The history of screening for cervical cancer is rich with implementing cutting-edge ideas and technologies. From the very first “Pap smear” to the semi-automated and computerized systems of today, the way we screen for cervical cancer has changed dramatically in the past 75 years. With the advent of new techniques and more advanced machine learning algorithms, we sought to understand the current and future applications of artificial intelligence in clinical pathology around cervical cancer screening, diagnosis, and treatment.

A structured narrative review was conducted to examine the historical evolution and contemporary advances in cervical cancer screening, diagnosis, excisional management, and artificial intelligence applications. Peer-reviewed articles, consensus guidelines, and global policy documents published between January 1990 and March 2025 were identified through targeted searches of PubMed and review of reference lists from relevant publications. Search terms included combinations of “cervical cancer screening,” “Papanicolaou test,” “liquid-based cytology,” “HPV testing,” “colposcopy,” “loop electrosurgical excision procedure,” “digital pathology,” “deep learning,” and “artificial intelligence.” Emphasis was placed on multi-center validation studies, systematic reviews, regulatory and implementation guidance, and global health frameworks. Publications lacking methodological transparency or direct relevance to clinical or translational practice were excluded.

Through a review of the literature, we describe how innovations in conventional and liquid-based cytology, human papillomavirus testing, and organized screening programs established the current prevention framework. Building on this foundation, recent studies demonstrate promising performance of deep learning algorithms applied to conventionally prepared cervical cytology slides, with systems capable of binary normal versus abnormal classification as well as more granular diagnostic categorization. Artificial intelligence-assisted colposcopy and computer-vision approaches have also shown improved diagnostic concordance, workflow efficiency, and potential to expand screening capacity in resource-limited environments.

There has been much work done in the past several years surrounding the implementation of deep learning algorithms in regard to cervical cancer screening. The work in this field shows promise in enhancing diagnostic accuracy, streamlining diagnostic workflow, and decreasing turnaround times from specimen collection to rendering a diagnosis. However, there are still many technical, legal, and ethical questions that must be answered prior to widespread adoption of these algorithms for patient care.

Metabolic dysfunction-associated fatty liver disease (MAFLD) has become one of the leading causes of chronic liver diseases in China, imposing a substantial and growing burden on the healthcare system. Considering the large number of individuals affected by MAFLD and the gap in disease management capacity at the primary care level, standardized guidance tailored to primary healthcare settings is urgently needed. In response, the Chronic Disease Management Branch of the China Medical Biotechnology Association convened a multidisciplinary working group incorporating hepatologists, general practitioners, and other specialists to initiate the first China national Guidelines for Diagnosis and Management of Metabolic Dysfunction-associated Fatty Liver Disease in Primary Care (2025). These guidelines provide recommendations and suggestions covering screening, risk assessment, diagnosis, treatment, referral pathways, and follow-up tailored for primary care institutions, thereby improving the long-term outcomes for the population with MAFLD and comprehensively strengthening the role of primary healthcare in chronic liver disease management.

Giant invasive spinal schwannoma (GISS) is a rare benign tumor that extends over two or more vertebral levels with myofascial invasion. No previous case of GISS with vertebral body collapse has been reported. A 44-year-old man presented with a one-year history of progressive limb weakness and difficulty with defecation. He was initially misdiagnosed with a metastatic spinal tumor. Imaging revealed a large extradural mass with C4 vertebral body collapse. Histological examination of tumor tissue from both operations confirmed the diagnosis of schwannoma. The postoperative course was uneventful, and the patient’s limb weakness gradually improved. One year after surgery, the patient was able to walk and write independently. Muscle strength recovered to 4/5 in the upper extremities and 5/5 in the lower extremities, with a modified Japanese Orthopaedic Association score of 15/15. The patient’s neurological function improved significantly, and one-year follow-up showed no recurrence and stable spinal fixation. Currently, the patient’s bowel function has improved; however, the patient still requires defecation in bed. When magnetic resonance imaging reveals giant spinal tumors with imaging features suggestive of malignancy, GISS should be considered. Preoperative biopsy is essential for accurate diagnosis.

Khat (Catha edulis) is a plant native to East Africa and the Arabian Peninsula, chewed for its stimulant effects by millions worldwide. Its sympathomimetic properties, primarily due to cathinone and other pyrrolizidine alkaloids, resemble those of amphetamine. Emerging reports have linked khat use to the development of autoimmune hepatitis, supported by elevated autoimmune markers, characteristic liver biopsy findings, and clinical resolution following khat cessation or a prompt response to corticosteroid therapy without recurrence. In this review, we aimed to update knowledge on both acute and chronic forms of khat-associated AIH. We discuss cathinone metabolism, pharmacokinetics, and proposed mechanisms of khat hepatotoxicity. We also provide an updated synthesis of published cases of khat-associated autoimmune hepatitis, including our calculated Roussel-Uclaf Causality Assessment Method analysis and the simplified Hennes AIH score where data were available. Case presentations, diagnostic criteria, histopathological findings, and treatment approaches are summarized to help guide management.

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.

Artemisia argyi H. Lév. & Vaniot essential oil (AAEO) holds significant pharmacological potential, but its application is constrained by hepatotoxicity. This study aimed to investigate the feasibility of reducing AAEO’s toxicity through storage and to evaluate changes in chemical composition, toxicity, and bioactivity.

Gas chromatography-mass spectrometry was used to analyze compositional changes during storage. Zebrafish acute toxicity tests and the liver-specific transgenic zebrafish model Tg(fabp10:EGFP) were used to assess toxicity. Antimicrobial, analgesic, and antioxidant assays evaluated variations in bioactivity.

Over the 150-day storage period, gas chromatography-mass spectrometry analysis identified 39 components. Zebrafish acute toxicity tests showed that the LD50 of AAEO stored for 0, 30, 60, 90, 120, and 150 days were 0.10 µL·mL−1, 0.10 µL·mL−1, 0.10 µL·mL−1, 0.11 µL·mL−1, 0.13 µL·mL−1, and 0.14 µL·mL−1, respectively, demonstrating a 40% reduction in acute toxicity after 150 days of storage. Using the liver-specific green fluorescent transgenic Tg(fabp10:EGFP) zebrafish model, the inhibition rates of AAEO on hepatic fluorescence intensity were measured at 68.5%, 43.5%, 42.6%, 37.8%, 34.6%, and 31.9% at different time points, confirming reduced hepatotoxicity after storage. Additionally, the antioxidant and analgesic activities of AAEO were significantly enhanced (p < 0.05) after storage, while the antibacterial activity decreased (p < 0.05).

After storage, AAEO significantly reduces hepatotoxicity, with a 40% decrease in acute toxicity after 150 days. Meanwhile, the antioxidant and analgesic activities of AAEO increase, while its antibacterial activity decreases after storage.

In the past decade, immune checkpoint inhibitors (ICIs) have dramatically changed cancer treatment, significantly improving outcomes for patients with various malignancies. Nonetheless, their widespread application has resulted in a rise in immune-related adverse events due to excessive immune activation, including immune-mediated hepatotoxicity (IMH). IMH can cause serious complications and even death, underscoring the need for early prediction and intervention. This review outlines the current understanding of risk factors and predictive biomarkers for IMH in cancer patients undergoing ICI therapy, with risk factors divided into patient-associated, tumor-associated, and agent-associated categories. Higher IMH risk is related to female sex, younger age, extreme BMI, Asian ethnicity, and chronic liver disease. Cancer type, prior ICI treatment, dual ICI combination therapy, and the concurrent use of chemotherapy, targeted agents, or other hepatotoxic drugs (e.g., acetaminophen, statins) also increase the risk of IMH. Potential predictive biomarkers encompass circulating blood cells, serum proteins, autoantibodies, cytokines, gene profiles, and the gut microbiome. Despite promising findings, the predictive value of these biomarkers remains inconsistent, and no definitive biomarker has been established for routine clinical use. Large-scale prospective studies are essential to verify the predictive value of these biomarkers and facilitate their integration into clinical practice, thereby providing deeper insights into the early identification and individualized management of IMH during ICI therapy.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and chronic kidney disease (CKD) have shown a significant increase in comorbidity on a global scale due to the prevalence of metabolic syndrome. In 2023, a number of academic societies formally proposed the concept of MASLD, superseding the previous terminology of “non-alcoholic fatty liver disease” and “metabolic dysfunction-associated fatty liver disease”. The diagnostic criteria have been revised to place greater emphasis on the association between hepatic steatosis and cardiometabolic risk factors. MASLD constitutes an independent risk factor for CKD, with this risk potentially increasing in line with the severity of fatty degeneration and the progression of hepatic fibrosis. CKD may represent a potential risk factor for the progression of fibrosis in patients with MASLD. The interaction between the two conditions may accelerate the occurrence of cardiovascular events and increase the risk of all-cause mortality. MASLD and CKD may share core pathophysiological mechanisms, including genetic variants, insulin resistance, lipid metabolism disorders, chronic inflammation, oxidative stress, and gut microbiota dysbiosis. However, the bidirectional causal relationship between the two conditions and the molecular dialogue between organs remains unclear. Furthermore, there are significant gaps in clinical prediction tools and targeted treatment strategies for comorbidities. This paper reviews common pathophysiological mechanisms in MASLD and CKD, the epidemiological and clinical evidence linking MASLD to the risk of CKD, biomarkers and clinical prediction models for coexisting conditions, and potential therapeutic strategies. Our aim is to provide a theoretical basis for early identification, mechanism exploration, and clinical treatment of comorbidities.

Acute-on-chronic liver failure (ACLF) is a life-threatening syndrome characterized by systemic inflammation and immune dysregulation, in which macrophages play a key role in organ injury. This study aimed to investigate the role and mechanism of pyruvate dehydrogenase kinase 4 (PDK4) in ACLF to identify therapeutic targets that modulate macrophage function and mitigate ACLF progression.

Single-cell RNA sequencing data from healthy and ACLF liver tissues were analyzed from the Sequence Read Archive database. Transcriptomic data of peripheral blood mononuclear cells from ACLF patients (GSE168048) were also examined. In vitro experiments assessed PDK4 expression and macrophage polarization, and conditioned-medium studies evaluated effects on LO2 hepatocytes. In vivo validation was performed in ACLF mouse models treated with a PDK4 inhibitor.

Single-cell analysis revealed a predominance of M1-polarized hepatic macrophages in ACLF with marked upregulation of PDK4. Peripheral blood mononuclear cell transcriptomics showed that higher PDK4 expression correlated with 28-day mortality. In vitro, PDK4 expression increased in M1 macrophages; PDK4 inhibition attenuated M1 polarization and reduced cytotoxic effects on LO2 cells. In vivo, pharmacologic inhibition of PDK4 suppressed M1 polarization in macrophages, alleviated liver inflammation, and reduced tissue injury. Mechanistically, PDK4 promoted M1 polarization via activation of signal transducer and activator of transcription 1 signaling.

PDK4 is a key pro-inflammatory regulator in ACLF by promoting M1 macrophage polarization. Targeting PDK4 may be a promising strategy to attenuate inflammation and improve clinical outcomes in ACLF.

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.