monitoring and timely instrumental diagnosis for early detection and management of MB metastases.

Early risk stratification of severe acute liver injury (SLI) that may progress to acute liver failure (ALF), is vital for timely intervention, but no universal prognostic assessment tool covers both conditions. This study aimed to develop a simplified prognostic model for early risk assessment in SLI/ALF patients.

A retrospective cohort study consecutively enrolled SLI patients (including those progressing to ALF) from July 1, 2020 to May 31, 2025. Baseline clinical and laboratory data on admission were collected, with 90-day transplant-free survival as the primary outcome. Independent prognostic factors were screened via Cox regression to build a simplified scoring model, whose performance was compared with the Model for End-Stage Liver Disease (MELD), King’s College Criteria (KCC), and the Acute Liver Failure Study Group Prognostic Index (ALFSG-PI).

Of 302 patients, 190 (62.9%) achieved 90-day transplant-free survival. Multivariate Cox regression identified international normalized ratio (hazard ratio [HR]: 1.118, 95% confidence interval [CI]: 1.050–1.191), platelet count (HR: 0.995, 95% CI: 0.993–0.998), and hepatic encephalopathy grade ≥ 2 (HR: 5.187, 95% CI: 3.403–7.907) as independent predictors, forming the HIP (derived from the above-mentioned three predictors) model. It showed good discrimination (area under the receiver operating characteristic curve [AUC]: 0.82), outperforming MELD (AUC: 0.76, P = 0.019) and KCC (AUC: 0.72, P = 0.002), and performing comparably to ALFSG-PI (AUC: 0.80, P = 0.429). The model also performed robustly in ALF subgroups defined by the American College of Gastroenterology and the 2024 Chinese Medical Association guidelines (AUCs: 0.80 and 0.76, respectively) and achieved an AUC of 0.85 in the validation set.

The HIP model is a simple and effective tool for prognostic risk stratification in SLI/ALF patients, suitable for emergency and primary care to facilitate timely intervention.

Amatoxin-containing mushroom poisoning causes fatal acute liver failure with >50% mortality despite maximal medical therapy. Interrupting the enterohepatic recirculation of amatoxins is a mechanistically rational but unproven therapeutic strategy. This study aimed to evaluate the efficacy and safety of biliary drainage (BD) in patients with pre-acute liver failure caused by amatoxin-containing mushroom poisoning.

In this prospective cohort study (ChiCTR2300073442), consecutive adults with amatoxin-induced pre-acute liver failure received standardized care (silibinin, N-acetylcysteine, dehydration). Patients undergoing percutaneous or endoscopic BD were compared to non-BD controls. The primary outcome was survival to hospital discharge.

Nine patients were enrolled (mean age: 63.3 ± 15.6 years; 44.4% female). All five patients who underwent BD (performed at a median of three days after ingestion) survived (100%), whereas only one of the four non-BD patients survived (25%; P = 0.048). BD initiated a rapid biochemical recovery: within 48 h, mean alanine and aspartate transaminase levels decreased by 67.6% and 91.6%, respectively, from their peak levels (P < 0.001), and the international normalized ratio decreased from 1.99 to 1.27 (P = 0.008). Non-survivors in the non-BD group progressed to multiorgan failure. Procedure-related complications (transient pancreatitis/amylasemia) occurred in three of the five BD patients but resolved with conservative management.

Timely BD was associated with 100% survival after amatoxin-induced pre-acute liver failure, contrasting sharply with 75% mortality in non-BD controls. The dramatic biochemical improvement after BD supports enterohepatic recirculation interruption as a mechanistic intervention. BD represents a potentially definitive, life-saving intervention for this lethal poisoning as a preliminary finding; larger, multicenter studies are required to confirm the observed association between BD and survival.

Micro- and nanoplastics (MNPs) are pervasive environmental contaminants with growing recognition as potential contributors to human disease. Widespread human exposure occurs primarily through ingestion of contaminated food and water, and MNPs have been detected in multiple human tissues, including the gastrointestinal tract. Experimental evidence provides a plausible biological basis for disease associations, including impairment of intestinal barrier integrity, activation of mucosal immune pathways, and alteration of gut microbial communities caused by MNP exposure. Although human data remain limited, early studies demonstrate MNP detection in stool and suggest potential correlations with inflammatory biomarkers such as fecal calprotectin. These findings, together with mechanistic data from in vitro and animal models, raise concern that MNP exposure represents a paradigm shift in the pathogenesis or modulation of inflammatory bowel disease (IBD); however, methodological variability, small sample sizes, and contamination challenges currently limit definitive conclusions. The aim of this review is to evaluate the current understanding of MNP exposure and its impact on intestinal health, particularly in relation to IBD. We synthesize mechanistic and early clinical evidence linking MNPs to IBD and highlight critical research gaps. Future standardized exposure assessment, mechanistic validation in human systems, and longitudinal studies are essential to clarify causal relationships. Given the modifiable nature of environmental plastic exposure, advancing this field may offer new opportunities for IBD prevention and intervention.