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.

Patients with chronic hepatitis B virus (HBV) infection in the immune-tolerant phase may still experience hepatic inflammation and disease progression, and could benefit from early antiviral treatment. This study aimed to investigate changes in the cumulative hepatitis B surface antigen (HBsAg)/HBV DNA ratio in immune-tolerant patients during the transition to the immune-active phase, and to evaluate its potential in predicting the risk of disease progression.

This longitudinal study included 127 untreated immune-tolerant patients, who were followed for up to 10 years. An independent cohort of 109 subjects was retrospectively enrolled for external validation. The relationship between the cumulative HBsAg/HBV DNA ratio and the duration of immune tolerance or transition to the immune-active phase was examined. The predictive value of the ratio was assessed and validated.

The relationship between the cumulative HBsAg/HBV DNA ratio and disease progression risk showed a non-linear pattern: below a ratio of 1.791, the risk of disease progression decreased rapidly as the ratio increased; above 1.791, the risk plateaued. The area under the curve for predicting disease progression was 0.67, 0.64, and 0.85 for cumulative HBsAg, HBV DNA, and the HBsAg/HBV DNA ratio, respectively. Multivariable Cox regression analysis revealed the cumulative HBsAg/HBV DNA ratio as an independent predictor of disease progression, with higher ratios associated with a lower risk. Prediction models incorporating this ratio were developed and externally validated, demonstrating strong performance and clinical utility.

The cumulative HBsAg/HBV DNA ratio is an independent factor influencing the duration of immune tolerance and shows superior predictive performance. It may serve as a valuable marker for assessing the risk of disease progression in patients with chronic HBV infection.

Lung metastasis is common in hepatocellular carcinoma (HCC) and is typically associated with a poor prognosis. In this report, we present a case of advanced HCC in a 46-year-old Chinese male with lung metastases. The patient received two cycles of sequential hepatic arterial infusion chemotherapy and transarterial embolization in combination with lenvatinib (a tyrosine kinase inhibitor) and tislelizumab (a programmed cell death protein 1 immune checkpoint inhibitor). After three months of treatment, the intrahepatic tumors showed a partial response, while the bilateral lung metastases exhibited a complete response. Concurrently, levels of alpha-fetoprotein and protein induced by vitamin K absence or antagonist-II decreased to normal levels. Systemic treatment with lenvatinib and tislelizumab was continued for 10 months. This case underscores the potential of combination therapies for advanced HCC with lung metastases and provides a novel perspective on a therapeutic approach involving sequential hepatic arterial infusion chemotherapy and transarterial embolization with immune checkpoint and tyrosine kinase inhibitors.

Coronary heart disease is an ischemic condition characterized by vascular stenosis or obstruction caused by coronary atherosclerosis, resulting in myocardial ischemia, hypoxia, or necrosis. It is one of the leading causes of death in both urban and rural populations in China. Safflower yellow pigments, the main active components of the traditional Chinese herbal medicine safflower, are primarily composed of quinochalcone compounds, including hydroxysafflor yellow A and anhydrosafflor yellow B—of which hydroxysafflor yellow A is the principal component. Studies have demonstrated that these pigments can improve myocardial ischemia, reduce ischemia-reperfusion injury, alleviate atherosclerotic damage, and address risk factors associated with coronary heart disease. This review aimed to systematically and comprehensively summarize the mechanisms of action of safflower yellow pigments and their active components in the context of coronary heart disease and its related risk factors.

Multimodal applications combining electroencephalogram (EEG) and functional near-infrared spectroscopy (fNIRS) are widely used in cognitive neuroscience and have progressively been applied to clinical applications, such as the joint diagnosis of amyotrophic lateral sclerosis, Alzheimer’s disease, and pediatric epilepsy. This study conducted a bibliometric analysis of EEG-fNIRS synchronization techniques over the past 20 years. The aim was to clarify their diagnostic and therapeutic value in clinical applications, particularly in the neurological system, and to guide future research and development trends.

This study utilized the Web of Science Core Collection database to analyze documents published between January 1, 2005, and May 13, 2024. CiteSpace and VOSviewer were employed for visual analyses of co-author relationships, keywords, citation patterns, and journal distributions. By overlaying dual-map diagrams and analyzing annual publication trends, the study identified research hotspots, development trends, and the evolution of EEG-fNIRS technology.

A total of 645 articles and reviews from 55 countries were analyzed. The USA contributed the most publications. The team led by Michela Balconi at the Catholic University of the Sacred Heart published the highest number of papers. Frontiers in Human Neuroscience had the greatest number of publications, while NeuroImage had the highest citation impact. Recent research has primarily focused on the application of neuroimaging and neurophysiological techniques (e.g., EEG, fNIRS, functional magnetic resonance imaging), brain activation, and brain-computer interface.

This study highlights the applications and developmental trends of dual-modality EEG-fNIRS technology. Specifically, this approach can assist in diagnosing neurological disorders, assessing activation and connectivity within functional brain regions, and evaluating therapeutic neuromodulation in clinical neurology. Overall, multimodal fusion is poised to advance neuroscience research significantly.

Laboratory-acquired infections (LAIs) have been documented since the first report of typhoid fever in 1885 and continue to endanger laboratory professionals despite decades of biosafety advances. This review provides a comprehensive overview of LAIs, emphasizing their history, modes of transmission, and strategies for prevention.

A systematic review of historical records, case series, and biosafety guidance (1885–2025) identified documented LAIs, their transmission routes, and preventive measures. Data were extracted on pathogen spectrum, geographic distribution, incident outcomes, and the effectiveness of biosafety interventions.

Historical analysis identified 50 laboratory-acquired typhoid infections with six deaths from 1885 to 1915, largely due to mouth pipetting and aerosol exposure. A sharp decline in fatal bacterial infections was observed following the introduction of Class II biosafety cabinets in the 1960s. From 2000 to 2021, 309 LAIs were reported across 94 studies, most commonly Salmonella enterica (56.6%), vaccinia virus (4.2%), and Brucella species (3.9%), with Brucella responsible for over half of hospital-laboratory cases (60 per 100,000 personnel-years). In Canada during 2023, 63 exposure events occurred, including three confirmed infections despite adherence to biosafety level protocols. Environmental persistence studies underscored surface-borne risks. The most effective preventative measures included abolishing mouth pipetting, mandatory use of gloves and eye/face protection, routine Class II biosafety cabinet use for aerosol-generating procedures, surface disinfection with 0.5% sodium hypochlorite, and annual competency-based biosafety training with incident reporting.

LAIs remain geographically widespread and pathogen-diverse. Quantitative historical trends and contemporary surveillance highlight critical transmission routes, including ingestion, inoculation, mucosal splash, and inhalation, while reinforcing evidence-based prevention strategies. Sustained investment in biosafety infrastructure, real-time exposure reporting, and pathogen-specific training is essential to further reduce LAI incidence and severity in the face of emerging antimicrobial resistance and novel agents.

Temporal lobe epilepsy (TLE) is the most common focal epilepsy, with many patients developing drug-resistant epilepsy. Surgical interventions, including stereoelectroencephalography (SEEG)-guided temporal lobe resection (TLR) and SEEG-guided responsive neurostimulation (RNS), are key treatment options. This systematic review compares the efficacy and safety of these interventions in drug-resistant TLE.

A systematic review was conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) 2020 guidelines. A comprehensive search of multiple databases was performed (January 23–February 14, 2025). Eligible studies included adult patients with drug-resistant TLE undergoing SEEG-guided TLR or RNS (where SEEG was used pre-implant for localization). Primary outcomes assessed included seizure freedom, seizure reduction, adverse events, and quality of life (QoL) improvements. Quality assessments were performed using appropriate tools for randomized and observational studies.

Fifteen studies met the inclusion criteria, with sample sizes ranging from 10 to 440 participants. SEEG-guided TLR achieved an average seizure freedom rate of 58.5% (range: 32–85%) and a mean seizure reduction of 75% (range: 60–90%). SEEG-guided RNS resulted in an average seizure freedom rate of 12.85% and seizure reduction of 63.2%, with variability across studies. QoL improvements were reported in 80–82% of patients. Adverse events were infrequent but varied between interventions.

This review highlights the effectiveness of SEEG-guided TLR and RNS in managing drug-resistant TLE. While both interventions reduce seizure burden and improve QoL, seizure freedom rates are higher with resection. However, gaps remain in understanding long-term cognitive outcomes and demographic influences on treatment response. Future research should address these factors to refine patient selection and optimize epilepsy care.

Breast cancer remains one of the most common cancers affecting women globally, with late detection frequently contributing to its high mortality rate. Multiple factors drive these delays, including a lack of awareness, financial constraints in low-income countries, and limited access to non-invasive and accurate biomarkers. This review aims to introduce biomarkers, particularly hematological and biochemical serum markers, as essential, non-invasive, and accurate tools for improving the diagnosis, prognosis, and therapeutic management of breast cancer. Hematological markers are measurable blood parameters that reflect physiological and pathological processes such as inflammation, infection, cardiovascular stress, autoimmune conditions, and cancer. Routinely measured hematological markers, such as the neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and red blood cell indices, are typically obtained from standard tests like the complete blood count. Regular monitoring through complete blood count is essential during cancer treatment to evaluate changes in blood cell counts and detect potential adverse effects. Because of their affordability, minimal infrastructure requirements, and broad accessibility, hematological parameters have been increasingly studied for their association with high-risk factors in breast cancer, particularly in resource-limited settings. Their utility underscores their critical role in improving patient outcomes across diverse healthcare environments. This review summarizes the clinical value of various hematological and serum-based biochemical markers in the screening and diagnosis of breast cancer. Prediction methods that incorporate hematological and serum-based biochemical parameters can support screening, diagnosis, and staging. Overall, individual or combined blood indicators hold significant potential to enhance diagnostic accuracy and effectiveness.

This review presents the latest evidence on the link between genetic single nucleotide polymorphisms and dental caries, highlighting key genes and pathways involved, introducing foundational concepts, and discussing essential methodological considerations for future research. Several genes have been identified as significantly associated with caries experience, including those related to tooth mineral tissues, taste perception, salivary composition and flow, and immune response. Epistatic interactions appear to be crucial in explaining genetic influence. Inconsistencies in the literature are attributed to variations in caries classification, age groups, ethnic backgrounds, limited statistical power, and linkage disequilibrium. Population stratification often confounds results, and few studies adequately control for genetic ancestry. Ensuring Hardy-Weinberg equilibrium and accounting for linkage disequilibrium are essential to avoid bias. Bonferroni corrections for multiple comparisons are fundamental but rarely applied, contributing to inconsistent findings. In conclusion, genetic epidemiology studies suggest that dental caries has a genetic component, accounting for significant individual differences in disease risk.

Metabolic-associated steatohepatitis (MASH) is an advanced and progressive liver disease that potentially causes cirrhosis and hepatocellular carcinoma. Exercise is a crucial and effective intervention for ameliorating metabolic dysfunction-associated steatotic liver disease. This study aimed to provide a comprehensive understanding of the underlying mechanisms of MASH, which benefit a broad spectrum of MASH patients, including those who have difficulty engaging in physical activity.

We established a mouse model of MASH and selectively knocked down L-type amino acid transporter 1 and alanine-serine-cysteine transporter 2. Mice were fed a high-fat high-cholesterol diet and subjected to either short- or long-term exercise regimens. We assessed the phosphorylation and activity of branched-chain alpha-keto acid dehydrogenase (BCKDH) as well as branched-chain amino acid (BCAA) content in skeletal muscle following exercise.

Short-term exercise significantly reduced hepatic steatosis and inflammation without causing notable changes in body weight. It also enhanced BCKDH activity in skeletal muscle and decreased hepatic BCAA accumulation. Muscle-specific overexpression of BCKDH further promoted BCAA catabolism and significantly attenuated hepatic steatosis and inflammation in high-fat high-cholesterol-fed mice. In contrast, muscle-specific L-type amino acid transporter 1 knockdown, which suppresses BCAA uptake, markedly abolished these beneficial effects. Interestingly, BCKDH overexpression in muscle increased glutamine levels in both the blood and liver. Hepatic alanine-serine-cysteine transporter 2 knockdown, which inhibited glutamine uptake, lessened the protective effect of exercise on MASH. Further in vitro study revealed that glutamine derived from myocytes improved redox homeostasis and inhibited lipid accumulation in hepatocytes.

Short-term exercise enhances BCAA catabolism in skeletal muscle and promotes glutamine production, which circulates to the liver to improve redox balance and alleviate MASH.