Epidemiological data on bacterial infections in cirrhosis in China remain limited. Therefore, we aimed to conduct a multicenter study to investigate the characteristics and outcomes of patients with cirrhosis and bacterial infections in China.

We retrospectively enrolled 1,438 hospitalized adult patients with cirrhosis and bacterial or fungal infections from 24 hospitals across China between January 2018 and September 2024. Data on demographics, clinical features, microbiology, treatment, and outcomes were collected.

A total of 1,783 infection episodes were recorded, including 1,668 first infections and 115 second infections. Most infections were community-acquired (86.6%). Pneumonia was the most common infection type (26.7%), followed by spontaneous bacterial peritonitis (19.5%) and spontaneous bacteremia (14.1%). Among 754 pathogens isolated from 620 patients, Klebsiella pneumoniae (20.1%) was nearly as common as Escherichia coli (21.7%). Multidrug-resistant (MDR) organisms accounted for 41.0% of all isolates, with extended-spectrum β-lactamase-producing Escherichia coli being the most prevalent MDR strain (8.9% of patients). Adherence to empirical antibiotic treatment guidelines from the European Association for the Study of the Liver was significantly lower in this cohort compared to the global study (21.5% vs. 61.2%, P < 0.001), accompanied by a lower clinical resolution rate (63.5% vs. 79.8%, P < 0.001).

The clinical and microbiological characteristics of bacterial infections in patients with cirrhosis in China differ substantially from those reported in other regions. These findings highlight the need for region-specific management and prevention strategies, particularly in light of the changing microbiological landscape, high MDR prevalence, and suboptimal antibiotic practices.

Given the high burden of hepatocellular carcinoma (HCC), risk stratification in patients with cirrhosis is critical but remains inadequate. In this study, we aimed to develop and validate an HCC prediction model by integrating radiomics and deep learning features from liver and spleen computed tomography (CT) images into the established age-male-ALBI-platelet (aMAP) clinical model.

Patients were enrolled between 2018 and 2023 from a Chinese multicenter, prospective, observational cirrhosis cohort, all of whom underwent 3-phase contrast-enhanced abdominal CT scans at enrollment. The aMAP clinical score was calculated, and radiomic (PyRadiomics) and deep learning (ResNet-18) features were extracted from liver and spleen regions of interest. Feature selection was performed using the least absolute shrinkage and selection operator.

Among 2,411 patients (median follow-up: 42.7 months [IQR: 32.9–54.1]), 118 developed HCC (three-year cumulative incidence: 3.59%). Chronic hepatitis B virus infection was the main etiology, accounting for 91.5% of cases. The aMAP-CT model, which incorporates CT signatures, significantly outperformed existing models (area under the receiver-operating characteristic curve: 0.809–0.869 in three cohorts). It stratified patients into high-risk (three-year HCC incidence: 26.3%) and low-risk (1.7%) groups. Stepwise application (aMAP → aMAP-CT) further refined stratification (three-year incidences: 1.8% [93.0% of the cohort] vs. 27.2% [7.0%]).

The aMAP-CT model improves HCC risk prediction by integrating CT-based liver and spleen signatures, enabling precise identification of high-risk cirrhosis patients. This approach personalizes surveillance strategies, potentially facilitating earlier detection and improved outcomes.

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.

Mitochondrial respiratory complexes (Complexes I–V) and their assembly into respiratory supercomplexes (SCs) are fundamental to liver bioenergetics, redox homeostasis, and metabolic adaptability. Disruption of these systems contributes to major liver diseases, including non-alcoholic fatty liver disease, alcoholic liver disease, drug-induced liver injury, viral hepatitis, and hepatocellular carcinoma, by impairing adenosine triphosphate synthesis, increasing oxidative stress, and altering metabolic pathways. Recent advances have clarified the structural-functional interdependence of individual complexes within SCs, revealing their dynamic remodeling in response to physiological stress and pathological injury. These insights open opportunities for clinical translation, such as targeting SC stability with pharmacological agents, nutritional strategies, or gene therapy, and employing mitochondrial transplantation in cases of severe mitochondrial failure. Precision medicine approaches, incorporating multi-omics profiling and patient-derived models, may enable individualized interventions and early detection using SC integrity as a biomarker. By linking molecular mechanisms to therapeutic strategies, this review underscores the potential of mitochondrial-targeted interventions to improve outcomes in patients with liver disease.

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.

The diagnosis of hepatic precancerous lesions (HPC) and early hepatocellular carcinoma (HCC) has significant public health implications and holds the potential to reduce the global burden of HCC. This study aimed to identify molecular features and biomarkers associated with HPC progression and early HCC development.

RNA sequencing was used to identify differentially expressed genes in mouse HPC tissues and normal liver tissues. Cyclin E1 (CCNE1) expression in HPC tissues and HCC cells was assessed using immunohistochemistry, Western blotting, and real-time polymerase chain reaction. The effects of CCNE1 on HCC cell proliferation, migration, invasion, and apoptosis were evaluated using colony formation, wound healing, Transwell assays, and flow cytometry. The mechanism of CCNE1 was explored through Kyoto Encyclopedia of Genes and Genomes pathway analysis and gene set enrichment analysis and further validated through in vitro experiments. The interaction between CCNE1 and tumor-associated macrophages (TAMs) was investigated by co-culturing HCC cells with macrophages.

RNA sequencing and TCGA database analysis showed that CCNE1 expression was significantly elevated in mouse HPC tissues and human HCC samples and was associated with reduced survival rates. In vitro assays demonstrated that CCNE1 promoted HCC cell proliferation, migration, invasion, and survival by activating the PI3K/Akt signaling pathway. Additionally, CCNE1 induced TAM polarization toward the M2 phenotype by promoting the expression of CCL2 and CCL5 in HCC cells.

CCNE1 promotes HPC progression and HCC cell proliferation, migration, invasion, and survival by activating the PI3K/Akt signaling pathway. Furthermore, CCNE1 enhances the secretion of CCL2 and CCL5 by HCC cells, promoting TAM infiltration and M2 polarization, thereby contributing to tumor progression.

Familial hypobetalipoproteinemia (FHBL), caused by apolipoprotein B (APOB) variants, disrupts APOB-containing lipoprotein synthesis, leading to reduced serum total cholesterol, low-density lipoprotein cholesterol, and APOB. Heterozygous carriers are often asymptomatic, while homozygotes exhibit severe manifestations like malabsorption, vitamin deficiencies, and hepatic steatosis. In recent years, FHBL has attracted increasing attention due to its association with liver disease and its role as a unique monogenic model of steatotic liver disease independent of cardiometabolic risk factors. Mechanistically, lipid overload, endoplasmic reticulum stress, oxidative damage, and impaired autophagy may drive hepatocellular injury and fibrosis. Challenges include insufficient diagnosis, sparse epidemiological data, and unclear disease progression. Enhanced genetic testing, mechanistic research, and longitudinal studies are critical to improving diagnosis, risk assessment, and therapies for FHBL-associated liver disease.

Fat mass and obesity-associated protein (FTO) has been linked to various cancers, though its role in hepatocellular carcinoma (HCC) remains unclear. This study aimed to investigate FTO expression, its clinical relevance, functional role in HCC progression, and the underlying molecular mechanisms.

Quantitative reverse-transcription polymerase chain reaction and immunohistochemical analysis were used to assess FTO expression in HCC. Functional assays, including proliferation, invasion, and epithelial-mesenchymal transition studies, were conducted using HCC cell lines with FTO knockdown. N6-methyladenosine (m6A) RNA immunoprecipitation and RNA stability assays further elucidated the role of FTO in BUB1 mRNA methylation and stability. Co-immunoprecipitation studies were employed to confirm the interaction between BUB1 and TGF-βR1. In vivo studies in nude mice were conducted to evaluate tumor growth following FTO knockdown.

FTO was significantly upregulated in HCC tissues compared to normal liver tissues, with higher expression observed in advanced tumor-node-metastasis stages and metastatic HCC. Elevated FTO correlated with poor overall survival in patients. Silencing FTO decreased HCC cell proliferation, colony formation, invasion, epithelial-mesenchymal transition, and tumor growth in nude mice. Mechanistically, FTO downregulation led to increased m6A modification of BUB1 mRNA, thereby promoting its degradation via the YTH domain family 2-dependent pathway and reducing BUB1 protein levels. Additionally, BUB1 physically interacted with TGF-βR1, activating downstream TGF-β signaling.

FTO is overexpressed in HCC and is associated with poor clinical outcomes. Mechanistically, FTO promotes HCC progression by stabilizing BUB1 mRNA through an m6A-YTH domain family 2–dependent pathway, which activates TGF-β signaling. Targeting the FTO–BUB1–TGF-βR1 regulatory network may offer a promising therapeutic strategy for HCC.

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents an escalating healthcare burden across the Middle East and North Africa (MENA) region; however, system-level preparedness remains largely undefined. This study aimed to assess existing models of care, clinical infrastructure, policy frameworks, and provider perspectives across 17 MENA countries.

A cross-sectional, mixed-methods survey was distributed to clinicians from MASLD-related specialties across the region. A total of 130 experts (87.2% response rate) from academic, public, and private sectors in 17 countries participated. The questionnaire addressed national policies, diagnostic and therapeutic practices, referral pathways, multidisciplinary team (MDT) integration, and patient/public engagement. Quantitative responses were analyzed descriptively, while qualitative inputs underwent thematic analysis.

Only 35.4% of respondents confirmed the presence of national clinical guidelines for MASLD, and 73.1% reported the absence of a national strategy. Structured referral pathways were reported by 39.2% of participants, and only 31.5% believed the current model adequately addresses MASLD. While 60% supported MDT approaches, implementation remained inconsistent. Limited access to transient elastography was reported by 26.2% of providers. Public education efforts were minimal: 22.3% reported no available tools, and 87.7% indicated the absence of patient-reported outcomes data. Nearly half (47.7%) cited poor patient adherence, attributed to low awareness, financial barriers, and lack of follow-up.

Significant policy, structural, and educational gaps persist in MASLD care across the MENA region. To address this rising burden, countries must adopt integrated national strategies, expand access to non-invasive diagnostic tests, institutionalize MDT care, and invest in both public and provider education as essential pillars of system-wide preparedness.

Acute coronary syndrome (ACS) in patients with SARS-CoV-2 infection is primarily driven by inflammation-induced myocardial injury through both direct and indirect mechanisms. Effective clinical management requires a dual approach: addressing cardiovascular lesions while also mitigating virus-induced local and systemic inflammation. This comprehensive approach is essential for improving the diagnosis and treatment of SARS-CoV-2-associated ACS. Emerging evidence highlights the potential of myocardial protective agents, including angiotensin-converting enzyme 2-modulating drugs and traditional Chinese medicine, which not only stabilize plaques and improve endothelial function but also confer cardioprotective effects. Furthermore, advancements in nanotechnology offer promising strategies for targeted therapy—particularly through angiotensin-converting enzyme 2 receptor modulation—by enhancing the precision and efficacy of herbal medicine delivery. This review explores the complex interplay between SARS-CoV-2 infection and ACS pathogenesis, and evaluates the therapeutic potential of pharmacological, herbal, and nanotechnology-based interventions in managing this multifaceted condition.